Osteomyelitis
*Inflammation of bone & marrow contents.
*Secondary changes due to inflammation of soft tissue content of bone.
*Predisposing Factors:
- trauma, accidents, gunshot wounds, radiation damage,Paget’s disease & osteoporosis.
- systemic conditions like malnutrition, acute leukemia,uncontrolled DM, sickle cell anemia & chronic
alcoholism.
*Types: 1. Acute suppurative osteomyelitis
2. Chronic suppurative osteomyelitis:
i. Chronic Focal Sclerosing Osteomyelitis
ii. Chronic Diffuse Sclerosing Osteomyelitis
ACUTE OSTEOMYELITIS
CHRONIC OSTEOMYELITIS
*Serious sequelae of periapical infection, results in
spread into medullary spaces with necrosis of bone.
* Develops from untreated, acute osteo. Or arise
from dental infection without preceeding acute
stage.
CLINICAL FEATURES
*Acute & subacute osteo. involve either
*Clinical features are similar to acute, except:
maxilla/mandible.
*Signs & symptoms – milder,with less pain.
*Some osteo. refered as neonatal maxillitis in
infants & young children - hematogenous origin.
* Leucocytes slightly greater than normal.
* Infants – seriously ill & may not survive disease.
* Adults - severe pain, trismus & parasthesia of lips
in mand. & elevated temperature with regional
lymphadenopathy.
*WBC count elevated.
*Teeth involved is loose,eating difficult.
* Pus exudate from gingival margins.
*Until periostitis, no swelling or no reddening on
skin/mucosa.
* Teeth may not be loose & sore, so mastication is
possible even though jaw
may not be perfectly comfortable.
* Acute exacerbation may occur periodically.
*Temperature still elevated, but mild.
* Suppuration may perforate bone & overlying skin
or mucosa to form fistulous tract & empty on
surface.
RADIOGRAPHIC FEATURES
* Evidence until disease for 1-2weeks.
* Single /multiple radiolucencies.
*Loss of continuity of lamina dura.
*Irregular margins.
*Trabeculae - fuzzy, indistinct & radiolucent.
*Root resorption.
*Saucer shaped irregularmargins.
* Lamina dura less apparent, blends with
surrounding granular sclerotic bone.
* Moth eaten appearance.
HISTOLOGIC FEATURES
*Inflam. Exudate in medullary spaces.
*Inflam. Cells – neutrophillic PMnuclear
leucocytes, occasional lymphocytes & plasma cells.
* Chronic inflam. Reaction in bone - exudate & pus
accumulation in medullary spaces.
* Lymphocytes, plasma cells & macrophages.
*Destroyed osteoblasts lining bony trabeculae.
* Depending duration of process – trabeculae loss
viability & undergo slow
* Osteoblastic & osteoclastic activity occur
parallely with irregular bony trabeculae
formation with reversal lines.
*Later stages – Sequestrum may develop
TREATMENT & PROGNOSIS:
*Drainage, debridement & antimicrobial therapy.
*When intensity of disease attenuated – sequestrum seperates from living bone & gradually exfoliates
through mucosa.
*If large – surgical removal.
*Acute SO may preceed to develop periosteitis, soft tissue abscess /cellulitis.
Chr.Focal Sclerosing O
Chr.Diffuse Sclerosing O
*A reaction to mild bacterial infection entering
bone through carious tooth in persons ’ving higher
degree of tissue resistance & tissue reactivity.
* Due to diffuse periodontal disease.
CLINICAL FEATURES
* Commonly in children & young adults & rarely
old age.
* Common in older, with edentulous mandibular
jaw.
* Common tooth: mand Ist molar.
*On exacerbation: vague pain, unpleasant taste &
mild suppuration many times with fistula formation
opening to mucosa & drains.
* No other signs & symptoms other than mild pain.
RADIOGRAPHIC FEATURES
* Well circumscribes radiopaque mass of sclerotic
bone extending below apex on
roots.
*Root outline nearly visible with intact lamina dura.
* PDL space widened & is important to distinguish
cementoblastoma.
*Lesion border: abutting normal bone, may smooth
& distinct or appear to blend
into surrounding bone in contrast to focal cement
osseus dysplasia.
* Cotton wool appearance.
*Sometimes bilateral.
* Bilateral involvement in both maxilla &
mandible.
*Border between sclerosis & normal bone is
indistinct.
* Pattern may actually mimic Paget’s disease or
cement osseus dysplasia.
* Radiopacity stands out
HISTOLOGIC FEATURES
*Dense mass of bony trabeculae with little
interstitial marrow tissue.
*Osteocytic lacunae is empty.
* Trabeculae show reversal & resting lines giving
Pagetoid appearance.
*If interstitial soft tissue present – fibrotic &
infiltrate of few lymphocytes .
*Dense irregular trabeculae, some borderd by
active layer of osteoblasts.
*Mosaic pattern, indicates periodic resorption &
repair.
*Soft tissue in between trabeculae – fibrous & show
proliferating fibroblast,capillaries with
lymphocytes & plasma cells.
*PMN leucocytes present, if lesion is in acute
*Osteoblastic activity ‘ve completely subsided.
phase.
*Sometimes, inflam component is completely
burned out, leaving sclerotic bone & fibrosis.
TREATMENT & PROGNOSIS
*Endodontic treatment
*Surgical removal
*Extraction
* If tooth is present, must extracted.
*Surgical removal of sclerotic lesion is not
indicated unless symptomatic.
*Sometimes sclerosed bone will remain after
resolution & remodelling.
Sclerotic Cemental Masses:*Benign fibro-osseous jaw lesions of unknown etiology, occurring predominantly in middle-aged black
females; lesions present as large painless radiopaque masses usually involving several quadrants of the
jaw
CLINICAL FEATURES:
*Just same as in Diffuse sclerosing osteomyelitis – present with multiple symmetric lesion, pain, drainage
& localized expansion.
RADIOGRAPHIC FEATURES:
*Same as in DSO - Lesions appear as multiple sclerotic masses, located in two or more quadrants, usually
in the tooth-bearing regions.
HISTOLOGIC FEATURES:
*Differences:
> Cemental masses instead of sclerotic bone
> Cementum – large solid masses with smooth, lobulated margins, with globular accretion pattern.
Florid Osseus Dysplasia:*Another disease similar to DSO & Sclerotic cemental masses; described by Melrose & his associates.
*characterized by lesions in upper/ lower jaw that occur when normal bone is replaced with a mix of CT
and abnormal bone. It affect middle age Black and Asian women .
*Cause – obstruction of normal interstitial fluid by fibro osseus proliferation.
RADIOGRAPHIC FEATURES:
*FOD appears as well-defined mixed (radiolucent-radiopaque) or totally radiopaque & has a radiolucent
periphery & surrounding sclerosing border similar to Periapical Cemental Dysplasia.
*“cotton wool” appearance or large amorphous regions of calcifications.
TREATMENT:
*Usually no treatment necessary.
Chronic Osteomyelitis with Proliferative Periosteitis (Garre’s
Chronic nonsuppurative sclerosing osteitis,periosteitis ossificans)
*A distinctive type of osteomyelitis with focal gross thickening of periosteum, & peripheral reactive bone
formation resulting from mild infection or irritation.
*It is essentially a periosteal osteosclerosis analogous to chronic focal endosteal sclerosis & diffuse
sclerosing osteomyelitis.
CLINICAL FEATURES:
*young age <25yrs, mostly involve anterior of tibia.
*Greater opportunity for infection enter maxilla & mandible, due to peculiar anatomic arrangement of
teeth.
*Cases in jaws; occurs in mandible bicuspid & molar region - children & young adults.
*Maxilla is seldom affected, reason not clear.
*Toothache or jaw pain & bony hard swelling on outer surface of jaw – usually for several weeks
duration.
*Due to overlying soft tissue infection/ cellulitis that involves periosteum cause reactive periosteitis.
RADIOGRAPHIC FEATURES:
*Reveals a carious tooth opp: to hard bony mass.
*Occlusal radiograph: focal overgrowth of bone on outer surface of cortex, which described as
duplication of cortical layer.
*Mass is smooth & well calcified & may show thin but definite cortical layer.
HISTOLOGIC FEATURES:
*Supracortical but subperiosteal mass is composed of much reactive new bone & ostoeid, with osteoblast
bordering many trabeculae.
*Trabeculae orient perpendicular to cortex, with trabeculae arranged in parellel to each other or reticular
form.
*CT between bony trabeculae is rather fibrous & show diffuse or patchy sprinkling of lymphocytes &
plasma cells.
*Periosteal reaction – infection from caries perforating cortical plate & become attenuated, stimulating
periosteum rather than producing usual suppurative periosteitis.
TREATMENT & PROGNOSIS:
* Endodontic treatment or extraction, with no surgical intervention for periosteal lesion except for biopsy.
*Periosteal bone formation /neoperiosteosis may occur in variety of other conditions & care must be
taken to exclude them from diagonosis.
*Include infantile cortical hyperosteosis (Caffey’s disease), hypervitaminosis A, syphilis, leukemia,
Ewing’s sarcoma, metastatic neuroblastoma & even a fracture callus.