Osseous in Latin means bony and Osteon in Greek means bone. Myelos is marrow. Itis in Greek means inflammation.
Osteomyelitis means inflammation of medullary portion of the bone or bone marrow or cancellous bone.
Osteomyelitis was common earlier but at present the incidence of jaws was less because of worldwide availability of
Few cases even occur
“An inflammatory condition of soft bone, that begins as an infection of medullary cavity and haversian systems of cortex and extends to involve the periosteum of the affected area”.
PREDISPOSING FACTORS :
Conditions that alters host defences and due to chronic debilitating systemic diseases:
Conditions that alter vascularity of bone :
Virulence of organisms:
Certain organisms precipitate thrombi formation by virtue of their destructive lysosomal enzymes.
Odontogenic infection from pulpal:
Infection of orofacial regions:
Infection derived by haematogenous route:
According to Topazian classification was done based on absence or presence of suppuration:
According to JOMS 1993: 51; 1994 by Hudson et al
iii) Odontogenic infection
iii) Vascular insufficiency
i) Developing skeleton (children)
ii) Developing dentition (children)
i) Developing skeleton (child)
ii) Escalated osteogenic activity (< age 25yrs)
i) Unique proliferative subperiosteal reaction
ii) Developing skeleton
i) Inadequately treated forms
ii) Systemically compromised forms
iii) Refractory forms
i) Fastidious microorganisms
ii) Compromised host and pathogen interface
i) Predominantly odontogenic
ii) Chronic localized injury
i) Haematogenous osteomyelitis
ii) Osteomyelitis secondary to a contiguous focus infection
iii) Osteomyelitis with or without peripheral vascular disease.
i) Stage I: medullary osteomyelitis – involved medullary without cortical, Haematogenous
ii) Stage II: superficial osteomyelitis – less than 2 cm bony defect without cancellous bone.
iii) Stage III: localized osteomyelitis – < 2 cm bony defect on radiograph, does not appear to involve both cortices.
iv) Stage IV: diffuse osteomyelitis – > 2 cm pathologic feature, infection, non-union.
i) Host – normal host
ii) Host – local compromise & systemic compromise
iii) Host – treatment is worse than disease
i) Systemic – malnutrition, renal and hepatic failure, diabetes mellitus, chronic hypoxia, immune deficiency, malignancy, old ages, tobacco, alcohol abuse.
ii) Local – chronic lymphedema, venous stasis, major vessel disease, arthritis, extensive scarring, radiation fibrosis, small vessel disease, local loss of sensation.
Periapical and periodontal infections localised by protective pyogenic membrane
⇓ Sufficient virulent M.O
Destroy this barrier
Infection into the bone
Pus (necrotic tissue, dead cells) accumulates in canals (Yolkman Haversian)
Vascular collapse (thrombosis) compression of neurovascular bundle
Ischemia mandibular anesthesia
The island of dead bone formed becomes place for precipitate of ionized calcium mobilized form surrounding osteolytic process (so sequestrum appears more opaque).
If pus continues to accumulate the periosteum is penetrated and mucosal and cutaneous abscess and fistula develop.
Mechanical trauma burnishes the bone causing ischemia and introduces organism initiated by acute inflammation – hyperemia increase capillary permeability.
As natural host defences and therapy begins to be effective the process becomes chronic, inflammation regresses, granulation tissue is formed and new blood vessels causes lyses of bone thus separating fragment of necrotic bone from viable involucrum.
The process leading to the formation of osteomyelitis is initiated by acute inflammation, hyperemia increase capillary permeability, and infiltration of granulocytes.
Tissue necrosis occurs as proteolytic enzymes are liberated and as destruction of bacteria and vascular thrombosis continues, there is pus formation.
The bone surrounding sequestrum appears less densely mineralized than sequestrum. Ischemia causes increase in CO2 level, which attracts calcium due to change in patient. The Ca deposition leads to increase in mineralization of the sequestrum.
Osteomyelitis in mandible: –
Osteomyelitis in mandible is common in adults. In craniofacial skeleton only the mandible and the calvarium have myeloid compartments.
The important factor in establishment of osteomyelitis is the compromise in the blood supply and venous drainage of mandible.
Secondary supply is periosteal supply through, which generally runs parallel to cortical surface of bone giving nutrient vessels those penetrate cortical bone and anastomoses with the branches of inferior alveolar artery.
It runs upwards and joins pharyngeal plexus.
It runs downwards and joins external jugular veins.
Walden (1943) gave a description of vascular morphology of mandibular and associated structures to account for spread of osteomyelitis. He described mandibular vascular support as being provided through multiple arterial loops from major vessels, which renders a large portion of bone susceptible to necrosis with the occurrence of major vessel infectious thrombosis.
Walsel Vogel (1970) describe,These tend to be segregation of terminal channels, which act like “end organs” due to lack of terminal collateral anastomoses, ultimately leading to vascular plugging by bacteria microthrombi or both. When afferent vessels anastomose with medullary channels there is a possibility of decrease in venous flow with associated areas of greater turbulence. These may be a reduction in host immune defence mechanism associated with these vascular channels in calcified tissue.
This is rare in adults due to
These preclude confinement of infections with in bone and permit dissipation of oedema and pus into soft tissue and paranasal air sinuses.
In past, the etiology of osteomyelitis was associated with skin surface bacteria, S. aureus and to lesser extent S. epidermidis, which was found that these organisms are found in bone not in skin.
However, aureus as primary offending pathogen does not hold true with regard to osteomyelitis.
Most of cases are caused by aerobic Streptococci (i.e., hemolytic streptococci, Streptococci viridans, anaerobic Streptococci, and Bacteroides)
Sometimes Klebsiella, Pseudomonas and Proteus are also found. Other organisms – M. tuberculosis, T. pallidium, Actinomyces, Coccidiodes, Tuberculosis bacilli, Treponema & Klebsei
Actinomycotic ostemyelitis classification of osteomyelitis defination of osteomyelitis etiology of osteomyelitis focal osteomyelitis garres osteomyelitis Garre’s sclerosing osteomyelitis inflammation of medullary portion of the bone inflammation of medullary portion of the bonemarrow microbiology of osteomyelitis Osteomyelitis pathogenesis of osteomyelitis predisposing factors of osteomyelitis Radiation osteomyelitis sclerosing osteomyelitis Specific infective osteomyelitis spread of osteomyelitis suppurative and non suppurative osteomyelitis suppurative osteomyelitis