OSTEOMYELITIS

 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.

 CASE REPORT

A 62-year-old woman referred to our clinic for treatment of chronic infection and pain following extraction of the left mandibular second molar under local anesthesia by her general dentist. She was in good general health and did not have a history of drug use. Her pre-extraction radiographic examination confirmed the presence of a deep distal periodontal pocket ). 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

3

.

            Tuberculous oral lesions are relatively rare occurrence. 

Oral manifestations occur in approximately 3% of cases 

involving long standing pulmonary and/ or systemic 

infection4

.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

5

.

               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

2

.

           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

a case of osteomyelitis

DISCUSSION

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.

CONCLUSION

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.