Bone pathology

Classification of bone pathology

1. Inflammatory.
2. Metabolic & hormonal.
3. Genetic & developmental.
4. Dystrophic.
5. Idiopathic.
6. Tumor and tumor-like lesions.
7. Cysts of the jaws.
Inflammatory bone diseases
 Osteomyelitis.
 Dry socket.
Metabolic/hormonal bone diseases
 Abnormal Hormonal:
1- Hyperparathyroidism.
2- Hyperthyroidism.
3- Acromegaly.
 Abnormal enzymes: Hypophosphatasia.
 Abnormal minerals : Rickets and osteomalacia.
 Abnormal matrix :Mucoplysacchridosises and
Osteoporosis.
Genetic bone diseases
 Cherubism.
 Osteoclast dysfunction:

Osteopetrosis.
 Abnormal metabolism of collagen:

Osteogenesis imperfecta
Developmental bone diseases
 Macrognathia.
 Micrognathia.
 Hemifacial hypertrophy.
 Hemifacial atrophy.
 Segmental odontomaxillary dysplasia.
 Syndromic.
Dystrophic bone disease
 Osteoclast dysfunction: Paget’s disease of
bone.
Idiopathic
 Infantile cortical hyperostosis.
 Phantom bone disease.
 Idiopathic osteosclerosis.
Tumor & tumor-like lesions
 Primary bone tumors.
 Metastatic bone tumors.
 Tumor-like lesions related to the bone :

1- Fibro-cemento-osseous lesions.
2- Giant cell lesions.
Cysts of the jaws
 Epithelialized cysts:
1- Odontogenic cysts.
2- Non-odontogenic cysts.
 Non-epithelialized cysts.
 Osteomyelitis
Definition:
It is the inflammation of bone and
bone marrow.
Classification
 According to the
cause:

Osteomyelitis

Specific Non-specific
Osteomyelitis
Specific osteomyelitis: caused by specific bacteria
1. Syphilitic.
2. Actinomycotic.
3. Tuberculous.
4. Osteoradionecrosis.
5. Osteochemonecrosis.
Non-specific osteomyelitis: caused by mixed bacteria
 Acute osteomyelitis.
 Chronic osteomyelitis.
Etio-pathogenesis of osteomyelitis
 Direct factors:
1. Following improper management of
odontogenic infection.
2. Following traumatic fracture (developed
countries).
3. Following NUG or noma (Africa).
4. Hematogenous.
Predisposing factors
 Chronic systemic disease (diabetes,
malnutrition, malignancy, radiation
immunocompromised status).
 Disorders associated with decreased
vascularity (osteopetrosis, late Paget’s
disease of bone, end stage cemento-
osseous dysplasia).
 Others: Tobacco, etc.
Clinical features of acute osteomyelitis
 Duration is less than one month.
 High & intermittent fever, leukocytosis.
 Painful soft tissue swelling,
lymphoadenopathy.
Chronic osteomyelitis
 Suppurative.
 Non-suppurative.
Chronic suppurative osteomyelitis
 Clinical features:
 Swelling and deep pain, fever.
 Sinus formation with discharge.
 Sequestrum formation.
 Periods of acute exacerbation.
 Pathologic fracture.
 paraesthesia of lower lip.
X-ray
 Acute: ill-defined radiolucency.
X-ray:Chronic: patchy, ragged, and ill-
defined radiolucency with central
radiopacity (sequestrum). Moth-eaten
appearance.
Histopathology
 Acute osteomyelitis :
 Necrotic bone with loss of osteocytes,
peripheral resorption, and bacterial
colonization.
 Peripheral bone contain PMNS
Histopathology
 Chronic osteomyelitis :
 Fibrous connective tissue with inflammatory
infiltrate.
 Scattered pockets of abscess formation.
Treatment
 Acute osteomyelitis :
 Drainage.
 Culture for sensitivity.
 Chronic osteomyelitis :
 Surgical removal of sequestrum and infected
material.
 Culture for sensitivity, antibiotic is given
intravenously.
Non-suppurative
osteomyelitis
Non-suppurative Osteomyelitis
 Diffuse sclerosing osteomyelitis.
 Focal sclerosing osteomyelitis.
 Osteomyelitis with proliferative periostitis.
Diffuse sclerosing osteomyelitis
 Definition:
It is a painful inflammatory bone process
characterized by bone destruction, bone
sclerosis, and periosteal hyperplasia.
Pathogenesis
 Caused by low virulent organism usually
Eikenella corrodons, aerobic Gram positive
bacilli and glucose non-fermenter.
Clinical features
 Adult.
 Mandible, may be the whole quadrants.
 Followed odontogenic or periodontal
infection.
 It may perforate cortical bone with
periosteal new bone formation.
X-ray
 Sclerosis around central area of infection
and bone resorption.
Histopathology
 Sclerosis and remodeling of bone.
 Marrow spaces filled with scattered
haversian canals.
 Sequestrum surrounded by subacutely
inflamed granulation tissue with secondary
bacterial colonization.
Focal sclerosing
osteomyelitis
Condensing osteitis
Definition
 It is a localized area of bone sclerosis
associated with the apex of a tooth with
pulpitis or pulpal necrosis.
Clinical features
 Children and young adult.
 No clinical swelling.
 Mandible, molar and premolar area.
X-ray
 Radiopacity related to the apex of the root
without radiolucent rim.
 Thickened lamina dura.
Osteomyelitis with
proliferative
periostitis
Garre’s osteomyelitis
Definition
 It is a periosteal reaction to the presence of
inflammation.
Pathogenesis
 Periapical inflammatory disease.
 Secondary to periodontal infections.
 Fractures.
 Buccal bifurcation cyst.
 Non-odontogenic infection.
Clinical features
 Children and young adult (mean age 13
years).
 No sex predilection.
 Common sites: mandibular molar and
premolar area.
 Mostly unifocal, but multiple quadrants may
be involved.
X-ray
 Parallel radiopaque laminations of bone
( onion skinning).
 Bony projection radiate perpendicular from
the underlying bone ( sun ray ).
 Specific
osteomyelitis
Tuberculous osteomyelitis
 Chronic granulomatous disease caused by
mycobacterium tuberculosis.
 Spine, knees, hips, and rarely jaws.
 It is more destructive with sinus drainage.
Syphilitic osteomyelitis
 Chronic granulomatous disease caused by
treponema pallidum.
 Acquired syphilis: nose, palate (saddle
nose), skull, and extremities. (gumma).
 Congenital syphilis: osteochondritis and
periostitis.
Actinomycotic osteomyelitis
 Chronic suppurative or granulomatous
disease caused by filamentous, branching,
G +ve, anaerobic bacteria: Actinomyces
israelii, A. naeslundii, A. viscosus.
 It is mainly infection of soft tissues but may
involve jaws.
 Multiple draining sinuses containing sulfur
granules ( organism colonies).
Dry socket
Alveolar osteitis
Pathogenesis
 Wash out of the clot.
 Failure of blood clot formation.
 Destruction of initial clot by activation of
plasminogen-plasmin fibrinolytic system.
*Activation is caused by:
Local trauma.
Estrogen.
Bacterial pyrogenes.
Predisposing factors
 Diseases associated with decrease
vascularity to the bone.
 Contraceptive bills.
 Smoking.
 History of dry socket.
 Existing sign of pericoronitis.
 Traumatic extraction.
Clinical features
 Prevelance: 1-3% for all extraction,
25-30% for impacted mandibular
third molar.
 Peak incidence 40-45 years of age.
 Socket with dirty gray clot that disintegrates
& leaves empty socket.
 Signs & symptoms: severe pain, foul odor,
swelling, lymphadenopathy.
 These signs may persist for 10-40 days.
Treatment
 Irrigation with warm saline.
 Idoform gause with eugenol.
Genetic bone diseases
 Cherubism.
 Osteopetrosis.
 Osteogenesis imperfecta.
 Syndromic:
 1- Cleidocranial dysplasia.
 2- Craniofacial dysostosis.
 3- Mandibulofacial dysostosis.
Osteopetrosis
(Marble bone disease)
 Definition:
It is a group of hereditary disorders
characterized by a marked increase in bone
density.
Pathogenesis
 A defect in remodeling caused by failure of
normal osteoclast function.
Classification
 There are two types:
 Infantile type (autosomal recessive).
 Adult type (autosomal dominant).
Infantile type
 Affect long bones.
 Normocytic anemia.
 Granulocytopenia = increased susceptibility
to infection.
 Facial deformity: broad face, hypertelorism,
snub nose, frontal bossing.
 Delayed tooth eruption.
 CNS : blindness, deafness, facial paralysis.
 Pathologic fracture.
 Osteomyelitis.
 Poor prognosis.
Adult type
 Affect axial bones.
 40 % asymptomatic.
 Symptomatic: either cranial compression or
bone fractures.
 Bone pain.
 Osteomyelitis.
Histopathology
 Dense bone formation. No Howship’s
lacunae.
Osteogenesis
imperfecta
Definition
 A heterogeneous group of heritable
disorder characterized by impairment of
collagen maturation.
Pathogenesis
 Mutation in one of two genes encoding for
type I collagen.
 It is either autosomal dominant or
recessive.
Classification
 It is divided in to four types:
 Type I : moderate / mild bone fragility, blue
sclera, opalescent teeth ( dentinogenesis
imperfecta type I ).
 Type II : fatal, died shortly after birth or in
utero.
 Type III, IV : may show opalescent teeth.
Histopathology
 Thin cortical bone.
 Reduced bone matrix.
 Persistent immature bone and no lamellar
bone.
X-ray
 Osteopenia.
 Bowing of long bones.
 Multiple fractures.
 Wormian bone in Skull.
Cleidocranial
dysplasia
Definition
 A hereditary disorder characterized by
dental and clavicular abnormalities.
Pathogenesis
 Defect in CBFA1 gene.
 Autosomal dominant.
Clinical features
 Clavicles are absent or hypoplastic.
 Abnormal shoulder mobility.
 Short stature with large head.
 Ocular hypertelorism.
 Wormian bones.
 Cleft palate or high arched palate.
 Delayed or failure of permanent teeth eruption.
 Presence of supernumerary teeth.
Craniofacial
dysostosis
Crouzon syndrome
Definition
 It is a rare syndrome characterized by
craniosynostosis ( premature closure of
cranial sutures).
Pathogenesis
 Mutation FGFR2 gene.
 Autosomal dominant.
Clinical features
 Premature closure of sutures ( boat or
triangle shape head).
 Ocular proptosis, total blindness.
 Hearing deficits.
 Headache.
 Hypoplastic maxilla, crowded maxillary
teeth.
 Pseudoclefts.
Mandibulofacial
dysostosis
Treacher-Collins syndrome
Definition
 It is a defect in structures derived from 1st
and 2nd branchial arches.
Clinical features
 Hypoplastic zygoma.
 Coloboma.
 Down-slanted palpebral.
 Deformed pinnae.
 Underdeveloped maxilla.
 Cleft palate (30%).
 Hypoplastic or underdeveloped parotid glands.
Dystrophic bone disease
Paget’s disease of bone.
Paget’s disease of
bone
Osteitis deformans
Definition
 It is a disease characterized by abnormal
and anarchic resorption and deposition of
bone resulting in distortion and weakening
of the affected bone.
 Pathogenesis
 Unknown….
 Inflammatory process.
 May be viral: Paramyxovirus was detected in osteoclasts
 Endocrine factors (hyperthyroidism).
 Genetic (15-30%), PDB1-7 genes.
 Inborn error of connective tissue metabolism.
Clinical features
 Common in English and French.
 Rare in Africa and Asia.
 Affect old people above 40 years.
 It could be symptomatic or asymptomatic.
 It could be monostotic or polyostotic(common).
 Common bones involved: lumbar vertebrae,
pelvis, skull, and femur.
Symptoms
 Bone pain.
 Osteoarthritis with joint pain.
 Limited mobility.
 Bowing deformity of weight-bearing bones
(monkey-like).
 Bone fracture.
Head & neck manifestation
 Progressive increase in the circumference of the head.
 Jaws affected in 17 % of cases, maxilla more than mandible
(2:1).
 Middle face enlargement (lion-like = leontiasis ossea).
 Obliteration of sinuses and enlarged alveolar bone (denture
tight).
 Spacing of teeth.
 Hypercementosis.
 Neurological signs: facial paralysis, visual and auditory
disturbances.
X-ray
 Osteolytic stage: large radiolucencies in
skull.

 Osteoblastic stage: cotton wool

appearance.
 Hypercementosis.
 Bone scintigraphy: high absorption.
 Histopathology
 Osteolytic stage: numerous osteoclasts
surrounding bone trabeculae with increased
activity.
 Vascular stage: bone marrow is replaced by
highly vascular & cellular fibrous connective.
 Sclerotic stage: large masses of dense
bone with prominent reversal lines ( mosaic
appearance).
Investigation
 High serum alkaline phosphatase.
 Normal calcium and phosphorus levels.
 Urine analysis:
1. N-telopeptides assays.
2. Pyridinoline cross-link assays.
Treatment
 Pain killer (aspirin).
 Biphosphonates.
 Calcitonin.
 Plicamycin , for resistant cases.
 Avoid surgical manipulation during vascular &
sclerotic stage ( bleeding or osteomyelitis).
 Hypercementosis cause difficulty in extraction.
 Malignant sarcoma in 0.9-13%.
Idiopathic bone diseases
 Infantile cortical hyperostosis.
 Phantom bone disease.
 Idiopathic osteosclerosis.
Infantile cortical
hyperostosis
Definition
 It is a self-limited, short-lived proliferative
bone disease characterized by cortical
thickening of various bones.
Pathogenesis
 Unknown.
 Genetic .
 Infection.
 Congenital abnormality.
Clinical features
 Firm tendered swelling , pain and fever.
 Common bones involved: mandible (75-
90%), clavicles, long bones, maxilla, ribs,
and scapulae.
 Affect infants at 7th month of life, mean age
9 weeks.
 Anemia and leukopenia.
X-ray
 Epensile hyperostotic process over cortical
surface.
 Rounded coronoid process.
Investigation
 Bone scan.
 High ESR.
 High alkaline phosphatase.
 Anemia.
Treatment
 Self-limited.
 Supportive care.
 Corticosteroids.
 Prognosis is good but may produce
malocclusion or mandibular deformity.
 Phantom bone
disease
Massive osteolysis, vanishing bone
disease
Definition
 It is a rare disease characterized by
spontaneous and progressive destruction of
one or more bones.
Pathogenesis
 Unknown.
 Vascular proliferation (hemangiomatosis of
bone).
Clinical features
 Children and young adult.
 50% have history of trauma.
 Common bones involved: pelvis, humeral
head and shaft, axial skeleton.
 30% affect maxillofacial bones.
 Mandible more than maxilla.
Oral manifestations
 Mobile teeth.
 Malocclusion.
 Obstructive apnea.
 Pathologic fracture.
 Deviation of the mandible.
X-ray
 Early: intramedullary radiolucent foci.
 Late: these foci coalesce to involve cortical
bone.
Histopathology
 Early stage: nonspecific vascular
proliferation with fibrous connective tissue
and chronic inflammatory cells.
 Late stage: more collagenous tissue.
Treatment
 Usually unsatisfactory.
 Some undergo spontaneous regress.
 Radiotherapy is the best but with hazards
of sarcomatous changes.
 Metabolic &
hormonal bone
diseases
Classification
 Abnormal Hormonal level:
1- Hyperparathyroidism.
2- Hyperthyroidism.
3- Acromegaly.
 Abnormal enzymes: Hypophosphatasia.
 Abnormal minerals : Rickets and osteomalacia.
 Abnormal matrix formation:
Mucoplysacchridosises and Osteoporosis.
Hyperthyroidism
 Abnormal high level of T3 & T4.
 Premature exfoliation of deciduous teeth
and eruption of permanent teeth.
 Osteoporosis of the jaws.
 Tooth erosion.
Acromegaly
 Abnormal high level of growth hormone
after plate closure.
 Mandibular prognathism.
 Condylar hyperplasia.
 Frontal bossing.
Hypophosphatasia
 Deficiency of alkaline phosphatase enzyme in
serum and tissues; characterized by skeletal
defects resembling those of rickets.
 Hereditary, autosomal recessive.
 Alveolar bone loss.
 Premature exfoliation.
 Large pulp chambers.
 Reduced cementum at the apex.
 Teeth hypoplasia.
Rickets & osteomalacia

 Vitamin D deficiency or abnormal calcium

and phosphorus homeostasis.
 Rickets:
frontal bossing, squared head, bowing legs.
 Osteomalacia:
loss of bone density, Milkman’s fracture.
Mucopolysaccharidoses
 Deficiency of lysosomal enzymes involved in
degradation of mucopolysaccharides in the matrix
leading to its accumulation.
 Hereditary, autosomal or X-linked recessive.
 There are 8 types.
 Coarse facial features.
 Malformed bones short stature.
 Joint stiffness.
 Clouding cornea.
 Mental retardation
Osteoporosis
 Reduced bone mass.
 Primary: postmenopausal, senile.
 Secondary: endocrine (hyperthyroid), GIT, drugs
steroids, neoplasia, immobilization.
Fibro-cemento-
osseous lesions
Definition
 A variety of disorders which histologically
characterized by replacement of bone by
cellular fibrous tissue within which islands
and trabeculae of metaplastic bone
develop.
Classification
 Neoplastic lesions: Cemento-ossifying fibroma.
 Developmental: Fibrous dysplasia.
 Genetic: Cherubism.
 Dysplastic ( reactive) lesions:
1. Periapical cemental dysplasia.
2. Focal cementosseous dysplasia.
3. Florid cementosseous dysplasia.
4. Gigantiform cementoma.
Cementifying/ossify
ing fibroma
Clinical features
 Common in mandible, molar-premolar area.
 Third and fourth decades of life.
 Female predilection.
X-ray
 Well-circumscribed radiolucency with
variable degree of calcification.
 Mixed ( intermediate stage).
 Root resorption.
Histopathology
 Collagenous stroma which arranged
haphazardly.
 Spindle or stellar cells with high
vasculature.
 Presence of calcification:bone, ovoid
basophilic cementum-like, or both.
 Osteoblastic rimming of trabeculae.
Fibrous dysplasia
Pathogenesis
 Mutation in GNAS1 gene.
 Endocrine disturbance.
Classification
 Monostotic fibrous dysplasia.
 Polyostotic fibrous dysplasia.
Monostotic fibrous dysplasia
 Much more common (80%).
 Iimb bone, ribs, skull bones, and jaws.
 Common in maxilla, in mandible affect body
of the mandible.
 Childhood and adolescent.
 Presented as painless fusiform gradually
increasing swelling.
 It may involve in addition to maxilla
adjacent bones (zygoma, sphenoid bone
maxillary sinus, floor of the orbit) called
craniofacial fibrous dysplasia.
 Equal gender distribution.
Polyostotic fibrous dysplasia
 It is uncommon.
 It is associated with other conditions or
syndromes:
1. Mc Cune – Albright syndrome.
2. Jaffe – Liechtenstein syndrome.
Mc Cune – Albright syndrome
 Multiple fibrous dysplasia
 Skin pigmentation ( café au lait spots).
 Precocious puberty in females.
 Endocrine disturbances ( acromegaly,
hyperthyroidism, hyperparathyroidism,
hyperprolactinemia.
Jaffe – Liechtenstein syndrome
 Multiple lesions of fibrous dysplasia.
 Skin pigmentation.
 Polyostotic is common in females with
segmental localization.
 Severe cases cause deformity and
pathological fracture.
Histopathology
 Early stage: fibroblastic richly cellular stroma,
storiform or whorled pattern,and little woven bone.
 Intermediate stage: delicate irregular bone
trabeculae ( Chinese letters), fusion of newly
formed bone with the surrounding normal bone,
occasionally multinucleated giant cells and
cementum-like material.
 Late stage: remodeling of bone, lamellar
bone are placed parallel to each other,
moderate cellular fibrous stroma.
X-ray
 Early stage: ill-defined radiolucency.
 Intermediate stage: Mixed ( mottled).
 Late stage: radiopaque with many delicate
trabeculae ( ground glass, or orange peel
stippling).
Periapical cemental
dysplasia
Clinical features
 Asymptomatic, self limiting,
 Site: incisal region of mandible.
 Involved teeth are vital.
 Female predilection M:F =1:10.
 Black predilection ( 70 %).
 Age: middle age, around 40 years.
X-ray
 Early stage: ill-defined periapical
radiolucency.
 Intermediate stage: mixed.
 Late stage: radiopaque with radiolucent
rim.
 No fusion to the tooth.
 Focal cemento-
osseous dysplasia
Clinical features
 Female predilection ( 90 %).
 Age: third to sixth decades, mean age 38
years.
 White predilection.
 Site: Posterior mandible.
 Asymptomatic, less than 1.5 cm.
X-ray
 Early: radiolucency.
 Intermediate: mixed.
 Late: radiopaque with radiolucent rim.
 Florid cemento-
osseous dysplasia
Clinical features
 Multifocal involvement.
 Black (90%).
 Female predilection.
 Age: middle age to elderly.
 Site: bilateral symmetrical or four posterior
quadrants.
 Asymptomatic, or dull pain with alveolar sinus
tract, exposing the yellowish avascular bone to
oral cavity.
X-ray
 Radiolucent.
 Mixed.
 Radiopaque with radiolucent rim.
Treatment
 No treatment but regular follow-up, strict
oral hygiene.
 Avoid extraction.
 Symptomatic patients: treat osteomyelitis.
Familial gigantiform
cementoma
Clinical features
 It is a disorder of gnathic bone that finally
leads to formation of massive sclerotic
masses of disorganized mineralized
material.
 A hereditary disorders, autosomal
dominant.
 Affect white and black.
 No gender predilection.
 Appear during first decade.
 Growth stop during fifth decade.
 Rapid expansive growth.
 Multifocal involvement.
 Impacted and malaligned teeth.
 High alkaline phosphatase.
 Anemia, polypoid adenoma of uterus.
Giant cell lesions
Definition
 Giant cell lesions are a variety of disorders,
which histologically characterized by
cellular fibrous tissue containing
multinucleated giant cells, foci of
hemorrhage, osteoid, and woven bone.
Classification
1. Reactive lesions: Giant cell granuloma.
2. Genetic: Cherubism.
3. Metabolic: Brown node tumor of
hyperparathyroidism.
4. Neoplastic: Giant cell tumor.
5. Cystic: Aneurysmal bone cyst.
Giant cell
granuloma
Pathogenesis
 Unknown etiology.
 Haemodynamic disturbance in bone
marrow following trauma.
 Counterpart of the giant cell tumor.
 Developmental anomaly.
Origin of multinucleated cells
 Osteoclast.
 Stromal mononuclear cells.
 Myofibroblast-like cells.
Clinical features
 Children and young adult, below 30 years.
 Female predilection (M:F = 1:2).
 Mandible, anterior to molar area.
 Non-aggressive form: painless swelling.
 Aggressive form : pain, paraesthesia, rapid
growth, occasionally perforate cortical
bone.
X-ray
 Well-defined multilocular radiolucency.
 Well-defined unilocular radiolucency ( less
common).
Histopathology
 Vascular stroma containing mononuclear
spindle cells with oval nuclei.
 Scattered or aggregated multinucleated
giant cells.
 Extravasated RBCs.
 Hemosiderin-laden macrophages.
 Osteoid or woven bone trabeculae.
Treatment
 aggressive curettage
It may recur especially aggressive form (11-
50 %).
 For aggressive:.
 Corticosteriods.
 Calcitonin.
 Interferon alpha-2a.
 Brown node tumor
of
hyperparathyroidism
Von Recklinghausen disease of
bone
Physiology
Hypocalcaemia:

P TH

G IT K id n e y s B one
C a a b s o r p t io n C a r e a b s o r t io n C a r e s o r p t io n
Classification
 Primary: hyperplasia (10-15%)
Adenoma (80-90%)
Adenocarcinoma (< 2%)
 Secondary: compensatory to renal failure.
 Hereditary: autosomal condition.
Clinical features
high ca & alkalinephophatase- low phosphate
 Primary affect older than 60 years, female.
 Symptoms: fatigue,anorexia.polyuria,
depression, bone pain, headache.
 Metastatic calcification, renal calculi,
nephrocalcinosis.
 Bone changes called osteitis fibrosa cystica.
 In GIT Produce peptic ulcer.
Oral manifestation
 Cyst-like changes (brown tumor).
 Osteoporotic appearance of bone.
 Loosening of teeth, generalized loss of
lamina dura.
 Pulp calcifications and obliteration.
Histopathology
 Similar to giant cell granuloma.
 Excessive hemosiderin pigment.
Treatment
 Surgical excision of PT gland.
 Monitor PTH, serum alkaline phosphatase,
serum Ca, and Phosphate.
Cherubism
Etiology
 An autosomal dominant with mutation in
SH3BP2 gene located in chromosome
4p16.3.
Clinical features
 Cherub appearance.
 Symmetrical involvement, bilateral
mandible or all quadrants.
 Male, M:F = 2:1.
 Age: 2-4 years, regresses at 7-12 years.
 Premature loss of deciduous teeth, lack of
eruption and development of some
permanent teeth.
X-ray
 Well-defined multilocular radiolucency.
 Soap bubble appearance (occlusal view).
 Perforation of cortical bone ( less common).
Histopathology
 Highly vascular loose fibrous tissue.
 Focal collection of multinucleated giant
cells around vascular channels.
 Cuffing of blood vessels by hyaline
eosinophilic collagen.
 Extravasated RBCs, hemosiderin.
 Metaplastic bone in old lesions.