ACUTE ODONTOGENIC OSTEOMYELITIS OF THE JAWS IN CHILDREN.DIAGNOSIS, CLINIC, EMERGENCY MEDICAL AND SURGICAL CARE, REHABILITATION OF THESE CHILDREN. PREVENTION OF THE DISEASE.

ACUTE NEODONTOHENNYY (HEMATOGENOUS, TRAUMATIC OSTEOMYELITIS) OF THE JAWS IN CHILDREN. REASONS DEVELOPMENT, CLINICAL COURSE. DIAGNOSIS, DIFFERENTIAL DIAGNOSIS, TREATMENT, COMPLICATIONS AND THEIR PREVENTION.

 

Summary

Osteomyelitis of the jaws is still a fairly common disease in maxillofacial clinics and offices, despite the introduction of antibiotics and the improvement of dental and medical care. The literature on this disease is extensive. Different terminologies and classification systems are used based on a variety of features such as clinical course, pathological–anatomical or radiological features, etiology, and pathogenesis. A mixture of these classification systems has occurred throughout the literature, leading to confusion and thereby hindering comparative

studies. An overview of the most commonly used terms and classification systems in osteomyelitis of the jaws is given at the beginning of this chapter.

The Zurich classification system, as advocated in this textbook, is primarily based on the clinical course and appearance of the disease as well as on imaging studies.

Subclassification is based on etiology and pathogenesis of the disease. Mainly three different types of osteomyelitis are distinguished: acute and secondary chronic osteomyelitis and primary chronic osteomyelitis. Acute and

secondary chronic osteomyelitis are basically the same disease separated by the arbitrary time limit of 1 month after onset of the disease. They usually represent a true bacterial infection of the jawbone. Suppuration, fistula formation, and sequestration are characteristic features of this disease entity. Depending on the intensity of the infection and the host bone response, the clinical presentation

and course may vary significantly. Acute and secondary chronic osteomyelitis of the jaws is caused mostly by a bacterial focus (odontogenic disease, pulpal

and periodontal infection, extraction wounds, foreign bodies, and infected fractures). Primary chronic osteomyelitis of the jaw is a rare, nonsuppurative, chronic inflammation of an unknown cause. Based on differences in age at presentation, clinical appearance and course, as well as radiology and histology, the disease may be subclassified into earlyand adult-onset primary chronic osteomyelitis. Cases with purely mandibular involvement are further distinguished from cases associated with extragnathic dermatoskeletalinvolvement such as in SAPHO syndrome or chronic recurrent multifocal osteomyelitis (CRMO).

2.2 Definition

The word “osteomyelitis” originates from the ancient Greek words osteon (bone) and muelinos (marrow) and means infection of medullary portion of the bone.

Common medical literature extends the definition to an inflammation process of the entire bone including the cortex and the periosteum, recognizing that the pathological process is rarely confined to the endosteum. It usually encompasses the cortical bone and periosteum as well. It can therefore be considered as an inflammatory condition of the bone, beginning in the medullar cavity and havarian systems and extending to involve the periosteum of the affected area. The infection becomes established in calcified portion of the bone when pus and edema in the medullary cavity and beneath the periosteum compromises or obstructs the local blood supply. Following ischemia, the infected bone becomes necrotic and leads to sequester formation, which is considered a classical sign of osteomyelitis (Topazian 1994, 2002). Although other etiological factors, such as traumatic

injuries, radiation, and certain chemical substances, among others, may also produce inflammation of the medullar space, the term “osteomyelitis” is mostly used in the medical literature to describe a true infection of the bone induced by pyogenic microorganisms (Marx 1991).

2.3 History

The prevalence, clinical course, and management of osteomyelitis of the jawbones have changed profoundly over the past 50 years. This is due to mainly one factor:

the introduction of antibiotic therapy, specifically penicillin. The integration of antibiotics into the therapeutic armamentarium has led to a complete renaissance

in the treatment of most infectious diseases, including osteomyelitis (Hudson 1993). Further factors, such as sophistication in medical and dental science as well as the widespread availability for adequate treatment, have additionally led to improvement in the management of this disease. Modern diagnostic imaging allows much earlier treatment of bone infections at a more localized

stage. In the preantibiotic era, the classical presentation of jawbone osteomyelitis was an acute onset, usually followed by a later transition to a secondary chronic process (Wassmund 1935; Axhausen 1934). Massive clinical symptoms with widespread bone necroses, neoosteogenesis, large sequester formation, and intra- and extraoral fistula formation were common presentations, sometimes leading to significant facial disfigurement (Fig. 2.1). After the introduction of antibiotics, acute phases were often concealed by these antimicrobial drugs without fully eliminating the infection. Subacute or chronic forms of osteomyelitis have therefore become more prominent, lacking an actual acute phase (Becker 1973;

Bьnger 1984).

 

Fig. 2.1a–c Elder case of advanced secondary chronic osteomyelitis of the left mandible. The massive affection of the left mandible demonstrates extraoral fistula

and scar formation (a). Intraoral view of the same patient with large exposure of infected bone and sequestra (b). Large sequester collected from surgery (c) (Courtesy of N. Hardt)

 

2.4 Overview of Currently Used Classification Systems and Terminology

One of the first widely accepted staging systems for osteomyelitis in long bones was first described by Waldvogel and Medoff (1970) and Waldvogel et al. (1970a,b). The authors distinguished three categories of osteomyelitis:

osteomyelitis from hematogenous spread; from a contagious focus; and due to vascular insufficiency. The classification is primarily based on etiology and pathogeneses of infection and does not readily lend itself to guiding therapeutic strategies such as surgery and antibiotic therapy. A more comprehensive classification proposed by Cieny et al. (1985) and Mader and Calhoun

(2000) is based upon the anatomy of the bone infection and the physiology of the host. It divides the disease into four stages combining four anatomical disease

types and three physiological host categories resulting in the description of 12 discrete clinical stages of osteomyelitis. Such a classification system, although it may be important in dealing with numerous sites of the skeletal system and allowing stratification of infection and the development of comprehensive treatment guidelines for each stage, is unnecessarily complex and impractical

when dealing with infections of the jawbones. Because of its unique feature bearing teeth and hence connecting to the oral cavity with the periodontal

membrane, osteomyelitis of the jaws differs in several important aspects from osteomyelitis of long bones. The specific local immunological and microbiological

aspects determine a major factor in the etiology and pathogenesis of this disease, and hence also have a direct impact on its treatment; therefore, to extrapolate

from long bone infections to disease of the jaws is only possible with limitations. This is reflected by the longstanding recognition of osteomyelitis of jawbones as a

clinical entity, which differs in many important aspects from the one found in long bones; hence, a wide variety of classifications, specifically for the jawbones, have

been established by several authors in the medical literature. Classifications proposed are based on different aspects such as clinical course, pathological–anatomical and/or radiological features, etiology, and pathogenesis. A mixture of these classification systems has been used in many instances, leading to confusion and thereby hindering comparative studies and obscuring classificationcriteria. An overview of the most commonly cited classifications of jawbone osteomyelitis are listed in Tables 2.1–2.4.

2

 

2.5 Currently Used Terms in Classification of Osteomyelitis of the Jaws

2.5.1 Acute/Subacute Osteomyelitis

Although acute forms of osteomyelitis are seen only rarely these days, most authors in common medical literature still describe this form as an entity of its own. Mercuri (1991) and Marx (1991) arbitrarily defined the time element as being 1 month after onset of symptoms. Endurance past this arbitrary set time limit is then considered as chronic osteomyelitis reflecting the inability of host defense mechanisms to eradicate the responsible pathogen. Many authors have agreed on this classification and have used the term likewise in their publications (Koorbusch et al. 1992; Hudson 1993; Schuknecht et al. 1997; Schuknecht and Valavanis 2003; Eyrich et al. 1999; Baltensperger et al. 2004). The term “subacute osteomyelitis” is not clearly defined in the literature. Many authors use the term interchangeably

with acute osteomyelitis, and some use it to describe cases of chronic osteomyelitis with more prominent (subacute) symptoms. In some instances, subacute osteomyelitis is referred to as a transitional stage within the time frame of acute osteomyelitis andcorresponds to the third and fourth week after onset of

symptoms (Schuknecht et al. 1997; Schuknecht and Valavanis 2003).

2.5.2 Chronic Osteomyelitis

The classification of chronic osteomyelitis is incoherent and confusing. Different disease processes have been described by this one term in some instances, whereas

several terms have been designated for lesions that represent the same entity in other instances (Groot et al. 1996; Eyrich et al. 1999).Many authors agree that chronic osteomyelitis involving the jawbone may be divided in two major categories: suppurative and nonsuppurative forms (Mittermayer 1976; Hudson 1993; Topazian 1994, 2002; Bernier et al. 1995).

2.5.3 Chronic Suppurative Osteomyelitis:

Secondary Chronic Osteomyelitis

Chronic suppurative osteomyelitis is an often preferred term in Anglo-American texts (Marx 1991; Bernier et al. 1995; Topazian 1994, 2002) and can mostly be used interchangeably with the term “secondary chronic osteomyelitis,” which is predominantly used in literature from continental Europe (Hjorting-Hansen 1970; Panders and Hadders 1970; Schelhorn and Zenk 1989). It is by far the most common osteomyelitis type, which is usually caused by bacterial invasion from a contagious focus. Most frequent sources are odontogenic foci, periodontal diseases and pulpal infections, extraction wounds, and infected fractures. Pus, fistula, and sequestration are typical clinical findings of this disease. Clinically and radiographically, a broad spectrum ranging from an aggressive osteolytic putrefactive phase to a dry osteosclerotic phase may be observed (Eyrich et al. 1999).

2.5.4 Chronic Non-suppurative Osteomyelitis

The term “nonsuppurative osteomyelitis” describes a more heterogenic group of chronic osteomyelitis forms, which lacks the formation of pus and fistula. Topazian (1994, 2002) includes chronic sclerosing types of osteomyelitis, proliferative periostitis, as well as actinomycotic and radiation-induced forms to this group, whereas Bernier et al. (1995) advocate a more restrictive use of this term. Hudson (1993) uses the term to describe a condition of prolonged refractory osteomyelitis due to inadequate treatment, a compromised host, or increased virulence and antibiotic resistance of the involved microorganisms. This classification therefore also incorporates those cases in which a suppurative

form of osteomyelitis can present as a nonsuppurative form in an advanced stage.

2.5.5 Diffuse Sclerosing Osteomyelitis, Primary Chronic Osteomyelitis,

Florid Osseous Dysplasia, Juvenile Chronic Osteomyelitis

One of the most confusing terms among the currently used osteomyelitis nomenclature is “diffuse sclerosing osteomyelitis” (DSO). This term has apparently led to great confusion in the medical literature. A variety of

denominations were used to describe this disease. One of the first descriptions was by Thoma in 1944, who used the term “ossifying osteomyelitis” and considered that a disease which was caused by a subpyogenic infection that could be found in tertiary syphilis. Sclerosing osteomyelitis was later described and divided into a focal and diffuse types (Shafer 1957; Shafer et al. 1974; Pindborg and Hjorting-Hansen 1974; Mittermayer 1976; Topazian 1994, 2002). The focal type, also known as periapical osteitis/osteomyelitis or condensing osteitis, is a rather common condition with a pathognomonic, well-circumscribed radioopaque mass of sclerotic bonesurrounding the apex of the root. Since the infection in these cases is limited to the apex of the root with the absence of deep bone invasion, sufficient endodontic treatment with or without apex surgery or extraction of the affected tooth usually leads to regression of these lesions or residual sclerosis may remain as a bone scar. True diffuse sclerosing osteomyelitis, however, is a rare disease of unknown etiology that can cause major diagnostic and therapeutic problems (Jacobson 1984). The absence of pus, fistula, and sequestration are characteristic. The disease shows an insidious onset, lacking an acute state. It is therefore considered to be primarychronic and has beeamed primary chronic osteomyelitis by several authors, predominantly in the German and continental European medical and dental literature (Hjorting-Hansen 1970; Panders and Hadders 1970; Schelhorn and Zenk 1989; Eyrich at al 1999). Periods of onset usually last from a few days up to several weeks and may demonstrate a cyclic course with symptomfreeintervals. Pain, swelling, and limitation of mouth

opening, as well as occasional lymphadenopathy, dominate the clinical picture.

The term DSO is primarily descriptive of the radiological appearance of the pathological bone reaction; however, although the term is usually used synonymously with primary chronic osteomyelitis, it represents a description of a strictly radiological appearance that can be caused by several similar processes. These processes include primary and secondary chronic osteomyelitis, chronic tendoperiostitis, and ossifying periostitis or Garrè’s osteomyelitis (Hjorting-Hansen 1970; Ellis et al. 1977; Eisenbund et al. 1981; Bьnger 1984; Van

Merkestyn et al. 1990; Groot et al. 1992b, 1996; Eyrich et al. 1999). This fact has most likely contributed to this diversity iomenclature, as the terms are often used interchangeably. A further pathological disease entity has been confused

with diffuse sclerosing osteomyelitis, since it may mimic DSO radiographically by presenting sclerosing opaque and dense masses: florid osseous dysplasia (FOD). These masses are, however, confined to the alveolar process of either or both jaws in cases of FOD. Florid osseous dysplasia is mostly observed in black women and in many cases lacks clinical symptoms. Patients suffering from this disease, similar to true DSO, may in some instances also experience cyclic episodes of unilateral pain and mild swelling. This is usually the case when superinfection occurs (Schneider et al. 1990; Groot et al. 1996) As with all pathologies of the bone which compromise local blood flow and host resistance, FOD makes the jaw more susceptible to secondary infection. In these instances pus and fistula formation may occur as well as sequestration (Carlson 1994). Many cases like these in the literature have, in retrospect, been incorrectly labeled as diffuse sclerosing osteomyelitis where these symptoms are by definition always absent. TheFOD should therefore be considered more a bone pathology facilitating osteomyelitis once infection of the bone has been established and not equated with the infection

itself. As mentioned above, the exact etiology of true DSO remains unknown. A common theory is a low-grade infection of some kind; however, most biopsy specimens taken from the enoral and extraoral approach have failed to be conclusive, showing either no growth in cultures or growth only from suspected contaminants (Jacobson et al. 1982; Jacobson 1984; Van Merkesteyn et al. 1988). A study by Marx et al. (1994) demonstrated a high frequency of Actinomyces, E. corrodens species, Arachnia and Bacteroides spp.in cortical and medullar samples from patients with DSO. This study, like many others, still demonstrated insufficiencies regarding the protocol for collecting bone specimens and therefore was inconclusive. Moreover, a variety of antibiotics used over a long period consistently failed to fully eradicate the disease or arrest the symptoms (Jacobson 1984; Van Merkesteyn et al. 1988, 1990). Van Merkesteyn et al. (1990) and Groot et al. (1992a) have advocated other etiologies such as aberrant jaw positioning and parafunction;however, their theory lacks an explanation for those cases of true DSO in edentulous patients. In our recent publications (Eyrich et al. 1999, 2003; Baltesperger et al. 2004) we used the term “juvenile chronic osteomyelitis,” which resembles the clinical and radiological picture of Garrè’s osteomyelitis as used

by various authors. Heggie et al. (2000, 2003) made a similar observation when analyzing his young osteomyelitis patients and used the term “juvenile mandibular

chronic osteomyelitis.” This disease usually peaks at puberty and is characterized mostly by voluminous expansion of the mandibular body, periosteal apposition

of bone (“periostitis ossificans”), and a mixed scleroticlytic appearance of the cancellous bone. The clinical picture resembles primary chronic osteomyelitis, sharing the lack of pus formation, fistulae, or sequestration. Juvenile chronic osteomyelitis is therefore considered to be an early-onset form of primary chronic osteomyelitis. A further and more detailed description of this disease entity is described later in this chapter.

2.5.6 SAPHO Syndrome, Chronic Recurrent Multifocal Osteomyelitis (CRMO)

In 1986 Chamot et al. described a syndrome associated with synovitis, acne, pustulosis, hyperostosis, and osteitis (SAPHO syndrome). Soon, several case reports and studies were published, concluding a possible relationship

between SAPHO syndrome and DSO of the mandible (Brandt et al. 1995; Kahn et al. 1994; Garcia- Mann et al. 1996; Suei et al. 1996; Schilling et al. 1999;

Eyrich et al. 1999; Roldan et al. 2001; Fleuridas et al. 2002). Kahn et al. (1994) presented a small series of seven patients with DSO of the mandible out of 85 cases of SAPHO syndrome. Eyrich et al. (1999) presented a series of nine patients with DSO, eight of which also represented a SAPHO syndrome, supporting the hypothesis of a possible association of the two. Chronic recurrent multifocal osteomyelitis (CRMO) is characterized by periods of exacerbations and remissions

over many years. This rare disease is noted in adults as in children, although it is predominant in the latter group. In several articles published in the past few years, a possible nosological relationship between diffuse sclerosing osteomyelitis and chronic recurrent multifocal osteomyelitis has been described (Reuland et al. 1992; Stewart et al. 1994; Suei et al. 1994, 1995; Flygare et al. 1997; Zebedin et al. 1998; Schilling 1998; Schilling et al. 1999). In correlation with advanced age, there seems to be an increased association with palmoplantar pustulosis, a part of the SAPHO syndrome (Shilling et al. 2000). Because of its possible relationship with otherdermatoskeletal associated diseases, CRMO has been integrated in the nosological heterogeneous SAPHO syndrome by several authors (Chamot et al. 1994; Schilling and Kessler 1998; Schilling et al. 2000).

2.5.7 Periostitis Ossificans, Garrès Osteomyelitis Strictly periostitis ossificans or ossifying periostitis is, like diffuse sclerosing osteomyelitis, a descriptive term

for a condition that may be caused by several similar entities. It is merely a periosteal inflammatory reaction to many nonspecific stimuli, leading to the formation of an immature type of new bone outside the normal cortical layer. Probably the most confusing and misinterpreted term regarding osteomyelitis is “Garrè’s osteomyelitis.” While most medical pathologists discard the term, it has still enjoyed great acceptance in the medical and dental literature, where occurrence in the jaws has been termed unequivocally (Eversole et al. 1979). Many

terms have been used synonymously in the literature and attributed to Garrè, such as periostitis ossificans, chronic nonsuppurative osteomyelitis of Garrè, Garrè’s

proliferative periostitis, chronic sclerosing inflammation of the jaw, chronic osteomyelitis with proliferative periostitis, and many more. Table 2.5 gives an overview of the use of the term “Garrè’s osteomyelitis” in the medical and dental literature; however, in his historical article in 1893, Carl Garrè did not actually describe a singular, specific type of osteomyelitis. Moreover he described special forms and complications of a single disease: acute infective osteomyelitis. He used 72 illustrative cases (98 sites) to discuss ten specific manifestations and complications of acute osteomyelitis. This is a direct contradiction to those authors who assume that he described a new form of chronic osteomyelitis (Wood et al. 1988).

2.5.8 Other Commonly Used Terms

2.5.8.1 Alveolar Osteitis (Dry Socket)

The clinical term “dry socket” or alveolar osteitis may also be regarded as a localized form of infection. Various authors have used this term differently. Hjorting- Hansen (1960) describes three principle forms of dry socket: alveolitis simplex; alveolitis granulomatosa; and an alveolitis sicca. Amler (1973) differentiates among alveolar osteitis, suppurative osteitis, and fibrous osteitis.

The author concludes that the three types of osteitis correspond to disturbances during the natural healing process of an extraction alveolus. Meyer (1971) took great effort in demonstrating the histopathological changes in alveolar osteitis. He classifies this condition according to the degree of local invasion of the surrounding bone and uses the terms “osteitis circumscripta superficialis”,

“media” and “profunda”. The term latter may be seen as a localized form of osteomyelitis; however, the term “alveolar osteitis” (dry socket) is generally used in the medical and dental literature to describe an absence of invasion into the bone. It should therefore not be regarded as a form of osteomyelitis (Marx 1991). In alveolar osteitis the commonly advocated theory suggests a clot breakdown due to the release of fibrinolysins either from microorganisms or trauma. In both situations the bacteria remain on the surface of the exposed bone, and an actual invasion does not occur. Although not considered a true infection, alveolar osteitis may lead to acute or secondary chronic osteomyelitis once the bacterial invasion into the medullar and cortical bone has occurred and a deep bone infection has been established.

2.5.8.2 Osteoradionecrosis and Radioosteomyelitis

Radiotherapy is considered a major column in the treatment of head and neck malignancies. Despite recent advances in radiotherapy, such as using modern threedimensional techniques, as well as hyperfractionation or moderately accelerated fractionation and consequent prophylactic dental treatment, osteoradionecrosis is still an observed condition in maxillofacial units.Aside from its effect on the tumor cells, radiation also has serious side effects on the soft and hard tissues adjacent to the neoplasm. Mucositis, atrophic mucosa, xerostomia, and radiation caries are well-known side effects of head and neck radiotherapy. Because of its mineral composition, bone tissue absorbs more energy than soft tissues and is therefore more susceptible to secondary radiation. In cases where the bone is irradiated exceeding a certain local dose, osteoradionecrosis may develop, leading to marked pain in the patient and possible loss of bone leading to functional and aesthetic impairment. Osteoradionecrosis was once considered an infection initiated by bacteria, which invaded the radiationdamaged bone; hence, the term “radiation-induced osteomyelitis” or radioosteomyelitis was commonly used. Marx (1983) conclusively identified this condition as a radiation-induced avascular necrosis of bone. He was able to demonstrate that radiation caused a hypoxic, hypocellular, and hypovascular tissue, leading to a spontaneous or trauma-initiated tissue breakdown. The result is a chronic nonhealing wound, susceptible to superinfection. As in florid osseous dysplasia and other bone

pathologies, microorganisms are responsible for contamination and, if invasion occurs, secondary infection of the bone, resulting in osteomyelitis.

2.5.8.3 Osteochemonecrosis

The medical literature describes several drugs and substances that facilitate or induce conditions known as osteonecrosis of the jaws, such as corticosteroids and

other cancer and antineoplastic drugs. Exposure to white phosphorous among workers in the matchmaking industry in the nineteenth century has led to unusual

necroses of the jaws, which became known in the literature as phossy jaw or phosphorous necrosis of the jaw. In the recent years bisphosphonate therapy has become a widely accepted mainstay of therapy in various clinical settings such as multiple myeloma, metastatic cancer therapy, and treatment of advanced osteoporosis. With the increased prescription of these drugs, the

incidence and prevalence of bisphosphonate-associated complications of the jaw continues to be elucidated. This trend seems to be even more the case in patients receiving injectable bisphosphonates, such as pamidronate and zoledronic acid, but cases involving osteochemonecrosis of the jaw associated with chronic peroral administered bisphosphonates have also been reported (Ruggiero etal. 2004, 2006). The pathophysiological mechanisms leading to bisphosphonate- induced osteochemonecrosis of the jaws are yet far from being fully understood; however, it seems apparent that important differences to the pathogenesis of osteoradionecrosis do occur (Hellenstein and Marek 2005). In bisphosphonate-induced osteochemonecrosis of the jaws osteoclastic action is reduced, but osteoblastic production continues, leading to an osteopetrosislike condition (Whyte et al. 2003). These alterations in bone physiology with eventual increase of the medullary bone as the disease progresses and the inability of osteoclasts to remove superinfected “diseased” bone are regarded as causative factors. In contrast to osteoradionecrosis, where a radiation-induced avascular necrosis is the major cause, avascularity does not appear to be a major cofactor to date; however, inhibition of angiogenesis is currently being actively investigated (Fournier et al. 2002; Wood et al. 2002), and further research will hopefully help fully understanding its role in pathogenesis of this disease. Regarding the current data and knowledge, we favor the term “bisphosphonate-induced osteochemonecrosis

of the jaw” because it is not restricted to a certain pathogenesis. The term “bisphosphonate osteomyelitis” should not be used for the same reasons as the term radioosteomyelitis should be abandoned. The jawbone with bisphosphonate-induced osteochemonecrosis is far more susceptible to bacterial invasion due to its strongly altered physiology; however, infection of the bone is to be considered a secondary phenomenon and not the primary cause of this disease entity.

2.6 Osteomyelitis of the Jaws: The Zurich Classification System

2.6.1 General Aspects of the Zurich Classification System

Osteomyelitis of the jaw as a clinical entity has long been recognized in the medical literature. As mentioned previously, various classification systems and nomenclatures of the disease have evolved with time. The heterogeneity of the classification systems is borne by the fact that several modalities are used to describe and define maxillofacial osteomyelitis. These modalities include etiology and pathogenesis, clinical presentation and course, radiology, and histopathology. Furthermore, most classification forms represent a mixture of these criteria, causing confusion, thereby hindering comparative studies. At the Department of Cranio-Maxillofacial Surgery at the University of Zurich, the classification system

for osteomyelitis of the jaws uses a hierarchical order of classification criteria. It is primarily based on clinical appearance and course of the disease, as well as on radiological features. Based on these criteria, three major groups of osteomyelitis can be distinguished:

1. Acute Osteomyelitis (AO)

2. Secondary Chronic Osteomyelitis (SCO)

3. Primary Chronic Osteomyelitis (PCO)

Within these major groups, the clinical presentation is similar in the majority of cases; however, as will be described later, a certain variety of the clinical course

is noted, especially in cases of primary and secondary chronic osteomyelitis.

Histopathology is considered a secondary classification criterion, taking into account that findings are mostly unspecific and nonconclusive when considered

by themselves; however, tissue examinations of biopsies are irreplaceable for confirmation of the diagnosis in cases of unclear and atypical clinical and radiological appearance, and moreover in excluding possible differential diagnosis. Furthermore, in some cases of osteomyelitis with an atypical appearance a synthesis of medical history, clinical presentation, imaging studies, histopathology, andother diagnostic tools may be necessary to achieve an appropriate diagnosis.

Analysis of the osteomyelitis patients treated in the Department of Cranio-Maxillofacial Surgery in Zurich using the abovementioned major classification groups showed a clear predominance of cases diagnosed as secondary chronic osteomyelitis at the time of presentation, whereas cases of acute osteomyelitis and primary chronic osteomyelitis were significantly less often diagnosed (Table 2.6). In a small group of nine patients, despite meticulous work-up of all data including clinical course and symptoms, diagnostic imaging, laboratory findings, and histopathology, no clear diagnosis was possible. Most of these cases showed a chronic courseresembling primary chronic osteomyelitis or a (diffuse) sclerosing form of secondary chronic osteomyelitis. In some of these cases the diagnosis of osteomyelitis was even questionable. The problems in diagnosis of these

challenging cases and possible related differential diagnosis are outlined later in this chapter. Further subclassification of these major osteomyelitis

groups is based on presumed etiology and pathogenesis of disease. These criteria are therefore considered tertiary classification criteria. These tertiary criteria are

helpful in determining the necessary therapeutic strategies which may differ somewhat among the subgroups. The nature of these subgroups are outlined in more detail later in this chapter. An overview of the Zurich classification of osteomyelitis of the jaws and the classification criteria are given in Fig. 2.2 and Table 2.7.

2.6.2 Acute Osteomyelitis and Secondary Chronic Osteomyelitis

2.6.2.1 Definitions

 

 

The basic terminology used in the Zurich classification of osteomyelitis of the jaws was promoted by Hugo Obwegeser, among others. The general principles of this classification system were described and published by E. Hjorting-Hanson, a former staff member at the Department of Cranio-Maxillofacial Surgery Zurich,

in 1970. Hjorting-Hanson, as many other authors before and after him, gave an excellent description of the clinical and radiological picture of acute and secondary

chronic osteomyelitis; however, he fell short of clearly defining at what stage an acute/subacute osteomyelitis should be considered chronic. To our knowledge, Marx (1991) and Mercuri (1991) were the first and only authors to define the duration for an acute osteomyelitis until it should be considered as chronic. They set an arbitrary time limit of 4 weeks after onset of disease. Pathological–anatomical onset of osteomyelitis corresponds to deep bacterial invasion into the medullar and cortical bone. After the period of 4 weeks, a persisting bone infection

should be considered as secondary chronic osteomyelitis (Fig. 2.3). Although the onset of the disease is a debatable point in time, it is still a simple and clear classification criterion and therefore of practical use for the clinician. This same definition was later used by several other authors (Eyrich et al. 1999; Schuknecht et al. 1997; Koorbusch et al. 1992). Because of its simplicity and clarity, this criterion is also used in the Zurich classification to differentiate acute osteomyelitis from secondary chronic osteomyelitis cases. The term “subacute osteomyelitis” is not clearly defined in the literature. Most clinicians would probably agree that this term describes a condition somewhat in between acute and chronic osteomyelitis with relatively moderate symptoms. To avoid confusion and keep the classification as simple as possible, this term has been abandoned in the Zurich classification.

According to this definition, acute and secondary chronic osteomyelitis are to be considered the same disease at different stages of their course; hence, both groups are presented and discussed together in this chapter.

2.6.2.2 Predisposing Factors, Etiology, and Pathogenesis

2.6.2.2.1 General Considerations

As mentioned previously, there are several etiological factors, such as traumatic injuries, radiation, and certain chemical substances, among others, which may

cause inflammation in the medullar space of the bone; however, acute and secondary chronic osteomyelitis, as these terms are generally used in the medical and dental literature and in this textbook, represent a true infection of the bone induced by pyogenic microorganisms. The oral cavity harbors a large number of bacteria, among which many may be identified as possible pathogens

to cause infection of the jawbone. Regarding the high frequency and sometimes severity of odontogenic infections in the daily dental and oral surgery practice,

and the intimate relationship of dental roots apices with the medullar cavity of the jawbone, it is remarkable that osteomyelitis cases are not more frequently observed. Explanation for the low incidence of osteomyelitis of the jawbones can be explained by four primary factors which are responsible for deep bacterial invasion into the medullar cavity and cortical bone and hence establishment

of the infection:

1. Number of pathogens

2. Virulence of pathogens

3. Local and systemic host immunity

4. Local tissue perfusion

Close interaction of these factors, as shown in Fig. 2.5, determine the pathological pathway of disease formation. In the healthy individual with sufficient host immunity mechanisms these factors form a carefully balanced equilibrium. If this equilibrium is disturbed by altering one or more of these factors, deep bone infection will be established (Figs. 2.4, 2.5).

2.6.2.2.2 Local and Systemic Host Immunity

Fig. 2.4 Chronic infection of the periapical bone as a sequel of endodontic disease. This frequently observed condition represents a classical equilibrium between microbiological aggressors and host factors hindering further spread of the bacteria. If this balance is disturbed and shifts toward the side of the microorganisms, deep invasion into the medullar and cortical bone may occur and

osteomyelitis is established

The oral cavity, like no other part of the human body, is constantly exposed to various potential aggressors. Many of these bacteria, given the chance, may cause severe infection and damage to the tissue if they are not kept at distance. Due to its unique environment, many potent strategies have been developed to prevent deep tissue invasion of bacteria. Specific local immunologicalmechanisms, potent barrier systems, such as the periodontal membrane and a rich local vascular supply, are the most important. A more detailed description of these and other defense systems is provided extensively in specific literature and is beyond the scope of this book. Every systemic disease with concomitant alterations in host defenses may influence profoundly the onset and course of acute and secondary chronic osteomyelitis. An alteration of some extent is probably the reason why osteomyelitis of the jaws develops in most cases, regardless of whether or not such deficiencies can be detected. Although the data is limited and lacks evidence-based

criteria in most instances, osteomyelitis has been associated with a variety of systemic diseases and pathological conditions. A list of such diseases and conditions, as well their mechanisms, are given in Tables 2.8 and

2.9. In our retrospective study of 244 cases of acute and secondary chronic osteomyelitis of the jaws, alcohol and tobacco consumption were observed in 33.2 and 47.5% of the cases, respectively, while other conditions, as shown in Table 2.8, were only observed in a scarce number of patients (Baltensperger 2003); however, more important in this study than the mentioned systemicfactors seemed to be the high prevalence of local infection in the examined patients with acute and secondary chronic osteomyelitis. Especially periodontal disease, which leads to a breakdown of the periodontal barrier membrane, facilitating deep invasion pathogens, seems to be an important condition leading to osteomyelitis. Significant periodontal disease was found in 51% of the patients of the same study. It is important for the treating physician to consider host compromise and treat any compromising condition, when feasible, concomitantly with the infection.

2.6.2.2.3 Local and Systemic Alterations in Bone Vascularity

Compromise of local blood supply must be considered a critical factor in the establishment of osteomyelitis. Systemic and local conditions that alter the vascularity of bone predispose the development of osteomyelitis. In these conditions immune cells and oxygen cannot reach the target area in an adequate manner. This facilitates the growth and spread of microorganisms, especially

anaerobes, leading to establishment and progression of osteomyelitis. An overview of conditions compromising blood supply of the jawbone is given in Table 2.10. In many cases of acute and secondary chronic osteomyelitis none of these factors may be apparent or detected; however, they must always be considered, looked for, and ultimately treated (Baltensperger 2003).

2.6.2.2.4 Microbiology

Acute and secondary chronic osteomyelitis are considered true infections of the bone induced by pyogenic microorganisms. As shown in Fig. 2.5, the number and

virulence of these pathogens are important factors in the establishment of a bone infection. Although until recently involvement of S. aureus, S. epidermidis, and Actinomyces were still discussed as the major pathogens in cases of osteomyelitis of the jaws, more recent studies favor the concept of a polymicrobic infection with several responsible pathogens.

This shift in doctrine is explained mainly by modern, sophisticated culture methods, especially involving anaerobic media, which enable identification of possible pathogens more accurately. Consequently, many pathogens, which are mostly found in the healthy oral flora, have been associated with cases of jawbone osteomyelitis; however, prolonged antibiotic therapy prior to harvesting of the specimen and possible oral contamination complicate the interpretation of each

result. A more detailed overview and in-depth information on this topic is provided in Chap. 7.

2.6.2.2.5 Etiology and Pathogenesis, Subclassification Groups

According to the classification criteria stated previously, subclassification of acute and secondary chronic osteomyelitis is based on presumed etiology and pathogenesis of disease (Tables 2.7 and 2.11). Acute and secondary chronic osteomyelitis are initiated by a contagious focus of infection or by hematogenous spread. In osteomyelitis of long bones, hematogenous spread is the leading cause, especially in infants and children, because of the distinct anatomy of the metaphyseal region. In most of these cases a single responsible pathogen can be isolated (Mader and Calhoun 2000). Staphylococcus spp. are the most common organisms isolated in adults and are also prominent in children and infants. Osteomyelitis of the jaws induced by hematogenous spread has become a rarity since the introduction of antibiotics; however, in regions of limited medical access

these forms may still be noted. Especially one form of osteomyelitis of hematogenous spread merits special mention: neonatal or tooth-germ-induced acute osteomyelitis of the jaws. Because of its risks of involvement of the

eye, spreading to the dural sinuses and creating loss of teeth and facial bone deformities if treated inadequately, this type of osteomyelitis should be remembered. Neonatal or tooth-germ-induced acute osteomyelitis occurs

most often within the first few weeks after birth, affecting the upper jaw in most instances. This infection showed a mortality rate of up to 30% before the advent of an tibiotics. The route of infection is considered by most clinicians to be hematogenous (Bass 1928; Lacey and Engel 1939; Heslop and Rowe 1956; Nade 1983), although a local infection caused by perinatal trauma of the oral

mucosa and local trauma to the overlying mucosa of the alveolar ridge (Hitchin and Naylor 1957; Nade 1983; Topazian 1994, 2002), as well as extension of infection from adjacent teeth or soft tissues, are also discussed (Loh and Ling 1993). Staphylococcus aureushas been implicated as the organism responsible for this type of acute osteomyelitis (Asherson 1939; Haworth 1947; McCasch and Rowe 1953; Niego 1970; Nade 1983; Loh and Ling 1993). The vast majority of cases of acute and secondary chronic osteomyelitis involving the jaws are usually

caused by infection primarily spreading by a contagious focus. The most common foci are odontogenic, originating from infected pulp or periodontal tissue or infected pericoronal tissue from retained teeth, especially third molars. Trauma, especially compound fractures, is also a major condition, which if not treated or treated inadequately, facilitates the development of osteomyelitis. But also every type of jawbone surgery, including surgical removal of impacted third molars, inevitably leads to a certain degree of local trauma to the bone, which causes local ischemia and may facilitate deep invasion of bacteria into the medullar cavity; hence, osteomyelitis can be established. Especially additional trauma to a preexisting chronic local infection carries a great risk of causingdeep bone infection. Foreign bodies as well as the various transplants and implants used in maxillofacial and dental surgery also may harbor microorganisms and hence

facilitate further spreading to the surrounding bone. Several types of bone pathologies and systemic conditions, as mentioned previously, influence local tissue perfusion and immunity and therefore are important cofactors in establishing bone infection. In rare cases, infections derived from periostitis after gingival ulceration, furuncles, and facial and oral lacerations may also be considered causative. In some instances the etiology and pathogenesis remains unclear or can only be speculated. These cases are subclassified as “other” in the classification system proposed in this book.

A distribution of acute and secondary chronic osteomyelitis cases, according to their etiology and pathogenesis, and their subclassification, respectively, is given

in Table 2.12. The distribution of acute and secondary chronic osteomyelitis shows a clear predominance of the mandible. In our patient data from 251 cases of acute and secondary chronic osteomyelitis only 16 patients (6.4%) demonstrated involvement of the upper jaw, whereas in the vast majority of cases (n=235; 93.6%) the mandible was the infected bone (Baltensperger 2003). Thedifferent anatomy of maxilla and mandible is probably the most important factor explaining the distribution of osteomyelitis involving the jawbones. The maxillary blood supply is more extensive than in the mandible. Additional thin cortical plates and the paucity of medullary tissues in the maxilla preclude confinement of infections within the bone and permit dissipation of edema and pus into the soft tissues of the midface and the paranasal sinuses (Topazian 1994, 2002). Maxillary osteomyelitis with tooth exfoliation after herpes zoster reactivation and concomitant cytomegalovirus infection has recently gained attention based on a review of

the literature and 27 previous reports of herpes zosterinduced jaw infections (Meer et al. 2006). The mandible is like a squashed long bone which has been shaped in a U-form. Like all long bones there is a clear distinction of a medullary cavity, dense cortical plates, and a well-defined periosteum on the outer border of the cortical bone. The medullary cavity is lined by the endosteum, which, like the periosteum, is a membrane of cells containing large numbers of osteoblasts. Within the medullary cavity a large variety of cells, such as reticuloendothelial cells, erythrocytes, granulocytes, platelets, and osteoblastic precursors, are harbored, as

well as cancellous bone, fat, and blood vessels. Bone spicules radiate centrally from cortical bone to produce a scaffold of interconnecting trabeculae (Copehaver et al. 1978). The architecture of mandibular cortical bone resembles that of other long bones. Longitudinally orientated haversian systems (osteons), each with a central canal and blood vessel that provide nutrients by means of canaliculi to osteocytes contained within lacunae. These canals communicate with adjunct haversian systems as well with the periosteum and the marrow space by Volkmann’s canals, thus forming a complex interconnecting vascular and neural network that nourishes bone and enables bone metabolism, necessary for repair, regeneration, and functional adaptation. Acute and secondary chronic osteomyelitis of the mandible affects most commonly the body of the mandible, followed by the symphysis, angle, ascending ramus, and condyle (Calhoun et al. 1988; Baltensperger 2003). The compromise of local blood supply is the critical factor and final common pathway in the establishment of acute and secondary chronic osteomyelitis (Fig. 2.7). Wannfors and Gazelius (1991) demonstrated by means of laser Doppler flowmetry (LDF) that long-standing local inflammation of the mandible was associated with a persistent reduction in blood flow. Except for the coronoid process, which is supplied primarily from the temporalis muscle and the mandibular condyle, which is supplied in part by vessels from the lateral pterygoid muscle and the temporomandibular joint (TMJ) capsule, the major blood supply of the rest of the mandible consists of the inferior alveolar artery(Fig. 2.6). A secondary source is provided by the vessels of the periosteum. These vessels are organized in a reticular manner and run alongside of the cortical surface, giving off small nutrient vessels that penetrate the cortical bone and anastomose with branches of the inferior alveolar artery (Fig. 2.6; Castelli 1963; Cohen 1959); however, the value of the periosteal circulation probably cannot be seen as full replacement of the vascular supply of the marrow space. Hence, despite this adjunctive vascularization of the mandible through the periosteum, the main blood supply is derived from the inferior alveolar artery which, especially in elderly patients, is a vessel of small caliber and most susceptible to damage. This context can be transferred to the clinical appearance of osteomyelitis of the mandible, where occlusion of the inferior alveolar artery inevitably boosts the progress of the infection even if an intact periosteum is still present. In most incidences periapical and periodontal infections are localized by a protective pyogenic membraneor soft tissue abscess wall which serves as a certain barrier (Schroeder 1991). As mentioned above, this condition represents a carefully balanced equilibrium between microorganisms and host resistance preventing further spreading of the infection. If the causative bacteria are sufficient iumber and virulence, this barrier can be destroyed. Furthermore, permanent or temporaryreduction of host resistance factors for various reasons mentioned previously facilitate deep bone invasion of the microorganisms. This invasion induces a cascade of inflammatory host responses causing hyperemia, increased capillary permeability, and local inflammation of granulocytes. Proteolytic enzymes are released during this immunological reaction creating tissue necrosis, which further progresses as destruction of bacteria and vascular thrombosis ensue. Accumulation of pus inside the medullary cavity, consisting of necrotic tissue and dead bacteria within white blood cells, increases intramedullary pressure. This leads to vascular collapse, venous stasis, thrombosis, and hence local ischemia (A in Fig. 2.7; Topazian 1994, 2002). Pus travels through the haversian and nutrient canals and accumulates beneath the periosteum, elevating it from the cortical bone and thereby further reducing the vascular supply (B in Fig. 2.7; Topazian 1994, 2002). Elevation of the periosteum is usually observed more extensively in children,presumably because the periosteum is less firmly attached to the cortical bone than in adults. When pus

accumulates continually underneath the periosteum, perforation may occur, leading to mucosal and cutaneous abscesses, and fistulas may develop. In mandibular osteomyelitis, the increased intramedullary pressure also leads to direct compression of theneurovascular bundle, accelerating thrombosis and ischemia resulting in dysfunction of the inferior alveolar nerve, known as Vincent’s symptom. The mandibular canal is also an anatomical pathway with no barrier function, alongside which pus can spread quickly (Fig. 2.8).

Fig. 2.6 a Condylar process arteries of an injected human head. Mandible soft parts

were discarded after injection was performed through the common carotid artery. A

artery coming from the lateral pterygoid muscle, B artery coming from vessels of the temporomandibular joint capsule (Teichmann’s paste injection; decalcified and cleared). b Coronoid process arterial vessels. Two arterioles (A and A’) are

present, both coming from the temporalis muscle (China-ink solution injection; decalcified and cleared). c Overall view of injected inferior alveolar artery

(Teichmann’s paste injection; decalcified and cleared). (From Castelli 1963)

 

2.6.2.2.6 Chronification of Bone Infection

The chronification of the disease reflects the inability of the host to eradicate the pathogen due to lack of treat ment or inadequate treatment, resulting in failure to

reestablish the carefully balanced equilibrium between host factors and pathogens found in a healthy oral environment. After the acute inflammatory process occurs and local blood supply is compromised, necrosis of the endosteal bone takes place. The bone fragments die and become sequestra (Fig. 2.9). Osteoclastic activity is then responsible for separating the dead bone from vital bone. Devital bone tissue clinically appears dirty, whitish- gray with an opaque appearance. Its fatty tissue has been destroyed and it does not bleed if scraped (Marx 1991). In some instances the bone sequester can demonstrate considerable dimensions (Fig. 2.10). The elevated periosteum involved in the inflammatory process still contains vital cells. These cells, once the acute phase has passed, form a new bony shell (involucrum) covering the sequester. The involucrum may be penetrated by sinuses called cloacae, through whichpus discharges, elevating the periosteum or forming

fistula. As chronification progresses this scenario may be repeated (Figs. 2.11, 2.12). The involucrum tends to hinder sequester from extruding, which perpetuates the process because the whole area is bathed in increasing amounts of pus unless treated promptly and adequately (Killey and Kay 1970). In secondary chronic osteomyelitis of the jaws, eventually a new equilibrium is established between the host and the aggressor causing the infection. The nature of this newly formed equilibrium is dependent on host immunitysupported by medical therapy and the causative bacteria. It dictates the further course of the infection:

• If adequate therapy is administered on time, balance is shifted in favor of the host, resulting in complete healing of the infection.

 • If no or inadequate therapy is provided, the disease may progress slowly or faster depending on the number and virulence of the bacteria and the remaining host defenses.

• If the number and virulence of the bacteria are small, host mechanisms may overwhelm, but still fail to fully eradicate the pathogen. In these instances a strong and diffuse sclerosis of the bone with or without a significant periosteal reaction can be noted. The clinical and radiological picture may then resemble primary chronic osteomyelitis.

Fig. 2.8a,b Patient with acute osteomyelitis, beginning secondary chronic osteomyelitis of the right mandible following extraction of the lower right second molar. Her chief complaint was a marked hypoesthesia of the right inferior alveolar nerve (Vincent’s symptom), which was documented preoperatively in a. b The intraoperative view after removal of the buccal cortical plate by decortication: note

the granulation tissue alongside the inferior alveolar nerve (arrows) as a primary pathway for spread of the infection. (This case is described in detail in Chap. 12, case report 4)

 

Fig. 2.9 a An OPG of a secondary chronic osteomyelitis case demonstrates osteolysis in the mandibular corpus around the alveolar region of the right first molar. A sequester is noted at the base of the right mandibular corpus with adjacent periosteal reaction. bSurgical specimen of the case shown in a: multiple sequesters and necrotic bone collected during debridement surgery

 

2.6.3 Clinical Presentation

2.6.3.1 Demographics

Acute and secondary chronic osteomyelitis may affect all ages and both sexes. In our retrospective analysis of  251 cases of acute and secondary chronic osteomyelitis there was a male predominance with a 2:1 ratio (Baltensperger 2003). Koorbush et al. (1992) described a male to female ratio of 3:1 in a survey of 35 patients. An equal gender distribution was noted by Daramola et al. (1982)

in a larger African patient population. The mean age of onset of disease in our studied cases was almost the same in cases of acute and secondary chronic osteomyelitis: 42.9 years (range 1–81 years) and 44.1 years (range 6–89 years; Baltensperger 2003),respectively. These figures are comparable with those

described by previous investigators (Adekeye 1985; Calhoun 1988; Koorbush 1992; Daramola 1982). 

Fig. 2.10a–c The CT scans of a patient with secondary chronic osteomyelitis of the left mandible developing a giant sequester on the bases of the mandibular corpus. The progressive infection has weakened the bone and hence a pathological fracture has resulted. Sagittal CT scan (a) and 3D reconstructions (b,c). (Courtesy of N. Hardt)

 

Fig. 2.11 Axial CT scan of an extended secondary chronic osteomyelitis of the left mandible. A strong periosteal reaction with neoosteogenesis has formed an involucrum over several sequestra. (This case is described in detail in Chap. 12, case report 6)

2.6.3.2 Acute Osteomyelitis

The clinical appearance of acute osteomyelitis of the jaws may show a great variety, depending on the intensity of the disease and the magnitude of imbalance

between the host and the microbiological aggressors. Three principal types of clinical courses of acute osteomyelitis can be distinguished:

• Acute suppurative

• Subacute suppurative

• Clinically silent with or without suppuration

Cases of acute osteomyelitis of the jawbone with an acute suppurative clinical course usually show impressive signs of inflammation. Pain can be intense and is

mostly described by a deep sensation within the bone by the patient, which may be a valuable clue in the patient’s history. Local swelling and edema due to abscess

formation can also be substantial causing trismus and limitation of jaw function. The patients experiences a general malaise caused by high intermittent fever with

temperatures reaching up to 39–40°C, often accompa nied by regional lymphadenopathy. In some instances paresthesia or anesthesia of the lower lip is described (Vincent’s symptom), indicating involvement of the inferior alveolar nerve. In most cases the cause of infection is odontogenic (Table 2.12) and can easily be identified. Pus may exude around the gingival sulcus and through mucosal and, possibly cutaneous, fistulas (Figs. 2.13–2.15). A fetid oral odor caused by anaerobic pyogenic bacteria often is present. Teeth in the affected

region may demonstrate increased mobility even leading to malocclusion and show decreased or loss of sensitivity. Sequester formation and appositional neoosteogenesis are limited, if not absent, due to the short period since establishment of deep bone infection, which is the definition of acute osteomyelitis (Fig. 2.16). Neonatal or tooth-germ-induced acute osteomyelitis of the jaws, as described previously, is a classical representative of this group, although this form of osteomyelitis has become a rarity in modern maxillofacial practice. But also in elderly patients this form of acute osteomyelitis has been seen much less frequently since the introduction of antibiotics and sophistication of medical and dental practice. In cases of a subacute or silent course, with or withoutsuppuration, the clinical presentation is by definition less impressive. This can make an early diagnosis increasingly difficult, and in many instances these cases are not detected until they have become secondary chronic. An overview of symptoms at initial presentation of our patient data is given in Table 2.13.

Fig. 2.12 Coronal view corresponding to axial CT scan shown in Fig. 2.11. (This case is described in detail in Chap. 12, case report 6)

Fig. 2.13 Acute odontogenic osteomyelitis with massive suppuration. Oral examination at initial presentation revealed pus in the sulci of the anterior incisors and canines on both sides, extending distally to the molars in the right lower jaw with multiple fistula formation

2.6.3.2.1 Laboratory Findings

Depending on the intensity of the infection, laboratory results in acute osteomyelitis may demonstrate a wide range. While in cases with little inflammation the laboratory will only reveal moderate evidence of acute infection, cases which are accompanied by abscessformation will show more pronounced findings. Examination of our own patient data is demonstrated in Table 2.14.

2.6.3.3 Secondary Chronic Osteomyelitis

As a sequel of acute osteomyelitis, the clinical presentation of secondary chronic osteomyelitis of the jaws may also show a great variety, depending on the intensity of the disease and the magnitude of imbalance between the host and the microbiological aggressors and the time (Fig. 2.16). Following an acute or subacute clinical phase with suppuration, the chronification of the disease is reflected by the clinical course and findings. Most symptoms, such as pain and swelling, are usually less extensive in the chronic than in the acute stage. The deep and intense pain frequently observed in the acute stage is replaced by a more dull pain. Painful swelling caused by local edema and abscess formation in the

acute stage is subsided by a harder palpable tenderness caused by periosteal reaction (see Figs. 2.11, 2.12). Other symptoms are somewhat more predominant in advanced stages, such as sequester and fistula formation, and are regarded as classical signs of secondary chronic osteomyelitis (see Figs 2.10, 2.11, 2.12). The

noted fetid odor ofteoted in cases of acute abscess formation is less frequent in patients with secondary chronic osteomyelitis. A disturbed occlusion can sometimes be noted when teeth of an affected region become more mobile and elongate due to rise of intraosseous pressure or a fracture present as a result or initiator of the osteomyelitic process. An overview of symptoms at initial presentation of our patient data is given in Table 2.15. In cases where the acute phase was clinically silent, secondary chronic osteomyelitis may begin as a hideous disease with little and somewhat unspecific clinical symptoms. In such instances the cause of the infection is considered to be a low-grade infection, which, however, cannot be fully eradicated by host defenses. These cases of secondary chronic osteomyelitis demonstrate less pus, fistula, and sequester formation, or may even lack these symptoms at a certain (progressive) stage of

the disease. Furthermore, their radiological appearance may predominantly show a diffuse sclerosis with little to no osteolysis. Probably a large portion of the cases

described in the literature as diffuse sclerosing osteomyelitis (DSO) falls into this category. A differentiation from primary chronic osteomyelitis may be difficult, if not impossible, in such cases (Figs. 2.17, 2.18); hence, it is most important to review the whole course of the disease and possibly obtain repeated imaging over time in such cases to establish the correct diagnosis.

Fig. 2.14 OPG at initial presentation (same patient as shown in Fig. 2.13). Osteolysis of the neighboring bone, derived from apical pathology, is noted in the incisor and canine region on both sides as well as in the molar region on the right

side

Fig. 2.15 Corresponding axial CT scan to OPG shown in Fig. 2.14 with a more detailed view of the osteolysis in the anterior and right sided alveolar bone

 

2.6.3.3.1 Actinomycotic and Other Rare Secondary Chronic Osteomyelitis of the Jaws Specific clinical findings can be found in acute and especially

in secondary chronic osteomyelitis caused by Actinomyces, Nocardia, and Mycobacteria. While Actinomyces is infrequently observed, the other pathogens are rarely associated with osteomyelitis of the jaws; however, if they are the causative pathogen, the clinical picture is somewhat atypical and hence deserves special recognition.

In our studied cases we identified 5 patients with actinomycotic secondary chronic osteomyelitis, while osteomyelitis cases associated with Nocardia and Myco Cervicofacial actinomycosis is a slowly progressive infection with both granulomatous and suppurative features. The disease predominantly affects the soft tissue of the head and neck with primary involvement of nearly every structure (Lerner 1988); however, in some instances the underlying bone, predominantly the mandible, can be infected by direct extension to the underlying bone or hematogenous spread (Topazian 1994, 2002). As in most cases of secondary chronic osteomyelitis, infection with Actinomyces is mostly of endogenous origin, since the pathogen is known to be an oral saprophyte,present in periodontal pockets, carious teeth, tonsillar crypts, and other structures. Local infection, as well as surgical or nonsurgical trauma, facilitates penetration of the mucosal and periodontal barrier structures and allows penetration of deep tissue and bone (Bowden 1984). Advanced cervicofacial Actinomycosis spreads without regard for fascial planes and typically appears on cutaneous, rather than mucosal,

surfaces. Firm soft tissue masses are present on the skin with purplish to dark-red oily areas and occasionally small zones of fluctuance (see Fig. 9.1, 9.2, Chap. 9). Spontaneous drainage of serous fluid containing granular material may occur. When placed on a piece of gauze, these granular, yellowish substances, also called sulfur granules, can be seen clearly and represent colonies ofbacteria (Topazian 1994, 2002). The underlying affected bone demonstrates the clinical and radiological picture of secondary chronic osteomyelitis with zones of osteolysis,

delayed healing of extraction sites, and sclerosis on radiographs. Occasionally sequester formation is also noted. Nocardiosis is also a chronic disease that may resemble actinomycotic infection. Although the primary target is usually the lungs, from where hematogenous spread leads the pathogen to other organs, the cervicofacial region, including bone, is occasionally involved (Schwartz and Tio 1987). Tuberculosis is still a widespread infectious disease worldwide with also an increasing incidence again in countries with poor socio-economic conditions, concomitant with the AIDS pandemic. The etiology, pathogenesis, diagnosis, and treatment of tuberculosis are well described in other textbooks and are beyond the

scope of this book. Osteomyelitis of the jaws caused by infection with

Mycobacterium tuberculosis is uncommon and, in most described instances, the tuberculosis infection is rarely confined to the bone. Adults are predominantly affected, although cases of affected children are also described (Bhatt and Jayakrishnan 2001; Hock-Liew et al. 1996; Kothari et al. 1998; Dimitrakopoulos et al. 1991; Fukuda et al. 1992). Oral tuberculous lesions are generally quite rare, despite the fact of high incidence of systemic involvement. A possible reason for this observation may be the inhibition ofMycobacterium tuberculosis by saliva and intact oral mucosa (Hock-Liew et al. 1996; McCarthy and Shklar 1980). The mechanisms of spread of infection are, in analogy to other osteomyelitis cases, caused by other bacteria, by direct inoculation, through tooth-extraction sockets, through any breach in the mucosa during tooth eruption, spread from adjacent soft tissue sites, or by hematogenous spread (Mishra and Bhoyar 1986). The clinical and radiological picture may resemble that of regular secondary chronic osteomyelitis with features similar to a dento-alveolar abscess; however, cervical lymphadenopathy, producing discrete or matted masses which are usually nontender, may be a distinctive presenting feature in some patients (Lee and Schecter 1995). This resemblance to conventional osteomyelitis cases underlines the importance of considering tuberculous osteomyelitis in the differentialdiagnosis of jaw lesions, especially if the patient’s medical history is suspicious for possible infection (Bhatt and Jayakrishnan 2001).Candida albicans has also been described as a potential microorganism to cause osteomyelitis in various

bones of the skeleton, especially in conjunction with prosthesis. In the facial skeleton, however, documented cases of osteomyelitis caused by Candida albicans

are extremely rare, despite the fact that Candida is known commensal of the oral cavity. Arranz-Caso et al. (1996) report of a case ofCandida albicans osteomyelitis of the zygomatic bone probably caused by self-inoculation of spores from muguet plaques on the oral mucosa to the exposed bone tissue by hand

contact. The authors conclude that such a mechanism should be considered especially in patients who frequently have oral candiasis (e.g., diabetic, cancer, and

HIV patients). Cases of acute and secondary chronic osteomyelitis of the jaws have also been reported by bacteria which are rarely or not considered to be oral commensals. These cases, however, are extremely scarce, and hence the literature on these infections consists mainly of case reports.

Fig. 2.17 Patient with secondary chronic osteomyelitis. After an initial phase of

pus and fistula formation with local surgical drainage and prolonged antibiotic therapy, the process advanced with little clinical symptoms and demonstrated a diffuse sclerosing pattern of the left and right mandibular corpus and symphyseal region in the further course mimicking primary chronic osteomyelitis

Fig. 2.18 Same as Fig. 2.17

 

2.6.3.3.2 Secondary Chronic Osteomyelitis Masquerading Malignancy

The clinical and radiological signs of secondary chronic osteomyelitis may share many similarities with malignancy complicated by secondary bone infection

(Figs. 2.19, 2.20). This may lead to delay definite diagnosis and appropriate treatment in certain instances (Vezeau et al. 1990).Lesions believed to be osteomyelitis that do not respond to treatment as expected within a short time

should be viewed with concern. The patient’s medical history, determining possible risk factors for developing oral carcinoma such as smoking, alcohol abuse, and poor oral hygiene, may be indicative, but imaging studies and representative biopsies should be performed to establish the diagnosis (Topazian 1994, 2002).

As much as the presence of a malignancy with invasion into the underlying jawbone may facilitate secondary infection, the opposite pathway may also be the case in rare instances. Ongoing bone infection may also lead to malignancy by neoplastic conversion of infectious tissue (Lemiиre et al. 2000; Niederdellmann et al. 1982).

2.6.3.3.3 Secondary Chronic Osteomyelitis Associated with Bone Pathology

As mentioned previously, there are several conditions which facilitate bone infection in the jaw. A summary of the most frequently involved pathological conditions enhancing the incidence of osteomyelitis of the jaws is given in Table 2.10; however, theoretically every pathological condition which alters bone physiology and/or vascularization of bone tissue may jeopardize host tissue

defense mechanisms and hence may promote secondary infection. The unique location of the jawbones with their proximity to the heavily contaminated oral

cavity makes them particularly vulnerable. Depending on the nature of the underlying bone pathology, the clinical picture of succeeding secondary chronic osteomyelitis may differ from the average osteomyelitis infection established in “healthy bone.” The initiation of infection is, like in regular acute and secondary chronic osteomyelitis, often a trauma such as extraction of a tooth or a dental infection leading to breakdown of the periodontal and/or mucosal barrier and promoting contamination and deep bone invasion of the jawbone. The further course of the disease is, however, strongly dependent on the reactive mechanisms

of the host tissue (e.g., bone). In general, underlying bone pathology will reduce the defensive abilities of the host tissue and infection may spread faster than in healthy bone. Clinical and radiological signs reflecting suppurative infection, such as abscess and fistulaformation, are similar to osteomyelitis cases without associated bone pathology. Bone reaction to infection, like osteolysis, sclerosis, sequester formation, and periosteal reaction, however, may strongly differ, making

correct diagnosis and determining the extent of the infection more challenging (Fig. 2.21). In cases were necrotic bone is exposed to the oral cavity, secondary

colonization of the bone and eventual deep bone invasion may occur (Fig. 2.22).

2.6.3.3.4 Laboratory Findings

In analogy to the clinical symptoms, the laboratory findings in secondary chronic osteomyelitis of the jaws are usually less prominent than in acute osteomyelitis.

The overall moderate systemic reactions are reflected by these results and indicate a more localized infectious process, especially in secondary chronic osteomyelitis

cases. This is especially true in cases with little or mild clinical symptoms where laboratory findings can be almost normal and hence are of little diagnostic or

monitoring value. Examination of our own patient data is demonstrated in Table 2.16.

2.6.4 Primary Chronic Osteomyelitis

2.6.4.1 Definition

Fig. 2.19a,b Patient with a squamous cell carcinoma of the left lower jaw with concomitant secondary chronic osteomyelitis. The patient was referred to the maxillofacial unit approximately 1 month after surgical removal of the lower left second molar with chronic local fistula formation and pus discharge from the extraction site. The medical history, clinical appearance, and initial radiologicalwork-up (OPG; Fig. 2.19 and corresponding axial CT scans in Fig. 2.20) were suspicious for secondary chronic osteomyelitis; however, initial bone and soft tissue biopsies revealed an invasive squamous cell carcinoma with a concomitant local bone infection

Fig. 2.20a,b Histology samples of the same patient shown in Figs. 2.19a and b.

Hematoxylin and eosin stains. a Infiltration of bone by moderately differentiated squamous cell carcinoma. Keratinization in center of tumor cell islands (arrow). Peritumoral fibrosis and infiltration by inflammatory cells are present (arrowheads)

 

Fig. 2.20 (continued) Histology samples of the same patient

shown in Figs. 2.19a and b. Hematoxylin and eosin stains. b Lamellar bone with preserved osteocyte nuclei is present besides signs of inflammation fibrosis of marrow spaces (arrows) and extensive infiltration by inflammatory cells (arrowheads)

 

Fig. 2.21 a A patient with a clinically extensive secondary chronic osteomyelitis of the frontal region with multiple fistula and abscess formations. The patient was

treated with i.v. bisphosphonates for metastatic breast cancer. (This case is described in detail in Chap. 12, case report 10.) b A CT scan corresponding to a: The bone and periosteal reaction is not as strong as would have been expected

from the clinical picture and compared with cases of secondary osteomyelitis of the mandible with no underlying bone pathology. (This case is described in detail

in Chap. 12, case report 10)

 

Acute and secondary chronic osteomyelitis of the jaw, as being the same disease at a different stage, share the same etiology, a bacterial or, in rare cases, a fungal infection. In the literature acute and secondary chronic osteomyelitis are often summarized by the term “suppurative osteomyelitis,” indicating a true bacterial infection with formation of pus. The term “primary chronic osteomyelitis,” as used in the Zurich classification of osteomyelitis of the jaws, refers to a rare inflammatory disease of unknown etiology. It is characterized as a strictly nonsuppurative chronic inflammation of the jawbone with the absence of pus

formation, extra- or intraoral fistula, or sequestration. The absence of these symptoms represents a conditio sine qua non and clearly differentiates primary from acute and secondary chronic osteomyelitis in most cases. The term “primary chronic osteomyelitis” also implies that the patient has never undergone an appreciable acute phase and lacks a definitive initiating event. The disease tends to a rise de novo without an actual acute phase and follows an insidious course. In

most cases of primary chronic osteomyelitis, periodic episodes of onset with varying intensity last from a few days to several weeks and are intersected by periods of silence where the patient may experience little to no clinical symptoms. In active periods dull to severe pain, limitation of jaw opening and/or myofacial pain, as well as variable swelling, may be observed. In certain cases regional lymphadenopathy and reduced sensation of the inferior alveolar nerve (Vincent’s symptom) are also accompanying symptoms.Primary chronic osteomyelitis of the jaws almost always targets the mandible. In our patient data all but one case of primary chronic osteomyelitis involved exclusively the lower jaw. In the remaining case, the zygoma demonstrated the clinical, radiological, andhistopathology findings as the mandible, indicating a possible spread of the pathological condition. The findings in the literature are similar to our data. Flygare et al. (1997) reported a case of primary chronic osteomyelitis with involvement of both jaws, which is considered to be a unique case.

2.6.4.2 Classification Problems of Primary Chronic Osteomyelitis of the Jaws

As mentioned previously, the classification of osteomyelitis of the jaws, and especially primary chronic osteomyelitis of the jaws, is somewhat confusing, mainly due to the wide variety of terms used to describe this disease entity.

 

Osteomyelitis is a rare complication of tooth-related infections (incidence of 25 in 100,000).  In most cases, it is the result of spread of infection from a dento-alveolar (tooth) or periodontal (pyorrhoea / gum disease) abscess or from the para-nasal sinuses, by way of continuity through tissue spaces and planes.  It occasionally occurs as a complication of jaw fractures or as a result of manipulations during 
surgical procedures.

Most patients are adult males with infection of the mandible (lower jaw).

Osteomyelitis of the maxilla (upper jaw) is a rare disease of neonates (newly born) or infants after either birth injuries or uncontrolled middle ear infection.

It is classified as acute or chronic osteomyelitis.

Acute Osteomyelitis

In the acute form (which rarely, may also be of hæmatogenous origin [i.e. seeded from the blood stream]), the infection begins in themedullary cavity (bone marrow) of the bone.  The resulting increase of intra-bony 
pressure leads to a decreased blood supply (and hence diminution of white blood cells and other immune components) and spread of the infection, by way of the Haversian canals of the bone, to the cortical bone (definition) and periosteum (below theperiosteum, a thick fibrous two-layered membrane covering the surface of bones).  This aggravates the ischæmia (decreased blood supply), resulting in necrosis (the death of cells or tissues 
from severe injury or disease, especially in a localised area of the body.  Causes of necrosis include inadequate blood supply [as ininfarcted tissue], bacterial infection, traumatic injury and hyperthermia) of the bone.

Acute Osteomyelitis of the Jaws — Potential Sources of 
Infection

• Peri-apical infection

• A periodontal pocket involved in a fracture

• Acute gingivitis or pericoronitis (even more rarely)

• Penetrating, contaminated injuries (open fractures or 
  gunshot wounds)

Important Predisposing Conditions for Osteomyelitis

Local Damage to / Disease of the Jaws

• Fractures, including gunshot wounds

• Radiation damage

• Paget’s disease

• Osteopetrosis

Impaired Immune Defences

• Acute leukaemia

• Poorly-controlled diabetes mellitus

• Sickle cell anaemia

• Chronic alcoholism or malnutrition

• AIDS

 

• Infection from micro-organisms with great virulence.  
  In such cases, even a peri-apical abscess may be 
  implicated in osteomyelitis.

Acute Osteomyelitis of the Jaws — Key Features

• Mandible mainly affected, usually in adult males

• Infection of dental origin – anærobes are important

• Pain and swelling of jaw

• Teeth in the area are tender; gingivæ (gums) are red 
  and swollen

• Sometimes paræsthesia of the lip

• Minimal systemic upset

• After about 10 days, X-rays show ‘moth-eaten’ 
  pattern of bone destruction

• Good response to prompt antibiotic treatment and 
  debridement

The mandible (lower jaw), due to decreased vascularity (blood supply & flow), is involved 6 times more often than the maxilla (upper jaw).
The mandible has a relatively limited blood supply and dense bone with thick bony (cortical) plates.  Infection causes acute inflammation in the medullary (bone marrow) soft tissues and inflammatory exudate (a fluid with a high content of protein and cellular debris which has escaped from blood vessels and has been deposited in tissues or on tissue surfaces, usually as a result of inflammation. It may be septic or non-septic) spreads infection through the marrow spaces.  It also compresses blood vessels confined in the rigid boundaries of the vascular canals.

Thrombosis (the formation or presence of a thrombus [a clot of coagulated blood attached at the site of its formation] in a blood vessel) and obstruction then lead to further bone necrosis.

Dead bone is recognisable microscopically by lacunae (a cavity, space, or 
depression, especially in a bone, containing cartilage or bone cells) empty of 
osteocytes (a cell characteristic of mature bone tissue.  It is derived from 
osteoblasts and embedded in the calcified matrix of bone. Osteocytes are found in small, round cavities called lacunae and have thin,cytoplasmic branches) but filled with neutrophils (white blood cells) and colonies of bacteria which proliferate in the dead tissue.

Pus, formed by liquefaction of necrotic soft tissue and inflammatory cells, is forced along the medulla and eventually reaches thesub-periosteal region by resorption (an organic process in which the substance of some differentiated structure that has been produced by the body undergoes lysis and assimilation) of bone.  Distension of the periosteum by pus stimulates sub-periostealbone formation but perforation of the periosteum by pus and formation of sinuses on the skin or oral mucosa are rarely seeow.

At the boundaries between infected and healthy tissue, osteoclasts (a specialised bone cell that absorbs bone) resorb the periphery of the dead bone, which eventually becomes separated as a sequestrum (a fragment of dead bone separated from healthy bone as a result of injury or disease).  Once infection starts to localise, new bone forms around it, particularly sub-periosteally.

Where bone has died and been removed, healing is by granulation with formation of coarse fibrous bone in the proliferating connective tissue.  After resolution, fibrous bone is gradually replaced by compact bone and remodelled to restore normal bone tissue and structure (and function).

Piercing, deep and constant pain predominates in the clinical presentation in adults, while low or moderate fever, cellulitis,lymphadenitis, or even trismus may also be noted.

In the mandible, changes in sensation affecting the lower lip (paræsthesia or 
dysæsthesia of the lower lip) may accompany the disease.  When the disease 
spreads to the peri-osteum (definition) and the surrounding soft tissues, a firm 
painful œdema (definition) of the region is observed, while the tooth becomes loose and there is discharge of pus from theperiodontium.  Radiographic examination reveals osteolytic (definition) or radiolucent (definition) regions

Therapy entails combined surgical (incision, drainage, extraction of the tooth and removal of sequestrum) and chemo-therapeutictreatment (with antibiotics).

Summary of Treatment of Osteomyelitis

Essential Measures

• Bacterial sampling and culture

• Vigorous (empirical) antibiotic treatment

• Drainage

• Give specific antibiotics based on culture and sensitivities

• Give analgesics

• Debridement

• Remove source of infection, if possible

Adjunctive Treatment

• Sequestrectomy

• Decortication if necessary

• Hyperbaric oxygen*

• Resection and reconstruction for extensive bone destruction

*Mainly of value for osteo-radionecrosis and possibly, anærobic infections.

Anæsthesia of the lower lip usually recovers with elimination of the infection.  Rare complications include pathological fracture caused by extensive bone destruction, chronic osteomyelitis after inadequate treatment, cellulitis due to spread of exceptionally virulent bacteria or septicæmia in an immuno-deficient patient.

Delayed Eruption of Teeth

Normal eruption of teeth is of primary importance to dentists. Eruption is the process which causes the tooth to move from its original position in the bone to its final position in the mouth. It must be corresponding with the growth of the jaws. Though deviations from normal time of eruption are often observed in clinical practice, delayed tooth eruption is the most commonly encountered deviation from normal eruption time.

Late eruption of a permanent tooth may be a significant concern for children in the mixed dentition stage and their parents. Late development and eruption can lead to disturbance to developing occlusion. Besides providing support for chewing, permanent molars eruption is very essential for organization of growth of face.

Normally, once milk tooth is shed off, permanent adult tooth should erupt within 6 months. But if the interval exceeds beyond 12 months, it may be of importance in a child. Therefore, most dentists consider eruption delayed if it goes beyond 12 months from its average time of eruption.

Delayed eruption can be identified if an affected tooth fails to move along the path that has been cleared for it and the normal time for eruption has crossed.

Also, if the tooth is not present in the oral cavity and shows no potential for eruption; the completely formed root of unerupted tooth recognizes condition as late eruption of tooth.

Causes of Delayed Eruption

Delayed or failure of eruption can also occur including a range of medical conditions and genetic alterations. Hindrances to tooth eruption can include bone, unfavorable tongue position, digit sucking habit or other teeth. The obstruction can also be important to the tooth in case if tooth joins to bone. This further result in ankylosis which then prevents further eruption of tooth.

The most common cause of delayed eruption of the upper permanent front teeth is the presence of supernumerary or extra tooth.

Local Conditions Which Can Cause Delayed Eruption

Localized causes can be dilacerations i.e, deformed root, malpositioning of the tooth, crowding, cysts, odontoma, or trauma to the corresponding milk tooth. The most common local cause of delayed eruption is physical obstruction. These can occur as a result of supernumerary teeth, mucosal barrier, and tumors.

Supernumerary (extra tooth) tooth can cause tooth irregularity, displacement, rotation, failure of eruption, or even delayed eruption of associated teeth. The most common supernumerary tooth is the mesiodens which is present between upper front teeth.

Tuberculate type of supernumerary is more common in patients with delayed eruption.

Tuberculate Supernumerary Tooth

Tumors have also been reported to be responsible for delayed eruption.

Disturbances during tooth development for example, Regional odontodysplasia, also called “ghost teeth,” can also lead to delayed eruption. Shapes of teeth are altered. Upper front teeth are most frequently involved. It can occur in either of the jaws and both milk and permanent teeth can be affected.

Severe gingival swelling can be a barrier to tooth eruption. Reasons for this could be hormonal or hereditary, vitamin C deficiency or drugs such as phenytoin.

Injuries to milk teeth have also been implicated as a cause of delayed eruption. Injured milk tooth might fuse with the bone and so this leads to it’s over retention and hence interferes with the eruption of permanent teeth.

X-ray radiation has also been shown to affect tooth eruption.

Normal eruption of the tooth usually resumes once the obstruction is removed

Systemic Conditions Which Can Cause Delayed Eruption

Delayed eruption is frequently reported in patients who are lacking in some essential nutrient. It might influence the eruptive process of tooth. Besides entire body, endocrine gland disturbances also affect human teeth. Hypothyroidism, hypopituitarism, hypoparathyroidism, and pseudohypoparathyroidism are the most common endocrine disorders associated with delayed tooth eruption. Endocrinal disturbances can cause medical delayed teeth eruption.  

In hypopituitarism or pituitary dwarfism, the eruption and shedding of the teeth are delayed along with growth of the body. The dental arch gets smaller thaormal; it cannot accommodate all the teeth, thus irregularity of teeth develops. The roots of the teeth are also shorter thaormal in dwarfism.

It is also common in preterm babies with respect to the milk teeth. In very low birth weight babies, maturation of permanent teeth delays.

HIV patients also reported to have delayed eruption of teeth. Unerupted milk and permanent teeth were more common in Children with cerebral palsy.

Some other systemic conditions such as anemia, renal failure, are also associated with delayed eruption and other abnormalities in dentofacial development.

Medical delayed teeth eruption occurs in these conditions.

Management of Delayed Teeth Eruption

Delayed teeth eruption might be a key indicator of local or systemic pathology. This delay in eruption can influence the precise diagnosis, treatment planning, and timing of treatment for the patient. Thus, it can have a considerable impact on patient’s proper health care.

Management depends on several factors, the most important being the age. Various options include observation, surgical exposure and luxation or removal of any obstacle and lastly extraction of tooth.

Any sort of surgical or orthodontic interventions should be avoided if the tooth is immature for eruption i.e, root formation is not complete. The most preferable method is tooth exposure and luxation. Patient has the most favorable prognosis with this.

Also if molars are luxated before completion of roots, they erupt spontaneously and continue to have their normal tooth development.

Criteria for Treatment of Delayed Eruption of Adult Teeth

There are certain criteria for treatment of delayed eruption of the permanent teeth.

If child’s chief complaint is delayed tooth eruption then the treatment is usually appropriate. Sooner or later, although the permanent tooth may erupt, but it can take up to a full year, and the parents and/or the child may not want to wait this long. Also, children are often the targets for teasing by their peers, so parents request for child’s treatment considering the esthetic grounds and the psychological benefit should not be neglected.

Teeth adjacent to the involved tooth may shift into the empty space and this can also further affect the eruption of tooth.  

The developmental stage of the unerupted tooth root will help in determining its treatment. If the tooth is fully formed and its erupting potential is lost, it will require orthodontic guidance.

Treatment Planning

Exact identification and scheduling of treatment is essential. Once the root tip is fully formed, it loses its tendency to erupt naturally. Therefore, when the cause of delayed eruption is the presence of supernumerary teeth, the unerupted tooth should be exposed.  

Surgical procedures and possible complications can be avoided by early diagnosis which helps to opt most appropriate treatment. After nonsurgical or surgical removal of the supernumerary tooth, the patient undergoes an initial stage of orthodontic treatment. Once the initial stage of orthodontic treatment is complete and sufficient arch space is available, then active treatment to extrude the unerupted permanent maxillary incisor can be started.

Conclusions

In patients with a delayed eruption, careful diagnosis and treatment planning allow the dentist to perform treatment at an early stage, rather than delaying treatment until the permanent teeth is in place.

 

WISDOM TEETH, PERICORONITIS

 

Third molars or wisdom teeth, as they are more commonly known, are the teeth which are most often missing, impacted and with altered morphology. Advances in dental anthropology states that there is a reduction in the number of teeth and size of jaws on evolutionary basis for the past 100000 years. Third incisors, third premolars and fourth molars have disappeared already. At present human third molars or wisdom teeth or wisdom teeth often fail to develop, which indicate that these teeth may be on their way out. Although there are some who advice the early removal of the third molars  or wisdom teeth, many strongly believe that the retention of asymptomatic third molars  or wisdom teeth may be useful in later years as a substitute for badly decayed teeth or may even be useful as a transplant.  

 

Development and Eruption of Wisdom Teeth or Third Molars

There is great variation in the timing of development, calcification, and eruption of third molars or wisdom teeth. Development of wisdom teeth may begin as early as 5 years or as late as 16 years, with the peak formation period at 8 or 9 years. Calcification can start at age 7 years in some children and as late as age 16 years in others. Enamel formation is normally complete between 12 and 18 years and root formation is normally completed between 18 and 25 years. Hellman reported that the average age of eruption was 20.5 years. In 1962, Fanning reported that average ages of eruption of 19.8 years for females and 20.4 years for males. Early formation of third molars  or wisdom teeth is generally regarded as predictive of early maturation but not always of early eruption. Most surveys report that more than 17% of lower third molars or wisdom teeth become impacted. Lower third molars  or wisdom teeth normally have their occlusal surfaces tilted slightly forwards and lingually during early calcification. As the mandible increases in length, with bone resorption at inner angulation between body and the ascending ramus of the mandible, the third molars or wisdom teeth become more upright. In contrast, upper wisdom teeth erupt downwards, backwards, and often outwards. There is, therefore, a possibility of crossbite, but tongue pressure on lower crowns and buccinator pressure on upper crowns will often correct this. If there is a lack of space, theormal eruptive paths cannot be followed, and crossbite can result.

 

Eruptive Pathways of Third molars or Wisdom Teeth

 

Richardson investigated the development of lower third molars  or wisdom teeth between ages 10 and 15 years, using models and four cephalometric radiographs (90 degree left lateral, straight posteroanterior and 60 degree’ left and right lateral views). She found that the angle of the occlusal surface of the lower third molars or wisdom teeth to the mandibular plane was 41 degree on average she found this decreased by 11 degree by age 15. Successful eruption of the lower third molar or wisdom teeth occurs by the tooth continuing to decrease its angle to the mandibular plane and moving occlusally into sufficient space.

 

J .N. Fayad et al in AJO 2004 determined the relationship between the maxillary molar’s sagittal inclination and the eruption of third molars  or wisdom teeth using CT scans. In their study the sagittal inclination of maxillary first and second molars were greater in the subjects with erupted maxillary third molars  or wisdom teeth than in those with impacted third molars or wisdom teeth and particularly in the younger subjects. They concluded that the vertical position of the first maxillary molar in the sagittal plane is a predictor of the eruption of the adjacent third molar and that the sagittal inclination of the maxillary molars increases with age which could be the effect of mesial drift.

 

Kahl et al when valuated ortho pantomograms of orthodontically treated 58 individuals in which the third molar was asymptomatic. He found out that with time some third molars or wisdom teeth became more upright while others showed more inclination either towards the mesial side or the distal side. They concluded that with third molars or wisdom teeth nothing can be predicted. It is not influences by age, amount of space, amount of bone, developmental stage.  

 

Assessment of Space for Third molars or Wisdom Teeth

Shortage of space between the second molar and the ramus has long been identified as a major factor in the etiology of lower third molar or wisdom teeth impaction. Henry and Morant suggested a technique for predicting impaction of lower third molar or wisdom teeth using their third molar space index obtained by expressing the mesiodistal width of the third molar as a percentage of the space available measured on bimolar radiographs, If this index, exceeded a value of 120 for a person at maturity, impact ion could be predicted. This index decreases as the growth continues and the space available increases. Ledyard, studying lateral jaw radiographs, found that less than a 2 mm increase in space between the lower second molar and the ramus could be expected after the age of 14 years and a negligible increase after 16 years. 

 

Ricketts claimed that, if 50% of the third molar crown lies ahead of the external oblique ridge at maturity, there is a 50% chance of eruption. Schulhof in 1976 claimed that growth prediction can estimate the adult dimension from Xi point to the mandibular second molar on a lateral cephalogram taken at the age of 9 years with a standard error of 2.8 mm. Schulhof suggested that lower third molars or wisdom teeth could not be classified as likely to erupt to good occlusion if the Xi point to lower second molar was measured less than 25mm.

 

Richard Olive et al in AJO 81 in a study on dried human skulls, examined the reproducibility of estimates of a space width ratio (space available between lower second molar and the ramus divided by mesiodistal width of mandibular third molar or wisdom teeth) on the lateral cephalogram, rotational tomograms (OPG), intraoral bitewings and 60 degree Cephalograms.

 

 

A template of cellulose acetate was prepared with a right angle T drawn in line through the lips of the most superior, anterior and posterior cusps of the first premolar to second molar section of buccal segment. The template was placed over the radiograph with the horizontal part of the T on the occlusal plane and the vertical pan touching the most distal part of second molar crown. The space available (AB), the mesiodistal width of the lower third moIar (CD) and space width ratio (AB/CD) were computed from the Digitized data. If this ratio is less than 120% then chances of third molar or wisdom teeth impaction are more. The rotational tomogram, intraoral bitewing and 60 degree rotated cephalogram were superior to the lateral cephalogram on the basis of reliability of results and reproducibility of radiograph technique for estimating the space width ratio.

 

The results suggested the difficulties in landmark location on lateral cephalogram. Locating anterior border of the ramus on lateral cephalogram is often difficult, which militates against good reproducibility of results. It was shown that the reliability for the lateral cephalogram technique alone was not as good as for the other techniques. The rotational tomograms yielded the most accurate estimates of space width ratio. Intraoral bitewings yielded the next best estimates.

 

Wisdom teeth or third molars are last teeth to come and can cause problems after they erupt in mouth. Wisdom teeth can cause change in dental structure which can further cause severe discomfort and pain. People may or may not have problems with their wisdom teeth. If wisdom teeth are impacted or are poking the cheeks or they are infected, then extraction of wisdom teeth is done. Most frequently asked questions by patients are enlisted here right from symptoms of wisdom tooth to wisdom tooth extraction and healing.

What are wisdom teeth?

Wisdom teeth are also known as third molars and are present distal to second molars. A person gets 4 wisdom teeth. There is 1 wisdom tooth present in every quadrant. Wisdom teeth are last teeth to erupt in dental arch.

What is the age of wisdom teeth eruption?

Wisdom teeth usually erupt in oral cavity in between the ages of 16-25 years with 17-21 years band being most common. In some people, wisdom teeth may erupt at 30-40 years of age.

When is extraction of wisdom teeth required?

If wisdom tooth is impacted that is there is not enough space for wisdom teeth to erupt, then wisdom tooth extraction is required. Impacted wisdom tooth can cause pain in the jaw and gums and can also cause damage to other teeth. Cyst can also form around wisdom tooth. If wisdom tooth is impacted, then extraction is required for the tooth. Wisdom teeth don’t aid in mastication so if they are infected, no treatment is required for them and tooth can be pulled out.

What is impacted wisdom tooth?

When there is not enough space for wisdom tooth to grow and wisdom tooth remains buried in gums or bone, due to decreased jaw size, then it is known as impacted wisdom teeth. Incidence of patients with at least 1 wisdom tooth being impacted is 16.7%.

What are various types of impactions of wisdom teeth?

Wisdom teeth impaction can either be bony or soft tissue impaction. If wisdom teeth have insufficient space to erupt and they are completely inside the bone, then it is known as bony wisdom tooth impactions and if wisdom tooth grows out of bone but has not erupted because of soft tissue on it, then it is known as soft tissue impaction. Impacted wisdom tooth can either be mesioangular in position, distoangular, vertical or horizontal. Mesioangular wisdom tooth impaction is most common.

What are the symptoms of impacted wisdom teeth?

Pain in gums and jaws, difficulty in mouth opening, swollen or inflamed gums, headache, bad taste in mouth, bad breath, crowding and decay of other teeth are symptoms of impacted wisdom teeth.

My wisdom teeth are erupting and causing severe pain. What can I do for some pain relief?

You can do warm saline rinses 3-4 times a day for some relief. Make sure that there are no food accumulates in back of jaw which can aggravate the pain.  You can avoid eating from side of erupting wisdom tooth and visit a dentist for evaluation. Dentist will take an x-ray to see the positioning of the wisdom tooth. If wisdom tooth is impacted, then surgical tooth extraction of wisdom tooth can be done.

What is Pericoronitis?

Pericoronitis is an acute infection which causes swelling or inflammation of gums and surrounding soft tissues of partially erupted teeth. It usually occurs in lower wisdom tooth area. For treatment of Pericoronitis, debridement of area, operculectomy or tooth extraction is required.

What is treatment of impacted wisdom tooth?

Surgical tooth extraction is done for impacted wisdom tooth. Cut is given on gums and if necessary bone cutting and or tooth sectioning is done to remove the tooth from socket. After surgical tooth extraction, stitches are given after tooth extraction to approximate flap margins.  

Who performs wisdom tooth extraction?

To remove wisdom tooth, mostly surgical tooth extraction is done. Surgical tooth extraction is often performed by an oral surgeon as opposed to a general dentist who mainly performs the simple tooth extraction procedure.

What type of anesthesia is used in surgical tooth extraction?

Surgical tooth extraction can be done after giving shots of local anesthesia. In case of difficult surgical tooth extractions or in patients with dental anxiety, procedure can be done under IV conscious sedation or general anesthesia.

Is Wisdom tooth extraction painful?

No pain occurs during wisdom tooth extraction. Before tooth extraction procedure, to numb the tooth extraction area, local anesthetic shot (Novocain), IV conscious sedation or general anesthesia is given. In case of surgical tooth extraction, cut is given on gums and bone cutting and or tooth sectioning is done to pull the tooth out of socket. After surgical tooth extraction, stitches are given to approximate the flap margins. If tooth is fully erupted in dental arch, then simple tooth extraction may also be done to pull the wisdom tooth out.

What types of stitches are given after wisdom tooth extraction?

In case of surgical tooth extractions or in extractions where much of trauma to the surrounding tissues have occurred, stitches are given. Resorbable or non-resorbable stitches can be given to the patient. Commonly used resorbable stitches are gut, polyglycolic acid and copolymer of glycolic and lactic acid. Resorbable stitches usually dissolve in 7-14 days. Non-resorbable stitches are silk, nylon, polyester or polypropylene. Non-resorbable stitches can be removed by dentist after a week of tooth extraction.  

What are the various complications which can occur during wisdom tooth extraction?

Various complications which can occur during wisdom tooth extraction are:

1.     Injury to nerve during tooth extraction

2.     Root displaced in fascial space

3.     Injury to adjacent teeth during wisdom tooth extraction

4.     Failure of anesthesia during tooth extraction

5.     Laceration of gums and mucosa during wisdom tooth extraction

6.     Tooth fracture or jaw fracture during tooth extraction

7.     Fracture of tooth during wisdom tooth extraction

8.     Jaw dislocation during tooth extraction

What are the various complications which can occur after wisdom tooth extraction?

Prolonged pain, swelling, bleeding and bruising can occur after wisdom tooth extraction. Limited mouth opening and TMJ dysfunction can also occur after wisdom tooth extraction.  Patient may also get burning or numbness sensation after wisdom tooth extraction due to nerve injury during tooth extraction. Osteomyelitis, Osteonecrosis, Ludwig’s angina are rare complications which may occur after wisdom tooth extraction.

Do I need to follow any precautions after wisdom tooth extraction?

After wisdom tooth extraction, take rest for a day. Don’t spit much after wisdom tooth extraction as it can lead to dislodgement of blood clot. Don’t drink anything with straw after 48 hours of tooth extraction and don’t smoke. Take the medicaments as prescribed by the oral surgeon and don’t chew from side of tooth extraction socket. After tooth extraction, you are advised to take soft foods such as mashed potatoes, smoothies and shakes and take more of fluids. You should not brush after 8 hours of tooth extraction and after that, you can brush your teeth gently avoiding area of surgery.

How can I control bleeding after wisdom tooth extraction?

Bleeding can occur up to 3 days after wisdom tooth removal. After third day, quantum of bleeding goes down and bleeding is very less or barely noticeable. Till the bleeding is continuing, one should avoid vigorous rinsing of mouth. To control bleeding, patient can bite on a gauze pack with equal pressure without irritating the tooth extraction socket area too much. After biting on gauze pack for half an hour, gauze pack can be changed. Patient can also bite on moist ice tea bag for bleeding to stop. Tea bags have tannic acid present which will cause vaso-constriction and will stop the bleeding.

After how long will swelling subside after wisdom tooth extraction?

Swelling usually lasts for 4-6 days after wisdom tooth extraction. Normally, the swelling subsides completely in 7 days. Swelling usually becomes pronounced on second or third day after wisdom tooth extraction and then it will subside. If swelling doesn’t reside even after 1 week, then one should call his oral surgeon for check-up. In some cases, swelling goes away initially and then sets in again. It occurs because of secondary infection.

What can I do to control swelling after wisdom tooth extraction?

Intermittent ice application can be done to reduce swelling after wisdom tooth extraction. Ice application can be done during first 24 hours after wisdom tooth extraction. After 1-2 days, heat in form of moist compresses can be applied. Pressure dressing can also be given to control the swelling after wisdom tooth extraction.

How long will healing take after wisdom tooth extraction?

After wisdom tooth extraction, socket may take 3 weeks to 3 months to heal completely depending on the procedure which is used for tooth extraction, angulation of wisdom tooth and amount of trauma to the investing tissues during tooth extraction. Duringhealing of extraction socket, firstly hematoma and clot formation takes place, then granulation tissue formation takes place. After granulation tissue formation, replacement of granulation tissue with connective tissue and then mature bone takes place. Smoking, alcohol consumption, poor nutrition, infection in socket will delay healing process after wisdom tooth extraction.  

What is the cost of wisdom tooth extraction without dental insurance?

There are different pricing for a wisdom tooth extraction. If the wisdom tooth is fully erupted, then tooth extraction will cost you in the range of $150 to $300. However, in the case of it only half erupted or impacted then the cost could be as much as $350 to $650. Extraction of a wisdom tooth requires more time and skill so the cost can be more. This fee is inclusive of all the follow up visits and the whole surgical procedure. Costs of initial consultation, X-rays and sedation will be additional. All in all, surgical wisdom tooth extraction costs about $1000 inclusive of all the costs.      

What is cost of wisdom tooth extraction with dental insurance?

Most dental plans cover for wisdom tooth extraction. Dental insurances cover 70-80% of cost of wisdom tooth extraction.  

Can wisdom tooth extraction be done during pregnancy?

Most of the obstetricians and gynecologists believe that wisdom tooth extraction can be done during pregnancy. Wisdom tooth should be removed with minimum of trauma during pregnancy. Antibiotics and pain pills may be prescribed by the dentist to reduce the infection and pain which can stress both mother and baby. Wisdom tooth Extraction should be done in the second trimester which is the safe period of pregnancy.

Pericoronitis is an acute infection which causes swelling or inflammation of gums and surrounding soft tissues of a partially erupted tooth. Pericoronitis usually occurs in lower wisdom tooth area. Wisdom teeth usually erupt in late teens. When there is not enough space for wisdom tooth to erupt, then tooth becomes impacted.  Wisdom tooth may be partially or completely impacted. A flap of gum tissue is created in partially erupted wisdom tooth where food impaction can occur. Soft tissue flap covering partially impacted tooth is known as operculum. Entrapment of food below operculum or injury by the opposing tooth on operculum can lead to Pericoronitis.  When the flap becomes inflamed and swollen, then it is known as Pericoronitis. Pericoronitis can also occur in relation to completely impacted wisdom tooth or partially impacted wisdom tooth.

 Signs and Symptoms of Pericoronitis

1.    Gum tissues in relation to partially impacted tooth become swollen and inflamed.

2.    Gum tissue will appear red and pus will discharge from gums in relation to tooth. Pus can result in increase in bulk of flap and can interfere with jaw closure.

3.    Lesion will be extremely tender and painful and pain may also radiate to ear, throat and floor of mouth.

4.    Bad taste and bad odor is present from oral cavity.   

5.    Patient will have difficulty in swallowing and will have difficulty in closing the jaws. Pain will aggravate on biting from opposite tooth as it will cause trauma to the flap present around the affected tooth.  

6.    Swelling of cheeks may also occur in Pericoronitis.

7.    Swelling of lymph nodes (Submandibular lymph nodes) and jaw muscles spasm may also occur in Pericoronitis.

8.    Fever, increase iumber of white blood cells (Leucocytes) and malaise indicate sever infection.

Diagnosis of Pericoronitis

Pain, swelling and redness in relation to partially erupted tooth will diagnose Pericoronitis.

Treatment of Pericoronitis

Treatment of Pericoronitis depends on many factors.

Treatment depends on:

1.   Severity of swelling which is present

2.   Whether  the involved tooth is to be extracted  or not and

3.   Whether systemic complications are present or not.

Debridement of area is done by cleaning the area. Flap is raised and pus and debris is removed by rinsing with water after giving topical anesthesia to the patient. If severe acute symptoms are present, then antibiotics are also prescribed to the patient to reduce the infection.

Patient is instructed to do hourly rinses with solution of tea spoonful of salt in glass of warm water. Patient should take more of fluids and should maintain good oral hygiene to avoid any food accumulates in wisdom tooth area. Patient should brush and floss properly to avoid any food deposits. Food deposits will aggravate the pain. Pericoronitis infection can regress in duration of 5-7 days. If tooth doesn’t erupt completely, then food accumulates will keep depositing below the gums and can cause Pericoronitis to recur.

Before                                             After

Operculectomy that is surgical removal of flap over partial erupted tooth can also be done in case of Pericoronitis.      

Dentist may or may not remove the involved tooth. Dentist will do examination and will make out that whether tooth can completely come or not.  If the tooth can erupt completely without any complication, then dentist may not do tooth extraction.

If tooth is to be retained and is not to be pulled out, then surgical procedures using periodontal knife or electro-surgery may also be required. After giving anesthesia to the patient, to remove the tissue, wedge shaped cut is made on gums. Periodontal pack is given after tissue removal.

Pericoronitis Home Remedy

1.    In initial stage of Pericoronitis, patient can do rinses with solution of tea spoonful of salt in glass of warm water. Rinse with this solution 2-3 times a day.

2.    Patient should brush his teeth after meals to remove the left over food particles in mouth. Food particles present over involved tooth site will aggravate the pain. 

Prevention of Pericoronitis

To prevent chances of Pericoronitis, patient should maintain good oral hygiene by brushing and flossing regularly. This is done to avoid deposits under gums. If Pericoronitis reoccurs, then flap of gum tissue is removed by the dentist. Flap of gum tissue may grow back again and in that case, extraction of wisdom tooth is required.

 
When to Consult an Oral Surgeon

If symptoms of Pericoronitis are present, then patient should visit his oral surgeon. If patient’s wisdom teeth are erupting, then he should visit his dentist twice a year for examination.

Complications of Pericoronitis

1.    It may become localized in form of pericoronal abscess.
2.    Cyst formation can occur in case of partially erupted vital tooth.
3.    Pericoronitis can cause difficulty in swallowing if it spreads to back soft tissue.
4.    Peritonsillar abscess formation, cellulitis, Ludwig’s angina are infrequent but can occur as a complication of Pericoronitis.  

If the involved tooth erupts completely or it is removed, then condition will not recur.

Third molar or wisdom Teeth retention may be beneficial in many situations. Some investigators maintain that third molars or wisdom teeth or wisdom Teeth could be used at a later date as replacements or for prosthetic abutments in case of loss of first and second molars. Third molars or wisdom teeth or wisdom Teeth could also be used as transplants. In shallow mesio angular impactions Richardson used a one stage method. A second molar tube caormally be bonded onto the buccal aspect of a partly erupted lower third molar, if enough enamel is visible. It is then possible to include the tooth in full treatment, if other teeth are already bonded and bracketed. If the case is not fully banded, then lower second or first molars alone can be used with a lingual arch for support.

 

In deep mesio angular impactions, a two stage method is used. If it is not possible to bond onto the buccal surface, a different technique is used which can be delayed until 18 -19 years of age to allow time for the tooth to improve its position. The first stage involves bonding a second molar tube onto the occlusal surface of the lower third molar. The hook is removed from the tube, before bonding. Lower first or second molars are banded with a lingual arch, using first molar bands and brackets. A small sectional archwire with a compressed coil spring, is used to provide a distalizing and up righting force to the crown of the impacted molars. After some up righting using this method, it is normally possible to bond a tube buccally for the second stage.

 

Ike Siodov et al in AIO 89 describes an orthodontic up righting technique similar to ‘Sling shot ‘ appliance described by Moyers and by Profitt. Modified impaction related surgical procedures provide easy application of techniques to facilitate exposure of unerupted and partially erupted third molars or wisdom teeth or wisdom teeth and allow orthodontic manipulation.

 

After surgical exposure a cleat is bonded in center of mesial marginal ridge. The wire port ion of the appliance is fabricated from0.032 inch stainless steel wire and adapted closely to the mucosa. The mesial hook is placed 3 mm distal to the distal portion of the third molar. Standard soldering techniques are used to attach the wire to the buccal (or lingual) surface of the band. Appliance is cemented in place and is activated with elastic modules.

 

By manipulation of the distal arm of the appliance either buccally or lingually, depending on the desired movement, teeth can be directed or rotated with some effectiveness. Variation can also be accomplished by alteration of the bond position of the cleat. Following activation, rapid up righting and distalisation will occur in 3 to 6 months in most cases. Grinding of occlusal surface is not necessary. When the third molars or wisdom teeth or wisdom teeth are upright, the appliances are removed and the third molars or wisdom teeth or wisdom teeth are banded, leveled and aligned with the rest of the teeth.

 

This procedure is contraindicated when the molar to the uprighted has no antagonist or is severely malformed or is abnormally large or small, and it should he done carefully when there is a tendency for open bite.

 

 

Advantages of Uprighting Impacted Third molars or Wisdom Teeth 

1.    Ease of fabrication and manipulation.

2.    Rapid treatment.

3.    Little discomfort.

4.    No demands for patient cooperation.

 

Orton and Jones in JCO 87 described a simple whip spring that is unobtrusive and fairly fast acting with a treatment time of 4 to 12 months. It is used for disimpacting mild to severe mesially impacted lower terminal molars (LTM). LTM crown must be accessible for an edgewise tube preferably on a band. Partial seating of the band on the mesial surface is acceptable at first, which can be fully seated as correction proceeds. If the impacted molar has not sufficiently erupted then surgically expose distobuccal surface and bond an attachment.

 

The whip spring is fabricated with 0.018 x 0.025 wire for 0.022 slot and 0.017 x 0.022 wire for 0.018 slot. A circular loop is placed mesial to the tube to prevent posterior displacement of the wire and to provide attachment of an elastic module that anchors the wire in the tube. Wire extends mesially from the loop. A vertical bend is pieced occlusally next to the midbuccal fissure of the anchor molar. The wire is curved lingually to pass through the midbuccal groove onto the occlusal surface. It is then contoured distally to run along the occlusal surface. Moving the whip to the occlusal surface of the anchor molar activates the appliance. The whip spring can be reactivated in the mouth by lifting the wire away from occlusal surface and gently squeezing the arm of the spring between loop and vertical bend with Tweeds loop forming plier. After initial adjustment of 3 to 4 weeks, adjustments every 6 weeks seem to be adequate. Over correction is advised.

 

The force of the whip tends to extrude the impacted molar and intrude the anchor molar. If there is too much intrusion of anchor molar, a new whip can be made that extends to another anchor tooth. The couple tends to disimpact the LTM by a combination of distal crown tipping and mesial root movement, resulting in root paralleling of the molars.

 

If the vertical development of the LTM is impeded by an upper molar, then the over erupted upper molar must be intruded by a removable appliance with an intrusive arm. 

 

Replacement of Third molars or Wisdom Teeth for Second Molars

During growth o f maxilla, space to accommodate the erupting first, second and third molars or wisdom teeth or wisdom teeth must be created by growth in the posterior region of the tuberosity. The maxillary growth in this area must normally be downward and forward to create room for the eruption of each succeeding molar. If growth in this region is insufficient, abnormal eruption or lack of eruption will be the result. According to Malcolm R Chipman in AJO 1961 the third molars or wisdom teeth or wisdom teeth can be substituted for the second molars in certain situations and solve some of the problems of maxillary tuberosity area. The indications for eliminating maxillary second molar and replacing it with third molars or wisdom teeth or wisdom teeth are: 

 

1.    Maxillary third molars or wisdom teeth or wisdom teeth are of fair size and shape with the possibility of good root development.

2.    Small, restricted maxillary tuberosities and the possibility of interference with distal movement in maxillary posterior region.

3.    Second molars erupted buccally.

4.    Second molars are decayed, badly decalcified or having large restorations.

5.    Maxillary third molars or wisdom teeth or wisdom teeth in favourable position and angulation relative to second molars and maxillary tuberosity.

6.    Maxillary third molars or wisdom teeth or wisdom teeth in favourable relation to mandibular second molars.

7.    Desirability of relieving the anchorage unit s of an overload.

 

The replacement of maxillary second molar will be considered in both Class I and Class II malocclusions. The contraindications for substitutions are:

 

1.    Maxillary third molars or wisdom teeth or wisdom teeth too high in the tuberosity.

2.    Maxillary third molars or wisdom teeth or wisdom teeth too low in relation to the second molars.

3.    Poor angulation in relation to second molar and the tuberosity.

4.    The possibility of third molars or wisdom teeth or wisdom teeth involving maxillary sinus.

5.    Small, odd shaped third molars or wisdom teeth or wisdom teeth or an indication of the formation of small roots.

 

There is a great variation in the time of development of third molars or wisdom teeth or wisdom teeth and this together with the amount of development in the tuberosity region, has a bearing on the decisions to be made in the event of a needed maxillary distal movement and a possible replacement of the second molar by third molar. For this reason the dental age as evidenced by the development of dental components, must be given as much considerations as chronological age.

 

The shape of third molar crowns is also considered. Small crowns with narrow width at the cervical margiot lend themselves to development of normal sized roots. Many third molars or wisdom teeth or wisdom teeth have odd shaped crowns with irregular cusp formations, and, while occlusal grinding frequently is needed, there is a limit to its use and these teeth cannot be recommended.

 

During its eruption following a second molar extraction, the third molar rotates or tip mesially as it descend. The amount of rotation is directly associated with the degree of angulation. The greater the degree of angulation, the greater is the amount of rotation, with the center of rotation being based on root apex. This rotation together with the downward and forward path of eruption is a major factor in determining when the second molar extraction may be planned. The ideal condition calls for the descending

third molar to come into contact with the maxillary first molar and into occlusion with the mandibular second molar at the same time.

 

In a Class I malocclusion, the third molar should have descended to the extent that the occlusal surface is approximately level with the vertical mid line of second molar root and the mesial surface of unerupted third molar is fairly in line horizontally with the distal

surface of mandibular second molar. Following extraction of second molar, the third molar will then descend in a downward and forward arc, rotating into contact and occlusion at the same time. If third molar is at a much higher point there is a possibility of impaction or premature cont act, before occlusion is attained. If it is at a lower level in relation to second molars, it is likely to erupt into occlusion before contact is established with first molar, resulting in open contacts and poor interproximal situations. In Class II malocclusions, the crown of maxillary third molar is horizontally advanced in relation to the mandibular second molar. In Class II cases in which second molar is to be extracted, the most ideal location of third molar is approximately at the junction of crown and root of second molar. The angulation of maxillary third molars or wisdom teeth or wisdom teeth to the plane of occlusion and their relation to the tuberosity must be carefully considered. The usable angulation will range from 0 to +30 degree (Distal tip) to occlusal plane.

 

Orton-Gibbs et al in AJO 2001 described the eruptive path of maxillary and mandibular third molars or wisdom teeth or wisdom teeth after extraction of second molars with the use of radiograph and assessed the final position from study models. They showed that the angulation o f the mandibular. Third molar crown long axis showed progressive uprighting from a mean of 55 degrees to the occlusal plane at the start of active treatment (SAT). Uprighting of mandibular third molars or wisdom teeth or wisdom teeth from SAT to end of active treatment (EAT) was limited (mean 6 Degrees). However the third molars or wisdom teeth or wisdom teeth continued to upright thereafter on average a further 13 degree. Clinically it is important to note that EAT radiographs will not give a true picture of the likely final mandibular third molar angulation. Approximately 50% of the space closure occurs by EAT. Interestingly space closure is not a result of mesial tipping but is due to significant horizontal translation. The relationship of the first and the third molar crown should be the most important indicator of successful outcome, not angulation of the whole tooth. The results confirm findings by Dacre and Richardson and Richardson that the original angulation of the third molar is not a reliable predictor of outcome for third molar position.

 

In contrast to the mandibular third molars or wisdom teeth or wisdom teeth, the maxillary third molars or wisdom teeth upright rapidly by 14 degrees on average, from SAT to EAT. Angular changes are minimal as the maxillary molars settle into occlusion. The rate of vertical change is rapid, with almost 7 mm of eruption occurring by the completion of active treatment and a further 6 mmafter active treatment.

 

The third molars or wisdom teeth in the study were invariably in a position that maintains a good functional occlusion. The periodontal health of the sample was excellent. There was no correlation between third molar position and the presence of gingivitis or periodontitis. The results showed that relief of crowding by removal of second molar is a realistic option in appropriate cases with mild to moderate crowding, particularly in patients in whom third molar impaction is predicted and in reducing the likelihood of increasing crowding through the teenage years.

 

Auto Transplantation of Third molars or Wisdom Teeth

Auto transplantation of teeth has become an accepted and reliable treatment modality in patients with early loss of teeth or aplasia. According to William Northway in AJO 80 autogenic tooth transplantation can give the concept of space management a much broader horizon. Third molars or wisdom teeth have been frequently used for transplantation. These teeth, which are often extracted, have served well as replacements, for cariously destroyed first molars. Their root development which continues into the late teen s and twenties makes these teeth suitable for use into adulthood. The last tooth in the arch may offer better access for removal and it is essential that the root not be damaged in any way during its relocation. The prognosis for successful transplantation is diminished as the root apex nears closure. Revascularisation must take place. While post operative resorption is rarely reported, the effective reduction in root length is minimized by allowing adequate development prior to transplantation. Hale believed that the most favorable time for transplanting was at 3 to 5 mm of root formation. Apfel stressed the need for delaying transplantation until after furcation formation. Andreasen, Baum, Peskin and Guralnick have contended that the results will be maximized if the operations are performed sometime between one third and three fourth of completion of root formation.

 

Proper alveolar architecture is essential for housing the transplant. The recipient site should be covered with adequate attached, keratinized tissue to allow proper coverage or approximation to the transplant and it should be free of chronic inflammation. Mesiodistal space deficiencies be eliminated prior to the surgical procedure, either by orthodontic means or by slicing of adjacent teeth. Also there should be adequate Iabiolingual width on the ridge to accommodate alveolar plates on both surfaces. 

 

Surgical Procedure for Transplantation of Third Molar or Wisdom Tooth

A full thickness muco-periosteal flap should be employed, allowing adequate exposure for atraurnatic preparation of the recipient site. A very gentle handling of the soft tissue is ensured. The socket is prepared with bone burs and rongeurs. Once the socket is judged to be of adequate depth and circumference, a trial insertion of pre sterilized dummy tooth can be made. Ideally, the preparation of the recipient site will allow insertion deep enough that the cusp tips will be at or apical to the alveolar crest height. This allows eruption and hence roots formation postoperatively. Now the transplant can be removed. Again, adequate flaps allow exposure and a minimum of trauma. With gentle manipulation of surgical instruments, the dental follicle is removed from around the crown. The tooth is removed and transferred immediately to the previously prepared crypt. It is preferable that the tooth be manipulated only by its crown. In the event that buccolingual width does not allow proper placement, it can he inserted in a rotated position. This wiII allow preservation of alveolar crest and the tooth can later be repositioned orthodontically as desired. Muco-periosteal flap is repositioned and sutures are placed over the crown to hold the tissues together and tooth in its crypt. After a week or 10 days sutures are removed and direct bonded stabilization can be employed for up to 6 weeks.

 

Oskar Bauss et al in AJO 2004 in their study determined the influence of orthodontic tooth movements on pulpal and periodontal conditions in transplanted immature third molars or wisdom teeth. The indication for transplantation was aplasia of premolars or early loss of molars.

 

In patients with horizontal atrophy of alveolar process with narrow alveolar ridges and unfavorable root morphology, transplants were placed in 45 to 90 degrees distally rotated positions. Derotation to a correct position in the dental arch was performed with

a couple of forces. The initial rotational force varied between 200 to 300 grams/mm. Mean rotation time was 12weeks. After complete derotation, all transplant s were integrated into a fixed appliance for leveling and approximal space closure. Average Orthodontic treatment time was 15.2 months.

 

In vertically atrophied jaw sections, transplants were fixed in distinct infraocclusion (average 5.1 mm). Transplants were leveled to the occlusal plane before closing the approximal spaces. Mean orthodontic treatment time was for 14.4months.

 

For determining pulpal and periodontal conditions, clinical and radiologic examinations were carried out. Autotransplanted third molars or wisdom teeth without subsequent orthodontic treatment had the best pulpal and periodontal results. All transplants were at the developmental stage with their open apices providing a high chance of pulp revascularization.

 

The results suggest that orthodontic extrusion and minor lateral tooth movement have no harmful effects on the pulpal and periodontal condition of autotransplanted immature third molars or wisdom teeth. Atrophy of the alveolar process did not affect pulpal and periodontal healing of the transplants in the extrusion group. A certain amount of spontaneous eruption had occurred in most patients by the time orthodontic treatment began. The formation of new alveolar processes wasobserved during subsequent orthodontic treatment.

 

Revascularisation started on the fourth postoperative day with an in growth of new vessels and was usually completed after 30 days, with the entire pulp containing new vessels. In contrast to pulpal revascularization, first signs of pulpal reinnervation cannot be demonstrated until at least a month after transplantation and are limited to the apical part of the pulp. Even after 2 years, the restored pulpal nerves are described as sparse, and the new axons are small in diameter. By postponing the onset of orthodontic treatment to the third to sixth month after transplantation and slower derotation of multi rooted transplants might increase the success rate.

Archer defined an impacted third molar or wisdom teeth as ‘One which was completely or partly erupted and positioned against another tooth, bone or soft tissue, so that its further eruption was unlikely. Dachi and Howell in their study found that the incidence of patients with at least one impacted tooth was 16.7%. Teeth most often impacted in order of frequency were the maxillary third molars or wisdom teeth, mandibular third molars or wisdom teeth, maxillary canines and mandibular premolars. No sex differences were noted. Bjork and colleagues identified 3 skeletal factors that are separately influencing third molar impaction.  

1)   Chances of impaction are more if the mandibular length is reduced which is measured from chin point to the condylar head.

 

2)   It is also influenced by the condylar growth. If condylar growth is in vertical direction, which is shown by mandibular base angle the chances of impaction are more.

 

3)   Backward directed eruption of mandibular dentition determined by the degree of alveolar prognathism of lower jaw. 

Types of Impaction of Wisdom Teeth or Third Molars  

Richardson suggested five categories of impaction.

 

Type A: The tooth can follow the pattern of an ideally developing third molar, by decreasing its angle to the mandibular plane and becoming more upright, but the up righting may not be enough to allow full eruption.

 

   

Type B: The angular developmental position relative to the mandibular plane may remain unchanged.

 

Type C: The tooth can increase its angulation to the mandibular plane and become more mesially inclined. There is at present no reliable way of predicting which teeth will follow this unfavorable pattern, which sometimes occurs unilaterally and leads to horizontal impaction.

 

Type D: The tooth can be seen to make favorable changes in angulation, but fail to erupt owing to lack of space. These are so called vertical impactions.

 

Type E: The tooth can continue to change its angulation beyond the ideal occlusal position, and show distoangular impaction or mesio angular impaction.

 

 

 

How Third molars or Wisdom Teeth Erupt and become Impacted

Differential root elongation might explain differences in eruptive behavior among lower third molars or wisdom teeth. Richardson offered a theoretical explanation for favourable or unfavourable rotational movement. Favorable change in angulation, to a more upright position, seemed to occur in teeth where the mesial root developed ahead of the distal crown surface and root. The typical root configuration showed a mesial root which was curved in a distal direction and was slightly longer than the distal root. Unfavorable mesial tipping, leading to horizontal impaction, seemed to occur when the distal root became the same length, and then longer than the mesial root. Th e distal root on such teeth was seen to appear to have a mesial curvature. 

 

What Influences Availability of Space for Eruption of Wisdom Teeth

Growth

 

Bjork et al measured the distance from the anterior border of the ramus to the second molar and concluded that the bigger the space, the better the chance of eruption. Richardson measured an average of 11.4 mm of growth between the age of 10 and 15 years.

 

Bone Resorption

 

In 1987 Richardson examined the creation of space for third molars or wisdom teeth in 51 patients and found that increased space was obtained from both the mesial movement of the dentition and bone remodeling along the anterior border of the ramus. On an average 2 mm of posterior space was created by bone remodeling.

 

Space Released by Attrition

 

In so called primitive dentition, where considerable attrition takes place, the third molars or wisdom teeth erupt to take up the space released. Begg felt that lack of this attrition due to highly refined diets, was a major cause of third molar impaction. Other authors such as Profitt have questioned this hypothesis. Early and extensive interproximal caries could also reduce the size of erupted teeth owing to disappearance of proximal contacts.

 

Second Molar Extraction

 

Richardson and Richardson in AJO 93 investigated 63 patients after extraction of lower second molars and found that all the lower third molars or wisdom teeth erupted more or less successfully after an average observation period o f 5.8 years. There was considerable variation in the time taken for eruption, ranging from 3 to 10 years and Richardsooted that it is not possible to predict how long eruption will take.

 

Bonham Magness in JCO 86 suggests that upper third molars or wisdom teeth have a much more predictable eruption pattern than lower third molars or wisdom teeth. He suggested the extraction of upper second molars in some cases to assist first molar positioning and increase space for upper third molars or wisdom teeth or wisdom Teeth.

 

Tae-Woo Kim et a l in AJO 2003 confirmed the findings of Faubion and Kaplan that impaction of mandibular third molars orwisdom teeth or wisdom Teeth occurs about twice as often in non extraction patients than in extraction patients. The mechanism may be that premolar extraction therapy is associated with an increase in the amount of mesial move ment of the maxillary and mandibular molars and an increase in the eruption space for the third molars or wisdom teeth or wisdom Teeth. Cephalometric growth studies suggest two important mechanisms for development of the retromolar space in the mandible. Resorption at the anterior border of the ascending ramus and the anterior migration of the posterior teeth during the functional phase of tooth eruption. More than 60% of the patients in the study with a distance of 23 mm or less from the distal of the mandibular second molar to the Ricketts’ Xi point at the end of the active treatment experienced eruption of the mandibular third molars or wisdom teeth or wisdom Teeth. The retromolar space can increase about 2 mm from age 15 to adulthood. They also showed that as many as 60% of the cases with distance from the anterior border of the ramus to the distal of the second molar of 5 mm or less experienced eruption space associated with a high risk of impaction might be smaller than previously suggested.

Following are the instructions which need to be followed by patients to avoid the complications after extraction of wisdom teeth and for faster healing.

Rest – Try to take some rest. You may feel great but don’t exercise at least for a day. When taking rest, keep your head lifted on a pillow

Do Not Chew from Extraction Side – Chewing of food from the side of extraction should be avoided as this can irritate the extraction wound which can cause bleeding and dislodgement of the clot and the infection. It is instructed to take liquid or semisolid diet.

Spitting – Do not spit for minimum for 24 hours because it can dislodge the clot. If the clot is dislodged you can have very painful condition known as dry socket. Afterwards one should spit 3-4 times in a day so that no food is lodged near the area where the tooth is removed.

No Smoking for 48 Hours – In smoking sucking action is involved and this can cause the dislodgement of the clot and can be the major cause of the dry socket which is a very painful condition.

No Sucking – Avoid sucking of any type. Do not drink anything with straw for 48 hours.  

Avoid Eating Hard Foods – Try taking soft and liquid food options such as soups, mashed potatoes, yogurts, milkshakes, smoothies etc. Avoid hot drinks, spicy foods, sodas, etc. Remember to take plenty of fluids.

Brushing – It is advised not to brush your teeth for the first 8 hours after surgery. After that one may brush one’s teeth but very gently, avoiding the area of surgery.

Warm Saline Rinses & Mouth Wash – Use of any kind of mouth washes or rinses should be done for first 24 hours as it can cause the dislodgement of the clot which is very essential for the proper healing of the extraction socket. After 24 hours one can use warm saline rinses or the mild antiseptic mouth wash as prescribed by the dentist. Warm saline rinses and mouthwash should be done gently and not vigorously.

Take your medicines as prescribed by your dentist. Don’t skip the medicines. If antibiotics are prescribed then they should be taken regularly. Pain killers and anti-inflammatory drugs help in reducing the pain and swelling.

There are certain problems related to removal of wisdom teeth, which the patients who undergo the surgical extraction of wisdom tooth have to face. These problems are not complications but are general ones which almost every body has to face. However if the patient is aware of these problems before hand then it becomes easier for them to minimize their effects and also helps mentally for the patients. These problems can sometimes lead to complications if not addressed properly like severe infection in the extraction site. However one can meet all the problems effectively by carefully following the instructions of dentists.

Bleeding after Wisdom Tooth Removal

The most important thing after the extraction of wisdom teeth is the formation of clot at the extraction site. Till then the bleeding and oozing of blood from there is common. This bleeding can occur up to 3 days after the removal of wisdom tooth; however after 3rd day its quantum goes down and should be very less or barely noticeable. Till the bleeding is continuing, one should avoid vigorous rinsing of the mouth as it can dislodge the colt formed at the extraction site. One should gently start doing warm saline rinses 2-3 times a day after 24 hours of extraction of wisdom tooth as it helps in faster healing of the wound. These should be continued till the healing is completed. This should stop the bleeding. But sometimes it does not stop. In such cases one can take sterilized gauge piece and gently bit down on it with equal pressure. This helps in stopping the bleeding. This should not be overdone as this can irritate the wound. After biting down for half an hour, when gauze piece is changed, there should be noticeable reduction in the bleeding. Another more effective way is to take iced tea bag instead of gauze piece as the tannic acid in the tea bag helps more in reducing the bleeding from wound. All the steps help in reducing the bleeding and oozing. However where in spite of all these steps it does not stop or reduce after one day then one should contact the Oral Surgeon as this is not normal and good and there can be some other reason for the same. During the period of formation of clot in the exposed extraction site of wisdom tooth and coupled with presence of bacteria in the mouth, one can have bad smell coming from there shortly after the surgery. Further this can be accompanied by bad tasting fluid seeping from extraction site. This bad smell and fluid can continue upto maximum 2 weeks after the surgery. All these increase the importance of follow up appointment with dentist within 7-10 days of surgery.  During this visit if the dentist feels that the infection has set in the extraction socket then he gently uses a plastic syringe without the hypodermic needle and fills it with a mixture of equal parts of hydrogen peroxide and water or Chlorhexidine Gluconate which also comes in the form of a mouth wash, into the sockets to remove any food or bacteria that may have collected in the back of the mouth.

Infection after Wisdom Tooth Removal

This is the most common complication after extraction. Our mouth is full of bacteria. One cannot sterilize it. Dentist decides whether to give antibiotics after the extraction or not. Usually for the simple extractions antibiotics may not necessary but in the case of patient having pain and swelling or pus then the dentist prescribes the antibiotics as a preventive measure.  In cases where bleeding continues after 48 hours along with acute pain and swelling, there could be infection after the extraction. In such cases the patient must contact dentist to avoid further complications.

Swelling after Wisdom Tooth Removal

Swelling is another common problem after the extraction of wisdom tooth. Rather the painful swelling is a good sign and is indicator of normal progress of healing process of wound. There is no fixed time frame for its duration and level of severity. These can be different from person to person. To reduce the amount of swelling one can do cold fermentation with ice. It should be done for 20 minutes and then take break of 20 minutes. Do this for one hour within 12 hours of surgery. Do not do hot fermentation.  The post operative instructions of the dentist explain all this including the start and reduction of swelling. Normally it takes 7 days for swelling to subside and if this does not happen within this expected time then one should call up the dentist to checkup. In cases where swelling once goes away and then sets in again, this can be due to infection in the wound.

Dry Socket after Wisdom Tooth Removal

Dry Socket is also one of the most common complications of wisdom tooth extraction. It is a very painful condition. In dry socket condition the pain is acute and it does not subside even after taking pain killer tablets and to complicate further food gets impacted in the socket. It happens when the blood clot formed over the extraction site gets dislodged or does not form or falls of prematurely. Dry Socket is not an infection rather it is a condition. This happens when the post extraction instructions given by the dentist are not followed by the patient. Smoking, drinking with straw, sucking, spitting or blowing nose dislodges the clot. Females taking contraceptives have higher risk of getting dry socket due to the high level of estrogen. Further sometimes sneezing, musical instruments played with mouth also can disturb the clot due to change in pressure in the mouth. In the cases where the patients are smokers or in the case of complicated extractions involving lot of effort on the part of dentist for cutting the bone or in the case of patients having previous history of dry socket, the chances of their having dry socket are higher than others. When all the symptoms are present and the patient suspects of having dry socket then he should contact the dentist. The dentist will clean the extraction socket and induce fresh bleeding for formation of clot. In case of infection, the antibiotics are prescribed along with pain killers.

Nerve Injury after Wisdom Tooth Removal

When the wisdom tooth is extracted by the dentist/Oral Surgeon, they have to be cautious so that to avoid the injury to nerve as these can be in close proximity to the tooth being extracted. The nerves of major concern are Inferior Alveolar Nerve and Lingual Nerve. The importance of these nerves is as under:

Inferior Alveolar Nerve – This nerve enters the mandible at the mandibular foramen and exits the mandible at the sides of the chin from the mental foramen. This nerve supplies sensation to the lower teeth on the right or left half of the dental arch, as well as sense of touch to the right or left half of the chin and lower lip.

Lingual Nerve – This nerve branches off the mandibular branches of the trigeminal nerveand courses just inside the jaw bone, entering the tongue and supplying sense of touch and taste to the right and left half of the anterior 2/3 of the tongue as well as the lingual gingiva. Such injuries can occur while lifting teeth but are most commonly caused by inadvertent damage with a surgical drill. Such injuries are rare and are usually temporary. Depending on the type of injury they can be prolonged or permanent.

Dental health and pericoronitis

Pericoronitis is a dental disorder in which the gum tissue around the molar teeth becomes swollen and infected. This disorder usually occurs as a result of impacted or partially erupted wisdom teeth, the third and final set of molars that most people get in their late teens or early twenties.

What causes pericoronitis?

Pericoronitis can develop when wisdom teeth only partially erupt (break through the gum). This allows an opening for bacteria to enter around the tooth and cause an infection. In cases of pericoronitis, food or plaque (a bacterial film that remains on teeth after eating) may get caught underneath a flap of gum around the tooth. If it remains there, it can irritate the gum and lead to pericoronitis. If the pericoronitis is severe, the swelling and infection may extend beyond the jaw to the cheeks and neck.

What are the symptoms of pericoronitis?

Symptoms of pericoronitis can include:

• Pain

• Infection

• Swelling in the gum tissue (caused by an accumulation of fluid)

• A “bad taste” in the mouth (caused by pus leaking from the gums)

• Swelling of the lymph nodes in the neck

• Difficulty opening the mouth.

How is pericoronitis diagnosed?

Your dentist will examine your wisdom teeth and how they are coming in, and see if any are partially erupted. He or she may take an X-ray periodically to determine the alignment of the wisdom teeth. Your dentist will also take note of any symptoms such as swelling or infection, and will check for the presence of a gum flap around a wisdom tooth.

How is pericoronitis treated?

If the pericoronitis is limited to the tooth (for example, if the pain and swelling has not spread), treat it by rinsing your mouth with warm salt water. You should also make sure that the gum flap has no food trapped under it.

If your tooth, jaw and cheek are swollen and painful, see your dentist right away. He or she can treat the infection with antibiotics (usually penicillin, unless you are allergic). You can also take pain relievers such as aspirin paracetamol or ibuprofen.

If the pain and inflammation are severe, or if the pericoronitis recurs, oral surgery to have the gum flap or wisdom tooth removed may be necessary. Your dentist can make the appropriate referral to the oral and maxillofacial surgeon. A low-level laser can be used to reduce pain and inflammation associated with pericoronitis.

Pericoronitis is a dental disorder wherein the gum tissues around the molar tooth become infected and swollen. This problem occurs when wisdom teeth is only partially erupt. This partial breakthrough of gum leaves opening for bacteria and causes infection. The possible causes of pericoronitis are poor hygiene and mechanical trauma on molar tissues that can cause inflammation.

When plaque or the bacterial layer (that remains on teeth after brushing) gets into flap of gums around teeth, it irritates the gums and leads to pericoronitis. In the severe stages of pericoronitis, swelling and infection extends beyond the jaw and also effect neck and cheeks.

 

Symptoms of Acute Phase of Pericoronitis

In its early stage pericoronitis is very similar to normal teething. The main symptoms of acute phase of pericoronitis include:

• Severe throbbing pain.

• Extra oral swelling

• Restricted mouth opening.

• Purulent discharge from pericoronal space.

• Halitosis, leucocytosis and malaise are also common in some cases of pericoronitis.

• In addition patient may also notice sloughing or ulceration around the operculum.

When the infection gets spread in sublingual and para- pharyngeal spaces then Dysphagia occurs. The person has difficulty in swelling food.

 

Symptoms of Sub-Acute Phase Pericoronitis

In the sub-acute phase of the systematic symptoms of pericoronitis become less acute.

• Jaw stiffness.

• Pus discharge.

• Swelling.

• Lymphadenopathy (in some cases)

Symptoms of Chronic Phase of Pericoronitis

Systemic features completely vanish till the chronic stage of pericoronitis, except for the state of severe exacerbation. In chronic phase of pericoronitis, patient report dull pain and bad taste in oral cavities.

• Dull pain.

• Unpleasant taste.

When intraoral periapical radiographs one can easily identify bony defect around the third molar.

 

Diagnosis of Pericoronitis

If you report pain or swelling iear your wisdom tooth then your dentist will first physically examine the area. If there is any partially erupted teeth or presence of a gum flap then you dentist will advise for an X-ray. This is done to determine the alignment of the wisdom teeth and the treatment is given accordingly.

 

ACUTE ODONTOGENIC OSTEOMYELITIS OF THE JAWS: CLINICAL COURSE, DIFFERENTIAL DIAGNOSIS, PREVENTION, TREATMENT (SURGICAL, MEDICATIONAL, PHYSIOTHERAPEUTICAL, ETC.), COMPLICATIONS. ACHIEVEMENT OF DEPARTMENT. CHRONIC ODONTOGENIC OSTEOMYELITIS OF THE JAWS: CLINICAL FEATURES, DIAGNOSIS, TREATMENT, COMPLICATIONS AND THEIR PREVENTION.

Osteomyelitis Jaw

Osteomyelitis is an infection of the bone. It can be caused by a variety of microbial agents (most common in staphylococcus aureus) and situations, including:

• An open injury to the bone, such as an open fracture with the bone ends piercing the skin.

• An infection from elsewhere in the body, such as pneumonia or a urinary tract infection that has spread to the bone through the blood (bacteremia, sepsis).

• A minor trauma, which can lead to a blood clot around the bone and then a secondary infection from seeding of bacteria.

• Bacteria in the bloodstream bacteremia (poor dentition), which is deposited in a focal (localized) area of the bone. This bacterial site in the bone then grows, resulting in destruction of the bone. However, new bone often forms around the site.

• A chronic open wound or soft tissue infection can eventually extend down to the bone surface, leading to a secondary bone infection.

Osteomyelitis affects about two out of every 10,000 people. If left untreated, the infection can become chronic and cause a loss of blood supply to the affected bone. When this happens, it can lead to the eventual death of the bone tissue.

Osteomyelitis can affect both adults and children. The bacteria or fungus that can cause osteomyelitis, however, differs among age groups. In adults, osteomyelitis often affects the vertebrae and the pelvis. In children, osteomyelitis usually affects the adjacent ends of long bones. Long bones (bones of the limbs) are large, dense bones that provide strength, structure, and mobility. They include the femur and tibia in the legs and the humerus and radius in the arms.

Osteomyelitis does not occur more commonly in a particular race or gender. However, some people are more at risk for developing the disease, including:

• People with diabetes

• Patients receiving hemodialysis

• People with weakened immune systems

• People with sickle cell disease

• Intravenous drug abusers

• The elderly

Symptoms of osteomyelitis

The symptoms of osteomyelitis can include:

• Pain and/or tenderness in the infected area

• Swelling and warmth in the infected area

• Fever

• Nausea, secondarily from being ill with infection

• General discomfort, uneasiness, or ill feeling

• Drainage of pus through the skin

Additional symptoms that may be associated with this disease include:

• Excessive sweating

• Chills

• Lower back pain (if the spine is involved)

• Swelling of the ankles, feet, and legs

• Changes in gait (walking pattern that is a painful, yielding a limp)

Diagnosing osteomyelitis

To diagnose osteomyelitis, the doctor will first perform a history, review of systems, and a complete physical examination. In doing so, the physician will look for signs or symptoms of soft tissue and bone tenderness and possibly swelling and redness. The doctor will also ask you to describe your symptoms and will evaluate your personal and family medical history. The doctor can then order any of the following tests to assist in confirming the diagnosis:

• Blood tests: When testing the blood, measurements are taken to confirm an infection: a CBC (complete blood count), which will show if there is an increased white blood cell count; an ESR (erythrocyte sedimentation rate); and/or CRP (C-reactive protein) in the bloodstream, which detects and measures inflammation in the body.

• Blood culture: A blood culture is a test used to detect bacteria. A sample of blood is taken and then placed into an environment that will support the growth of bacteria. By allowing the bacteria to grow, the infectious agent can then be identified and tested against different antibiotics in hopes of finding the most effective treatment.

• Needle aspiration: During this test, a needle is used to remove a sample of fluid and cells from the vertebral space, or bony area. It is then sent to the lab to be evaluated by allowing the infectious agent to grow on media.

• Biopsy: A biopsy (tissue sample) of the infected bone may be taken and tested for signs of an invading organism.

• Bone scan: During this test, a small amount of Technetium-99 pyrophosphate, a radioactive material, is injected intravenously into the body. If the bone tissue is healthy, the material will spread in a uniform fashion. However, a tumor or infection in the bone will absorb the material and show an increased concentration of the radioactive material, which can be seen with a special camera that produces the images on a computer screen. The scan can help your doctor detect these abnormalities in their early stages, when X-ray findings may only show normal findings.

Treating and managing osteomyelitis

The objective of treating osteomyelitis is to eliminate the infection and prevent the development of chronic infection. Chronic osteomyelitis can lead to permanent deformity, possible fracture, and chronic problems, so it is important to treat the disease as soon as possible.

Drainage: If there is an open wound or abscess, it may be drained through a procedure called needle aspiration. In this procedure, a needle is inserted into the infected area and the fluid is withdrawn. For culturing to identify the bacteria, deep aspiration is preferred over often-unreliable surface swabs. Most pockets of infected fluid collections (pus pocket or abscess) are drained by open surgical procedures.

Medications: Prescribing antibiotics is the first step in treating osteomyelitis. Antibiotics help the body get rid of bacteria in the bloodstream that may otherwise re-infect the bone. The dosage and type of antibiotic prescribed depends on the type of bacteria present and the extent of infection. While antibiotics are often given intravenously, some are also very effective when given in an oral dosage. It is important to first identify the offending organism through blood cultures, aspiration, and biopsy so that the organism is not masked by an initial inappropriate dose of antibiotics. The preference is to first make attempts to do procedures (aspiration or bone biopsy) to identify the organisms prior to starting antibiotics.

Splinting or cast immobilization: This may be necessary to immobilize the affected bone and nearby joints in order to avoid further trauma and to help the area heal adequately and as quickly as possible. Splinting and cast immobilization are frequently done in children, although motion of joints after initial control is important to prevent stiffness and atrophy.

Surgery: Most well-established bone infections are managed through open surgical procedures during which the destroyed bone is scraped out. In the case of spinal abscesses, surgery is not performed unless there is compression of the spinal cord or nerve roots. Instead, patients with spinal osteomyelitis are given intravenous antibiotics. After surgery, antibiotics against the specific bacteria involved in the infection are then intensively administered during the hospital stay and for many weeks afterward.

With proper treatment, the outcome is usually good for osteomyelitis, although results tend to be worse for chronic osteomyelitis, even with surgery. Some cases of chronic osteomyelitis can be so resistant to treatment that amputation may be required; however, this is rare. Also, over many years, chronic infectious draining sites can evolve into a squamous-cell type of skin cancer; this, too, is rare. Any change in the nature of the chronic drainage, or change of the nature of the chronic drainage site, should be evaluated by a physician experienced in treating chronic bone infections. Because it is important that osteomyelitis receives prompt medical attention, people who are at a higher risk of developing osteomyelitis should call their doctors as soon as possible if any symptoms arise.

Osteomyelitis for Jaw Treatment

Osteomyelitis occurs when a bone becomes infected. Though osteomyelitis most often occurs in the bones of the limbs, spine and pelvis, it can also affect the jaw. Osteomyelitis in the jaw is a rare condition that once had been thought incurable, however advances in medicine make the condition treatable. It can present itself in either acute or chronic forms. Osteomyelitis is a serious condition and if proper treatment is not sought, it can destroy your bones.

Symptoms

The symptoms for people with osteomyelitis in the jaw include pain and tenderness, swelling around the jaw, drainage in the sinus cavity, loss of teeth, discharging of pus and necrotic bones. Factors that can lead to osteomyelitis include tobacco, anaemia, viral infections and malnutrition. Since the condition exhibits symptoms that are common in many other diseases, osteomyelitis can be difficult to diagnose at first. If you have chronic osteomyelitis, debilitating fatigue is also very common symptom.

Diagnosis

If your doctor suspects osteomyelitis, he will order various tests before he can make a firm diagnosis. Though a blood test does not define an osteomyelitis diagnosis, a high level of white blood cells will indicate that body is fighting off an infection. If your osteomyelitis is advanced, an X-ray will show the extent of the damage. If you need a better image, your doctor may recommend a CAT scan or MRI. Your doctor may also remove a piece of your bone for a biopsy. This biopsy will check for the strain of bacteria that has infected your bone.

Treatment

Most often infections of the jaw are polymicrobial oral flora so a regimen of antibiotics are used to treat the infection. You doctor may prescribe penicillin, clindamycin and metronidazole. Depending on the extent of the infection, surgery may be required. Your doctor will decide which procedure is best based on the damage caused by the infection. Some bone and tissue may need to be removed, fractures repaired and rotten teeth extracted. You may also want to consult with an oral-maxillofacial surgeon to see if facial reconstruction is required.

Osteomyelitis
Osteomyelitis is a rare complication of tooth-related infections (incidence of 25 in 100,000).  In most cases, it is the result of spread of infection from a dento-
alveolar (tooth) or periodontal (pyorrhoea / gum disease) abscess or from the para-nasal sinuses, by way of continuity throughtissue spaces and planes.  It occasionally occurs as a complication of  jaw fractures or as a result of manipulations during surgical procedures.
Most patients are adult males with infection of the mandible (lower jaw).
Osteomyelitis of the maxilla (upper jaw) is a rare disease of neonates (newly born) or infants after either birth injuries or uncontrolled middle ear infection.
It is classified as acute or chronic osteomyelitis.
Acute Osteomyelitis
In the acute form (which rarely, may also be of hæmatogenous origin [i.e. seeded from the blood stream]), the infection begins in themedullary cavity (bone marrow) of the bone.  The resulting increase of intra-bony pressure leads to a decreased blood supply (and hence diminution of white blood cells and other immune 
components) and spread of the infection, by way of the Haversian canals of the bone, to the cortical bone (definition) andperiosteum (below the periosteum, a thick 
fibrous two-layered membrane covering the surface of bones).  This aggravates the ischæmia (decreased blood supply), resulting innecrosis (the death of cells or tissues from severe injury or disease, especially in a localised area of the body.  Causes of necrosisinclude inadequate blood supply [as in infarcted tissue], bacterial infection, traumatic injury and hyperthermia) of the bone.
Acute Osteomyelitis of the Jaws — Potential Sources of 
Infection

• Peri-apical infection

• A periodontal pocket involved in a fracture

• Acute gingivitis or pericoronitis (even more rarely)

• Penetrating, contaminated injuries (open fractures or 
  gunshot wounds)

Important Predisposing Conditions for Osteomyelitis
Local Damage to / Disease of the Jaws

• Fractures, including gunshot wounds

• Radiation damage

• Paget’s disease

• Osteopetrosis

Impaired Immune Defences

• Acute leukaemia

• Poorly-controlled diabetes mellitus

• Sickle cell anaemia

• Chronic alcoholism or malnutrition

• AIDS

 

• Infection from micro-organisms with great virulence.  
  In such cases, even a peri-apical abscess may be 
  implicated in osteomyelitis.

Acute Osteomyelitis of the Jaws — Key Features

• Mandible mainly affected, usually in adult males

• Infection of dental origin – anærobes are important

• Pain and swelling of jaw

• Teeth in the area are tender; gingivæ (gums) are red 
  and swollen

• Sometimes paræsthesia of the lip

• Minimal systemic upset

• After about 10 days, X-rays show ‘moth-eaten’ 
  pattern of bone destruction

• Good response to prompt antibiotic treatment and 
  debridement

The mandible (lower jaw), due to decreased vascularity (blood supply & flow), is 
involved 6 times more often than the maxilla (upper jaw).
The mandible has a relatively limited blood supply and dense bone with thick bony 
(cortical) plates.  Infection causes acute inflammation in the medullary (bone 
marrow) soft tissues and inflammatory exudate (a fluid with a high content of 
protein and cellular debris which has escaped from blood vessels and has been 
deposited in tissues or on tissue surfaces, usually as a result of inflammation. It 
may be septic or non-septic) spreads infection through the marrow spaces.  It also 
compresses blood vessels confined in the rigid boundaries of the vascular canals.

Thrombosis (the formation or presence of a thrombus [a clot of coagulated blood 
attached at the site of its formation] in a blood vessel) and obstruction then lead to 
further bone necrosis.

Dead bone is recognisable microscopically by lacunae (a cavity, space, or 
depression, especially in a bone, containing cartilage or bone cells) empty of 
osteocytes (a cell characteristic of mature bone tissue.  It is derived from 
osteoblasts and embedded in the calcified matrix of bone. Osteocytes are found in 
small, round cavities called lacunae and have thin, cytoplasmic branches) but filled 
with neutrophils (white blood cells) and colonies of bacteria which proliferate in the 
dead tissue.

Pus, formed by liquefaction of necrotic soft tissue and inflammatory cells, is forced 
along the medulla and eventually reaches the sub-periosteal region by resorption 
(an organic process in which the substance of some differentiated structure that 
has been produced by the body undergoes lysis and assimilation) of bone.  
Distension of the periosteum by pus stimulates sub-periosteal bone formation but 
perforation of the periosteum by pus and formation of sinuses on the skin or oral 
mucosa are rarely seeow.

At the boundaries between infected and healthy tissue, osteoclasts (a specialised 
bone cell that absorbs bone) resorb the periphery of the dead bone, which eventually becomes separated as a sequestrum (a fragment of dead bone separated from healthy bone as a result of injury or disease).  Once infection starts to localise, new bone forms around it, particularly sub-periosteally.
Where bone has died and been removed, healing is by granulation with formation of 
coarse fibrous bone in the proliferating connective tissue.  After resolution, fibrous 
bone is gradually replaced by compact bone and remodelled to restore normal 
bone tissue and structure (and function).
Piercing, deep and constant pain predominates in the clinical presentation in adults, 
while low or moderate fever, cellulitis, lymphadenitis, or even trismus may also be 
noted.
In the mandible, changes in sensation affecting the lower lip (paræsthesia or 
dysæsthesia of the lower lip) may accompany the disease.  When the disease 
spreads to the peri-osteum (definition) and the surrounding soft tissues, a firm 
painful œdema (definition) of the region is observed, while the tooth becomes loose 
and there is discharge of pus from the periodontium.  Radiographic examination 
reveals osteolytic (definition) or radiolucent (definition) regions.
Therapy entails combined surgical (incision, drainage, extraction of the tooth and 
removal of sequestrum) and chemo-therapeutic treatment (with antibiotics).
Summary of Treatment of Osteomyelitis
Essential Measures

• Bacterial sampling and culture

• Vigorous (empirical) antibiotic treatment

• Drainage

• Give specific antibiotics based on culture and sensitivities

• Give analgesics

• Debridement

• Remove source of infection, if possible

Adjunctive Treatment

• Sequestrectomy

• Decortication if necessary

• Hyperbaric oxygen*

• Resection and reconstruction for extensive bone destruction

*Mainly of value for osteo-radionecrosis and possibly, anærobic infections.

Anæsthesia of the lower lip usually recovers with elimination of the infection.  Rare 
complications include pathological fracture caused by extensive bone destruction, 
chronic osteomyelitis after inadequate treatment, cellulitis due to spread of 
exceptionally virulent bacteria or septicæmia in an immuno-deficient patient.

Chronic Osteomyelitis

 

Formation of a sequestrum: (A), sound bone; (B), new bone; (C), granulations lining involucrum; (D), cloaca; (E), sequestrum.

Chronic osteomyelitis is characterised by a clinical course lasting over a month.  It 
may occur after the acute phase or it may be a complication of tooth-related 
infection without a preceding acute phase.  The clinical presentation is milder, with 
painful exacerbations and discharge of pus or sinus tracts.

Osteomyelitis – Inflammation of the Bone

The terms osteomyelitis, periostitis and ostitis are frequently used as synonyms for inflammation of the bone.

Let’s have a quick look at the definition of the terms. Since the bone itself (the calcium structure) cannot get inflamed osteomyelitis(meaning bone marrow inflammation) and periostitis (meaning bone lining inflammation) would be the correct descriptions for an inflammation of the bone. Nevertheless ostitis is becoming more and more the term used.

The cause of an inflammation of the bone can come from outside – (exogenous factors) or from inside (endogenous factors). When both factors occur at the same time then we speak of combined forms. The so called idiopathic factors may also be regarded as a fourth form, consisting of bone inflammations of unidentifiable origin. Exogenous factors include, for example, numerous bacteria, viruses and fungi. They are potential pathogenic agents. If these pathogens find their way into our body they can cause an inflammation. If the inflammation gets into the bone then it’s a bone inflammation.

In the case of endogenous factors the cause lies in our own bodies. For example, in the case of diabetics the raised level of sugar of a diabetic leads to ever-increasing thickening of the walls of the blood vessels and thus an ever-poorer flow of blood.

The flow of blood can get so bad that certain areas of the body are no longer reached by it any more and the affected tissues die due to lack of oxygen and will be destroyed as a consequence of an inflammatory reaction – this can also occur in the bones, as shown in the animation and that would be an example of an endogenous osteomyelitis.

X-ray of Jaw Structure

Idiopathic osteomyelitis means to the patient that, at the end of the day the doctor cannot find an adequate explanation for it.

In the area of the jaw the most common causes of bone inflammation are exogenous or, more accurately, iatrogenous (caused by the doctor). Thus often extractions and/or badly root-treated teeth lead to bone infections.

In the picture you can see an x-ray of an extraction wound (circled in blue), the bone in this area is inflamed (circled in red) – osteomyelitis. In order to diagnose osteomyelitis an x-ray is usually required. In the same picture you can see a tooth (circled in green), which has an inflammation of the bone going on at the tip of the root (circled in red), as can be seen from the dark spot.

An x-ray can provide a lot of information about the bone but if precision is needed then a CT or MRT scan is very useful. This brings us to the diagnosis of osteomyelitis – CT and MRT scans are very reliable diagnostic aids at a certain stage of the osteomyelitis but at a very early stage of the illness their usefulness is rather limited.

Nuclear medical examinations such as skeletal cintography (Tc-99m) are frequently being made use of in order to detect osteomyelitis. The radioactive element technetium will be seen to be concentrated in the areas with raised bone metabolism after being applied intravenously. This increased concentration can be seen from the outside by means of a special camera (the darker spots in the exposure). Unfortunately it is not possible with this method to distinguish between the different causes of the raised bone metabolism.

Is the cause an inflammation or only an innocent build-up of bone after all?

With the addition of special factors (marked anti-granulocyte antibodies for additional investigation) the examination can however be made more specific. Blood tests are likewise not specific and unfortunately the blood values of the inflammation do not always correlate with the values of the osteomyelitis – especially in the jaw area. A bone biopsy is usually the most reliable means of diagnosis, as this way the bone can be viewed very precisely under the microscope (histological examination), and it may be possible to isolate the offending pathogen on the culture glass (bacteriology). If this succeeds then an antibiogram can be carried out in order to find the antibiotic with which to destroy the pathogen.

Bone Scan Scintigraphy

However, biopsy has a couple of disadvantages. The examination is invasive (therefore a wound is unavoidable) and not all areas of bone can be biopsied easily. Sometimes the bacteriological investigations are not successful or it may happen that during the taking of the sample there is contamination of the sample, for example by non-specific bacteria from the mouth.

Finally, let us take a look at the treatment options for osteomyelitis. There are various treatment options available – in the worst case the affected bone must be removed but this is very seldom necessary. The most frequent and simplest treatment option is the prescription of antibiotics, which can be swallowed or applied intravenously. The latter gives a higher concentration of the active ingredient in the blood.

By means of oxygen therapy we enrich the concentration of oxygen in the blood, since within the inflamed bone there is frequently insufficient blood supply and consequently, too little oxygen, ideal conditions for the multiplication of bacteria which do not tolerate oxygen – anaerobic bacteria as they are known. Oxygen-rich blood should have an effect on them, as per the motto: a little blood but very rich.

Another very much talked about treatment is the removal of the sick bone and the filling of the resultant gap with replacement donor bone which has been enriched with an antibiotic. In the animation you can see how the donor bone with the antibiotic (shown in green here) is put in place. The inflamed bone (shown in red here) will be removed and the donor bone will be inserted in the resulting cavity. The antibiotic will then pass continually into the body over months and simultaneously the replacement bone can regenerate.

The advantage of this treatment is that far higher concentrations of medication can be placed specifically in the affected area unlike with the usual means of application (orally or intravenously). Examination over a long period of time is still needed in order to evaluate this treatment over several years.

Ideally you want to avoid it getting to that stage. At least the iatrogenic forms of osteomyelitis can be avoided through sterilisation and cleanliness in the dental clinic.

Osteomyelitis

Odontogenic infection via a root canal, a periodontal pocket or an extraction wound is the most common local cause of osteomyelitis of the jaws. Rarely, a fracture serves as in infection route. Haematogenous spread of an infective agent from another part of the body also occurs. A distinct type of osteomyelitis, osteoradionecrosis, occurs after therapeutic irradiation of oral and neck malignancies.

Figure 20. 
An ill-defined periapical and interdental osteolytic lesion in the mandibular anterior region three weeks after onset of clinical symptoms of osteomyelitis.

Figure 21.
Chronic suppurative osteomyelitis with three sequestra (arrows). Osteolytic as well as sclerotic areas are present.

Osteomyelitis is more common in the mandible than in the maxilla. In the mandible, it occurs predominantly in the posterior parts, the ramus included, whereas in the maxilla, it is more frequent in the anterior than in the posterior parts. In the acute phase, osteolysis is not visible radiographically until one or two weeks after the onset of clinical symptoms which are: pain, fever, local lymphadenopathy, increased white blood cell count, and teeth sensitive to percussion. Numbness of the lower lip is another common sign of mandibular osteomyelitis.

The initial radiographic changes are blurring and thinning of the trabeculae and subsequent enlargement of the bone marrow spaces. Without treatment, large volumes of the bone tissue can rapidly become involved, causing loosening of the teeth (Fig. 20).

If acute osteomyelitis becomes chronic, it is frequently possible to distinguish between chronic suppurative osteomyelitis (Fig. 21) and chronic sclerosing osteomyelitis (Fig. 22), both of which have ill-defined borders. In the suppurative form, radiolucent areas alternate with sclerotic, giving the bone a “moth-eaten” appearance. This is further enhanced when sequestra develop. In chronic sclerosing osteomyelitis, radiolucent areas occur, but there is a predominance of radiopaque changes due to the formation of sclerotic bone. The bone is often enlarged through periosteal bone formation (Figs. 22, 23). Over time, the distribution of sclerotic and radiolucent areas varies, indicating disease activity.

Figure 22.
Chronic sclerosing osteomyelitis of right mandible with some osteolytic areas. Ramus is enlarged.

b

Figure 23.
a) Right mandibular molars in a young patient. The alveolar bone is unevenly sclerotic; chronic sclerosing osteomyelitis.
b) Occlusal view of the same patient. Periosteal bone formation (arrow) on the buccal side of the mandible.

Fig. 1.

Cropped panoramic radiograph of suppurative osteomyelitis at the right mandible. Osteolytic change is observed from around the molar tooth roots to the body of the mandible (arrows).

How to Diagnose Osteomyelitis

Osteomyelitis is an infection of the bone, generally caused by the Staphylococcus Aureus bacteria. This bacteria infects the bones because it travels through the blood from other infected areas. It can also come directly from a wound and travel straight to the bone. A common cause of Osteomyelitis is an open fracture, where not only the bone breaks, but the skin breaks too.

 

Instructions

1.       Perform a physical examination of the patient. Be sure to take a complete medical history and list any medications the patient is already taking. Also ask about any recent problems with the area the patient says is painful.

2.       Take a blood sample to perform a blood test to pinpoint if the patient’s white blood cell count is high, which is often a sign of infection. Look for signs of infection in the body, such as areas that are inflamed, red and warm.

3.       Send the patient for a bone x-ray. A bone x-ray can show if there is an infection in the bone, but might not be as accurate for someone who has just started complaining of pain. If the bone x-ray does not come back positive, but the patient exhibits signs of Osteomyelitis, send them for a bone scan, which gives you a more detailed view of the bone.

4.       Follow up with an MRI, if the bone scan indicates osteomyelitis. MRIs are a valuable test to run. In addition to diagnosing osteomyelitis, the MRI can also help determine how long the infection has been in the bone.

Osteomyelitis may manifest itself in acute, subacute, or chronic forms. Chronic osteomyelitis will result in variable sclerosis and deformity of the affected bone. After the age of 50, the majority of the blood supply to the mandible comes from the overlying periosteum and attached musculature, due to age and atherosclerosis-related involution of the inferior alveolar artery. With an infection of the bone, the subsequent inflammatory response will elevate this overlying periosteum, leading to a loss of the nourishing vasculature, vascular thrombosis, and bone necrosis, resulting occasionally in formation of sequestra. These become areas that are more resistant to systemic antibiotic therapy due to lack of the normal Haversian canals that are blocked by scar tissue, inflammatory exudate, and necrotic bone. At this point, not only systemic antibiotic therapy, but also surgical debridement maybe required to remove the affected bone and prevent disease propagation to adjacent areas. The relative hypoxia seen in infected bone will impair leukocyte bacterial killing, and impede fibroblastic collagen production that is required to support angiogenesis. Thus, it is not surprising that the concomitant use of hyperbaric oxygen therapy maybe beneficial in cases refractory to medical management alone or in patients with a severely compromised immune response. Generally, 20 dives (2.8-3.0 at 100% oxygen for 90 minutes) are administered preoperatively, followed by 20 dives after the debridement of necrotic tissue.

Radiographic imaging may be deceptively unremarkable in acute osteomyelitis, particularly with plain x-rays. Computed tomography (CT) scanning is the standard for evaluating the bone for sequestrum formation. Generally, one sees areas of lytic destruction and overlying periosteal reaction. It is much more common to find cortical plate disruption in the buccal plate than in the lingual plate. Technetium⁹⁹ bone scanning is often positive within 24 hours of an acute infection. Unfortunately, persistent uptake maybe present for 2 years after eradication of osteomyelitis. Gallium^-67 scanning normalizes after successful treatment of mandibular osteomyelitis.

In acute osteomyelitis, or in chronic forms without evidence of formation of sequestra, culture-driven antibiotic therapy is important to allow for disease eradication and decrease the likelihood of formation of antibiotic resistant strains resulting from inadequate subtherapeutic antibiotic therapy. Occasionally, repeated cultures may be required to allow for pathogen isolation, especially in cases of chronic osteomyelitis. Open biopsy of the bone allows for the most accurate culture results. Alpha hemolytic streptococcus, often in conjunction with oral anaerobes, is the most commonly isolated organism noted today. Although acute osteomyelitis is often adequately treated with a culture-driven 6- to 8-week course of antibiotic therapy, chronic osteomyelitis generally requires surgical debridement as well. Antibiotic therapy should be continued for 4 to 6 weeks from the date of last debridement, from resolution of the patient’s symptom complex and/or normalization of the gallium scan (if performed). Refractory osteomyelitis may benefit from the addition of hyperbaric oxygen therapy. Vancomycin or clindamycin are generally effective in the treatment of group A or B streptococci. However, as stated, culture-driven antibiotic therapy is required. With the propagation of multidrug-resistant varieties, treatment with nontraditional antibiotic regimens, such as fluroquinolones, may be required. Attention to optimal management of any underlying systemic immunocompromising conditions, such as diabetes mellitus, steroid usage, and HIV infection is important in all cases.

Clinical features, Radiographic features and treatment of Chronic Osteomyelitis of mandible

Clinical feature:
1. Site: Mandible
2. At early stage:
a. General constitutional symptoms:
• Intermittent fever
• Malaise
• Nausea, vomiting
• Anorexia
b. Pain:
• Deep seated
• Paresthesia of the lower lip

Radiology of Chronic OML• Facial cellulitis

• Trismus
• Swelling
3. Established case of OML:
a. Deep pain
b. Loosening of involved teeth
c. Pain on percussion
d. Sensitivity
e. Purulent discharge of pus
f. Regional lymphadenopathy
g. Trismus
Radiological feature:
1. In early stage, there are no findings
2. The changing begins 4-6 weeks after infection
3. In ate stage of Osteomyelitis, we find sequesterum, involucrum, scattered area, moth eaten appearance in conventional radiograph.
4. For specialized image, we do: CT scan, Radionucleido bone scan, Positron emission tomography.

Treatment:
1. Conventional treatment:
a. Complete bed rest
b. Supportive therapy:
• Nutritional support
• High protein diet
• High calorie and multivitamin diet
c. Rehydration by IV fluid
d. Blood transfusion
e. IV antimicrobial agent
2. Surgical treatment:
a. Incision and drainage   b. Extraction of the offending tooth   c. Debridement of the affected area by irrigating with H2O2 and normal saline  d. Sequestrectomy e. Decortication f. Saucerisation  g. Resection
Post operative care:
1. Continuous use of antibiotics
2. Analgesics
3. Adequate hydration
4. Complete bed rest
5. Follow up

Suppurative mandibular osteomyelitis

Suppurative mandibular osteomyelitis refers to agents that invasion of the mandible, the bone tissue as a whole, including the periosteum, cortical bone, bone marrow and the blood vessels, nerves, inflammation, alveolar abscess, periodontitis, and the third molar crown weeks go far odontogenic infection from which the highest incidence of mandibular osteomyelitis.

Disease Overview

When agents that invaded the jaw, will cause the entire jaw organizations, including the periosteum, cortical bone, bone marrow, and one of the blood vessels, nerve inflammation range of leisure, known as purulent maxillary osteomyelitis. Classification of Diseases 1 performance classification, according to the clinical pathology of suppurative odontogenic mandibular osteomyelitis lesions originating in the maxillary central cancellous bone and bone marrow, known as the Central osteomyelitis, lesions originating in the periosteum and cortical bone of the jaw around the , called the edge of osteomyelitis, according to the nature of the lesions can be divided into acute and chronic phase, the scope of the validation can be divided into localized or diffuse suppurative disease cause of mandibular osteomyelitis of up to alveolar abscess, periodontitis, third molar pericoronitis go far odontogenic infection from, followed by invasive infection due to a comminuted fracture or gunshot wound in open injury to bone by the blood circulation of sepsis or sepsis infection. this situation occurred in the maxilla of the infants and young children, very few of the infection of facial skin or oral mucosa directly affect the jaw. put the treatment of oral cancer or nasopharyngeal carcinoma, osteomyelitis common major pathogens Staphylococcus aureus bacteria, followed by Streptococcus, a few other pyogenic bacteria, stereotypes of mixed infections. pathophysiology of mandibular osteomyelitis compared with the previous mandibular osteomyelitis is more common condition than maxillary bone marrow serious, this is because the upper jaw bone dense fascia and strong muscles, present jaw infection, pus is not left around the puncture drainage poor blood supply of the mandible, infection of vascular thrombosis, it is easy to form a large sequestrum. diagnostic tests 1, details incidence and its treatment, consultation, attention to the relationship with the teeth, identify pathogen teeth. 2, with or without empyema sense of volatility, can be used to puncture confirmed suspicious when pus for bacterial culture and antibiotic sensitivity determination. fistula, exploration probes and other instruments with or without sequestrum sequestrum separation, X-ray, chronic identifying bone destruction, with or without sequestrum formation or infection of the low toxicity to the bone cortical hyperplasia. .

Clinical symptoms

Symptoms characteristic of central mandibular osteomyelitis, acute early inflammation is often restricted to the alveolar bone or bone marrow of the mandibular body, and then invasion of mandible, from the center to the edges of cortical bone and periosteum. 2. stage, patients may feel a severe toothache, pain along the trigeminal nerve distribution area for radiation lesions of the gingival mucosa hyperemia and edema, teeth percussion pain and loose, and may have gingival sulcus overflow pus or the formation of alveolar abscess , this stage of the lesion has not been timely drainage, the infection will continue to spread to the medullary cavity, can cause diffuse osteomyelitis or perforation of cortical bone formation in subperiosteal abscess, then patients with systemic poisoning symptoms became worse, and this when patients with serious manifestations of anemia, dehydration, exhaustion, body temperature increased to 39 ~ 40 ℃, blood test white blood cells increased significantly, local pain and soft tissue swelling in the affected region of the majority of teeth to loosen, some patients would be a serious concurrent disease, such as sepsis, intracranial infections, such as inflammation has not yet been brought under control, the maxilla infection can cause suppurative maxillary sinusitis and infraorbital cheek, or zygomatic, or pterygopalatine concave, temporal, concave and other regional proliferation. mandibular infection can spread to the inferior alveolar nerve caused by the lower lip numbness spread to the jaw weeks, stimulate the open jaw muscles, causing limited mouth opening, can be complicated by the jaw weeks more space infection, so that the face was seen in the swelling, and finally inflammation in the formation of blood clots within the jaw, resulting in jaw nutritional disorders and necrosis, and thus transferred to the chronic phase. 6, transferred from the acute to the chronic phase of about 2 to 3 weeks later, the pain and other systemic symptoms have begun reduced, but the mouth gums can form multiple fistula and pus. sequestrum with healthy bone will be in about a month later, new bone layer, caused by the separation of the sequestrum with healthy bone. this stage without surgical removal of involved regional fistula pus prolonged unhealed, can sometimes have a small piece of sequestrum discharged from the fistula osteomyelitis of the mandible can cause large sequestrum formation of pathogenic pathologic fracture, marginal mandibular osteomyelitis clinical features , limitations with young people, the lesions occurred, with chronic symptoms, does not appear large sequestrum. 2, occurred in young people under the jaw, the lesion is more limited spread of the infection pathway is not the first damage to bone marrow, but in the periosteum inflammation or subperiosteal abscess on the basis of the first involving the cortical bone, but also to the deep development involving the bone marrow, but rarely large sequestrum formation of the infections originated in the mandibular third molar crown Zhou Yan, can cause masseter muscle space infection subperiosteal abscess, resulting in the mandible of the ascending branch and corner Nutrition disorders of the cortical bone necrosis, showing chronic symptoms, local mild chronic inflammatory swelling and pitting edema due to masseter muscle and pterygoid muscle involvement, and limited mouth opening. pericoronitis infection if not controlled, often repeatedly made. 5, the edge of mandibular osteomyelitis after repeated anti-inflammatory medication, could easily lead to pathogen resistance, the formation of low toxicity and infection jaw inflammation.

Signs and symptoms

In particular, according to the clinical pathology of suppurative odontogenic mandibular osteomyelitis lesionsoriginating in the maxillary centralBone trabecular and bone marrow, known as the Central osteomyelitis lesions originating in the periosteum and cortical bone of the jaw around, known as the edge of osteomyelitis according to the nature of the lesions can be divided into acute and chronic phase, according to The scope of the validation can be divided into localized or diffuse. central mandibular osteomyelitis: the maxilla than the mandible more common in teeth with severe pain, persistent, and radiating pain along the trigeminal nerve distribution. teeth and adjacent teeth loose, percussion pain, vestibular groove fullness, cheek swelling. mandibular alveolar abscess, the pus is not easy worn develop into acute diffuse osteomyelitis and lack of drainage, the patients with systemic symptoms get worse, fever, chills, leukocyte, dehydration and other toxic manifestations. mandibular osteomyelitis refers to agents that invaded the jaw, causing the entire bone tissue, including periosteum, cortical bone, bone marrow and the blood vessels, nerve inflammation, Chinese medicine called ‘bone slot wind ‘or’ wear gills were sharply acute onset of high fever, increased white blood cells, can shift to the left. body poisoning, and with general malaise, headache, loss of appetite and other symptoms can occur in patients toothache, and the pain along the trigeminal nerve distribution area of ​​radiation, and can quickly spread to the adjacent teeth. the short term, there may be multiple tooth mobility, periodontal pocket pus, inferior alveolar nerve by inflammatory damage to the lower lip numbness due to the spread of inflammation to the surrounding maxillofacial swelling which can occur, such as infection spread to the masticatory muscles can be trismus such as infection control in a timely and quickly to the infraorbital, inferior temporal, the pterygopalatine concave and by the mandibular foramen caused the wing jaw space infection. systemic complications such as sepsis, and intracranial infection may also occur.

Disease etiology

Suppurative osteomyelitis of jaw up to the alveolar abscess, periodontitis, the third molar pericoronitis go far odontogenic infection from, followed by open injury due to comminuted or anger injury caused by bone invasive infection, sepsis or infections, sepsis and blood circulation more than occurred in the maxilla of infants and young children, very few of the infection of facial skin or oral mucosa directly affect the jaw. major pathogens Staphylococcus aureus, followed by Streptococcus few other pyogenic bacteria stereotypes mixed infection.

Pathophysiological

Mandibular osteomyelitis compared with maxillary osteomyelitis more common condition than the maxilla bone marrow serious, this is because the upper jaw bone is dense, and some surrounding fascia and strong muscles, present jaw infection, pus left After puncture drainage poor blood supply of the mandible, infection of vascular thrombosis, easy to form a large sequestrum.

Diagnostic tests

A detailed consultation incidence after treatment, and attention teeth identify pathogen teeth.

2, with or without empyema sense of volatility suspicious can be used for puncture confirmed. 3, pus for bacterial culture and antibiotic sensitivity determination, with or without fistula, probes and other instruments to probe whether the sequestrum sequestrum separation. 5, X-ray, the chronic phase to identify bone destruction, with or without sequestrum formation or infection of the low toxicity of the bone cortex hyperplasia type.

Disease Prevention

No special

Safety Tips

 1, the disease mostly occurs in the infant’s maxillary marginal mandibular osteomyelitis: more common in young people, the acute phase is difficult to find common chronic phase 2, the timely treatment of the crown Zhou Yan, the periapical Yandeng odontogenic infection to prevent occurrence of mandibular osteomyelitis. has formed should be a thorough treatment to avoid to chronic osteomyelitis, in the acute phase.

 

Treatment programs

 Acute systemic antibiotics, local incision and drainage or removal of loose teeth, diffuse patient performance Decline thirsty, systemic poisoning, severe anemia, in addition to general supportive therapy, but also a small amount of multiple transfusions and enhance systemic resistance to the chronic phase sequestrum curettage and extraction of teeth lesions mainly purulent maxillary bone marrow after a course of inflammation, and generally can be divided into two phases of acute and chronic phase. to The sequestrum began to take shape used to be collectively referred to as the acute phase by the onset, generally about 3 to 4 weeks if the infection fails to be completely controlled in the acute phase, into the chronic phase. must be used in sufficient quantities and effective antimicrobial treatment. use drugs in order to control the infection in the acute phase, use of antibiotics against Staphylococcus aureus and mixed infections, the other based on bacterial culture and susceptibility to choose effective antibiotics. In the initial stages of infection, but also with the physical therapy. When the infection into the suppuration of Early incision and drainage. wait for his condition slightly eased, the mouth opening slightly improved, should try to extraction, so that the pus from the socket to get the drainage, to prevent the spread of infection in the bone of acute suppurative osteomyelitis oncoming acute, severe illness, can cause blood and brain complications, and therefore close observation, as early as the appropriate emergency treatment of acute systemic application of antibiotics, local incision and drainage removal of loose teeth mainly diffuse patient performance decline thirsty, systemic poisoning, severe anemia, in addition to general supportive therapy, but also a small amount of multiple transfusions, enhanced systemic resistance to the chronic phase to sequester scrape and lesions in tooth extraction based. 1, the disease occurred in the maxilla of infants and young children. marginal mandibular osteomyelitis: more common in young people, the acute phase is difficult to find common chronic phase. and timely treatment of pericoronitis, periapical go far odontogenic infection, on the prevention of mandibular osteomyelitis. such as formation of osteomyelitis in the acute phase should be a thorough treatment so as not to become chronic. acute phase of infection control, enhance the body resistance-based, anti- infection drugs should be selected according to the sensitivity of pathogenic bacteria. mandibular osteomyelitis more mixed bacterial infection, it is appropriate in order to use broad-spectrum antibiotics. In addition, as has been clear for odontogenic infection, early removal of the lesions teeth in order to facilitate drainage, to avoid more extensive bone destruction. case of subperiosteal abscess or infection jaw week gap, it is timely incision in chronic phase, the lesion has been limited or has been sequestrum formation, while the surgical treatment of the main supplemented by drug treatment. marginal mandibular osteomyelitis are generally large sequestrum formation, mostly for the proliferation of subperiosteal cortical bone, the texture is more loose, and should be completely clear, pus foci of cortical bone surface where infection and the granulation organizers should be scraping, postoperative use of antibiotics to control infection in 7 to 14 days to avoid relapse.

Clinical manifestations

Clinical presentation of osteonecrosis of the jaw. (A) Typical lesion of osteonecrosis of the jaw showing exposed infected bone involving the mylohyoid ridge. (B) Osteonecrotic bone below a dental implant. (C) Spontaneous exfoliated teeth with underlying exposed dead bone. (D) Operative picture showing well-demarcated dead bone involving the whole alveolus. (From Badros A, Weikel D, Salama A, et al. Osteonecrosis of the jaw in multiple myelomoa patients: clinical features and risk factors. J Clin Oncol 2006;24:948; with permission. Copyright © 2006 by American Society of Clinical Oncology.)

Suppurative mandibular osteomyelitis from the clinical course of disease, pathogens, routes of infection and lesions involving the siteCan be manifested as acute and chronic stages, and often divided into two types of central and edge (a central mandibular osteomyelitis is usually odontogenic inflammation spread to the bone marrow, spread to the bone from the jaw center around cortex and periosteum in the bone marrow of early acute inflammation is often restricted to the alveolar bone or the mandibular body, patients feel severe toothache, pain along the trigeminal nerve distribution of radiation lesions of the gingival mucosa hyperemia and edema, teeth that is, obvious pain and loose, and can gingival sulcus septic overflow or the formation of alveolar abscess. acute phase has not been timely drainage, infections continue to spread to the medullary cavity can cause disseminated osteomyelitis or perforation of cortical bone formation in subperiosteal abscess. exacerbate symptoms of systemic poisoning at this time, the body temperature to 39 ~ 40 ℃, blood test white blood cells increased significantly, local pain and soft tissue swelling the affected regions the majority of loose teeth. If the inflammation is not brought under control, the maxillary infection can cause purulent maxillary sinusitis and infraorbital, buccal, zygomatic or pterygopalatine concave, temporal concave and other areas to spread. mandibular infection can spread to the inferior alveolar nerve caused by the lower lip numbness spread to the jaw week to stimulate the open jaw muscles, causing limitation of mouth opening can be complicated by the infection of the jaw week more than the gap, so that the face was seen in the swelling, and finally inflammation in the formation of blood clots within the jaw, resulting iutritional disorders of the jaw and necrosis, and thus transferred to the chronic phase. turn by the acute phase into the chronic phase of about two to three weeks later, pain and other systemic symptoms began to ease, but the mouth gums can form more than one fistula and pus out about a month later, the sequestrum with healthy bone between the new bone layer, causing the separation of the sequestrum with healthy bone without surgical removal of involved regional fistula pus prolonged unhealed, can sometimes have a small piece of sequestrum discharged from the fistula. osteomyelitis of the mandible can cause large piece of dead bone formation, can be pathogenic pathological fractures appear bite (occlusal disorders. Suppurative mandibular osteomyelitis (two marginal mandibular osteomyelitis spread of the infection pathway is not the first damage to bone marrow, but the basis of periostitis or subperiosteal abscess the first involving the cortical bone occurred in adolescents mandible, more limited lesions, infections originated in the mandibular third molar pericoronitis inflammation, caused by the masseter muscle space infection and subperiosteal abscess, resulting in lower jaw of the ascending branch and the corner of cortical bone nutritional barriers necrosis. clinical manifestations of chronic symptoms, the symptoms of the acute phase of infection and jaw week gap coexist but often overlooked in local mild chronic inflammatory swelling and pitting edema due to the chewing muscles and wing muscle involvement and limited mouth opening. lesions confined to the cortical bone, or to the deep development involving the bone marrow, but rarely large sequestrum formation. pericoronitis infections if not controlled, often repeatedly made by anti-inflammatory drugs after treatment, could easily lead to pathogen resistance, the formation of low toxicity and infection, no obvious purulent and sequestrum formation process and significant cortical hyperostosis, sclerosis and periosteal thickening of cortical bone lysis little part the formation of small abscess and granulation tissue. cortical hyperplasia of the mandibular ascending branch of the Ministry of mandibular angle can cause facial asymmetry, X-ray showed obvious subperiosteal hyperostosis.

Osteomyelitis is an infection of the bone. It can be caused by a variety of microbial agents (most common in staphylococcus aureus) and situations, including:

• An open injury to the bone, such as an open fracture with the bone ends piercing the skin.

• An infection from elsewhere in the body, such as pneumonia or a urinary tract infection that has spread to the bone through the blood (bacteremia, sepsis).

• A minor trauma, which can lead to a blood clot around the bone and then a secondary infection from seeding of bacteria.

• Bacteria in the bloodstream bacteremia (poor dentition), which is deposited in a focal (localized) area of the bone. This bacterial site in the bone then grows, resulting in destruction of the bone. However, new bone often forms around the site.

• A chronic open wound or soft tissue infection can eventually extend down to the bone surface, leading to a secondary bone infection.

Osteomyelitis affects about two out of every 10,000 people. If left untreated, the infection can become chronic and cause a loss of blood supply to the affected bone. When this happens, it can lead to the eventual death of the bone tissue.

Osteomyelitis can affect both adults and children. The bacteria or fungus that can cause osteomyelitis, however, differs among age groups. In adults, osteomyelitis often affects the vertebrae and the pelvis. In children, osteomyelitis usually affects the adjacent ends of long bones. Long bones (bones of the limbs) are large, dense bones that provide strength, structure, and mobility. They include the femur and tibia in the legs and the humerus and radius in the arms.

Osteomyelitis does not occur more commonly in a particular race or gender. However, some people are more at risk for developing the disease, including:

• People with diabetes

• Patients receiving hemodialysis

• People with weakened immune systems

• People with sickle cell disease

• Intravenous drug abusers

• The elderly

Symptoms of osteomyelitis

The symptoms of osteomyelitis can include:

• Pain and/or tenderness in the infected area

• Swelling and warmth in the infected area

• Fever

• Nausea, secondarily from being ill with infection

• General discomfort, uneasiness, or ill feeling

• Drainage of pus through the skin

Additional symptoms that may be associated with this disease include:

• Excessive sweating

• Chills

• Lower back pain (if the spine is involved)

• Swelling of the ankles, feet, and legs

• Changes in gait (walking pattern that is a painful, yielding a limp)

Diagnosing osteomyelitis

To diagnose osteomyelitis, the doctor will first perform a history, review of systems, and a complete physical examination. In doing so, the physician will look for signs or symptoms of soft tissue and bone tenderness and possibly swelling and redness. The doctor will also ask you to describe your symptoms and will evaluate your personal and family medical history. The doctor can then order any of the following tests to assist in confirming the diagnosis:

• Blood tests: When testing the blood, measurements are taken to confirm an infection: a CBC (complete blood count), which will show if there is an increased white blood cell count; an ESR (erythrocyte sedimentation rate); and/or CRP (C-reactive protein) in the bloodstream, which detects and measures inflammation in the body.

• Blood culture: A blood culture is a test used to detect bacteria. A sample of blood is taken and then placed into an environment that will support the growth of bacteria. By allowing the bacteria to grow, the infectious agent can then be identified and tested against different antibiotics in hopes of finding the most effective treatment.

• Needle aspiration: During this test, a needle is used to remove a sample of fluid and cells from the vertebral space, or bony area. It is then sent to the lab to be evaluated by allowing the infectious agent to grow on media.

• Biopsy: A biopsy (tissue sample) of the infected bone may be taken and tested for signs of an invading organism.

• Bone scan: During this test, a small amount of Technetium-99 pyrophosphate, a radioactive material, is injected intravenously into the body. If the bone tissue is healthy, the material will spread in a uniform fashion. However, a tumor or infection in the bone will absorb the material and show an increased concentration of the radioactive material, which can be seen with a special camera that produces the images on a computer screen. The scan can help your doctor detect these abnormalities in their early stages, when X-ray findings may only show normal findings.

Treating and managing osteomyelitis

The objective of treating osteomyelitis is to eliminate the infection and prevent the development of chronic infection. Chronic osteomyelitis can lead to permanent deformity, possible fracture, and chronic problems, so it is important to treat the disease as soon as possible.

Drainage: If there is an open wound or abscess, it may be drained through a procedure called needle aspiration. In this procedure, a needle is inserted into the infected area and the fluid is withdrawn. For culturing to identify the bacteria, deep aspiration is preferred over often-unreliable surface swabs. Most pockets of infected fluid collections (pus pocket or abscess) are drained by open surgical procedures.

Medications: Prescribing antibiotics is the first step in treating osteomyelitis. Antibiotics help the body get rid of bacteria in the bloodstream that may otherwise re-infect the bone. The dosage and type of antibiotic prescribed depends on the type of bacteria present and the extent of infection. While antibiotics are often given intravenously, some are also very effective when given in an oral dosage. It is important to first identify the offending organism through blood cultures, aspiration, and biopsy so that the organism is not masked by an initial inappropriate dose of antibiotics. The preference is to first make attempts to do procedures (aspiration or bone biopsy) to identify the organisms prior to starting antibiotics.

Splinting or cast immobilization: This may be necessary to immobilize the affected bone and nearby joints in order to avoid further trauma and to help the area heal adequately and as quickly as possible. Splinting and cast immobilization are frequently done in children, although motion of joints after initial control is important to prevent stiffness and atrophy.

Surgery: Most well-established bone infections are managed through open surgical procedures during which the destroyed bone is scraped out. In the case of spinal abscesses, surgery is not performed unless there is compression of the spinal cord or nerve roots. Instead, patients with spinal osteomyelitis are given intravenous antibiotics. After surgery, antibiotics against the specific bacteria involved in the infection are then intensively administered during the hospital stay and for many weeks afterward.

With proper treatment, the outcome is usually good for osteomyelitis, although results tend to be worse for chronic osteomyelitis, even with surgery. Some cases of chronic osteomyelitis can be so resistant to treatment that amputation may be required; however, this is rare. Also, over many years, chronic infectious draining sites can evolve into a squamous-cell type of skin cancer; this, too, is rare. Any change in the nature of the chronic drainage, or change of the nature of the chronic drainage site, should be evaluated by a physician experienced in treating chronic bone infections. Because it is important that osteomyelitis receives prompt medical attention, people who are at a higher risk of developing osteomyelitis should call their doctors as soon as possible if any symptoms arise.

What is jaw osteomyelitis?

Osteomyelitis is an inflammatory condition of bone that begins from an infection within the bone cavity. The infection is generally bacterial in origin and is most commonly caused by Staphylococcus aureus. Osteomyelitis can affect any bone in the body but has a predilection towards long bones and the jaw bones. Osteomyelitis affecting jaws is generally associated with dental complications. It was once a very serious disease with life threatening complication but these days it can be adequately treated with prompt medical intervention.

Jaw Osteomyelitis Symptoms

Osteomyelitis can be acute, subacute or chronic iature. The acute form of osteomyelitis of the jaws generally affects the mandible, the lower jaw. Common symptoms include fever, malaise, nausea, vomiting and dehydration. The affected area of jaws is associated with continuous, intense and deep bony pain. The lower lip is associated with tingling sensations or loss of sensations.

Acute Jaw Osteomyelitis

Facial cellulitis and a hard swelling over the affected area develops in acute forms of the disease. The teeth become tender on percussion. Difficulty in jaw opening is often present. A pus discharge into the oral cavity and over the skin through an opening is present in established cases of osteomyelitis. It may also be associated with a fetid odor.

Chronic Jaw Osteomyelitis

The chronic forms of osteomyelitis present with pain and tenderness over the affected area. Pain is minimal in such cases. It may also be associated with bony and overlying soft tissue wounds with firm to hard consistency. In chronic osteomyelitis the bone has a thickened, woody characteristic appearance. The teeth present in the region of the infection often become loose.

Jaw Osteomyelitis Causes

Acute osteomyelitis of the jaws is caused by pyogenic organisms. The chronic form occur secondary to untreated or incompletely treated acute infections. The commonly involved bacteria are Staphylococcus aureus but Streptococcus pyogenes and Spirochetesare also responsible.

The most common causes of infections are as follows :

• Dental infections including dental abscess ,periodontal disease, pericoronitis and infected cysts and tumor.

• Local traumatic injuries.

• Peritonsillar abscess (quinsy).

• Furuncle of skin.

• Blood borne infections.

Risk Factors

The risk factors for developing osteomyelitis are :

• Lowered immunity.

• Malnourished children.

• Systemic disease including diabetes and leukemia.

• Acute illnesses such as influenza, scarlet fever and pneumonia.

• Radiation to the head and neck.

Treatment of Jaw Osteomyelitis

The treatment includes antibiotic therapy, supportive masures, complete bed rest and surgery if necessary.

• Antibiotics that are generally prescribed include penicillins, penicillinase-resistant penicillins, clindamycin, cephalosporins, metronidazole and erythromycins.

• In acute forms of the disease analgesics or sedation may be given to reduce the pain.

• Intravenous fluids are administered to avoid dehydration.

• Blood transfusions may be required in cases with low hemoglobin levels.

• High protein diet and nutritional support is also recommended.

• Hyperbaric oxygen therapy is also very useful in treating osteomyelitis. It involves intermittent inhalation of 100% oxygen, humidified under pressure.

Surgery

Surgical procedures include :

• extraction of the offending tooth

• incision and drainage of an existing abscess

The infected portion of the bone can be surgically removed or entire segment of the jaw can be excised according to the extent of the disease. Immediate or delayed jaw reconstruction is carried out subsequently.

Primary Chronic Osteomyelitis Associated with Extraction of a Periodontally Involved Tooth

INTRODUCTION

Osteomyelitis (OM) is an inflammatory condition of bone that involves the medullary cavity and the adjacent cortex. It occurs more frequently in mandible than in the maxilla and is often associated with suppuration and pain.1 The osseous spaces are usually filled with exudates that can lead to pus formation. Chronic osteomyelitis can be the result of a non-treated acute mild inflammation or emerge without a precursor. When osteomyelitis occurs in the mandible, it is usually more diffused and widespread.1-6 Clinical examination alone is often enough to diagnose chronic mandibular osteomyelitis due to the progression of this disease and suppuration.1,2 In cases of chronic osteomyelitis, a radiolucent circumscribed image can be seen encapsulating central radiopaque sequestra, as well as radiopacities of the surrounding bone due to a local osteogenic reaction.7 Patients who present active chronic osteomyelitis usually require long-term use of antibiotic therapy and surgical intervention.7 Treatment requires both antibiotic therapy and surgical debridement, meaning the necrotic bone must be completely removed until the underlying bone starts bleeding.7 Although most cases of OM of the jaws result from dental origins, other sources of infection are possible.2 Although primary OM following extraction of periodontally involved teeth is rare, it is, however, of concern to both the patient and dentist. The following case report describes the presentation of OM and how it was managed.

CASE REPORT

A 62-year-old woman referred to our clinic for treatment of chronic infection and pain following extraction of the left mandibular second molar under local anesthesia by her general dentist. She was in good general health and did not have a history of drug use. Her pre-extraction radiographic examination confirmed the presence of a deep distal periodontal pocket (Figure 1). She then developed pain, chronic infection, and discharge following the extraction (Figure 2). She returned to her general dentist who prescribed amoxicillin 500 mg every 8 hours for 10 days. After multiple visits to her dentist, and no abatement of her symptoms after 5 months, she was referred to our clinic.

Intraoral clinical examination revealed that the socket of the left mandibular second molar tooth had chronic infection and a malodorous discharge. A sample of this fluid was collected for culture and antibiotic sensitivity. Culture was positive for non-A non-D streptococci sensitive to cephalexin. Radiographic examination confirmed the presence of a sequestrum in the socket (Figure 3).

Considering the clinical and radiographic presentation, a diagnosis of chronic osteomyelitis was made and the patient was scheduled for surgery. After general anesthesia, preparation, draping and packing the oropharynx; a flap was reflected and the sequestrum was removed with a curette. The socket was cleaned and irrigated. Nonvital necrotic bone was shaved using a round bur until vital bone was apparent (confirmed clinically by bone bleeders). The lesion was sent to the pathology laboratory and their report confirmed the diagnosis of chronic osteomyelitis. The patient was given cephalexin and metronidazole 500 mg every 6 hours for 2 weeks. A radiograph was that taken 3 months postoperatively showed bony consolidation of the socket (Figure 4). The patient has been symptom-free since the completion of the surgical treatment and antibiotic regimen.

DISCUSSION

Osteomyelitis may result from the direct extension of pulpal or periodontal infection without the formation of a granuloma or from acute exacerbation of a periapical lesion. It may also occur following penetrating trauma or various surgical procedures. Extension of the infection into adjacent soft tissue and fascial spaces is common, and often the presenting clinical symptoms are swelling, pain and suppuration. Sequelae to transcortical extension of the inflammatory process can include cortical destruction, fistulization and periosteal reaction. These changes can be evaluated by imaging techniques.5

Histopathology. The bone pathology presents various forms, depending on the virulence of the infecting microorganism, the host capacity of effective immune response and the kind of reaction of the periosteal and osseous tissues. Chronic osteomyelitis histopathology depicts irregular fragments of devitalized bone surrounded by dense fibrous tissue heavily infiltrated by plasma cells, lymphocytes, and only a few granulocytes (Figure 5).

Imaging. Appropriate evaluation of radiographic types of osteomyelitis is necessary for treatment planning. Kazunori Yoshiura6 classified mandibular osteomyelitis into four basic patterns, as lytic, sclerotic, mixed and sequestrum patterns. Our case presented with the latter pattern. In some cases computerized tomography or scintography may be necessary.1

Presentation. Patients can have swelling of the face, tenderness and pain (localized), draining sinus tracts, suppuration, tooth loss, possible necrotic bone fragment formation, and a low-grade fever. New bone and oral mucosa will occasionally regenerate beneath the sequestra, probably because of activation of periosteal osteoblasts. According to Reinert,6 clinical examination alone can be enough to diagnose mandibular chronic osteomyelitis, particularly at the onset of the disease. The radiographic characteristics of the osteomyelitis presented were a radiolucent area circumscribing a central bone sequestrum and radiopacity in the surrounding bone. Due to the characteristics of the pathology and the clinical history, there was no need for other exams.

Predisposing factors. Viral fevers (eg, measles), malaria, anemia, malnutrition, and use of tobacco are found to contribute to the development of osteomyelitis.

Management. Treatment goals include reversal of any predisposing conditions, long-term antibiotic therapy. Antibiotic therapy alone is not enough for the treatment of osteomyelitis, since the devitalized osseous tissue in combination with the capsule of the surrounding fibrous connective tissue protects the microorganisms from the drug action. Corticotomy can be used as treatment, and if not effective, bone resection can be done as a more radical alternative. However, aggressive treatment may cause loss of function, exposure of the inferior alveolar nerve and problems regarding the reconstruction.7 High doses of antibiotics should accompany any aggressive surgical treatment. Some authors feel that penicillin G is the medication of choice, followed by clindamycin.7 Since most of the osteomyelitis infections are polymicrobial oral flora (primarily facultative streptococci, Bacteroides spp, Peptostreptococcus,and Peptococcus), antibiotic treatment includes penicillin, metronidazole, and clindamycin. Operative interventions such as sequestrectomy, decortication, removal of nonviable bone (ie, mandibulectomy or maxillectomy), and dental extractions, are also needed. A wide incision to remove all the diseased tissue, as well as primary closure of the surgical wound is performed to ensure a successful operation.

Figure 1. Pre-extraction radiograph confirmed the presence of a deep periodontal pocket distal to the left lower molar tooth.

Figure 2. Postextraction radiograph showing the nonhealing socket.

Figure 3. Radiograph depicting the presence of a sequestrum in the socket.

Figure 4. Radiograph, at 3 months postoperatively, shows bony consolidation in the socket.

Figure 5. Chronic osteomyelitis histopathology (H&E x 400). Note the irregular fragment of devitalized bone. This is surrounded by dense fibrous tissue which is infiltrated heavily by lymphocytes, plasma cells, and a few granulocytes.

Mandibular osteomyelitis

 

     

[Introduction]

Overview: mandibular suppurative osteomyelitis can be divided into, specificity, radioactive and other types. Clinically, the most common pyogenic osteomyelitis jaw.

[Cause]

mandibular osteomyelitis is caused by what the?

mandibular osteomyelitis main sources of infection in three ways, namely tooth-borne, injury and blood-borne. Blood-borne mandibular osteomyelitis is less common, occurring mainly in children. The most common odontogenic mandibular osteomyelitis, accounting for 90% of all mandibular osteomyelitis. China due to medical conditions improve, the incidence rate has dropped significantly. Common odontogenic mandibular osteomyelitis, which is the mandible cortical bone bone density, muscle hypertrophy and around the fascia attached to the compact, easy to puncture the drainage canal accumulation of pus and other factors.

[Symptoms]

What are the early symptoms of Mandibular osteomyelitis?

(a) acute Mandibular osteomyelitis

rapid onset, systemic symptoms. Sense of pathogen local first tooth pain, and rapid extension of the adjacent teeth, causing pain and diffuse to the ipsilateral temporal. The corresponding parts of the facial swelling, gums and vestibular swelling, loose teeth more affected areas. Since periodontal pus often overflow. Mandibular osteomyelitis, due to masticatory muscle involvement, often with varying degrees of limitation of mouth opening. Inferior alveolar nerve involvement, may have affected the lower lip numbness. Maxillary osteomyelitis more common iewborns, infants, often the source of blood-borne infection. The local performance of the Ministry of significantly inferior orbital swelling, and often cause the eye until the eye could not open. The latter can, including canthus, nasal and oral puncture septic overflow.

(b) of chronic Mandibular osteomyelitis

acute maxillary osteomyelitis who fail to complete treatment, can be converted chronic. Common reason is simply the use of conservative medical treatment, pus worn on their own, poor drainage. During chronic maxillary osteomyelitis, most acute symptoms subside, have obvious symptoms, pain significantly reduced. Local fibrosis, swelling, stiff. Fistula, often overflow pus, discharge even small sequestrum. Lesions of multiple loose teeth, gum abscess overflow gap. When the lower body resistance or poor drainage can be acute. Such as delays in the course of time, can cause weight loss, anemia, physical weakness.

[Diet]

mandibular osteomyelitis ate?

therapeutic mandibular osteomyelitis (The following information is for reference only, details need to consult a doctor)

1, Daphne 15 g, 3 eggs, boil eggs with cooked, fresh eggs to the soup. 1 day, taken fasting, pediatric dosage reduce it.

2, wax gourd 500 grams, mussels 25 grams, 50 grams of mushrooms. To sub-cut melon, with mussels, mushrooms together spoil the broth.

3, cucumber 500 grams. Salted cucumber slices for 15 minutes, squeeze the water into the amount of sugar, vinegar mixed with food.

4, broiler 1, Panax 15 grams. Broiler hair removal to debris, 37 into the abdominal chicken, add wine, salt, ginger and other spices after the stew cook until the chicken when you can Decoction and fresh chicken Sulan.

5, wax gourd 500 grams tomatoes 200 grams. Peeled and diced melon, tomato slices, both with the soup, add salt, MSG seasoning.

mandibular osteomyelitis in patients with eating what does a body good?

1, the diet should be light.

2, eat more fresh fruits and vegetables.

3, eat more alkaline foods, alkaline foods, such as: tea, cabbage, persimmon, cucumber, carrots, spinach, cabbage, lettuce, taro, seaweed, citrus, figs, watermelon, grapes, raisins, chestnut, coffee, wine, and so on. Alkaline foods: tofu, peas, soybeans, green beans, bamboo shoots, potatoes, mushrooms, mushrooms, rape, pumpkin, tofu, celery, sweet potato, lotus root, onion, eggplant, pumpkin, carrots, milk, apples, pears, bananas, cherries and so on.

mandibular osteomyelitis patients what to eat is unhealthy?

1, eat fatty foods Hun , non-digestible food.

2, eat spicy food, such as pepper.

3, avoid alcohol and tobacco.

[Prevention]

mandibular osteomyelitis should be how to prevent?

health tips

1, for the prevention of radiatioecrosis and osteomyelitis of the jaw occurred, to take appropriate preventive measures.

2, before radiotherapy to eliminate both inside and outside the mouth all foci. full-mouth scaling; removal of incurable Bingya; treatment still retained dental caries, periodontal Bingya; remove the existing metal dentures in the mouth; dentures to be a period of time after termination of radiotherapy and then wear line, to avoid causing mucosal injury.

3, radiation therapy, the application of non-irradiated zone barrier material to be isolated; mouth ulcers, local antibiotic ointment applied to prevent infection in radiation therapy should be to strengthen the protection of non-radiation field organization, the organization, especially to reduce the radioactive teeth, jaw injury.

4, after radiation therapy , in the event of odontogenic inflammation, surgery or tooth extraction must be to minimize the surgical injury; surgery before and after effective antibiotics should be used to control secondary infection in radiation therapy, attention to oral hygiene, regular inspection, timely filling of dental caries, to avoid radiation therapy after three years in the extraction, in order to avoid radioactive maxillary osteomyelitis, such as teeth must be removed, and should try to reduce surgical trauma, the use of an appropriate amount of antibiotics to control secondary infection.

[Treatment]

mandibular osteomyelitis treatment considerations?

for the prevention of radiatioecrosis and osteomyelitis of the jaw occurred, to take appropriate preventive measures. According to the nature of the tumor to select the appropriate radiation type, dose and radiation field. Inside and outside the mouth before radiotherapy to eliminate all foci. Full-mouth scaling; removal of incurable Bingya; treatment still retained dental caries, periodontal Bingya; remove the existing metal dentures in the mouth; dentures to be a period of time after termination of radiotherapy re-wear, to avoid causing mucosal injury. Radiotherapy for non-application of barrier material to be irradiated zone isolation; mouth ulcers, local antibiotic ointment applied to prevent infection. After radiation therapy, in the event of odontogenic inflammation, surgery or tooth extraction must be carried out, should minimize the surgical injury; before and after surgery should be the use of effective antibiotics to control secondary infection.

mandibular osteomyelitis Chinese medicine treatment methods

No information

mandibular osteomyelitis Western medicine treatment

treated pericoronitis, periapical dental sources go far infection, osteomyelitis of the jaw to prevent the occurrence of positive significance. Such as osteomyelitis has been formed, in order to avoid a thorough treatment of the acute phase should be chronic.

systemic treatment of acute maxillary osteomyelitis and cellulitis jaw the same week, mainly to enhance the body’s resistance to drugs to control infection (metronidazole, spiramycin). Treatment focuses on timely local incision and drainage, removal of pathogenic teeth.

chronic mandibular osteomyelitis should be efforts to improve patient body condition, maintaining unobstructed drainage, timely removal of pathogenic teeth to remove lesions, scaling or removal of sequestrum.

[Check]

mandibular osteomyelitis should be how?

detailed history, partial inspection, possible X-ray examination to confirm the diagnosis.

white blood cell count was elevated, a larger proportion of neutrophils. Abscess has formed, the needle can be removed from theAbscess pus center.

[Confused]

mandibular osteomyelitis and the diseases easily confused?

chronic phase of the X-ray diagnosis in maxillary sinus cancer and should be noted, with the central mandibular carcinoma should be differentiated, proliferative type of marginal bone osteomyelitis should be with osteosarcoma and ossifying fibroma and other similar identification, where necessary, for biopsy.

Infant maxillary osteomyelitis

infants and young children with acute maxillary osteomyelitis are infection, the most common pathogen was Staphylococcus aureus. Routes of infection are: from the mother’s infection, blood-borne infections, such as local infection spread directly. Damage caused by forceps delivery, reproductive tract infections, umbilical cord infection, nipple and sucking dirty pacifier when artificial feeding, sucking action may damage gum infection. Cavernous maxillary bone is extremely rich in blood vessels, is easy to cause disease.

prognosis: early use of effective antibiotic treatment may be cured. However, if treatment is not timely or inadequate treatment, can produce a variety of complications, such as maxillofacial fistula, brain abscess, sepsis, etc.

Osteomyelitis

Definition

Osteomyelitis is an acute inflammatory process within bone, bone marrow, and surrounding soft tissue that develops secondary toinfection with bacterial organisms (and, rarely, fungi). The disease may be either current, requiring immediate treatment (acute), or long term (chronic); acute cases may become chronic (or recurrent) if treatment is delayed or unsuccessful. Chronic osteomyelitis tends to persist regardless of its initial cause and despite aggressive treatment.  Osteomyelitis is differentiated into two primary categories based on how the infective organisms enter the bone (mechanism of infection). In hematogenous osteomyelitis, bacteria enter directly through the bloodstream.  In direct inoculation or contiguous inoculation osteomyelitis, secondary infection is caused by bacteria coming into contact with bone during surgery or trauma. In individuals with lack of sufficient blood supply (vascular insufficiency), direct-inoculation osteomyelitis may result from bacteria entering through a specific route such as infected nail beds.  The causative bacteria will vary in people of different ages and according to the mechanism of infection. The most common cause of hematogenous osteomyelitis is pus-forming (pyogenic) bacteria, including the tuberculosis bacterium.  In direct-inoculation osteomyelitis, multiple organisms from the site of surgery or trauma may cause secondary local infection in the involved bone. Organisms may be introduced into the bone during surgery, from a compound or open fracture, from a contaminated wound over exposed bone, or from a foreign object penetrating the skin and bone, such as puncture of the foot. Hardware or prosthetic implants may carry infection into a bone where bacteria multiply rapidly, causing it to become a focus of infection. Because the metal is not affected by circulating blood, antibiotics may not have any effect on that type of infection.  Infection may also spread from a soft tissue injury caused by trauma, pressure ulcers, or burns. The bone itself is not initially injured, but the infection spreads through the layers of soft tissue into the bone. This type of osteomyelitis is more common in the elderly. Bones may also become predisposed to infection in individuals with peripheral vascular disease, which is characterized by formation of blood clots that may block the blood supply to a given area. Other diseases and conditions may also predispose individuals to secondary bone infection, including diabetes, sickle cell anemia, AIDS, intravenous drug abuse, alcoholism, chronic use of steroids, immunosuppression, and chronic joint disease. Individuals on hemodialysis and those who have had orthopedic surgery or open fracture or who have a prosthetic orthopedic device are also more susceptible to developing osteomyelitis.  In acute osteomyelitis, bacteria lodge in bones, where circulation is sluggish. The bacteria then multiply, resulting in secondary infection, abscess formation, and eventual bone destruction. Because the abscess deprives the bone of its blood supply, the bone will die (necrosis). As the disease progresses, areas of healthy bone may become isolated by the infection and areas of necrotic bone. Chronic osteomyelitis may develop when these necrotic areas of bone form islands or segments (sequestra) that remain infected, becoming a source of recurrent infection and, often, draining wounds (sinus tracts). The infection can also spread to other areas of the body. This pattern of recurring infection results in failure of the bone to heal. When some areas of the bone die, circulation throughout the bone stops, maintaining the cycle of infection and bone destruction. The osteomyelitis that develops from direct inoculation with vascular insufficiency is most common in diabetics and occurs in adults over age 45 (King). The target bones in osteomyelitis are primarily the spine and pelvis; children most often have their long bones affected. Risk: Osteomyelitis can affect individuals of all ages and all races. The risk of developing osteomyelitis is higher in individuals with diabetes, sickle cell disease, AIDS, immunosuppression, and chronic joint disease. Alcoholism, chronic use of steroids, and the use of intravenous drugs are also risk factors. Orthopedic surgery, open fracture, or the presence of a prosthetic orthopedic device increase risk. Men are twice as likely as women to develop osteomyelitis (King). Incidence and Prevalence: The incidence of osteomyelitis in the US is under 2% a year (Paluska). Incidence increases with every decade of life. Acute hematogenous osteomyelitis is most commonly seen in children, with 85% of affected individuals usually under the age of 1; the prevalence among children is 1 in 5,000 (King). Among individuals who have been treated for an episode of acute osteomyelitis, the prevalence of chronic osteomyelitis is about 5% to 25% in the US (Khan). Prevalence can be as high as 30% to 40% in individuals with diabetes and 16% after foot puncture (King).  In developing countries, the overall incidence is higher (King).

Diagnosis

History: In individuals with acute osteomyelitis, the main complaint is pain in the bone or bone tenderness, localized swelling and warmth, and perhaps redness of the area. The individual may avoid using or have a reduced ability to use the affected body part. In acute cases, individuals may report a generalized feeling of illness (malaise), loss of appetite, fatigue, nausea, irritability, and fever. There may be a history of recent trauma, surgery, or infection of another organ (i.e., lungs, bladder). Individuals with chronic osteomyelitis will have a history of an acute episode (if it was recognized initially), and often have a recurrence of pus draining out through the skin, pain, and swelling. They may also have generalized complaints of fever, loss of appetite, and fatigue. Additional symptoms may include excessive sweating (diaphoresis), chills, and low back pain. These individuals may have an underlying immune system disease or peripheral vascular disease. Individuals must be questioned about IV drug abuse and alcoholism. A complete health history is obtained, including all current and prior illnesses and injuries Physical exam: An examination will reveal local pain and tenderness. Redness over the area (erythema), swelling (edema), draining wounds, draining sinuses, or chronic skin ulcers may also be evident. Fever, signs of dehydration, or other signs of blood infection (sepsis) may be evident. Range of motion of joints may be reduced. Generally, direct inoculation osteomyelitis presents more local signs, whereas hematogenous osteomyelitis presents more generalized signs and symptoms that tend to progress slowly. Tests: Blood tests include a complete blood count (CBC), erythrocyte sedimentation rate (ESR), and a test for C-reactive protein. Samples of blood and wound drainage (or samples taken directly from the infected bone or sinus tract) may be cultured to identify the causative organism and determine antibiotic (or antifungal) sensitivities, although causative bacteria are identified in only about 35% to 40% of cases (King). Other possible tests include needle aspiration (lumbar puncture) within the vertebral space for culture, tuberculin skin test, open bone biopsy, bone culture, Doppler studies in cases of peripheral vascular disease, plain x-rays,ultrasound (in soft tissue abnormalities), gallium bone scan, CT scan, and MRI. Specialized tests may be ordered to evaluate the individual for the presence of a primary underlying illness or monitor ongoing treatment for a known chronic illness.

Treatment

The treatment goal is to eliminate the infection and prevent the development of a chronic infection. Because early treatment is critical, high-dose antibiotic intravenous (IV) therapy is usually started immediately, before test results are known. Antibiotics can be changed later, depending upon results of cultures. Hospitalization is necessary, at least during the early stages of treatment. The IV antibiotics continue for 4 to 6 weeks and may be followed with oral treatment for several months (the usual treatment duration for acute osteomyelitis is about 6 weeks, but the duration is longer for chronic and vertebral osteomyelitis). Analgesics are prescribed as needed. Wound care, if applicable, may include removal of dying or dead tissue (débridement) and frequent dressing changes. Bed rest and immobilization of the infected body part are essential. If improvement is not evident after 24 hours of antibiotic treatment, surgery may be done to relieve pressure in the bone (surgical decompression) by drilling into the bone and removing pus. Open spaces left by the removed bone will be filled with bone graft, or left with packing material in to promote regrowth of new bone tissue. If a prosthetic implant or hardware is suspected as the cause, the device may be removed; the infection should be eradicated before a replacement device is inserted. In cases in which there is reduced oxygen tension or vascular supplies, hyperbaric oxygen therapy may be used, but it is not recommended for routine use. In vertebral osteomyelitis, if the infection persists, it might be necessary to perform surgery, such as vertebral fusion. Chronic osteomyelitis will require surgical removal of the sequestra (sequestrectomy) and surrounding tissue, followed by antibiotic therapy. In severe cases, amputation may be necessary. Dehydration, protein deficiency, and anemia caused by draining wounds require nutritional supplementation. Education is very important to ensure compliance with long-term therapy. Home care services are necessary when patients require IV medication administration and wound care after discharge from the hospital.

Prognosis

Acute episodes have a good prognosis with timely diagnosis and aggressive antibiotic treatment. Chronic cases often have a poor outcome, especially when chronic underlying illness (e.g., diabetes, peripheral vascular disease, sickle cell disease, or chronic bone disease) is present. In vertebral osteomyelitis, approximately 10% to 15% develop neurological deficits (King). Mortality rates associated with osteomyelitis are generally low unless serious or chronic concomitant illness is present.

Rehabilitation

The type of rehabilitation for osteomyelitis depends on the location of the infected bone and the underlying cause of infection. For rehabilitation purposes, osteomyelitis is subdivided into five types. Depending on the type of osteomyelitis (ranging from type I to type V, according to the degree of tibia and fibula involvement and the bone’s ability to withstand functional loads), the rehabilitation time required varies. For type I osteomyelitis (in which both tibia and fibula are intact and can withstand functional loads), the rehabilitation time is from 6 to 12 weeks. In type II osteomyelitis (in which the tibia is intact, but a bone graft is needed), the rehabilitation time required is from 3 to 6 months. For type III osteomyelitis (in which the fibula is intact, but there is a tibial defect of no more than 6 cm), 6 to 12 months of rehabilitation are needed. In type IV osteomyelitis (in which the fibula is intact, but there is a tibial defect of more than 6 cm), 12 to 18 months of rehabilitation are required. Finally, for type V osteomyelitis (in which there is no usable intact fibula, and there is a tibial defect of more than 6 cm), 18 months or longer are required for rehabilitation. In general, rehabilitation is aimed at restoring normal range of motion, flexibility, strength, and endurance. The goal of rehabilitation for progressive osteomyelitis is to maintain function and enhance mobility. Active range of motion physical therapy initially helps maintain flexibility and strength and relieves the musculoskeletal pain associated with muscular weakness, paralysis, and immobility. As the therapy progresses, passive range of motion exercises are preferable to avoid overexertion or possible damage to the muscles. In the event of muscle weakness to the legs, balance exercises may be utilized. As strength continues to progress, endurance becomes a focus in the individual’s rehabilitation program for osteomyelitis. Aerobic exercises that increase cardiovascular fitness are recommended. The American Heart Association recommends 30 to 60 minutes of aerobic activity 3 or 4 times a week. Learning how to avoid injury is another important intervention in the rehabilitation of progressive osteomyelitis. Occupational therapyhelps individuals arrange their homes and organize their lives in ways that support their physical and mental well-being. Activities are also provided to relieve the mental boredom of inactivity. Devices and techniques that help the individual communicate are invaluable in maintaining peace of mind. The rehabilitation program varies among individuals with progressive osteomyelitis as the intensity and progression of the exercise depends on the stage of the disease and individual’s overall health.

Source: Medical Disability Advisor

 

Complications

An acute condition may become chronic. Soft tissue abscess formation, soft tissue cellulitis, bone abscess, septic arthritis, a prosthetic implant coming loose, the spread of a localized infection, chronic drainage (development of draining soft-tissue sinus tracts), toxic shock syndrome, joint contracture, and amputation can all result from acute or chronic osteomyelitis. Bone resorption can weaken bone and lead to fractures. Osteomyelitis of the spine can be complicated by paraplegia or inflammation of the membranes that surround the spinal cord and brain (meningitis). Untreated or inadequately treated osteomyelitis can lead to blood poisoning (septicemia), which can be fatal. Deep venous thrombosis (DVT) may occur in up to 30% of children with long-bone osteomyelitis, sometimes indicating disseminated infection (King).

Source: Medical Disability Advisor

 

Return to Work (Restrictions / Accommodations)

Individuals may be able to receive intravenous (IV) therapy at work if a clean space that permits privacy, equipment to handle infusion, and refrigeration of medication can be made available. A home health nurse may be brought to the workplace to assist in this treatment plan. The individual may require frequent breaks to rest and eat. Depending on the affected bone and whether the individual had an amputation, restrictions on weight lifting may be necessary. Other restrictions and accommodations relate to the specific body part involved.

Source: Medical Disability Advisor

 

Failure to Recover

If an individual fails to recover within the expected maximum duration period, the reader may wish to consider the following questions to better understand the specifics of an individual’s medical case. Regarding diagnosis: Has diagnosis of osteomyelitis been confirmed? What was the mechanism of infection? Was the causative organism identified? Were antibiotic (or antifungal) sensitivities determined? Does individual have an underlying condition (e.g., disorders associated with a disabled immune system [organ transplantation, AIDS, cancer], diabetes, obesity, general debility, suboptimal nutrition, sleep dysfunction or apnea, tuberculosis, cardiovascular disease) that may affect recovery? Regarding treatment: Was treatment with broad-spectrum antibiotics initiated immediately once osteomyelitis was suspected? Have antibiotic-resistant organisms been ruled out? Did the initial therapy consist of oral or IV antibiotics? Was antibiotic therapy discontinued before 4 to 6 weeks of treatment were completed? Was surgical decompression required? Is the osteomyelitis associated with some type of fixation device (screw, plate, prosthesis)? Has the device been removed? Have home care services been employed to provide necessary intravenous medication administration and wound care? Has individual received the education and support services necessary to ensure compliance with long-term therapy? Regarding prognosis: Did osteomyelitis result from a bone fracture? Has permanent bone damage occurred? If the osteomyelitis is associated with some type of fixation device (screw, plate, prosthesis) and the device has been removed, how does that affect function? Is the osteomyelitis considered chronic? Has individual experienced complications related to the osteomyelitis? Did the individual need an amputation? Is so, how did that affect overall function? If the individual smoked or abused alcohol or IV drugs, was the individual instructed to stop these habits, and was the individual able to comply? Is an underlying chronic illness being treated effectively?

Infected fractures with or without bone loss

1. Diagnosis

Definition

Open fractures can generally be regarded as contaminated. Since fractures in the dentate area have communication with the oral cavity, these are considered open fractures.
Infections with clinical relevance show swelling, pain, fever, reddening, and secretion of pus. In the case of acute infection radiographic signs can be absent. Chronic cases exhibit the typical signs of osteomyelitis.

Special conditions influencing adequate internal fixation
Instability produces and maintains the infectious process.

Osteosynthesis of an acutely infected fracture or pseudarthrosis must be a safe procedure. Under these conditions, high rigidity (absolute immobility) is mandatory. Therefore the locking reconstruction system 2.4 is recommended. It is important not to place any screws into the infected bone area which must be spared from screw insertion. The reconstruction plate functions as a bridging device. Large areas of infected or necrotic bone require curettage and either immediate or delayed cancellous bone grafting. Antibiotic therapy alone does not eliminate the infection as long as the fracture is unstable.

Clinical findings
Fractures in the dentate area are regarded as open fractures because the gingiva is usually lacerated. These fractures are contaminated. An acute infection is not reflected in the x-ray examination. In chronic cases the bone becomes infected exhibiting the typical clinical and radiographic signs of osteomyelitis.

In addition there will be inflammatory signs such as swelling, pain, fever, reddening, and secretion of pus.

Clinical photograph showing an infected fracture between the first and second molar. The pericoronal gingiva of the second molar contains pus and the swelling fills the vestibular sulcus.

Imaging

OPG confirming the clinical diagnosis of an infected fracture site in the posterior mandibular body with radiolucency around the second molar and an extended fracture zone containing several bone sequestra.

PA view of the same case.

CT scans of the same patient detailing the condition of the fracture zone.

Additional considerations

Patients with infected fractures often present a constellation of problems:

• Noncompliance

• Alcohol addiction

• Drug abuse

• Self-neglect and social deprivation

• Imprisonment

• Dementia

Medical risk factors:

• Chronic corticoid medication

• Immune deficiency

• Diabetes mellitus

• Osteopathy

2. Principles

Formal pathogenesis

A predilection zone for infected fractures is the posterior mandibular body or the angle region. Contributing factors in this area are due to the occurrence of impacted or partially impacted wisdom teeth. The chronic infection leads to osteomyelitis with inflammatory resorption and sequestration of the bone in the proximity of the fracture line.

The current concept is that the infection and osteomyelitis are propagated by the instability and mobility of the fracture fragments.

When dealing with osteomyelitis, the infected fracture will be debrided and leave the patient with a defect fracture situation.

If the bony defect extends throughout the entire fracture, grafting will be necessary.

Choice of implant

Since the rigidity of large plates is defined by the number and diameter of the inserted screws, it is recommended to use reconstruction plates compatible with large diameter screws only, ie, 2.4 or 3.0 mm screws.

The span of the plate has to cover such a length that at least three screws on either side of the defect can be inserted into intact bone. Very often, with large span defects, it is advisable to have four or more screws on either side of the defect.

3. Sequestrectomy and debridement

Clearing of the infected area

After wide exposure of the outer bony surface the infected area must be cleared of any granulation tissue.
The extent of the exposure must anticipate the application of a large reconstruction plate allowing for the placement of at least three screws on either side away from the defect.

Sequestrectomy

Remove the dead bone (sequestra) and decorticate the bony surfaces of the fractured ends.

Smoothing bony edges

Sharp bony edges should be burred away. The remaining bone surfaces should have bleeding patches to make sure that the vascularization is maintained.
This will define the size of the eventual defect.

The mandibular nerve should be preserved, if not irreversibly damaged by the chronic infectious process.

Tooth and sequestra removed.

4. Load-bearing osteosynthesis

MMF and preliminary fragment fixation

The tooth bearing distal part of the fracture is secured via MMF. The condyle bearing part is positioned arbitrarily by pushing the condyle into the fossa and a small (adaptation) plate is applied onto the superior border of the defect in order to maintain the position of the fragments while the reconstruction plate is adapted and secured.

Contouring the plate

The load-bearing bridging plate is contoured to the lower border with the help of a malleable template.

The contour of the plate must match the template in all three dimensions.

Plate fixation

The bridging plate is firmly applied to the bone with plate forceps and the screws are inserted in the usual manner, starting with the screws closest to the defect zone.

Option: remove adaptation plate
After all screws are inserted, optionally, remove the adaptation plate at the superior border of the mandible.

Occlusion check

Load-bearing osteosynthesis is stable and cannot be influenced postoperatively using elastic tractions. Therefore, the occlusion must be checked after applying the plate. If it does not fit it must be decided whether the occlusion can be corrected by minimally grinding the teeth or repositioning of the bone and plate. The revision of the osteosynthesis may be difficult because of reduced quality of the bone and reduced bony buttressing.

Removal of arch bars
Usually, this type of fracture occurs in compromised or noncompliant patients. Therefore, one might consider removal of all MMF appliances prior to intraoral wound closure (at the tooth extraction site). This can facilitate oral hygiene.

5. Intraoral plastic soft-tissue coverage

The intraoral mucoperiosteum is closed using the envelope technique with a flap derived from the lateral vestibule.
This is done prior to any bone grafting in order to separate the defect from the oral cavity.

6. Same stage bone grafting

Bone harvesting

If immediate bone grafting is desired, bone is harvested from the anterior iliac crest or the tibial head according to preference and the amount of bone graft needed.

In this case a corticocancellous piece and cancellous chips were taken from the inner table of the iliac crest.

The corticocancellous piece was shaped approximately to the size of the defect. Holes were drilled to increase the bony surface in order to enhance revascularization.

Cancellous chips were harvested to augment and fill in the defect.

Applying the bone graft

All bone grafts are inserted through the external approach.
The shape of the corticocancellous bone graft is checked and introduced into the defect.

The remaining dead space is filled with cancellous chips which are further used to augment the area.

7. Extraoral wound closure

The use of suction drain is at the discretion of the surgeon. The external wound is closed in layers.

8. Completed osteosynthesis

Panoramic x-ray showing the plate osteosynthesis bridging the defect zone in the left posterior mandibular body.

Note: there are three screws on each side of the defect and these are placed away from the fracture. The defect zone appears opaque because of the bone graft.

A nasogastric tube is used to feed the patient to enhance intraoral hygiene.

9. Aftercare

If arch bars or MMF screws are used, they may be removed at the conclusion of surgery or may be maintained for several weeks at the discretion of the surgeon.
Postoperative x-rays are taken within the first days after surgery. In an uneventful course, follow-up x-rays are taken at the 4–6 week interval.
It will be necessary to see the patient after approximately 1 week to assess the stability of the occlusion. In an infected mandibular fracture, the aftercare has to include the observation of a number of factors including the special wound situation, the general health condition (nutritional status, diabetes, and particular medication), psychosocial status, economical situation and specific local regimens. The surgeon must also evaluate patient response to the current antibiotic regimens and check for systemic parameters (for example, CRP, white cell blood count, erythrocyte sedimentation rate). Patients will have to be re-examined periodically to rule out recurring signs of infection. At each visit, the surgeon must evaluate patient ability to perform adequate oral hygiene and wound care. It may be necessary to provide additional instruction to assure appropriate hygiene and wound care.

If a malocclusion is detected, the surgeon must ascertain the etiology of it (using the appropriate imaging technique). If the malocclusion is secondary to surgical edema or muscle splinting, training elastics may be beneficial. The lightest elastics possible are used for guidance, because active motion of the mandible is desirable. Patients should be shown how to place and remove the elastics using a hand mirror.

If the malocclusion is secondary to a bony problem due to inadequate reduction or hardware failure or displacement, elastic training will be of no benefit. The patient must return to the operating room for revision surgery.
Follow-up appointments are at the discretion of the surgeon, and will also depend on the stability of the occlusiooted on the first visit. If a malocclusion is noted and treatable by using training elastics, at weekly appointments to determine the progression are recommended.

Postoperatively, patients will have to follow three basic instructions:

1. Diet
Depending upon the stability of the internal fixation, the diet can vary between liquid and semi-liquid to “as tolerated”, at the discretion of the surgeon. Any elastics are removed during eating.

2. Oral hygiene
Patients having only extraoral approaches are not compromised in their routine oral hygiene measures and should continue with their daily schedule.
Patients with intraoral wounds must be instructed in appropriate oral hygiene procedures. The presence of the arch-bars and any elastics makes this a more difficult procedure thaormal. A soft toothbrush (dipping in warm water makes it softer) should be used to clean the surfaces of the teeth and arch-bars. Any elastics are removed for oral hygiene procedures. Chlorhexidine oral rinses should be prescribed and used at least three times each day to help sanitize the mouth. For larger debris, a 1:1 mixture of hydrogen peroxide/chlorhexidine can be used. The bubbling action of the hydrogen peroxide helps remove debris. A Waterpik® is a very useful tool to help remove debris from the wires. If a Waterpik is used, care should be takeot to direct the jet stream directly over intraoral incisions as this may lead to wound dehiscence.

3. Physiotherapy
Physiotherapy can be prescribed at the first visit and opening and excursive exercises begun as soon as possible. Goals should be set, and, typically, 40 mm of maximum interincisal jaw opening should be attained by 4 weeks postoperatively. If the patient cannot fully open his mouth, additional passive physical therapy may be required such as Therabite or tongue-blade training.

 CHRONIC (ODONTOGENIC AND NEODONTOHENNYY) OSTEOMYELITIS OF THE JAWS IN CHILDREN. CLINICAL AND RADIOGRAPHIC FORMS OF THE DISEASE. PRIMARY CHRONIC OSTEOMYELITIS. DIAGNOSIS, DIFFERENTIAL DIAGNOSIS, TREATMENT, COMPLICATIONS AND THEIR PREVENTION.

 

 

Osteomyelitis Jaw

Osteomyelitis is an infection of the bone. It can be caused by a variety of microbial agents (most common in staphylococcus aureus) and situations, including:

• An open injury to the bone, such as an open fracture with the bone ends piercing the skin.

• An infection from elsewhere in the body, such as pneumonia or a urinary tract infection that has spread to the bone through the blood (bacteremia, sepsis).

• A minor trauma, which can lead to a blood clot around the bone and then a secondary infection from seeding of bacteria.

• Bacteria in the bloodstream bacteremia (poor dentition), which is deposited in a focal (localized) area of the bone. This bacterial site in the bone then grows, resulting in destruction of the bone. However, new bone often forms around the site.

• A chronic open wound or soft tissue infection can eventually extend down to the bone surface, leading to a secondary bone infection.

Osteomyelitis affects about two out of every 10,000 people. If left untreated, the infection can become chronic and cause a loss of blood supply to the affected bone. When this happens, it can lead to the eventual death of the bone tissue.

Osteomyelitis can affect both adults and children. The bacteria or fungus that can cause osteomyelitis, however, differs among age groups. In adults, osteomyelitis often affects the vertebrae and the pelvis. In children, osteomyelitis usually affects the adjacent ends of long bones. Long bones (bones of the limbs) are large, dense bones that provide strength, structure, and mobility. They include the femur and tibia in the legs and the humerus and radius in the arms.

Osteomyelitis does not occur more commonly in a particular race or gender. However, some people are more at risk for developing the disease, including:

• People with diabetes

• Patients receiving hemodialysis

• People with weakened immune systems

• People with sickle cell disease

• Intravenous drug abusers

• The elderly

Symptoms of osteomyelitis

The symptoms of osteomyelitis can include:

• Pain and/or tenderness in the infected area

• Swelling and warmth in the infected area

• Fever

• Nausea, secondarily from being ill with infection

• General discomfort, uneasiness, or ill feeling

• Drainage of pus through the skin

Additional symptoms that may be associated with this disease include:

• Excessive sweating

• Chills

• Lower back pain (if the spine is involved)

• Swelling of the ankles, feet, and legs

• Changes in gait (walking pattern that is a painful, yielding a limp)

Diagnosing osteomyelitis

To diagnose osteomyelitis, the doctor will first perform a history, review of systems, and a complete physical examination. In doing so, the physician will look for signs or symptoms of soft tissue and bone tenderness and possibly swelling and redness. The doctor will also ask you to describe your symptoms and will evaluate your personal and family medical history. The doctor can then order any of the following tests to assist in confirming the diagnosis:

• Blood tests: When testing the blood, measurements are taken to confirm an infection: a CBC (complete blood count), which will show if there is an increased white blood cell count; an ESR (erythrocyte sedimentation rate); and/or CRP (C-reactive protein) in the bloodstream, which detects and measures inflammation in the body.

• Blood culture: A blood culture is a test used to detect bacteria. A sample of blood is taken and then placed into an environment that will support the growth of bacteria. By allowing the bacteria to grow, the infectious agent can then be identified and tested against different antibiotics in hopes of finding the most effective treatment.

• Needle aspiration: During this test, a needle is used to remove a sample of fluid and cells from the vertebral space, or bony area. It is then sent to the lab to be evaluated by allowing the infectious agent to grow on media.

• Biopsy: A biopsy (tissue sample) of the infected bone may be taken and tested for signs of an invading organism.

• Bone scan: During this test, a small amount of Technetium-99 pyrophosphate, a radioactive material, is injected intravenously into the body. If the bone tissue is healthy, the material will spread in a uniform fashion. However, a tumor or infection in the bone will absorb the material and show an increased concentration of the radioactive material, which can be seen with a special camera that produces the images on a computer screen. The scan can help your doctor detect these abnormalities in their early stages, when X-ray findings may only show normal findings.

Treating and managing osteomyelitis

The objective of treating osteomyelitis is to eliminate the infection and prevent the development of chronic infection. Chronic osteomyelitis can lead to permanent deformity, possible fracture, and chronic problems, so it is important to treat the disease as soon as possible.

Drainage: If there is an open wound or abscess, it may be drained through a procedure called needle aspiration. In this procedure, a needle is inserted into the infected area and the fluid is withdrawn. For culturing to identify the bacteria, deep aspiration is preferred over often-unreliable surface swabs. Most pockets of infected fluid collections (pus pocket or abscess) are drained by open surgical procedures.

Medications: Prescribing antibiotics is the first step in treating osteomyelitis. Antibiotics help the body get rid of bacteria in the bloodstream that may otherwise re-infect the bone. The dosage and type of antibiotic prescribed depends on the type of bacteria present and the extent of infection. While antibiotics are often given intravenously, some are also very effective when given in an oral dosage. It is important to first identify the offending organism through blood cultures, aspiration, and biopsy so that the organism is not masked by an initial inappropriate dose of antibiotics. The preference is to first make attempts to do procedures (aspiration or bone biopsy) to identify the organisms prior to starting antibiotics.

Splinting or cast immobilization: This may be necessary to immobilize the affected bone and nearby joints in order to avoid further trauma and to help the area heal adequately and as quickly as possible. Splinting and cast immobilization are frequently done in children, although motion of joints after initial control is important to prevent stiffness and atrophy.

Surgery: Most well-established bone infections are managed through open surgical procedures during which the destroyed bone is scraped out. In the case of spinal abscesses, surgery is not performed unless there is compression of the spinal cord or nerve roots. Instead, patients with spinal osteomyelitis are given intravenous antibiotics. After surgery, antibiotics against the specific bacteria involved in the infection are then intensively administered during the hospital stay and for many weeks afterward.

With proper treatment, the outcome is usually good for osteomyelitis, although results tend to be worse for chronic osteomyelitis, even with surgery. Some cases of chronic osteomyelitis can be so resistant to treatment that amputation may be required; however, this is rare. Also, over many years, chronic infectious draining sites can evolve into a squamous-cell type of skin cancer; this, too, is rare. Any change in the nature of the chronic drainage, or change of the nature of the chronic drainage site, should be evaluated by a physician experienced in treating chronic bone infections. Because it is important that osteomyelitis receives prompt medical attention, people who are at a higher risk of developing osteomyelitis should call their doctors as soon as possible if any symptoms arise.

Osteomyelitis for Jaw Treatment

Osteomyelitis occurs when a bone becomes infected. Though osteomyelitis most often occurs in the bones of the limbs, spine and pelvis, it can also affect the jaw. Osteomyelitis in the jaw is a rare condition that once had been thought incurable, however advances in medicine make the condition treatable. It can present itself in either acute or chronic forms. Osteomyelitis is a serious condition and if proper treatment is not sought, it can destroy your bones.

Symptoms

The symptoms for people with osteomyelitis in the jaw include pain and tenderness, swelling around the jaw, drainage in the sinus cavity, loss of teeth, discharging of pus and necrotic bones. Factors that can lead to osteomyelitis include tobacco, anaemia, viral infections and malnutrition. Since the condition exhibits symptoms that are common in many other diseases, osteomyelitis can be difficult to diagnose at first. If you have chronic osteomyelitis, debilitating fatigue is also very common symptom.

Diagnosis

If your doctor suspects osteomyelitis, he will order various tests before he can make a firm diagnosis. Though a blood test does not define an osteomyelitis diagnosis, a high level of white blood cells will indicate that body is fighting off an infection. If your osteomyelitis is advanced, an X-ray will show the extent of the damage. If you need a better image, your doctor may recommend a CAT scan or MRI. Your doctor may also remove a piece of your bone for a biopsy. This biopsy will check for the strain of bacteria that has infected your bone.

Treatment

Most often infections of the jaw are polymicrobial oral flora so a regimen of antibiotics are used to treat the infection. You doctor may prescribe penicillin, clindamycin and metronidazole. Depending on the extent of the infection, surgery may be required. Your doctor will decide which procedure is best based on the damage caused by the infection. Some bone and tissue may need to be removed, fractures repaired and rotten teeth extracted. You may also want to consult with an oral-maxillofacial surgeon to see if facial reconstruction is required.

Osteomyelitis
Osteomyelitis is a rare complication of tooth-related infections (incidence of 25 in 100,000).  In most cases, it is the result of spread of infection from a dento-
alveolar (tooth) or periodontal (pyorrhoea / gum disease) abscess or from the para-nasal sinuses, by way of continuity throughtissue spaces and planes.  It occasionally occurs as a complication of  jaw fractures or as a result of manipulations during surgical procedures.
Most patients are adult males with infection of the mandible (lower jaw).
Osteomyelitis of the maxilla (upper jaw) is a rare disease of neonates (newly born) or infants after either birth injuries or uncontrolled middle ear infection.
It is classified as acute or chronic osteomyelitis.
Acute Osteomyelitis
In the acute form (which rarely, may also be of hæmatogenous origin [i.e. seeded from the blood stream]), the infection begins in themedullary cavity (bone marrow) of the bone.  The resulting increase of intra-bony pressure leads to a decreased blood supply (and hence diminution of white blood cells and other immune 
components) and spread of the infection, by way of the Haversian canals of the bone, to the cortical bone (definition) andperiosteum (below the periosteum, a thick 
fibrous two-layered membrane covering the surface of bones).  This aggravates the ischæmia (decreased blood supply), resulting innecrosis (the death of cells or tissues from severe injury or disease, especially in a localised area of the body.  Causes of necrosisinclude inadequate blood supply [as in infarcted tissue], bacterial infection, traumatic injury and hyperthermia) of the bone.
Acute Osteomyelitis of the Jaws — Potential Sources of 
Infection

• Peri-apical infection

• A periodontal pocket involved in a fracture

• Acute gingivitis or pericoronitis (even more rarely)

• Penetrating, contaminated injuries (open fractures or 
  gunshot wounds)

Important Predisposing Conditions for Osteomyelitis
Local Damage to / Disease of the Jaws

• Fractures, including gunshot wounds

• Radiation damage

• Paget’s disease

• Osteopetrosis

Impaired Immune Defences

• Acute leukaemia

• Poorly-controlled diabetes mellitus

• Sickle cell anaemia

• Chronic alcoholism or malnutrition

• AIDS

 

• Infection from micro-organisms with great virulence.  
  In such cases, even a peri-apical abscess may be 
  implicated in osteomyelitis.

Acute Osteomyelitis of the Jaws — Key Features

• Mandible mainly affected, usually in adult males

• Infection of dental origin – anærobes are important

• Pain and swelling of jaw

• Teeth in the area are tender; gingivæ (gums) are red 
  and swollen

• Sometimes paræsthesia of the lip

• Minimal systemic upset

• After about 10 days, X-rays show ‘moth-eaten’ 
  pattern of bone destruction

• Good response to prompt antibiotic treatment and 
  debridement

The mandible (lower jaw), due to decreased vascularity (blood supply & flow), is 
involved 6 times more often than the maxilla (upper jaw).
The mandible has a relatively limited blood supply and dense bone with thick bony 
(cortical) plates.  Infection causes acute inflammation in the medullary (bone 
marrow) soft tissues and inflammatory exudate (a fluid with a high content of 
protein and cellular debris which has escaped from blood vessels and has been 
deposited in tissues or on tissue surfaces, usually as a result of inflammation. It 
may be septic or non-septic) spreads infection through the marrow spaces.  It also 
compresses blood vessels confined in the rigid boundaries of the vascular canals.

Thrombosis (the formation or presence of a thrombus [a clot of coagulated blood 
attached at the site of its formation] in a blood vessel) and obstruction then lead to 
further bone necrosis.

Dead bone is recognisable microscopically by lacunae (a cavity, space, or 
depression, especially in a bone, containing cartilage or bone cells) empty of 
osteocytes (a cell characteristic of mature bone tissue.  It is derived from 
osteoblasts and embedded in the calcified matrix of bone. Osteocytes are found in 
small, round cavities called lacunae and have thin, cytoplasmic branches) but filled 
with neutrophils (white blood cells) and colonies of bacteria which proliferate in the 
dead tissue.

Pus, formed by liquefaction of necrotic soft tissue and inflammatory cells, is forced 
along the medulla and eventually reaches the sub-periosteal region by resorption 
(an organic process in which the substance of some differentiated structure that 
has been produced by the body undergoes lysis and assimilation) of bone.  
Distension of the periosteum by pus stimulates sub-periosteal bone formation but 
perforation of the periosteum by pus and formation of sinuses on the skin or oral 
mucosa are rarely seeow.

At the boundaries between infected and healthy tissue, osteoclasts (a specialised 
bone cell that absorbs bone) resorb the periphery of the dead bone, which eventually becomes separated as a sequestrum (a fragment of dead bone separated from healthy bone as a result of injury or disease).  Once infection starts to localise, new bone forms around it, particularly sub-periosteally.
Where bone has died and been removed, healing is by granulation with formation of 
coarse fibrous bone in the proliferating connective tissue.  After resolution, fibrous 
bone is gradually replaced by compact bone and remodelled to restore normal 
bone tissue and structure (and function).
Piercing, deep and constant pain predominates in the clinical presentation in adults, 
while low or moderate fever, cellulitis, lymphadenitis, or even trismus may also be 
noted.
In the mandible, changes in sensation affecting the lower lip (paræsthesia or 
dysæsthesia of the lower lip) may accompany the disease.  When the disease 
spreads to the peri-osteum (definition) and the surrounding soft tissues, a firm 
painful œdema (definition) of the region is observed, while the tooth becomes loose 
and there is discharge of pus from the periodontium.  Radiographic examination 
reveals osteolytic (definition) or radiolucent (definition) regions.
Therapy entails combined surgical (incision, drainage, extraction of the tooth and 
removal of sequestrum) and chemo-therapeutic treatment (with antibiotics).
Summary of Treatment of Osteomyelitis
Essential Measures

• Bacterial sampling and culture

• Vigorous (empirical) antibiotic treatment

• Drainage

• Give specific antibiotics based on culture and sensitivities

• Give analgesics

• Debridement

• Remove source of infection, if possible

Adjunctive Treatment

• Sequestrectomy

• Decortication if necessary

• Hyperbaric oxygen*

• Resection and reconstruction for extensive bone destruction

*Mainly of value for osteo-radionecrosis and possibly, anærobic infections.

Anæsthesia of the lower lip usually recovers with elimination of the infection.  Rare 
complications include pathological fracture caused by extensive bone destruction, 
chronic osteomyelitis after inadequate treatment, cellulitis due to spread of 
exceptionally virulent bacteria or septicæmia in an immuno-deficient patient.

Chronic Osteomyelitis

Chronic osteomyelitis is characterised by a clinical course lasting over a month.  It 
may occur after the acute phase or it may be a complication of tooth-related 
infection without a preceding acute phase.  The clinical presentation is milder, with 
painful exacerbations and discharge of pus or sinus tracts.

Osteomyelitis – Inflammation of the Bone

The terms osteomyelitis, periostitis and ostitis are frequently used as synonyms for inflammation of the bone.

Let’s have a quick look at the definition of the terms. Since the bone itself (the calcium structure) cannot get inflamed osteomyelitis(meaning bone marrow inflammation) and periostitis (meaning bone lining inflammation) would be the correct descriptions for an inflammation of the bone. Nevertheless ostitis is becoming more and more the term used.

The cause of an inflammation of the bone can come from outside – (exogenous factors) or from inside (endogenous factors). When both factors occur at the same time then we speak of combined forms. The so called idiopathic factors may also be regarded as a fourth form, consisting of bone inflammations of unidentifiable origin. Exogenous factors include, for example, numerous bacteria, viruses and fungi. They are potential pathogenic agents. If these pathogens find their way into our body they can cause an inflammation. If the inflammation gets into the bone then it’s a bone inflammation.

In the case of endogenous factors the cause lies in our own bodies. For example, in the case of diabetics the raised level of sugar of a diabetic leads to ever-increasing thickening of the walls of the blood vessels and thus an ever-poorer flow of blood.

The flow of blood can get so bad that certain areas of the body are no longer reached by it any more and the affected tissues die due to lack of oxygen and will be destroyed as a consequence of an inflammatory reaction – this can also occur in the bones, as shown in the animation and that would be an example of an endogenous osteomyelitis.

X-ray of Jaw Structure

Idiopathic osteomyelitis means to the patient that, at the end of the day the doctor cannot find an adequate explanation for it.

In the area of the jaw the most common causes of bone inflammation are exogenous or, more accurately, iatrogenous (caused by the doctor). Thus often extractions and/or badly root-treated teeth lead to bone infections.

In the picture you can see an x-ray of an extraction wound (circled in blue), the bone in this area is inflamed (circled in red) – osteomyelitis. In order to diagnose osteomyelitis an x-ray is usually required. In the same picture you can see a tooth (circled in green), which has an inflammation of the bone going on at the tip of the root (circled in red), as can be seen from the dark spot.

An x-ray can provide a lot of information about the bone but if precision is needed then a CT or MRT scan is very useful. This brings us to the diagnosis of osteomyelitis – CT and MRT scans are very reliable diagnostic aids at a certain stage of the osteomyelitis but at a very early stage of the illness their usefulness is rather limited.

Nuclear medical examinations such as skeletal cintography (Tc-99m) are frequently being made use of in order to detect osteomyelitis. The radioactive element technetium will be seen to be concentrated in the areas with raised bone metabolism after being applied intravenously. This increased concentration can be seen from the outside by means of a special camera (the darker spots in the exposure). Unfortunately it is not possible with this method to distinguish between the different causes of the raised bone metabolism.

Is the cause an inflammation or only an innocent build-up of bone after all?

With the addition of special factors (marked anti-granulocyte antibodies for additional investigation) the examination can however be made more specific. Blood tests are likewise not specific and unfortunately the blood values of the inflammation do not always correlate with the values of the osteomyelitis – especially in the jaw area. A bone biopsy is usually the most reliable means of diagnosis, as this way the bone can be viewed very precisely under the microscope (histological examination), and it may be possible to isolate the offending pathogen on the culture glass (bacteriology). If this succeeds then an antibiogram can be carried out in order to find the antibiotic with which to destroy the pathogen.

Bone Scan Scintigraphy

However, biopsy has a couple of disadvantages. The examination is invasive (therefore a wound is unavoidable) and not all areas of bone can be biopsied easily. Sometimes the bacteriological investigations are not successful or it may happen that during the taking of the sample there is contamination of the sample, for example by non-specific bacteria from the mouth.

Finally, let us take a look at the treatment options for osteomyelitis. There are various treatment options available – in the worst case the affected bone must be removed but this is very seldom necessary. The most frequent and simplest treatment option is the prescription of antibiotics, which can be swallowed or applied intravenously. The latter gives a higher concentration of the active ingredient in the blood.

By means of oxygen therapy we enrich the concentration of oxygen in the blood, since within the inflamed bone there is frequently insufficient blood supply and consequently, too little oxygen, ideal conditions for the multiplication of bacteria which do not tolerate oxygen – anaerobic bacteria as they are known. Oxygen-rich blood should have an effect on them, as per the motto: a little blood but very rich.

Another very much talked about treatment is the removal of the sick bone and the filling of the resultant gap with replacement donor bone which has been enriched with an antibiotic. In the animation you can see how the donor bone with the antibiotic (shown in green here) is put in place. The inflamed bone (shown in red here) will be removed and the donor bone will be inserted in the resulting cavity. The antibiotic will then pass continually into the body over months and simultaneously the replacement bone can regenerate.

The advantage of this treatment is that far higher concentrations of medication can be placed specifically in the affected area unlike with the usual means of application (orally or intravenously). Examination over a long period of time is still needed in order to evaluate this treatment over several years.

Ideally you want to avoid it getting to that stage. At least the iatrogenic forms of osteomyelitis can be avoided through sterilisation and cleanliness in the dental clinic.

Osteomyelitis

Odontogenic infection via a root canal, a periodontal pocket or an extraction wound is the most common local cause of osteomyelitis of the jaws. Rarely, a fracture serves as in infection route. Haematogenous spread of an infective agent from another part of the body also occurs. A distinct type of osteomyelitis, osteoradionecrosis, occurs after therapeutic irradiation of oral and neck malignancies.

Figure 20. 
An ill-defined periapical and interdental osteolytic lesion in the mandibular anterior region three weeks after onset of clinical symptoms of osteomyelitis.

Figure 21.
Chronic suppurative osteomyelitis with three sequestra (arrows). Osteolytic as well as sclerotic areas are present.

Osteomyelitis is more common in the mandible than in the maxilla. In the mandible, it occurs predominantly in the posterior parts, the ramus included, whereas in the maxilla, it is more frequent in the anterior than in the posterior parts. In the acute phase, osteolysis is not visible radiographically until one or two weeks after the onset of clinical symptoms which are: pain, fever, local lymphadenopathy, increased white blood cell count, and teeth sensitive to percussion. Numbness of the lower lip is another common sign of mandibular osteomyelitis.

The initial radiographic changes are blurring and thinning of the trabeculae and subsequent enlargement of the bone marrow spaces. Without treatment, large volumes of the bone tissue can rapidly become involved, causing loosening of the teeth (Fig. 20).

If acute osteomyelitis becomes chronic, it is frequently possible to distinguish between chronic suppurative osteomyelitis (Fig. 21) and chronic sclerosing osteomyelitis (Fig. 22), both of which have ill-defined borders. In the suppurative form, radiolucent areas alternate with sclerotic, giving the bone a “moth-eaten” appearance. This is further enhanced when sequestra develop. In chronic sclerosing osteomyelitis, radiolucent areas occur, but there is a predominance of radiopaque changes due to the formation of sclerotic bone. The bone is often enlarged through periosteal bone formation (Figs. 22, 23). Over time, the distribution of sclerotic and radiolucent areas varies, indicating disease activity.

Figure 22.
Chronic sclerosing osteomyelitis of right mandible with some osteolytic areas. Ramus is enlarged.

b

Figure 23.
a) Right mandibular molars in a young patient. The alveolar bone is unevenly sclerotic; chronic sclerosing osteomyelitis.
b) Occlusal view of the same patient. Periosteal bone formation (arrow) on the buccal side of the mandible.

Fig. 1.

Cropped panoramic radiograph of suppurative osteomyelitis at the right mandible. Osteolytic change is observed from around the molar tooth roots to the body of the mandible (arrows).

How to Diagnose Osteomyelitis

Osteomyelitis is an infection of the bone, generally caused by the Staphylococcus Aureus bacteria. This bacteria infects the bones because it travels through the blood from other infected areas. It can also come directly from a wound and travel straight to the bone. A common cause of Osteomyelitis is an open fracture, where not only the bone breaks, but the skin breaks too.

 

Instructions

1.       Perform a physical examination of the patient. Be sure to take a complete medical history and list any medications the patient is already taking. Also ask about any recent problems with the area the patient says is painful.

2.       Take a blood sample to perform a blood test to pinpoint if the patient’s white blood cell count is high, which is often a sign of infection. Look for signs of infection in the body, such as areas that are inflamed, red and warm.

3.       Send the patient for a bone x-ray. A bone x-ray can show if there is an infection in the bone, but might not be as accurate for someone who has just started complaining of pain. If the bone x-ray does not come back positive, but the patient exhibits signs of Osteomyelitis, send them for a bone scan, which gives you a more detailed view of the bone.

4.       Follow up with an MRI, if the bone scan indicates osteomyelitis. MRIs are a valuable test to run. In addition to diagnosing osteomyelitis, the MRI can also help determine how long the infection has been in the bone.

Osteomyelitis may manifest itself in acute, subacute, or chronic forms. Chronic osteomyelitis will result in variable sclerosis and deformity of the affected bone. After the age of 50, the majority of the blood supply to the mandible comes from the overlying periosteum and attached musculature, due to age and atherosclerosis-related involution of the inferior alveolar artery. With an infection of the bone, the subsequent inflammatory response will elevate this overlying periosteum, leading to a loss of the nourishing vasculature, vascular thrombosis, and bone necrosis, resulting occasionally in formation of sequestra. These become areas that are more resistant to systemic antibiotic therapy due to lack of the normal Haversian canals that are blocked by scar tissue, inflammatory exudate, and necrotic bone. At this point, not only systemic antibiotic therapy, but also surgical debridement maybe required to remove the affected bone and prevent disease propagation to adjacent areas. The relative hypoxia seen in infected bone will impair leukocyte bacterial killing, and impede fibroblastic collagen production that is required to support angiogenesis. Thus, it is not surprising that the concomitant use of hyperbaric oxygen therapy maybe beneficial in cases refractory to medical management alone or in patients with a severely compromised immune response. Generally, 20 dives (2.8-3.0 at 100% oxygen for 90 minutes) are administered preoperatively, followed by 20 dives after the debridement of necrotic tissue.

Radiographic imaging may be deceptively unremarkable in acute osteomyelitis, particularly with plain x-rays. Computed tomography (CT) scanning is the standard for evaluating the bone for sequestrum formation. Generally, one sees areas of lytic destruction and overlying periosteal reaction. It is much more common to find cortical plate disruption in the buccal plate than in the lingual plate. Technetium⁹⁹ bone scanning is often positive within 24 hours of an acute infection. Unfortunately, persistent uptake maybe present for 2 years after eradication of osteomyelitis. Gallium^-67 scanning normalizes after successful treatment of mandibular osteomyelitis.

In acute osteomyelitis, or in chronic forms without evidence of formation of sequestra, culture-driven antibiotic therapy is important to allow for disease eradication and decrease the likelihood of formation of antibiotic resistant strains resulting from inadequate subtherapeutic antibiotic therapy. Occasionally, repeated cultures may be required to allow for pathogen isolation, especially in cases of chronic osteomyelitis. Open biopsy of the bone allows for the most accurate culture results. Alpha hemolytic streptococcus, often in conjunction with oral anaerobes, is the most commonly isolated organism noted today. Although acute osteomyelitis is often adequately treated with a culture-driven 6- to 8-week course of antibiotic therapy, chronic osteomyelitis generally requires surgical debridement as well. Antibiotic therapy should be continued for 4 to 6 weeks from the date of last debridement, from resolution of the patient’s symptom complex and/or normalization of the gallium scan (if performed). Refractory osteomyelitis may benefit from the addition of hyperbaric oxygen therapy. Vancomycin or clindamycin are generally effective in the treatment of group A or B streptococci. However, as stated, culture-driven antibiotic therapy is required. With the propagation of multidrug-resistant varieties, treatment with nontraditional antibiotic regimens, such as fluroquinolones, may be required. Attention to optimal management of any underlying systemic immunocompromising conditions, such as diabetes mellitus, steroid usage, and HIV infection is important in all cases.

Clinical features, Radiographic features and treatment of Chronic Osteomyelitis of mandible

Clinical feature:
1. Site: Mandible
2. At early stage:
a. General constitutional symptoms:
• Intermittent fever
• Malaise
• Nausea, vomiting
• Anorexia
b. Pain:
• Deep seated
• Paresthesia of the lower lip

Radiology of Chronic OML• Facial cellulitis

• Trismus
• Swelling
3. Established case of OML:
a. Deep pain
b. Loosening of involved teeth
c. Pain on percussion
d. Sensitivity
e. Purulent discharge of pus
f. Regional lymphadenopathy
g. Trismus
Radiological feature:
1. In early stage, there are no findings
2. The changing begins 4-6 weeks after infection
3. In ate stage of Osteomyelitis, we find sequesterum, involucrum, scattered area, moth eaten appearance in conventional radiograph.
4. For specialized image, we do: CT scan, Radionucleido bone scan, Positron emission tomography.

Treatment:
1. Conventional treatment:
a. Complete bed rest
b. Supportive therapy:
• Nutritional support
• High protein diet
• High calorie and multivitamin diet
c. Rehydration by IV fluid
d. Blood transfusion
e. IV antimicrobial agent
2. Surgical treatment:
a. Incision and drainage   b. Extraction of the offending tooth   c. Debridement of the affected area by irrigating with H2O2 and normal saline  d. Sequestrectomy e. Decortication f. Saucerisation  g. Resection
Post operative care:
1. Continuous use of antibiotics
2. Analgesics
3. Adequate hydration
4. Complete bed rest
5. Follow up

Suppurative mandibular osteomyelitis

Suppurative mandibular osteomyelitis refers to agents that invasion of the mandible, the bone tissue as a whole, including the periosteum, cortical bone, bone marrow and the blood vessels, nerves, inflammation, alveolar abscess, periodontitis, and the third molar crown weeks go far odontogenic infection from which the highest incidence of mandibular osteomyelitis.

Disease Overview

When agents that invaded the jaw, will cause the entire jaw organizations, including the periosteum, cortical bone, bone marrow, and one of the blood vessels, nerve inflammation range of leisure, known as purulent maxillary osteomyelitis. Classification of Diseases 1 performance classification, according to the clinical pathology of suppurative odontogenic mandibular osteomyelitis lesions originating in the maxillary central cancellous bone and bone marrow, known as the Central osteomyelitis, lesions originating in the periosteum and cortical bone of the jaw around the , called the edge of osteomyelitis, according to the nature of the lesions can be divided into acute and chronic phase, the scope of the validation can be divided into localized or diffuse suppurative disease cause of mandibular osteomyelitis of up to alveolar abscess, periodontitis, third molar pericoronitis go far odontogenic infection from, followed by invasive infection due to a comminuted fracture or gunshot wound in open injury to bone by the blood circulation of sepsis or sepsis infection. this situation occurred in the maxilla of the infants and young children, very few of the infection of facial skin or oral mucosa directly affect the jaw. put the treatment of oral cancer or nasopharyngeal carcinoma, osteomyelitis common major pathogens Staphylococcus aureus bacteria, followed by Streptococcus, a few other pyogenic bacteria, stereotypes of mixed infections. pathophysiology of mandibular osteomyelitis compared with the previous mandibular osteomyelitis is more common condition than maxillary bone marrow serious, this is because the upper jaw bone dense fascia and strong muscles, present jaw infection, pus is not left around the puncture drainage poor blood supply of the mandible, infection of vascular thrombosis, it is easy to form a large sequestrum. diagnostic tests 1, details incidence and its treatment, consultation, attention to the relationship with the teeth, identify pathogen teeth. 2, with or without empyema sense of volatility, can be used to puncture confirmed suspicious when pus for bacterial culture and antibiotic sensitivity determination. fistula, exploration probes and other instruments with or without sequestrum sequestrum separation, X-ray, chronic identifying bone destruction, with or without sequestrum formation or infection of the low toxicity to the bone cortical hyperplasia. .

Clinical symptoms

Symptoms characteristic of central mandibular osteomyelitis, acute early inflammation is often restricted to the alveolar bone or bone marrow of the mandibular body, and then invasion of mandible, from the center to the edges of cortical bone and periosteum. 2. stage, patients may feel a severe toothache, pain along the trigeminal nerve distribution area for radiation lesions of the gingival mucosa hyperemia and edema, teeth percussion pain and loose, and may have gingival sulcus overflow pus or the formation of alveolar abscess , this stage of the lesion has not been timely drainage, the infection will continue to spread to the medullary cavity, can cause diffuse osteomyelitis or perforation of cortical bone formation in subperiosteal abscess, then patients with systemic poisoning symptoms became worse, and this when patients with serious manifestations of anemia, dehydration, exhaustion, body temperature increased to 39 ~ 40 ℃, blood test white blood cells increased significantly, local pain and soft tissue swelling in the affected region of the majority of teeth to loosen, some patients would be a serious concurrent disease, such as sepsis, intracranial infections, such as inflammation has not yet been brought under control, the maxilla infection can cause suppurative maxillary sinusitis and infraorbital cheek, or zygomatic, or pterygopalatine concave, temporal, concave and other regional proliferation. mandibular infection can spread to the inferior alveolar nerve caused by the lower lip numbness spread to the jaw weeks, stimulate the open jaw muscles, causing limited mouth opening, can be complicated by the jaw weeks more space infection, so that the face was seen in the swelling, and finally inflammation in the formation of blood clots within the jaw, resulting in jaw nutritional disorders and necrosis, and thus transferred to the chronic phase. 6, transferred from the acute to the chronic phase of about 2 to 3 weeks later, the pain and other systemic symptoms have begun reduced, but the mouth gums can form multiple fistula and pus. sequestrum with healthy bone will be in about a month later, new bone layer, caused by the separation of the sequestrum with healthy bone. this stage without surgical removal of involved regional fistula pus prolonged unhealed, can sometimes have a small piece of sequestrum discharged from the fistula osteomyelitis of the mandible can cause large sequestrum formation of pathogenic pathologic fracture, marginal mandibular osteomyelitis clinical features , limitations with young people, the lesions occurred, with chronic symptoms, does not appear large sequestrum. 2, occurred in young people under the jaw, the lesion is more limited spread of the infection pathway is not the first damage to bone marrow, but in the periosteum inflammation or subperiosteal abscess on the basis of the first involving the cortical bone, but also to the deep development involving the bone marrow, but rarely large sequestrum formation of the infections originated in the mandibular third molar crown Zhou Yan, can cause masseter muscle space infection subperiosteal abscess, resulting in the mandible of the ascending branch and corner Nutrition disorders of the cortical bone necrosis, showing chronic symptoms, local mild chronic inflammatory swelling and pitting edema due to masseter muscle and pterygoid muscle involvement, and limited mouth opening. pericoronitis infection if not controlled, often repeatedly made. 5, the edge of mandibular osteomyelitis after repeated anti-inflammatory medication, could easily lead to pathogen resistance, the formation of low toxicity and infection jaw inflammation.

Signs and symptoms

In particular, according to the clinical pathology of suppurative odontogenic mandibular osteomyelitis lesionsoriginating in the maxillary centralBone trabecular and bone marrow, known as the Central osteomyelitis lesions originating in the periosteum and cortical bone of the jaw around, known as the edge of osteomyelitis according to the nature of the lesions can be divided into acute and chronic phase, according to The scope of the validation can be divided into localized or diffuse. central mandibular osteomyelitis: the maxilla than the mandible more common in teeth with severe pain, persistent, and radiating pain along the trigeminal nerve distribution. teeth and adjacent teeth loose, percussion pain, vestibular groove fullness, cheek swelling. mandibular alveolar abscess, the pus is not easy worn develop into acute diffuse osteomyelitis and lack of drainage, the patients with systemic symptoms get worse, fever, chills, leukocyte, dehydration and other toxic manifestations. mandibular osteomyelitis refers to agents that invaded the jaw, causing the entire bone tissue, including periosteum, cortical bone, bone marrow and the blood vessels, nerve inflammation, Chinese medicine called ‘bone slot wind ‘or’ wear gills were sharply acute onset of high fever, increased white blood cells, can shift to the left. body poisoning, and with general malaise, headache, loss of appetite and other symptoms can occur in patients toothache, and the pain along the trigeminal nerve distribution area of ​​radiation, and can quickly spread to the adjacent teeth. the short term, there may be multiple tooth mobility, periodontal pocket pus, inferior alveolar nerve by inflammatory damage to the lower lip numbness due to the spread of inflammation to the surrounding maxillofacial swelling which can occur, such as infection spread to the masticatory muscles can be trismus such as infection control in a timely and quickly to the infraorbital, inferior temporal, the pterygopalatine concave and by the mandibular foramen caused the wing jaw space infection. systemic complications such as sepsis, and intracranial infection may also occur.

Disease etiology

Suppurative osteomyelitis of jaw up to the alveolar abscess, periodontitis, the third molar pericoronitis go far odontogenic infection from, followed by open injury due to comminuted or anger injury caused by bone invasive infection, sepsis or infections, sepsis and blood circulation more than occurred in the maxilla of infants and young children, very few of the infection of facial skin or oral mucosa directly affect the jaw. major pathogens Staphylococcus aureus, followed by Streptococcus few other pyogenic bacteria stereotypes mixed infection.

Pathophysiological

Mandibular osteomyelitis compared with maxillary osteomyelitis more common condition than the maxilla bone marrow serious, this is because the upper jaw bone is dense, and some surrounding fascia and strong muscles, present jaw infection, pus left After puncture drainage poor blood supply of the mandible, infection of vascular thrombosis, easy to form a large sequestrum.

Diagnostic tests

A detailed consultation incidence after treatment, and attention teeth identify pathogen teeth.

2, with or without empyema sense of volatility suspicious can be used for puncture confirmed. 3, pus for bacterial culture and antibiotic sensitivity determination, with or without fistula, probes and other instruments to probe whether the sequestrum sequestrum separation. 5, X-ray, the chronic phase to identify bone destruction, with or without sequestrum formation or infection of the low toxicity of the bone cortex hyperplasia type.

Disease Prevention

No special

Safety Tips

 1, the disease mostly occurs in the infant’s maxillary marginal mandibular osteomyelitis: more common in young people, the acute phase is difficult to find common chronic phase 2, the timely treatment of the crown Zhou Yan, the periapical Yandeng odontogenic infection to prevent occurrence of mandibular osteomyelitis. has formed should be a thorough treatment to avoid to chronic osteomyelitis, in the acute phase.

 

Treatment programs

 Acute systemic antibiotics, local incision and drainage or removal of loose teeth, diffuse patient performance Decline thirsty, systemic poisoning, severe anemia, in addition to general supportive therapy, but also a small amount of multiple transfusions and enhance systemic resistance to the chronic phase sequestrum curettage and extraction of teeth lesions mainly purulent maxillary bone marrow after a course of inflammation, and generally can be divided into two phases of acute and chronic phase. to The sequestrum began to take shape used to be collectively referred to as the acute phase by the onset, generally about 3 to 4 weeks if the infection fails to be completely controlled in the acute phase, into the chronic phase. must be used in sufficient quantities and effective antimicrobial treatment. use drugs in order to control the infection in the acute phase, use of antibiotics against Staphylococcus aureus and mixed infections, the other based on bacterial culture and susceptibility to choose effective antibiotics. In the initial stages of infection, but also with the physical therapy. When the infection into the suppuration of Early incision and drainage. wait for his condition slightly eased, the mouth opening slightly improved, should try to extraction, so that the pus from the socket to get the drainage, to prevent the spread of infection in the bone of acute suppurative osteomyelitis oncoming acute, severe illness, can cause blood and brain complications, and therefore close observation, as early as the appropriate emergency treatment of acute systemic application of antibiotics, local incision and drainage removal of loose teeth mainly diffuse patient performance decline thirsty, systemic poisoning, severe anemia, in addition to general supportive therapy, but also a small amount of multiple transfusions, enhanced systemic resistance to the chronic phase to sequester scrape and lesions in tooth extraction based. 1, the disease occurred in the maxilla of infants and young children. marginal mandibular osteomyelitis: more common in young people, the acute phase is difficult to find common chronic phase. and timely treatment of pericoronitis, periapical go far odontogenic infection, on the prevention of mandibular osteomyelitis. such as formation of osteomyelitis in the acute phase should be a thorough treatment so as not to become chronic. acute phase of infection control, enhance the body resistance-based, anti- infection drugs should be selected according to the sensitivity of pathogenic bacteria. mandibular osteomyelitis more mixed bacterial infection, it is appropriate in order to use broad-spectrum antibiotics. In addition, as has been clear for odontogenic infection, early removal of the lesions teeth in order to facilitate drainage, to avoid more extensive bone destruction. case of subperiosteal abscess or infection jaw week gap, it is timely incision in chronic phase, the lesion has been limited or has been sequestrum formation, while the surgical treatment of the main supplemented by drug treatment. marginal mandibular osteomyelitis are generally large sequestrum formation, mostly for the proliferation of subperiosteal cortical bone, the texture is more loose, and should be completely clear, pus foci of cortical bone surface where infection and the granulation organizers should be scraping, postoperative use of antibiotics to control infection in 7 to 14 days to avoid relapse.

Clinical manifestations

Clinical presentation of osteonecrosis of the jaw. (A) Typical lesion of osteonecrosis of the jaw showing exposed infected bone involving the mylohyoid ridge. (B) Osteonecrotic bone below a dental implant. (C) Spontaneous exfoliated teeth with underlying exposed dead bone. (D) Operative picture showing well-demarcated dead bone involving the whole alveolus. (From Badros A, Weikel D, Salama A, et al. Osteonecrosis of the jaw in multiple myelomoa patients: clinical features and risk factors. J Clin Oncol 2006;24:948; with permission. Copyright © 2006 by American Society of Clinical Oncology.)

Suppurative mandibular osteomyelitis from the clinical course of disease, pathogens, routes of infection and lesions involving the siteCan be manifested as acute and chronic stages, and often divided into two types of central and edge (a central mandibular osteomyelitis is usually odontogenic inflammation spread to the bone marrow, spread to the bone from the jaw center around cortex and periosteum in the bone marrow of early acute inflammation is often restricted to the alveolar bone or the mandibular body, patients feel severe toothache, pain along the trigeminal nerve distribution of radiation lesions of the gingival mucosa hyperemia and edema, teeth that is, obvious pain and loose, and can gingival sulcus septic overflow or the formation of alveolar abscess. acute phase has not been timely drainage, infections continue to spread to the medullary cavity can cause disseminated osteomyelitis or perforation of cortical bone formation in subperiosteal abscess. exacerbate symptoms of systemic poisoning at this time, the body temperature to 39 ~ 40 ℃, blood test white blood cells increased significantly, local pain and soft tissue swelling the affected regions the majority of loose teeth. If the inflammation is not brought under control, the maxillary infection can cause purulent maxillary sinusitis and infraorbital, buccal, zygomatic or pterygopalatine concave, temporal concave and other areas to spread. mandibular infection can spread to the inferior alveolar nerve caused by the lower lip numbness spread to the jaw week to stimulate the open jaw muscles, causing limitation of mouth opening can be complicated by the infection of the jaw week more than the gap, so that the face was seen in the swelling, and finally inflammation in the formation of blood clots within the jaw, resulting iutritional disorders of the jaw and necrosis, and thus transferred to the chronic phase. turn by the acute phase into the chronic phase of about two to three weeks later, pain and other systemic symptoms began to ease, but the mouth gums can form more than one fistula and pus out about a month later, the sequestrum with healthy bone between the new bone layer, causing the separation of the sequestrum with healthy bone without surgical removal of involved regional fistula pus prolonged unhealed, can sometimes have a small piece of sequestrum discharged from the fistula. osteomyelitis of the mandible can cause large piece of dead bone formation, can be pathogenic pathological fractures appear bite (occlusal disorders. Suppurative mandibular osteomyelitis (two marginal mandibular osteomyelitis spread of the infection pathway is not the first damage to bone marrow, but the basis of periostitis or subperiosteal abscess the first involving the cortical bone occurred in adolescents mandible, more limited lesions, infections originated in the mandibular third molar pericoronitis inflammation, caused by the masseter muscle space infection and subperiosteal abscess, resulting in lower jaw of the ascending branch and the corner of cortical bone nutritional barriers necrosis. clinical manifestations of chronic symptoms, the symptoms of the acute phase of infection and jaw week gap coexist but often overlooked in local mild chronic inflammatory swelling and pitting edema due to the chewing muscles and wing muscle involvement and limited mouth opening. lesions confined to the cortical bone, or to the deep development involving the bone marrow, but rarely large sequestrum formation. pericoronitis infections if not controlled, often repeatedly made by anti-inflammatory drugs after treatment, could easily lead to pathogen resistance, the formation of low toxicity and infection, no obvious purulent and sequestrum formation process and significant cortical hyperostosis, sclerosis and periosteal thickening of cortical bone lysis little part the formation of small abscess and granulation tissue. cortical hyperplasia of the mandibular ascending branch of the Ministry of mandibular angle can cause facial asymmetry, X-ray showed obvious subperiosteal hyperostosis.