Acute, chronic osteomyelitis of the jaws. X-ray diagnostic. Physiotherapy and comprehensive treatment of osteomyelitis. Actinomycosis, tuberculosis, syphilis and AIDS
Osteomyelitis
Osteomyelitis is defined as an inflammation of the bone marrow with a tendency to progression. This is what differentiates it in the jaw from the ubiquitous dentoalveolar abscess, “dry socket” and “osteitis,” seen in infected fractures. It involves adjacent cortical plates and often periosteal tissues. In the preantibiotics era, osteomyelitis of the mandible was not uncommon.With the advent of antibiotics, it became a rare disease. In recent years antimicrobials have become less effective and there has been a re-emergence of the disease, presenting major diagnostic and therapeutic challenges for practicing surgeons. Despite modern therapy it can still remain a major source of morbidity to the patient, requiring multiple surgeries and resulting in prolonged treatment with loss of teeth and/or jawbone. The incidence of osteomyelitis is much higher in the mandible due to the dense poorly vascularized cortical plates and the blood supply primarily from the inferior alveolar neurovascular bundle. It is much less common in the maxilla due to the excellent blood supply from multiple nutrient feeder vessels. In addition the maxillary bone is much less dense than the mandible. Diminished host defenses, both local and systemic, can contribute significantly to the emergence and clinical course of the disease. Osteomyelitis has been associated with multiple systemic diseases including diabetes, autoimmune states, malignancies, malnutrition, and acquired immunodeficiency syndrome.1 The medications linked to osteomyelitis are steroids, chemotherapeutic agents, and bisphosphonates. 1–3 Local conditions that adversely affect the blood supply can also predispose the host to a bony infection. Radiation therapy, osteopetrosis, and bone pathology can alter the blood supply to the area and provide a potential foothold for osteomyelitis to set in (Figure 17-1).
Pathogenesis In the maxillofacial region, osteomyelitis primarily occurs as a result of contiguous spread of odontogenic infections or as a result of trauma. Primary hematogenous osteomyelitis is rare in the maxillofacial region, generally occurring in the very young. The adult process is initiated by an inoculation of bacteria into the jawbones. This can occur with the extraction of teeth, root canal therapy, or fractures of the maxilla or mandible. This initial insult results in a bacteria-induced inflammatory process 
or cascade. In the normal healthy host, this process is self-limiting and is a component of healing. Occasionally, however, in the normal host, and certainly in the compromised host, there is the potential for this process to progress to the point where it is considered pathologic. With inflammation there is hyperemia and increased blood flow to the affected area. Additional leukocytes are recruited to this area to fight off infection. Pus is formed when there is an overwhelming supply of bacteria and cellular debris that cannot be eliminated by the body’s natural defense mechanisms. When the pus and subsequent inflammatory response occur in the bone marrow, an elevated intramedullary pressure is created which further decreases the blood supply to this region. The pus can travel via haversian and Volkmann’s canals to spread throughout the medullary and cortical bones. Once the pus has perforated the cortical bone and collects under the periosteum, the periosteal blood supply is compromised and this further aggravates the local condition. The end point occurs when the pus exits the soft tissues either by intraoral or extraoral fistulas.
Microbiology
More than 500 bacterial taxa have been identified in the mouth.4–6 The mouth and the anus are opposing ends of the same alimentary tube, and many clinicians consider them to be the most highly contaminated areas of the human body. In the past, staphylococcal species were considered the major pathogen in osteomyelitis of the jaws. However, with refinements in the collection and processing of microbiologic specimens, we are able to get a true picture of the disease-causing organisms. As with most oral infections the prime pathogenic species are streptococci and anaerobic bacteria. The anaerobes responsible are generally bacteroides or peptostreptococci species. Often, the infections are mixed, growing several pathogens on final culture. The clinician must begin empiric antibiotic treatment based on the most likely pathogens. This could include penicillin and metronidazole as dual-drug therapy or clindamycin as a single-drug treatment. Definitive antimicrobial therapy should be based on the final culture and sensitivities for optimal medical management results.
Classification
Over the years many ways of classifying osteomyelitis have been presented. A rather complex classification system was proposed by Cierny and colleagues.7 Osteomyelitis was classified as being either suppurative or nonsuppurative by Lew and Waldvogel.8 This classification was modified by Topazian.9 Additional authors classified osteomyelitis as being either hematogenous or secondary to a contiguous focus of infection.10 Another system proposed by Hudson essentially divided the presentation of osteomyelitis into acute and chronic forms.11 With the multitude of classification systems, the controversy involved in adequately classifying osteomyelitis is clearly evident. However, for simplicity’s sake, the classification system offered by
d. Sclerosing (Figure 17-6)
Clinical Presentation
Very often, as with any infection, the patient with osteomyelitis of the maxillofacial region will present with classic symptoms: • Pain • Swelling and erythema of overlying tissues • Adenopathy • Fever • Paresthesia of the inferior alveolar nerve • Trismus • Malaise • Fistulas The pain in osteomyelitis is often described as a deep and boring pain, which is often out of proportion to the clinical picture. In acute osteomyelitis it is very common to see swelling and erythema of the overlying tissues, which are indicative of the cellulitic phase of the inflammatory process of the underlying bone. Fever often accompanies acute osteomyelitis, whereas it is relatively rare in chronic osteomyelitis. Paresthesia of the inferior alveolar nerve is a classic sign of a pressure on the inferior alveolar nerve from the inflammatory process within the medullary bone of the mandible. Trismus may be present if there is inflammatory response in the muscles of mastication of the maxillofacial region. The patient commonly has malaise or a feeling of overall illness and fatigue, which would accompany any systemic infection. Lastly both intraoral and extraoral fistulas are generally present with the chronic phase of osteomyelitis of the maxillofacial region. Often these patients will have a laboratory work-up as part of their initial examination. In the acute phase of osteomyelitis it is common to see a leukocytosis with left shift, common in any acute infection. Leukocytosis is relatively uncommon in the chronic phases of osteomyelitis. The patient may also exhibit an elevated erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP). Both the ESR and CRP are very sensitiveindicators of inflammation in the body and they are very nonspecific. Therefore, their main use is to follow the clinical progress of the osteomyelitis. Nearly all patients will have some form of maxillofacial imaging. The orthopanoramic view is indispensable in the initial evaluation of osteomyelitis. This view is easily obtainable in most dental offices and can yield valuable information as to the radiographic changes with osteomyelitis, potential sources of the disease, and predisposing conditions such as fractures and underlying bone disease. One must bear in mind that radiographic images lag behind the clinical presentation since cortical involvement is required for any change to be evident. Therefore, it may take several weeks before the bony changes appear radiographically. Hence, it is possible to see a patient with acute osteomyelitis that has a normal-appearing orthopantomogram. However, one can often see the appearance of “moth-eaten” bone or sequestrum of bone, which is the classic appearance of osteomyelitis. Computerized tomography (CT) scans have become the standard in evaluating maxillofacial pathology such as osteomyelitis. They provide threedimensional imaging not available on an orthopanoramic view. The CT scan can give very detailed images as to early cortical erosion of bone in ostemyelitis. One can often see the extent of the lesion and bony sequestra along with pathologic fractures. CT scanning, like plain films, requires 30 to 50% demineralization of bone before changes can be seen, thus presenting an essential delay in diagnosis of osteomyelitis.12 Magnetic resonance imaging (MRI) is generally considered more valuable in the evaluation of soft tissue lesions of the maxillofacial region. However, MRI can assist in the early diagnosis of osteomyelitis by loss of the marrow signal before cortical erosion or sequestrum of the bone appears. Thus, MRI may benefit in identifying the earlier stages of osteomyelitis.12 Nuclear medicine has evolved to aid in the diagnosis of osteomyelitis. Technetium 99 has been the workhorse of nuclear medicine imaging of the maxillofacial region. The technetium 99 bone scan is very sensitive in highlighting areas of increased bone turnover; however, the scan is not very specific to areas of infection. With the addition of gallium 67 or indium 111 as contrast agents, one can differentiate areas of infection from trauma or postsurgical healing as these agents specifically bind to white blood cells.
Treatment
The management of osteomyelitis of the maxillofacial region requires both medical and surgical interventions. In rare cases of infantile osteomyelitis, intravenous antibiotic therapy alone may eradicate the disease. Antibiotic therapy is rarely curative in later-onset cases, and the overwhelming majority of osteomyelitis cases require surgical intervention. Clearly the first step in the treatment of osteomyelitis is diagnosing the condition correctly. The tentative diagnosis is made from clinical evaluation, radiographic evaluation, and tissue diagnosis. The clinician must be aware that malignancies can mimic the presentation of osteomyelitis and must be kept in the differential diagnosis until ruled out by tissue histopathology (Figure 17-7).
Tissues from the affected site should be sent for Gram stain, culture, sensitivity, and histopathologic evaluations. The clinical response to the treatment of any patient will be compromised unless altered host factors can be optimized. Medical evaluation and management in defining and treating any immunocompromised state is indicated and often helpful. For example, glucose control in a diabetic patient should be stabilized for best response to therapy. Empiric antibiotic treatment should be started based on Gram stain results of the exudate or the suspected pathogens likely to be involved in the maxillofacial region. Definitive culture and sensitivity reports generally take several days or longer to be obtained but are valuable in guiding the surgeon to the best choice of antibiotics based on the patient’s specific causative organisms.13 Infectious disease consultation may illustrate the most current antimicrobials and/or regimens.
Surgical Options
Classic treatment is sequestrectomy and saucerization. The aim is to debride the necrotic or poorly vascularized bony sequestra in the infected area and improve blood flow. Sequestrectomy involves removing infected and avascular pieces of bone—generally the cortical plates in the infected area. Saucerization involves the removal of the adjacent bony cortices and open packing to permit healing by secondary intention after the infected bone has been removed. Decortication involves removal of the dense, often chronically infected and poorly vascularized bony cortex and placement of the vascular periosteum adjacent to the medullary bone to allow increased blood flow and healing in the affected area. The key element in the above procedures is determined clinically by cutting back to good bleeding bone. Clinical judgment is crucial in these steps but can be aided by preoperative imaging that shows the bony extent of the pathology. It is ofteecessary to remove teeth adjacent to an area of osteomyelitis. In removing adjacent teeth and bone the clinician must be aware that these surgical procedures may weaken the jaw bone and make it susceptible to pathologic fracture (see Figure 17-6). Supporting the weakened area with a fixation device (external fixator or reconstruction type plate) and/or placing the patient in maxillomandibular fixation is frequently used to prevent pathologic fracture. Indeed, we have primarily grafted such areas when the sequestrectomy and saucerization have been deemed adequate. Some authors have proposed adjunctive treatment methods that deliver high doses of antibiotic to the area using antibiotic impregnated beads or wound irrigation systems.14–16 This therapy works on the premise that high local levels of antibiotics are made available and the overall systemic load is very low, thus reducing the possible side effect and complication rate. Hyperbaric oxygen (HBO) treatment has also been advocated for the treatment of refractory osteomyelitis. This treatment method works by increasing tissue oxygenation levels that would help fight off any anaerobic bacteria present in these wounds. The widespread use of HBO treatment of osteomyelitis still remains controversial. Resection of the jaw bone has traditionally been reserved as a last-ditch effort, generally after smaller debridements have been performed or previous therapy has been unsuccessful or to remove areas involved with pathologic fracture. This resection is generally performed via an extraoral route, and reconstruction can be either immediate or delayed based on the surgeon’s preference. Rigid internal fixation
has simplified the postoperative course by providing a means for immediate function of the jaws. We believe that early resection and reconstruction shorten the course of treatment. Once the patient develops paresthesia in mandibular osteomyelitis, resection and immediate reconstruction are indicated. At this point preservation of the mandible is highly unlikely and one should attempt to shorten the course of the disease and treatment (Figure 17-8).
Actinomycosis Definition Actinomycosis is an infection primarily caused by the bacterium Actinomyces israelii. Infection most often occurs in the face and neck region and is characterized by the presence of a slowly enlarging, hard, red lump. Description Actinomycosis is a relatively rare infection occurring in one out of 300,000(1/300,000) people per year. It is characterized by the presence of a lump or mass that often forms, draining sinus tracts to the skin surface. Fifty percent of actinomycosis cases are of the head and neck region (also called “lumpy jaw” and “cervicofacial actinomycosis“), 15% are in the chest, 20% are in the abdomen, and the rest are in the pelvis, heart, and brain. Men are three times more likely to develop actinomycosis than women. Causes and symptoms Actinomycosis is usually caused by the bacterium Actinomyces israelii. This bacterium is normally present in the mouth but can cause disease if it enters tissues following an injury. Actinomyces israelii is an anaerobic bacterium which means it dislikes oxygen but grows very well in deep tissues where oxygen levels are low. Tooth extraction, tooth disease, root canal treatment, jaw surgery, or poor dental hygiene can allow Actinomyces israelii to cause an infection in the head and neck region. The main symptom of cervicofacial actinomycosis is the presence of a hard lump on the face or neck. The lump may or may not be red. Fever occurs in some cases. Diagnosis Cervicofacial actinomycosis can be diagnosed by a family doctor or dentist and the patient may be referred to an oral surgeon or infectious disease specialist. The diagnosis of actinomycosis is based upon several things. The presence of a red lump with draining sinuses on the head or neck is strongly suggestive of cervicofacial actinomycosis. A recent history of tooth extraction or signs of tooth decay or poor dental hygiene aid in the diagnosis. Microscopic examination of the fluid draining from the sinuses shows the characteristic “sulfur Granules” (small yellow colored material in the fluid) produced by Actinomyces israelii. A biopsy may be performed to remove a sample of the infected tissue. This procedure can be performed under local anesthesia in the doctor’s office. Occasionally the bacteria can be cultured from the sinus tract fluid or from samples of the infected tissue.
Key terms Biopsy — The process that removes a sample of tissue for microscopic examination to aid in the diagnosis of a disease. Sinus tract — A narrow, elongated channel in the body that allows the escape of fluid.
Actinomycosis in the lungs, abdomen, pelvis, or brain can be very hard to diagnose since the symptoms often mimic those of other diseases. Actinomycosis of the lungs or abdomen can resemble tuberculosis or cancer. Diagnostic x-ray results, the presence of draining sinus tracts, and microscopic analysis and culturing of infected tissue assist in the diagnosis. Treatment Actinomycosis is difficult to treat because of its dense tissue location. Surgery is often required to drain the lesion and/or to remove the site of infection. To kill the bacteria, standard therapy has included large doses of penicillin given through a vein daily for two to six weeks followed by six to twelve months of penicillin taken by mouth. Tetracycline, clindamycin, or erythromycin may be used instead of penicillin. The antibiotic therapy must be completed to ensure that the infection does not return. However, a report in 2004 on several cases of actinomycosis said that therapy depends on the individual case and that many patients today will be diagnosed in earlier stages of the disease. Sometimes, shorter courses of antibiotic treatment are effective, with close diagnostic x-ray monitoring. Hyperbaric oxygen (oxygen under high pressure) therapy in combination with the antibiotic therapy has been successful
.
Prognosis Complete recovery is achieved following treatment. If left untreated, the infection may cause localized bone destruction. Prevention The best prevention is to maintain good dental hygiene. Scrofula is the term used for lymphadenopathy of the neck, usually as a result of an infection in the lymph nodes, known as lymphadenitis. It can be caused by tuberculous or non tuberculous mycobacteria. About 95% of the scrofula cases in adults are caused by Mycobacterium tuberculosis, most often in immunocompromised patients (about 50% of cervical tuberculous lymphadenopathy). In immunocompentent children, scrofula is often caused by atypical mycobacteria (Mycobacterium scrofulaceum) and other nontuberculous mycobacteria (NTM). Unlike the adult cases, only 8% of cases in children are tuberculous. With the stark decrease of tuberculosis in the second half of the 20th century, scrofula became a less common disease in adults, but remained common in children. With the appearance of AIDS, however, it has shown a resurgence, and presently affects about 5% of severely immunocompromised patients.[citatioeeded] Signs and symptoms The most usual signs and symptoms are the appearance of a chronic, painless mass in the neck, which is persistent and usually grows with time. The mass is referred to as a “cold abscess”, because there is no accompanying local color or warmth and the overlying skin acquires a violaceous (bluish-purple) color. NTM infections do not show other notable constitutional symptoms, but scrofula caused by tuberculosis is usually accompanied by other symptoms of the disease, such as fever, chills, malaise and weight loss in about 43% of the patients. As the lesion progresses, skin becomes adhered to the mass and may rupture, forming a sinus and an open wound. Diagnosis Diagnosis is usually performed by needle aspiration biopsy or excisional biopsy of the mass and the histological demonstration of stainable acid-fast bacteria in the case of infection by M. tuberculosis (Ziehl-Neelsen stain), or the culture of NTM using specific growth and staining techniques. Pathology The classical histologic pattern of scrofula features caseating granulomas with central acellular necrosis (caseous necrosis) surrounded by granulomatous inflammation with multinucleated giant cells. Although tuberculous and non tuberculous lymphadenitis are morphologically identical, the pattern is somewhat distinct from other causes of bacterial lymphadenitis. [1] Therapy Treatments are highly dependent on the kind of infection. Surgical excision of the scrofula does not work well for M. tuberculosis infections, and has a high rate of recurrence and formation of fistulae. Furthermore, surgery may spread the disease to other organs. The best approach is to use conventional treatment of tuberculosis with antibiotics. Scrofula caused by NTM, on the other hand, responds well to surgery, but is usually resistant to antibiotics. The affected nodes can be removed either by repeated aspiration, curettage or total excision (with the risk in the latter procedure, however, often causing unsightly scarring, damage to the facial nerve, or both). Prognosis With adequate treatment, clinical remission is practically 100%. In NTM infections, with adequate surgical treatment, clinical remission is greater than 95%. It is recommended that persons in close contact with the diseased person, such as family members, be tested for tuberculosis. History Scrofula (scrophula or struma) is any of a variety of skin diseases; in particular, a form of tuberculosis, affecting the lymph nodes of the neck. In adults it is caused by Mycobacterium tuberculosis and in children by nontuberculous mycobacteria. The word comes from the Latin scrofula, meaning brood sow. In the Middle Ages it was believed that “royal touch”, the touch of the sovereign of
Bilozetskyi Ivan
