Osteomyelitis (OM) is an inflammatory condition of bone that involves the medullary cavity and the adjacent cortex. It occurs more frequently in mandible than in the maxilla and is often associated with suppuration and pain.1 The osseous spaces are usually filled with exudates that can lead to pus formation. Chronic osteomyelitis can be the result of a non-treated acute mild inflammation or emerge without a precursor. When osteomyelitis occurs in the mandible, it is usually more diffused and widespread.1-6 Clinical examination alone is often enough to diagnose chronic mandibular osteomyelitis due to the progression of this disease and suppuration.1,2 In cases of chronic osteomyelitis, a radiolucent circumscribed image can be seen encapsulating central radiopaque sequestra, as well as radiopacities of the surrounding bone due to a local osteogenic reaction.7 Patients who present active chronic osteomyelitis usually require long-term use of antibiotic therapy and surgical intervention.7 Treatment requires both antibiotic therapy and surgical debridement, meaning the necrotic bone must be completely removed until the underlying bone starts bleeding.7 Although most cases of OM of the jaws result from dental origins, other sources of infection are possible.2 Although primary OM following extraction of periodontally involved teeth is rare, it is, however, of concern to both the patient and dentist.
Osteomyelitis may result from the direct extension of pulpal or periodontal infection without the formation of a granuloma or from acute exacerbation of a periapical lesion. It may also occur following penetrating trauma or various surgical procedures. Extension of the infection into adjacent soft tissue and fascial spaces is common, and often the presenting clinical symptoms are swelling, pain and suppuration. Sequelae to transcortical extension of the inflammatory process can include cortical destruction, fistulization and periosteal reaction. These changes can be evaluated by imaging techniques.5
Histopathology. The bone pathology presents various forms, depending on the virulence of the infecting microorganism, the host capacity of effective immune response and the kind of reaction of the periosteal and osseous tissues. Chronic osteomyelitis histopathology depicts irregular fragments of devitalized bone surrounded by dense fibrous tissue heavily infiltrated by plasma cells, lymphocytes, and only a few granulocytes (Figure 5).
Imaging. Appropriate evaluation of radiographic types of osteomyelitis is necessary for treatment planning. Kazunori Yoshiura6 classified mandibular osteomyelitis into four basic patterns, as lytic, sclerotic, mixed and sequestrum patterns. Our case presented with the latter pattern. In some cases computerized tomography or scintography may be necessary.1
Presentation. Patients can have swelling of the face, tenderness and pain (localized), draining sinus tracts, suppuration, tooth loss, possible necrotic bone fragment formation, and a low-grade fever. New bone and oral mucosa will occasionally regenerate beneath the sequestra, probably because of activation of periosteal osteoblasts. According to Reinert,6 clinical examination alone can be enough to diagnose mandibular chronic osteomyelitis, particularly at the onset of the disease. The radiographic characteristics of the osteomyelitis presented were a radiolucent area circumscribing a central bone sequestrum and radiopacity in the surrounding bone. Due to the characteristics of the pathology and the clinical history, there was no need for other exams.
Predisposing factors. Viral fevers (eg, measles), malaria, anemia, malnutrition, and use of tobacco are found to contribute to the development of osteomyelitis.
Management. Treatment goals include reversal of any predisposing conditions, long-term antibiotic therapy. Antibiotic therapy alone is not enough for the treatment of osteomyelitis, since the devitalized osseous tissue in combination with the capsule of the surrounding fibrous connective tissue protects the microorganisms from the drug action. Corticotomy can be used as treatment, and if not effective, bone resection can be done as a more radical alternative. However, aggressive treatment may cause loss of function, exposure of the inferior alveolar nerve and problems regarding the reconstruction.7 High doses of antibiotics should accompany any aggressive surgical treatment. Some authors feel that penicillin G is the medication of choice, followed by clindamycin.7 Since most of the osteomyelitis infections are polymicrobial oral flora (primarily facultative streptococci, Bacteroides spp, Peptostreptococcus,and Peptococcus), antibiotic treatment includes penicillin, metronidazole, and clindamycin. Operative interventions such as sequestrectomy, decortication, removal of nonviable bone (ie, mandibulectomy or maxillectomy), and dental extractions, are also needed. A wide incision to remove all the diseased tissue, as well as primary closure of the surgical wound is performed to ensure a successful operation.
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A 62-year-old woman referred to our clinic for treatment of chronic infection and pain following extraction of the left mandibular second molar under local anesthesia by her general dentist. She was in good general health and did not have a history of drug use. Her pre-extraction radiographic examination confirmed the presence of a deep distal periodontal pocket ). She then developed pain, chronic infection, and discharge following the extraction . She returned to her general dentist who prescribed amoxicillin 500 mg every 8 hours for 10 days. After multiple visits to her dentist, and no abatement of her symptoms after 5 months, she was referred to our clinic.
Intraoral clinical examination revealed that the socket of the left mandibular second molar tooth had chronic infection and a malodorous discharge. A sample of this fluid was collected for culture and antibiotic sensitivity. Culture was positive for non-A non-D streptococci sensitive to cephalexin. Radiographic examination confirmed the presence of a sequestrum in the socket .
Considering the clinical and radiographic presentation, a diagnosis of chronic osteomyelitis was made and the patient was scheduled for surgery. After general anesthesia, preparation, draping and packing the oropharynx; a flap was reflected and the sequestrum was removed with a curette. The socket was cleaned and irrigated. Nonvital necrotic bone was shaved using a round bur until vital bone was apparent (confirmed clinically by bone bleeders). The lesion was sent to the pathology laboratory and their report confirmed the diagnosis of chronic osteomyelitis. The patient was given cephalexin and metronidazole 500 mg every 6 hours for 2 weeks. A radiograph was that taken 3 months postoperatively showed bony consolidation of the socket The patient has been symptom-free since the completion of the surgical treatment and antibiotic regimen.
Tuberculosis is a chronic infectious granulomatous disease
caused by Mycobacterium tuberculosis
1 which is an aerobic,
slender, non-motile, non-encapsulated, non-sporing, rod
shaped organism ranging from 2 to 5 µm2
. The World
Health Organization (WHO) estimates that worldwide
there are approximately 20 million active cases, of them
approximately 3 million people die each year from
tuberculosis, of which 80 % are in developing countries
Tuberculous oral lesions are relatively rare occurrence.
Oral manifestations occur in approximately 3% of cases
involving long standing pulmonary and/ or systemic
.Oral clinical presentation may be as ulcers,
erythematous patches, and indurated lesions with granular
surface, nodules, and fissures or as jaw lesions. The most
common sites involved are tongue, gingiva, tooth sockets
and jaw involvement may present as osteomyelitis
Two main types of tubercular infections of oral
tissues are recognized - Primary and Secondary. Primary
lesions develop when tuberculosis bacilli are directly
inoculated into the oral tissues of a person who has not
acquired immunity to the disease and in fact, any area that
is vulnerable to direct inoculation of bacilli from
exogenous source can be a potential site. These frequently
involve gingiva, tooth extraction sockets and buccal folds.
Secondary infection of oral tissues can result from either
haematogenous or lymphatic spread or from
autoinoculation by infected sputum and direct extensions
from neighbouring structures. Intraoral sites frequentlyinvolved include the tongue, palate, lips, alveolar mucosa
and jaw bones
With myriad presentations and sometimes lack of
specific systemic symptoms, oral tubercular lesions may
present as puzzle for us and may escape our eyes. Hence,
we document a case of primary tuberculous osteomyelitis
of mandible in an old male individual who was initially
suspected for dental abscess with nonspecific chronic
osteomyelitis and later proved as primary tubercular osteomylitis
are predisposing factors to infection 5
Bone TB is a relatively uncommon form of
extrapulmonary tuberculosis seen in approximately 1% of
children with TB
. It is more frequently seen in children
as compared to adults because of highly vascularized
bone in infants and children
. Tuberculous osteomyelitis
is quite rare and constitutes less than 2% of skeletal TB.
Jaw involvement is even rarer and affects older individual
and also children
The involvement of the mandible by TB infection is
extremely rare as it contains less cancellous bone. But the
mandibular involvement is more frequent than maxilla
and the alveolar and angle regions have greater affinity.
The infection may extend to the mandible by:
1) Direct transfer from infected sputum or infected raw milk
of cow through an open pulp in carious tooth, an
extraction wound or gingival margin or perforation of an
2) Regional extension of soft tissue lesion to involve the
3) Haematogenous route
12 described four clinical forms of
tuberculosis of the mandible.
1. The superficial or alveolar form in which the alveolar process
is involved either by direct extension of the tuberculous
gingival tissues or by way of a deep carious tooth. The
course is usually chronic, and necrosis of bone is
progressive, with the formation of abscesses and fistulae.
2. The deep or central form, in which the lesion involves the
angle of the mandible. It is found, according to Chapotel,
almost exclusively in children during the period of eruption of molar teeth.
Brown recluse spider bites cause significant trauma via their tissue toxic venom. Diagnosis of these injuries and envenomation is difficult and many times presumptive. Treatment is varied and dependent upon presentation and course of injury.
Materials and Methods:
We present a case of a previously unreported incidence of osteomyelitis of the mandible as a result of a brown recluse spider bite. A review of the literature and discussion of diagnosis and treatment of brown recluse spider bites are presented.
Osteomyelitis of the mandible causing a chronic wound was the presenting finding of a patient with a history of spider bite and exposure to brown recluse spiders. Operative debridement and wound closure resulted in successful treatment. Brown recluse spider envenomation varies in its presentation and treatment is based on the presenting clinical picture. Conclusion: Treatment regimens for brown recluse spider bite envenomation should include the basics of wound care. Systemic antibiotics, topical antimicrobials, dapsone, and surgical debridement are valuable adjuncts of treatment, as indicated, based on the clinical course.
Brown recluse spider bite envenomation can be a significant traumatic injury. Probably overreported, brown recluse spider bites and their resultant tissue injury patterns are well documented; however, treatment regimens are somewhat controversial. We present an unusual case of a presumed brown recluse spider bite injury of the face, which developed into chronic osteomyelitis of the mandible, and discuss the evaluation and further management of this interesting clinical presentation.
A 52-year-old white male presented with a 6-month history of a tender, open wound in the submental area. The chronic wound had been draining serous and purulent material for 4 to 6 weeks prior to evaluation. The wound began as a “pimple” on his chin that progressed in a few days to erythema, skin breakdown, and then, eventually, purulent drainage. The patient related a history of having encountered multiple “fiddleback” spiders at his place of work. He also claimed to have suffered multiple spider bites on the extremities in the past, all of which healed without sequelae. Physical examination was significant for a 5-mm open wound of the mandible, slightly to the right of the midline of his chin (Fig 1). The area was tender and a small amount of murky fluid was expressed. The wound probed to bone, using a sterile hemostatic clamp. There was no palpable regional lymphadenopathy. Computed tomography revealed a large bony cavity eroding through the inferior cortex of the mandibular symphysis anteriorly and abutting the lingual cortex. The mandibular integrity was intact with no evidence, clinically or radiographically, of a pathological fracture (Fig 2). The bony destruction appeared chronic, as evidenced by the sclerotic margins of the cavity. Differential diagnosis included possible odontogenic infection, neoplastic process, and traumatic wound infection. An odontogenic infection was excluded because of the viability of associated dentition and lack of demonstrable dental pathology. As a soft tissue or bony neoplasm appeared unlikely because of the smooth, sclerotic margins seen on computed tomographic scan and the lack of a demonstrable soft tissue lesion, this was attributed most likely to a wound infection secondary to traumatic injury.
Operative debridement was planned with a presumptive diagnosis of traumatic infection. The patient underwent excision of the wound and the chronic granulation/soft tissue inflammatory reaction within the bony cavity. The bone cavity was aggressively curetted and debrided to healthy bleeding bone (Fig 3). The mandibular symphysis was found to be extremely stable with adequate stock of bone to maintain its integrity without the need for mechanical reinforcement, either by plating or bone graft. The soft tissue was extensively mobilized and reapproximated in layers. The pathology report revealed chronic osteomyelitis. At 6 weeks follow-up, the wound had healed without complication or further sequelae (Fig 4).
The brown recluse spider, Loxosceles recluseis the most common of the Loxosceles species in the United States. Clinical sequelae of Loxosceles bites were described in the literature as early as 1879. According to the Centers for Disease Control and Prevention, approximately 10,000 spider bites are annually reported to poison control centers, of these, 1835 bites were attributed to the brown recluse in 1994. The brown recluse spider mainly populates the southern central states, due to a preferred habitat of mild climates. The spiders prefer dark, quiet environments such as closets, basements, attics, and sheds. Brown recluse spiders do not usually bite unless provoked or threatened. The spider is generally 1 to 5 cm in length and has a tan to light brown color. Distinguishing features include fiddle-shaped brown markings on its dorsum and characteristic 3 dyads (6 eyes as opposed to the usual 8 for most spiders). Brown recluse spiders commonly bite exposed lower or upper extremities, but bites to the face have been reported.
Brown recluse spider bite injuries cause envenomation leading to major tissue destruction. Pain and erythema are apparent within the first few hours after the bite. Progression to skin necrosis with purplish blue cyanotic bullae within 24 to 48 hours soon follows. The site of injury undergoes a cycle of erythema, ischemia, and thrombosis, referred to as the “red, white, and blue sign.”(p565) This is due to brown recluse venom components, including hyaluronidase, elastase, sphingomyelinase D, lipase, and serum amyloid protein.8 Each of these enzymes contribute to the extent of tissue necrosis.8 The envenomation attracts polymorphonuclear cells, which further propagate the necrosis. The polymorphonuclear cells degranulate within the vasculature leading to vessel thrombosis followed by tissue ischemia. The underlying area of necrosis is generally extensive in comparison to the minimal surface lesion as seen in our patient. The clinical picture may progress to signs of fever, chills, malaise, vomiting, and arthralgias. There have even been reports of brown recluse spider bite envenomation leading to multisystem organ failure and death.9
The diagnosis and treatment of brown recluse bites is controversial: a classification system proposed by Anderson has been favored by expert entomologists to facilitate the diagnosis and, perhaps, to decrease overdiagnosis in nonendemic areas. A number of entomologists have collected data from reported brown recluse spider bites, but they noted that positive identification of the spider has been absent. Laboratory tests using enzyme-linked immunosorbent assay techniques have been developed in attempt to accurately diagnose brown recluse envenomation but none have been widely accepted or approved for clinical use.
The differential diagnosis of brown recluse spider bite envenomation includes thromboembolic disease; focal vasculitis; drug reactions; pyoderma gangrenosum; Lyme disease, bacterial, viral, or fungal infections; neoplasms; chemical burns; and factitious injections. Attempts to exclude other potential causes before attributing necrotic skin lesions to the probably overused diagnosis of brown recluse bite should be made. Nonendemic regions are especially unlikely to encounter the problem and other more probable diagnoses should be entertained.
Treatment includes basic wound care measures, such as rest, ice compresses, and elevation of the involved extremity. Antibiotics are typically not indicated unless there is skin breakdown with secondary infection caused by typical skin flora. Dapsone, a leukocyte inhibitor, has shown some promise, if administered early. Dapsone's efficacy is based on its inhibitory effect on the polymorphonuclear cells that infiltrate and further propagate thrombosis, leading to further ischemia and tissue necrosis. Dapsone is usually reserved for severe cases because of its adverse effects, including dose-related hemolysis, agranulocytosis, aplastic anemia, cholestatic jaundice, and methemoglobinemia.
Operative intervention is indicated when frank abscess formation occurs, tissue necrosis is extensive or severe, or deep vital structures are involved or exposed. Incision and drainage of a defined abscess is always indicated; however, as intense tissue inflammation and edema are more common findings than discrete abscesses, indiscriminate incision without the presence of an underlying abscess should be avoided. Debridement of necrotic tissue is necessary to avoid the negative metabolic effects of the breakdown products of cell death on wound healing. Deep exposed structures such as bone or vital tissues may require soft tissue coverage by an appropriate flap or graft after adequate wound bed preparation.
Our patient presented with a prolonged course of a chronic, open wound with deep soft tissue and bone involvement. There was chronic infection manifested by osteomyelitis of the mandible. Appropriate soft tissue debridement and bone debridement were performed and primary wound closure was obtained. Long-term follow-up demonstrated resolution of the chronic draining wound with surgical management and antibiotic therapy. Although the spider is not considered endemic to Florida, the patient did identify environmental exposure and clinical presentation consistent with a brown recluse spider bite.
Brown recluse spider bites and envenomations may be overreported. The course of injury may vary from mild erythema to frank necrosis of soft tissue and bone. The treatment regimen should include the basics of wound care and consideration of systemic antibiotics and topical antimicrobials as indicated. Dapsone may be of value if given early in the course of treatment. Surgical intervention is warranted in cases of abscess formation, extensive tissue necrosis, or deep tissue involvement. Injuries to the face are rare but follow the course of injury to other more common areas of the body.
|Figure 1. Preoperative photograph of presenting wound.|
|Figure 2. Computed tomographic scan demonstrating infection of mandibular symphyseal bone.|
|Figure 3. Intraoperative photograph of debrided, stable mandibular symphysis.|
|Figure 4. Postoperative photograph demonstrating healed, stable wound.|