ACUTE ODONTOGENIC JAW OSTEOMIYELITIS: ETIOLOGY, PATHOGENESIS, CLASSIFICATION. DISEASES OF THE TEETH ERUPTION. DETAINED AND HALF DETAINED TEETH. PERICORONITIS: CLINIC, DIAGNOSTICS, TREATMENT, COMPLICATIONS.

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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 presentationand 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 dermatoskeletal involvement such as in SAPHO syndrome or chronic recurrent multifocal osteomyelitis (CRMO).

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).

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).

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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)

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 classification criteria. An overview of the most commonly cited classifications of jawbone osteomyelitis are listed in Tables 2.1–2.4.

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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 and corresponds to the third and fourth week after onset of

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

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).

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).

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.

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 bone surrounding 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 primary chronic and has been named 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 symptomfree intervals. 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 in nomenclature, 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. The FOD 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 other dermatoskeletal 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).

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).

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.

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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.

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 et al. 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.

Osteomyelitis of the Jaws: The Zurich Classification System

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)

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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, and other 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 course resembling 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.

Acute Osteomyelitis and Secondary Chronic Osteomyelitis

Definitions

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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.

Predisposing Factors, Etiology, and Pathogenesis

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).

Local and Systemic Host Immunity

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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 immunological mechanisms, 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.

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 systemic factors 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.

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).

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.

Etiology and Pathogenesis, Subclassification Groups

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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 aureus has 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 causing deep 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.

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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). The different 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 membrane or 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 in number and virulence, this barrier can be destroyed. Furthermore, permanent or temporary reduction 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 the neurovascular 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).

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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)

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 which pus 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 immunity supported 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.

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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)

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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. b Surgical specimen of the case shown in a: multiple sequesters and necrotic bone collected during debridement surgery

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).

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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)

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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)

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 without suppuration, 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.

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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)

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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

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 abscess formation will show more pronounced findings. Examination of our own patient data is demonstrated in Table 2.14.

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 often noted 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.

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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

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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

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 of bacteria (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 of Mycobacterium 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 differential diagnosis 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 of Candida 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.

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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

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Fig. 2.18 Same as Fig. 2.17

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).

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 fistula formation, 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).

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.

Primary Chronic Osteomyelitis

Definition

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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 radiological work-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

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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)

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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)

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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, and histopathology 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.

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 the medullary 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 the periosteum, 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 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

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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 seen now.

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.

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.

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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.

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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.

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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.

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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 than normal; it cannot accommodate all the teeth, thus irregularity of teeth develops. The roots of the teeth are also shorter than normal 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.

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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, then normal 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.

Опис : Assessment of Space for Third molars or Wisdom Teeth

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.

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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.

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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.

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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.

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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.

Опис : http://www.identalhub.com/images/images/precautions%20after%20wisdom%20tooth%20extraction.JPG

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.

Опис : http://www.identalhub.com/images/images/tooth%20extracted1.JPG

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. During healing 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.

Опис : http://www.identalhub.com/images/images/healing%20take%20after%20wisdom%20tooth%20extraction.JPG

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 in number of white blood cells (Leucocytes) and malaise indicate sever infection.

Опис : http://www.identalhub.com/images/images/Pericoronitis.JPG

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.

Опис : http://www.identalhub.com/images/images/Debridement%20of%20area.JPG

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 can normally 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.

Опис : Dental Procedures for Impacted Wisdom Teeth or Third molars

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 from 0.032 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.

Опис : Dental Procedures for Impacted Wisdom Teeth or Third molars

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 margin not 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 mm after 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.

Опис : Types of Impaction of Wisdom Teeth or Third Molars

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.

Опис : Types of Impaction of Wisdom Teeth or Third Molars

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.

Опис : Types of Impaction of Wisdom Teeth or Third Molars

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 Richardson noted 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 or wisdom 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

Опис : http://www.identalhub.com/images/files/Rest%281%29.jpg

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.

Опис : http://www.identalhub.com/images/files/Spitting.jpg

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.

Опис : http://www.identalhub.com/images/files/No%20Smoking.JPG

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.

Опис : http://www.identalhub.com/images/files/Brushing%281%29.jpg

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.

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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

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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

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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.

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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.

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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)

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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

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If you report pain or swelling in near 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.