OSTEOMYELITIS

OSTEOMYELITIS Definition Osteomyelitis can be defined as the inflammation of bone and bone marrow along with the surrounding periosteum. The inflammatory condition involves all the structures of bone, e.g. the bone marrow, haversian systems, periosteum, blood vessels, nerves and epiphyses, etc. Classification There are various types of Osteomyelitis lesions occurring in the jawbones, which can be broadly divided into two groupsacute osteomyelitis and chronic osteomyelitis. According to the specificity of the causative microorganisms, osteomyelitis may be of two typesspecific osteomyelitis and non-specific osteomyelitis. A. Acute Osteomyelitis Most commonly encountered (Nonspecific) lesions in this category includea. Acute suppurative osteomyelitis b. Acute subperiosteal osteomyelitis c. Acute periosteitis B. Chronic Osteomyelitis i. Nonspecific type a) Chronic intramedullary osteomyelitis. b) Chronic focal sclerosing osteomyelitis. c) Chronic diffuse sclerosing osteomyelitis. d) Chronic osteomyelitis with proliferative periosteitis. e) Chronic subperiosteal osteomyelitis. f) Chronic periosteitis. ii. Specific type a) Tuberculous osteomyelitis. b) Syphilitic osteomyelitis. c) Actinomycotic osteomyelitis.

C. Radiation Induced Osteomyelitis D. Idiopathic Osteomyelitis Aetiology of Osteomyelitis: Numerous etiological factors have been identified which can cause osteomyelitis and these factors are as: Direct spread of infection from dental pulp into the jawbone. Spread of infection in the bone from the preexisting suppurative odontogenic infections, e.g. Periapical abscess. Infected periapical granuloma Infected periapical cyst. Periodontal abscess. Pericoronitis Infected and fractured tooth/retained root tip. Spread of infection following removal of tooth without proper asepsis and antibiotic coverage. Compound fracture of the jaw bone with exposure of bone outside the skin or mucosa. Gunshot injuries in the jaw with soft tissue laceration and exposure of bone. Spread of microorganisms from overlying soft tissue (skin or mucosa) infecti9ns. Post radiation secondary infection. Infection to the pre-existing bony diseases, e.g. Paget's disease of bone, fibrous dysplasia and osteoporosis, etc. Phosphorus poisoning. Anachoretic infections. Idiopathic factors. Being an inflammatory disease, development of osteomyelitis depends mainly upon the balance between the virulence and number of microorganisms present in the bone and the local or systemic defense capacity of the patient's body to infection.

PREDISPOSING FACTORS OF OSTEOMYELITIS: Local Factors: Anatomical site of the disease: The mandibular bone has poor blood supply in comparison to that of the maxilla, besides this it has more compact bony pattern due to which, osteomyelitis occurs far more commonly in mandible than maxilla. Pre-existing bone disease: Long standing bony disease like Paget's disease of bone, fibrous dysplasia, cystic lesions, osteoporosis, etc. many render the jaw bones more susceptible to osteomyelitis, when infections occur in the tissue. Radiation injury: Radiotherapy to the head and neck area often produces obliterative endarteritis, which results in impaired blood supply to the jawbones. Therefore in such conditions possibility of osteomyelitis is increased once the infection in the bone sets-in. Systemic Factors: Predisposing factors (systemic) in osteomyelitis favor the development of the disease by lowering the body resistance to infections. These factors include the following: Malnutrition. Drug addiction. Anemia. Diabetes. Leukemia. Agranulocytosis. Syphilis. Measles and typhoid fever. HIV infection and AIDS. Extremes of age Urinary tract infections. Micro-organisms in Osteomyelitis: Microorganisms responsible for this type of infections are as follows: Aerobic organisms Staphylococcus aureus Haemolytic Streptococcus Anaerobic organisms Bacteroids Anaerobic Streptococcus.

Pathogenesis of Osteomyelitis: In osteomyelitis inflammation and destruction of bone take place by the following mechanisms. 1) Infection from the periapical lesions or infected pulp or other foci enters into bone marrow first and from there it extends into the cancellous bony spaces. 2) As the infection is established, the lumina of the nutrient vessels of the living bone are occluded by the formation of thrombus. (The thrombus consists of dead or viable neutrophils, microorganisms and necrotic tissue debris, etc). 3) Due to thrombosis of the nutrient vessels and excessive pressure from the inflammatory exudates against the rigid and confined space in the bone, the nutrition supply to the bone cells is completely disturbed resulting in death of cancellous bony trabeculae with formation of `sequestrum'. 4) The infection then spreads via the Volkmanns canals in the cortical plates and reaches to the external surface of bone below the periosteum, inflammation at this area results in periosteitis. Accumulation of more and more exudates and pus cause separation between the cortical plates of bone and the periosteum. 5) Further extension of the inflammation may lead to single or multiple sinus tracts formation, which communicate between the bone and the external surface of the skin and mucous membrane. 6) As the cortical plates of the bone get the blood supply from the overlying periosteum, separation between the cortical plates and the periosteum results in necrosis of the cortical bone. 7) Although the periosteum is infected and elevated from the cortical bone, a few bone- forming cells still survive and when the acute phase of the disease subsides, a new layer of bone is often formed over the sequestrum which is called `involucrum'. 8) Pus discharges from the involucrum through sinuses called cloacae and bathe the surface of the sequestra.