Presented by:Dr . Gaurav S. Salunkhe

Oral & Maxillofacial Pathology 23th September 2014

Introduction Bone is a living tissue, which makes up the body

skeleton and is one of the hardest structures of the animal body.

Bone possesses a certain degree of toughness and elasticity.

It provides shape and support for the body.It also provides site of attachment for tendons and

muscles, which are essential for locomotion.It also protects vital organs in the body.It also provides site for development and storage for

blood cells.

CLASSIFICATION OF BONE

ALVEOLAR BONE ALVEOLAR BONE PROPER

A) LAMELLATED BONE: It is the outer most part of

the alveolar bone proper.Some lamellae of the

lamellated bone are arranged roughly parallel to the surface of the adjacent marrow spaces, whereas others forms haversian system.

ALVEOLAR BONE BUNDLE BO NE

Bundle bone is the part of alveolar bone, into

which the fiber bundles of the PDL insert.

It is characterized by scarcity of fibrils in

intercellular substance.

Fibrils arranged at right angles are

Sharpey’s Fibers

Bundle bone is formed in areas of recent

bone deposition.

Lines of rest seen in bundle bone.

Radiographically it is called as Lamina Dura

because of increased radiopacity which is due

to the presence of thick bone without

trabeculations.

DENTIN

CEMENTUM

PDL SPACE

BUNDLE BONE

The lamina dura (arrows) appears as a thin opaque layer of bone around teeth, A, and around a recent extraction socket, B.

RADIOGRAPHICALLY

SUPPORTING ALVEOLAR BONE It consists of two parts –

Cortical plates (Outer and inner) Spongy bone

Cortical plates: these are made up of compact bone & form the outer and inner plates of alveolar bone.

Cortical bone varies in thickness in different areas – it is thicker in the mandible than in the maxilla and thicker in the premolar-molar region than in the anterior.

Spongy bone: it fills the area between the cortical plates and the alveolar bone proper.

It contains trabaculae of bone and marrow spaces.

Types of spongy bone (spongiosa) :- Type I: the trabaculae are regular

and horizontal like a ladder. This is seen most commonly in the mandible.

Type II: irregularly arranged delicate and numerous trabaculae. This is seen most commonly in the maxilla.

The spongy bone is very thin or absent in the anterior regions of

both the jaws.

A. DEVELOPMENTAL DISEASES:- Cheurbism- Osteopetrosis- Osteogenesis imperfecta- Cleiodocrainal dysplasia

B. ENDOCRINAL DISEASES:- Hyperparathyroidism

C. IDIOPATHIC DISEASES:- Idiopathic osteosclerosis- Massive osteolysis- Langerhan’s cell disease (Histiocytosis-X)- Paget’s disease

D. REACTIVE DISEASES:- Giant cell lesion of bone - Aneurysmal bone cyst- Simple / Traumatic bone cyst

E. FIBRO-OSSEOUS LESIONS:(i) Non-neoplastic lesions -

- Fibrous dysplasia - Cemento-osseous dysplasia

(ii) Neoplasms –- Ossifying fibroma

F. INFLAMMATORY DISEASES: -(i) Specific:

- Tuberculosis- Actinomycosis

(ii) Non specific- Osteomyelitis- Dry socket- Periapical cyst / abscess / granuloma- Osteoradionecrosis

G. NEOPLASTIC DISEASES: -(i) Benign:

- Osteoma- Osteoid osteoma & osteoblastoma - Chondroma- Chondromyxoid fibroma

(ii) Malignant: - Osteosarcoma- Ewing’s sarcoma- Chondrosarcoma

1. CHERUBISM 2. OSTEOPETROSIS3. OSTEOGENESIS IMPERFECTA4. CLEIODOCRANIAL DYSPLASIA.

CHERUBISMRare developmental jaw condition, first described by

Jones in 1933.Jones called it as familial multilocular disease of the jaw.Transmitted as an autosomal dominant trait.Causes characteristic posterior mandibular swelling due

to which the child appears as a plump cheeked angels called “CherubCherub” in Renaissance paintings.

The jaw lesion remit spontaneously when the child reaches puberty, but reason for this remission is still unknown.

The appearance of people with the disorder is caused by a loss of bone, which the body replaces with excessive amounts of fibrous tissue.

Pathogenesis The gene for cherubism was mapped to chromosome

4p16. Mutation were identified in the SH3BP2 gene within this

locus. The protein encoded by this gene is believed to function

in signal transduction pathway and to increase the activity of osteoclasts and osteoblasts during normal tooth eruption.

It has been suggested that mutation in the SH3BP2 gene may led to pathologic activation of osteoclasts and disruption of jaw morphogenesis.

CLINICAL FEATURES: -Age incidence: Affected children, are normal at the birth and

are without any clinically or radiographically evident disease until 14 months to 3 yrs of age.

Sex incidence: males = femalesSite predilection: Mostly bilateral involvementMandible affected more commonly than maxilla.In maxilla, tuberosity region is affected frequently, resulting

in respiratory obstruction and impairment of vision & hearing.

The lesion are painless and symmetrical.Cervical lymphadenopathy contributes to the patients full

faced appearance, it is said to be caused due to lymphoid hyperplasia with fibrosis.

Signs & symptoms:Begins as painless bilateral

expansion of affected bone. Skin of upper face is stretched.A rim of sclera may be seen beneath

the iris, giving a classical “ e ye s upturne d to he ave n” appearance.

This feature is due to involvement of the infraorbital rim and orbital floor that tilts the eyeball upwards, as well as to stretching of the upper facial skin that pulls the lower lid downwards.

Progressive, extensive bone involvement causes widening and distortion of alveoli.

As a result, developing teeth displaced, fail to erupt.

Numerous dental abnormalities have been reported, such as agenesis of the 2nd & 3rd mandibular molars, displacement of the teeth, premature exfoliation of the primary teeth, delayed eruption of the permanent teeth, and transposition and rotation of the teeth.

The permanent dentition is often defective. In sever cases root resorption occurs. It is been connected to NOONAN’S

SYNDROME.

RADIOGRAPHIC FEATURES: -

Appear as expansile, multilocular radiolucency.

The presence of numerous unerupted teeth and the destruction of the alveolar bone may displace the teeth, producing a radiographic appearance referred as FLOATING TOOTH SYNDROME.

With adulthood, the cystic areas in the jaws become re-ossified, which results in irregular patchy sclerosis.

There is classic but non specific ground glass appearance because of the small, tightly compressed trabecular pattern.

HISTOLOGICAL FEATURES:

Features are similar to giant cell tumors. In cherubism, normal bone is partly replaced

by pathologic tissue. Under the microscope, it contains numerous

randomly distributed multinucleated giant cells and vascular spaces within a fibrous connective tissue stroma.

An increase in osteoid and newly formed bone matrix is found in the peripheral region of the fibrotic stroma in patients above the age of 20 years.

An eosinophilic perivascular cuffing is seen.

The multinucleated giant cells are positive for tartrate resistant acid phosphatase an

expressed the vitronectin receptor.

Multinucleated giant cells are scattered in vascular fibrous stroma. Osteoid and newly formed bone matrix are visible

Multinucleated giant cells are scattered around blood vessels

Multinucleated giant cells in cherubism are positive for tartrate resistant acid phosphatase

DIFFERENTIAL DIAGNOSIS Giant cell granulomas of the jaw

Osteoclastomas

Aneurysmal bone cyst

Fibrous dysplasia

Hyperparathyroidism

IT IS BASED ON THE KNOWN NATURAL COURSE OF THE DISEASE AND THE CLINICAL BEHAVIOUR OF THE INDIVIDUAL CASE.IF NESSARY SURGERY IS UNDERTAKEN ONLY AFTER PUBERTY.

Key features:-Inherited autosomal dominant trait.Jaw swelling appears in infancy.Angle regions of mandible affected symmetrically

giving typical chubby face.Symmetrical involvement of maxillae also seen in

sever cases.Radiographically- multilocular cystic lesion.Histologically- consist of giant cells in vascular

connective tissue.Lesion regress with skeletal maturation and nornal

contour is restored.

OSTEOGENESIS IMPERFECTAMost common type of developmental, inherited bone

disorder, showing both autosomal dominant and recessive pattern.

Comprises heterogeneous group of heritable CT disorder in which bone fragility is the primary feature.

It is a condition resulting from abnormality in the type I collagen.

It is characterized by impairment of collagen maturation.

Co llag e n fo rms a majo r po rtio n o f bo ne , de ntine , scle rae , lig aments, and skin, OI demo nstrate s a varie ty o f chang e s that invo lve s the se site s.

Abnormal collagenous maturation results in bone with thin cortex, fine trabeculation, and diffused osteoporosis.

Upon fracture, healing will occurs but may be associated with exuberant callus formation.

Several different forms of OI have been reported and they represent the most common type of inherited bone disease.

Structurally, this protein is made of a left handed helix formed by intertwining of pro-α1 and pro-α2 chains. Mutation in the loci coding for these chains causes osteogenesis imperfecta.

CLINICAL FEATURESThe chief clinical feature is the extreme fragility and

porosity of the bones, with an attended proneness to fracture.

Fractures heals readyly but with the same quality of bone.

AGE: Varies with the type.The other characteristic feature of OI is the

occurrence of blue sclera. The sclera is abnormally thin, and for this reason the

pigmented choroid shows through and produces the bluish colour.

Other condition in which blue sclera can be seen OsteopetrosisFetal ricketsTurner syndromePagets diseaseMarfan syndrome &Ehlers-Danlos syndrome.Some times in normal infants.

Additional signs & symptomsDeafness- due to osteosclerosis.Abnormalities of teeth.Laxity of ligaments.A peculiar shape of the skull.Abnormal electrical reaction of the muscles.Tendency towards capillary bleeding.

CLINICAL FEATURES: -Four types present, each having several subtypes.TYPE I Osteogenesis imperfecta:Commonest type – autosomal dominant.Mild to moderate bone fragility – onset is highly

variable – may be present at birth also.Hearing loss develops before 30 years.Some patients may show dentinogenesis imperfecta

sub type B.Blue sclera is seen.KyphoscoliosisEasy bruisingShort stature

Deformity of long bones

Dentinogenesis imperfecta

TYPE II Osteogenesis imperfecta:

Extreme bone fragility with frequent fractures.

Many patients stillborn – 90% die before 4 weeks of age.

Blue sclera present.Dentinogenesis

imperfecta present.Hearing loss present.Micrognathia Short trunk.

TYPE III Osteogenesis imperfecta:Moderate to severe bone fragility.Blue sclera present in infants but fades by adulthood.Mortality rate higher in older children.Death from cardiopulmonary complications caused

by kyphoscoliosis (backward & lateral curvature of spine).

Dentinogenesis imperfecta.Short limbs.Triangluar face, with frontal bossing

TYPE IV Osteogenesis imperfecta: -Mild to moderate bone fragility.Sclera pale in early life, but fades in later life.Fractures present in 50 % case – frequency of

fractures decreases after puberty.Some patients may have dentinogenesis imperfecta,

some may not.

•Both the dentitions are affected, and demonstrate blue to brown translucency. •Radiographically reveals premature obliteration of pulp. •Although the altered teeth closely resemble dentinogenesis imperfecta , the two disease are the result of different mutations and should be considered as separate processes. •Head size is large.•Frontal and temporal bossing is seen.•Class III malocclusion is seen due to maxillary hypoplasia rather than mandibular hyperplasia.•Anterior and posterior cross bite and open bites can be seen.•Large numbers of impacted and ectopic teeth can be reported.•Unerupted 1st and 2nd molar is very common feature.

Radiographic featuresHallmarks of OI includes:OsteopeniaBowing AngulationDeformity of long bonesMultiple fratures Wormian bone in the skull.

HISTOLOGICAL FEATURES: -Anomaly due to abnormal collagen

synthesis by abnormal osteoblasts.Mass of cortical and cancellous bone is

abnormal and greatly reduced.Cortical bone is extremely thin while

the cancellous bone is delicate and shows micro fractures.

Osteoblasts are present but bone matrix synthesis is reduced, for this reason the thickness of long bone is deficient.

Bone architecture remains immature throughout life.

Treatment No known treatment.Only treatment of the infection when they occur.

Key features:-Thin fragile bones due to inadequate type I collagen.Inherited as an autosomal dominant trait.Multiple features typically lead to gross deformities.Jaw fractures are uncommon.

CLEIDOCRANIAL DYSPLASIABone defects primarily involve skull and clavicle – defects

seen in other bone also.Inherited as autosomal dominant trait, but almost 40%

cases show spontaneous mutation. It is caused due to defect in CBFA 1 gene also called as RUNX

2 gene of chromosome 6p21. (Runt-related transcription factor 2 (RUNX2 ) a ls o kno wn a s c o re -bind ing fa c to r s ubunit a lpha -1 (CBF-a lpha -1 ) is a p ro te in tha t in hum ans is e nc o d e d by the RUNX2 g e ne . RUNX2 is a ke y tra ns c rip tio n fa c to r a s s o c ia te d with o s te o bla s t d iffe re ntia tio n)

This gene normally guides osteoblastic differentiation and appropriate bone formation.

CLINICAL FEATURES: -Age incidence: Children

Sex incidence: Nil

Site predilection: Skull, clavicles and jaw bones.

Signs & symptoms: Short height with large heads

showing pronounced frontal and parietal bossing.

Nose is broad with depressed nasal bridge.

Shoulders narrow and droop excessively.

Sagittal suture is sunken giving the skull a flat appearance.

Paranasal sinuses are under developed

Patients show unusual mobility of shoulders due to absence / hypoplasia of clavicles.

Oral manifestations: Narrow, high arched palate.Increased prevalence of cleft

palate.Maxilla is underdeveloped and

smaller than mandible. Prolonged retention of deciduous

teeth and delay / complete failure of eruption of permanent teeth.

OPG and dental radiographs show multiple impacted and supernumerary teeth.

The roots of the teeth are short and thinner than usual, and might be deformed.

Treatment No treatment exists for the skull, clavicular, and other

bone anomalies associated with CCD. Most patient function well with out any significant

problem.

Key features:-Rare genetic disorder causing defective formation of

clavicle, delayed closure of fontanells and other defects.

Many or most permanent teeth typically remains embedded in the jaw.

Many additional unerupted teeth also present.Sometimes many dentigerous cytes.

OSTEOPETROSIS(Albers - Schönberg Disease, Marble bone disease)

Rare hereditary bone disorder characterized by increase in bone density due to defect in bone remodeling caused by failure of normal osteoclast function.

Clinical types – infantile, intermidiate and adult osteopetrosis.

PATHOGENESIS: -Osteoclasts fail to function normally.As a result, bone remodeling is affected.Defective bone resorption combined with continued bone

deposition results in thickening of cortical bone and sclerosis of cancellous bone.

The exact mechanism is unknown. However, deficiency of carbonic anhydrase in osteoclasts is noted. The absence of this enzyme causes defective hydrogen ion pumping by osteoclasts, and this, in turn, causes defective bone resorption by osteoclasts, as an acidic environment is needed for dissociation of calcium hydroxyapatite from bone matrix. Hence, bone resorption fails while its

formation persists. Excessive bone is formed.

I. INFANTILE OSTEOPETROSISCLINCAL FEATURES: - Autosomal recessive trait. Diffusely sclerotic skeleton, marrow failure and

signs of cranial nerve compression present. Initial signs – normocytic normochromic anemia

and hepatosplenomegaly, due to compensatory extramedullary heamatopoiesis.

Increased susceptibility to infections due to granulocytopenia.

Intermediate OsteopetrosisAffected patients have a short stature and are often

asymptomatic at birth, but frequently exhibit fractures by the end of their first decade of life.

Marrow failure and hepatosplenomegaly are rare. Some present with cranial nerve deficits,

macrocephaly, mild or moderately severe anemia and ankylosed teeth that may predispose them to osteomyelitis of the jaws.

III. ADULT OSTEOPETROSISCLINICAL FEATURES: -Discovered late in life – milder

symptoms.Autosomal dominant trait.About 40% cases are asymptomatic.Axial skeleton shows sclerosis, while

long bones show little or no defects.Bone pain is seen10% shows osteomyelitis of mandible

Oral manifestations: Facial deformity leading to hypertelorism, snub nose,

frontal bossing etc.Delayed tooth eruption and osteomyelitis of jaws.Sclerosis of skull bones leads to narrowing of foramina

which causes compression of various cranial nerves – blindness, deafness, facial paralysis etc.

The medullary spaces of the jaws are reduced.Fracture of jaws during extraction procedure can occur

without undue force, due to fragility of the bone.

Common orofacial findings in infantile osteopetrosis

Common orofacial findings in adult osteopetrosis

Facial deformity (broad face, hypertelorism, snub nose and frontal bossing)

Optic atrophy, nystagmus and blindness, deafness and facial paralysis (due to failure of resorption and remodeling of skull bones with resultant narrowing of skull foramina and pressure on various cranial nerves)

Nasal stuffiness (due to malformation of mastoid and paranasal sinuses)

Delayed tooth eruption Tooth roots often difficult to visualize

due to density of surrounding bone Osteomyelitis as a complication of

tooth extraction

Congenitally absent, delayed or unerupted malformed teeth

Increased susceptibility to caries due to reduced calcium–phosphorus ratio in both enamel and dentin that may decrease hydroxyapatite crystal formation.

Most serious complication is increased susceptibility to develop osteomyelitis. As the vascular supply to the jaws is compromised, avascular necrosis and infection after dental extractions may lead to osteomyelitis

HISTOLOGICAL FEATURES:A failure of osteoclasts to resorb skeletal tissue, with remnants of mineralized

primary spongiosa that persist as islands of calcified cartilage within mature bone, is characteristic of osteopetrosis. Several patterns of abnormal endosteal bone formation may be seen

tortuous lamellar trabeculae replacing the cancellous portion of bone globular amorphous bone deposition in marrow spaces osteophytic bone formation.The number of osteoclasts may be increased,

normal or decreased, but there is no evidence of functional osteoclast as Howship’s lacunae are not visible.

RADIOGRAPHIC FEATURES: -• Wide spread increase in bone density.• Distinction between cortical and cancellous

bone is lost.• Dental X rays – difficult to distinguish

roots.

Key features:-Rare genetic defect of osteoclastic activity.Bone lack medullary caities but are fragile.Extramedullary haemopoiesis in liver and spleen but

anemia common.Osteomyelitis a recognised complication.

- Idiopathic osteosclerosis- Massive osteolysis- Langerhan’s cell disease - Paget’s disease

PAGET’S DISEASE OF BONE(Osteitis deformans)

Characterized by abnormal resorption and deposition of bone, resulting in distortion and weakening of bone.

ETIOLOGY: -Unknown, but predisposing factors could be –

inflammatory, genetic, endocrine factors or a slow virus infection, autoimmune, connective tissue or vascular disorder.

CLINICAL FEATURES: -Age incidence: Middle aged

individualsSex incidence: Male to female

ratio is 2:1Site predilection: Bones of skull, lumbar

vertebrae ,pelvis, femur and tibia.

Common in England, France and Germany. Rare in Middle and Far East Asia and

Africa.

Signs & symptoms:Severe bone pain and

limitation of movement, especially of joints.

Affected bones – thickened, enlarged and weak.

Weight bearing joints/bones become bowed.

Skull involvement – increase in head circumference.

Signs & symptoms: Maxilla affected more than

mandible. Maxilla – enlargement of middle

third of face (leontiasis ossea)Nasal obstruction, obliterated

sinuses and deviated septum also occur.

In dentulous patients spacing of teeth is seen, while edentulous patients complains of tightness of the dentures.

Mandible involved rarely – may cause prognathism.

RADIOGRAPHIC FEATURES:

Early stage (lytic) -radiolucency and alteration of trabecular pattern.

Late stage (osteoblastic) – patchy areas of sclerotic bone is formed, called “cotton wool” appearance.

Dental radiographs also show the classical cotton wool appearance.

Extensive hypercementosis can be noted.

DIFFERENTIAL DIAGNOSIS: -Acromegaly.Florid cemento- osseous dysplasia.Sclerosing osteomyelitis (diffuse

type).Osteosarcoma.Adult osteopetrosis

LABORATORYFINDINGS: -Abnormally elevated serum alkaline

phosphatase level upto 250 Bodansky units (normal – 30 to 40).

But normal calcium and phosphorous levels).

Increased urinary calcium and hydroxyproline levels.

HISTOLOGICAL FEATURES: -Alternating bone resorption and

deposition seen.Thus osteoclastic resorption seen

surrounding the trabeculae.Simultaneously, osteoblastic

activity also seen with formation of osteoid rims around trabeculae.

Surrounding stroma is highly fibro-vascular.

This hypervascular bone combined with cutaneous vasodilation causes an increase in regional blood flow resulting in rise in skin temperature.

A characteristic feature is presence of basophilic reversal lines in the bones.

This indicates junction between the alternating resorptive and formative phases of bone.

It gives a “jigsaw puzzle” or “mosaic” appearance of the bone.

The new bone is disordered, poorly mineralized, and lacks structural integrity.

Treatment It is a chronic and slow growing diease, it is seldom

the cause of death.In patient with no symptom and less involvement

treatment is not required. Bone pain is mostly controlled by anti-inflammatory

drugs.

Key features are:-Person past middle age affected.Enlargement of skull, thickening but weakness of long

bone and bone pain.Maxilla occasionally, but mandible rarely affected.Hypercementosis.Radiographically- cotton wool appearance. Histologically- mosaic/ jigsaw puzzle pattern. Serum alkaline phosphatase upto 250 Bodansky units

(normal – 30 to 40).

LANGERHANS CELL DISEASEThe term HISTOCYTOSIS was introduce as a collective

designation for a spectrum of clinicopathologic disorders characterized by proliferation of histiocytes-like cells.

It is an idiopathic disease characterized by proliferation of histiocyte like cells (Langerhan's cells), that are accompanied by varying numbers of eosinophils, lymphocytes, plasma cells & multinucleated giant cell.

Believed to be a non neoplastic process.Langerhan’s cells are dendritic, mononuclear cells

normally found in epidermis, mucosa , lymph nodes & bone marrow. They are known as antigen presenting cells.

TYPES: -1. Eosinophilic granuloma of bone: solitary / multiple

bone involvement without systemic organ involvement. It causes localized bone destruction with swelling and often pain.

2. Hand-Schüller-Christian disease: Chronic disseminated disease involving bones, viscera and skin. It shows triad of lytic skull lesion, exophthalmous, and diabetes insipidus.

3. Letter-Siwe disease: acute disseminated disease with bone, visceral and skin involvement, occurring mainly in infants.

CLINICAL FEATURES: -Age incidence: Predominantly children

below 10 years of age.Sex incidence: Definite male

predilection.Site predilection: Bones - Skull, ribs, vertebrae, femur and

mandible most frequently.Oral – gingiva and lips most commonly.

Signs & symptoms:Involved bones manifest dull pain

and tenderness.

Visceral involvement results in decreased or failure of affected organ.

Jaw bone involvement results in loosening of teeth which resembles aggressive periodontitis, and the appearance of teeth “floating in air” are typical.

Oral mucosa may show ulcerative / proliferative masses on gingiva.

RADIOGRAPHIC FEATURES: -

Multiple, well / poorly defined punched out radiolucent areas seen.

Extensive alveolar bone loss occurs, causing the teeth to appear as if they are “floating in air”.

HISTOLOGICAL FEATURES: -Lesion shows diffuse infiltration of

pale staining, mononuclear cells containing ill defined cell borders and vesicular nuclei.

Darker staining eosinophils, plasma cells and lymphocytes and multinucleated giant cells also seen.

Electron microscopy shows rod / racquet shaped characteristic birbeck granules within cytoplasm of Langerhan's cells.

Birbeck granules, also known as Birbeck bodies, are rod shaped or "tennis-racket" cytoplasmic organelles with a central linear density and a striated appearance. They are a characteristic microscopic finding in Langerhans cell histiocytosis

• Immunohistochemical studies are needed to confirm the diagnosis as these cells cannot be distinguished from normal histiocytes.• Langerhan’s cells stain positively for S-100 protein.

DIFFERENTIAL DIAGNOSIS: -Other lesions with multifocal,

multilocular radiolucency are- Cemento-osseous dysplasia- Hyperparathyroidism- Cherubism- Multiple myeloma

Central giant cell granuloma Aneurysmal bone cystTraumatic bone cyst

CENTRAL GIANT CELL GRANULOMA

Considered to be a non neoplastic lesion.Can be grouped under two types –1.Non aggressive type = slow growth, no

symptoms, no cortical perforation, no root resorption.

2.Aggressive type = pain, rapid growth seen, cortical perforation, root resorption. Has a tendency to recur.

CLINICAL FEATURES: -Age incidence: 60% cases occur below

20 years of age.Sex incidence: Predominantly females.Site predilection: 70% cases occur in mandible. Mandibular

lesions often crosses the midline. Most lesions occur in anterior portions of

jaws.

Signs & symptoms: Mostly asymptomatic and

diagnosed only during routine radiographic examination.

Manifest usually as painless expansion of affected bone.

Some aggressive cases may manifest with pain, paresthesia and perforation of cortical plate.

Occasionaly shows ulceration of the mucosal surface.

RADIOGRAPHIC FEATURES: -

Present as well defined, unilocular / multilocular radiolucent defects, but the margins are usually noncorticated.

Lesions may vary in size from small unilocular radiolucencies to large multilocular radiolucencies.

DIFFERENTIAL DIAGNOSIS: -Small unilocular lesions can be

confused radiographically with periapical cyst / granuloma.

Large multilocular lesions should be differentiated from other multilocular radiolucencies like– ameloblastoma, aneurysmal bone cyst, Pindborg tumor etc

HISTOLOGICAL FEATURES: -Few to large number of small / large multinucleated giant

cells seen in a background of ovoid / spindle shaped mesenchymal cells.

Giant cells believed to represent osteoclasts, and vary in size from few to many nuclei.(20 nuclei or more )

Foci of osteoid and newly formed bone may also be seen.Areas of hemorrhage and hemosiderin deposition are

common.

ANEURYSMAL BONE CYSTPrimarily seen in long bones or

vertebrae, and rarely in jaws.Cause and pathogenesis are not yet

clear.Controversy – whether it arises de

novo or occurs as a result of some “vascular accident” in a pre-existing lesion.

Aneurysmal bone cyst is an intraosseous accumulation of variable sized, blood filled spaces surrounded by cellular fibrous connective tissue that is often admixed with trabeculae of reactive woven bone.

Pathogenesis is not clear, but some investigators believe that it arises from a traumatic event, vascular malformation, or neoplasm that disrupts the normal osseous hemodynamics and leads to an enlarging, hemorrhagic extravassation.

An aneurysmal bone cyst may form when an area of hemorrhage maintain connection with the disrupted feeding vessels, subsequently, giant cell granuloma like area can develop after loss of connection with the original vascular source.

CLINICAL FEATURES: -Age incidence: First 3 decades.Sex incidence: Mainly females.Site predilection: molar regions of

mandible & maxilla.

Signs & symptoms: Hard, rapidly growing swelling

which can cause malocclusion. Mobility of teethMigration of teethRoot resorptionPain is often present.Paresthesia is presentIf lesion perforates cortical

plates, can cause “egg shell crackling”.

RADIOLOGICAL FEATURES: -

Classically seen as a unilocular, ovoid / fusiform radiolucency which balloons the cortical plates.

Teeth displacement and root resorption also observed.

HISTOLOGICAL FEATURES: Cyst cavity shows many

capillaries and blood filled spaces, of various sizes separated by delicate loose CT.

Blood filled spaces are not lined by endothelium.

Many small multinucleated giant cells and trabeculae of osteoid / woven bone cab be seen.

Key features:-Rare in jawsJaw lesions are mostly seen in ramus and angle regionAffected patient usually between 10 and 20 years.Unknown etiology.Soap- bubble radiolucencies –mistaken –

ameloblastoma or OKC.Histologically consist of a mass of blood-filled spaces

with scattered giant cells.Treated by curettage, but sometimes recur.

SIMPLE BONE CYST(Solitary / Traumatic / Hemorrhagic bone cyst}

The simple bone cyst is a benign, empty, or fluid containing cavity within bone that is devoid of an epithelial lining.

Commonly seen in mandible, rare in maxilla.

Identical to solitary bone cyst of humerus in children and adolescents.

PATHOGENESIS: -None of the theories are certain about exact cause.

First theory – cyst may follow trauma to bone that is insufficient to cause fracture which results in intra medullary hemorrhage which fails to organize and repair. This clot subsequently liquefies - resulting in CYST.

Recent theory – osteogenic cells fail to differentiate locally and thus instead of bone, the undifferentiated cells form synovial tissue.

CLINICAL FEATURES: -Age incidence: Young individuals

10-20 yrsSex incidence: Equal

Site predilection: Body and symphysis of

mandible.

Signs & symptoms:Asymptomatic.Rarely, swelling, pain & paresthesia may be seen.

Common in premolar and molar region of mandible

Half of all patients give a history of trauma to the area.

RADIOGRAPHICAL FEATURES: -

Appears as a radiolucency with irregular but well defined edges and slight cortication.

When many teeth involved – radiolucency scallops between roots.

Teeth involved in lesion – usually vital, no root resorption seen.

HISTOLOGICAL FEATURES:-

Wall shows loose fibrovascular CT.

Hemorrhage and hemosiderin pigment usually present.

Multinucleated giant cells scattered within the CT.

Adjacent bone shows osteoclastic resorption on inner surface.

Fibro-osseous lesions are a diverse group of lesions characterized by replacement of normal bone by a fibrous tissue containing a newly formed, mineralized product. It is not a specific diagnosis and described only as a process.

These lesions include developmental, reactive and even neoplastic lesions.

Histologic features can be very similar in lesions of different etiology and biological behavior.

Clinical, pathological and radiographic correlation is required to establish a specific diagnosis.

CLASSIFICATION: -(i) Non-neoplastic lesions - a. Fibrous dysplasia b. Cemento-osseous dysplasia

→ Periapical cement-osseous dysplasia→ Focal cemento-osseous dysplasia→ Florid cemento-osseous dysplasia

(ii) Neoplasms –- Ossifying fibroma

FIBROUS DYSPLASIACondition in which normal medullary bone is

gradually replaced by an abnormal fibrous connective tissue proliferation.

This mesenchymal tissue contains varying amounts of osteoid that presumably arises through metaplasia. The resultant fibro-osseous tissue is poorly formed and structurally inadequate.

▪ The condition tends to stabilize and stops growing as skeletal maturity is reached.

ETIOLOGY: -1. Hamartomatous 2. Abnormal reaction of bone to a localized traumatic

episode.3. Endocrine disturbance: the recent description of

presence of estrogen receptors in osteogenic cells of a patient with FD suggests that this process may reflect a defect in the regulation of these receptors and consequently of cellular activity.

TYPES OF FIBROUS DYSPLASIA: -1. Monostotic: Fibrous dysplasia (FD) limited to one

single bone. Accounts for 80% – 85% of all cases.2.Polyostotic: FD affects several bones.

(a) Jaffe type – severe FD with almost entire skeleton involved.(b) McCune-Albright syndrome – along with polyostotic FD, multiple cutaneous pigmentations and hyperfunction of one or more endocrine glands.

MONOSTOTIC FIBROUS DYSPLASIACLINICAL FEATURES: -Age incidence: 1st or 2nd decade of life.Sex incidence: equalSite predilection: Maxilla involved more than mandible.Maxillary lesions often involve adjacent bones like

zygoma, sphenoid etc (called Craniofacial FD).

Signs & symptoms:Affected bone / bones

show a painless, gradually enlarging swelling.

Teeth within affected jaws remain firm but may be displaced by the mass.

RADIOGRAPHIC FEATURES: -Early stages – mixed

radiopaque-radiolucent appearance.

Later stages show a characteristic “ground glass / orange peel” appearance of affected bones.

Lesions not well defined and blend into adjacent bone – limits of lesion cannot be defined.

DIFFERENTIAL DIAGNOSIS: -Clinically, FD must be differentiated from1. Ossifying fibroma2. Paget’s disease.Though, its radiographic appearance is typical, it

must be distinguished from1. Hyperparathyroidism.2. Paget’s disease (early stage).

POLYOSTOTIC FIBROUS DYSPLASIACLINICAL FEATURES: -Age incidence: 1st decade of life or

earlier.Sex incidence: equal.Site predilection: Can affect any bone

in skeleton, but primarily the skull bones and long bones of skeleton.

Signs & symptoms: -Even though skull and jaws

commonly affected, symptoms are mostly related to involvement of long bones – pain, pathological fractures etc.

Patients with McCune-Albright syndrome have café-au-lait (coffee with milk) pigmentation.

Typically, margins of the spots are irregular, unlike those of neurofibromatosis, where the spots have smooth borders

HISTOLOGICAL FEATURES: -Lesion shows typical irregular, shaped

trabeculae of immature woven bone in a cellular, vascular stroma.

Theses trabeculae are not connected to each other.

They often assume curvilinear shape, which have been linked to Chinese script writing.

These trabeculae believed to arise due to metaplasia and are not bordered by osteoblasts.

The surrounding stroma is highly cellular and vascular.

Fibrous dysplasia typically demonstrates a rather monotonous pattern throughout the lesion rather than being a haphazard mixture of woven bone, lamellar bone, and spheroid particles.

The lesional bone fuses directly to normal bone at the periphery of the lesion, so that no capsule or line of demarcation is involved.

Jaw & skull lesions tends to be more ossified than other counterparts in the rest of the skeleton.

Some jaw lesion which rarely undergo maturation shows lamellar bone in a cellular connective tissue stroma.

CEMENTO-OSSEOUS DYSPLASIASCommonest type of fibro-osseous

lesions in head and neck region, occurring in the tooth bearing area.

Believed to represent some form of reactive process.

Histopathological features similar to FD and ossifying fibroma.

Cemento-osseous dysplasia arises in close approximation to the periodontal ligament and exhibits histopathological similarities with the structure. Hence some investigators have suggested these lesion are of periodontal ligament origin.

Other investigators believe it is triggered by local factors and possibly correlated to hormonal imbalance.

TYPES OF CEMENTO-OSSEOUS DYSPLASIAS: -

Based on their clinical and radiological features, grouped into

1.Periapical cemento-osseous dysplasia2.Focal cemento-osseous dysplasia3.Florid cemento-osseous dysplasia

PERIAPICAL CEMENTO-OSSEOUS DYSPLASIAIt a reasonably well-defined clinical-radiologic entity

CLINICAL FEATURES: -Age incidence: 30 – 50 yearsSex incidence: marked female predilection

(female : male ratio is 14 : 1)Racial predilection: Predominantly blacksSite predilection: predominantly

mandibular anteriors.

Signs & symptoms:Can occur either as solitary lesion,

but mostly as multiple lesions.Almost always asymptomatic.Teeth associated with the lesions

are always vital.

RADIOGRAPHIC FEATURES: -

(a) Early stage: well circumscribed radiolucency involving apices of vital teeth (cannot be distinguished from periapical granuloma / cyst)

(b) Intermediate stage: as mineralized areas begin to appear in the lesion, mixed radiopaque radiolucent appearance seen.

(c) Late stage: the entire lesion becomes radiopaque surrounded by a narrow radiolucent rim.

FOCAL CEMENTO-OSSEOUS DYSPLASIA

Benign cemento-osseous lesion.Features intermediate between those

of periapical and florid cemento-osseous dysplasia.

Believed to be the commonest fibro-osseous lesion.

CLINICAL FEATURES: -Age incidence: 4th and 5th decades.Sex incidence: 80 % cases in females.Racial predilection: more in whites.Site predilection: mostly posterior

mandible.Signs & symptoms: asymptomatic,

detected during routine radiographic examination.

RADIOGRAPHIC FEATURES: -

Lesion may be completely radiolucent / radiopaque.

Most commonly, it is mixed radiopaque-radiolucent.

Borders are usually irregular.

FLORID CEMENTO-OSSEOUS DYSPLASIA

Widespread disease affecting greater area of jaw bones.

Secondary infections commonly occur (low grade osteomyelitis) due to exposure of abnormal mineralized material to oral cavity.

CLINICAL FEATURES: -Age incidence: 2nd and 3rd decades.Sex incidence: predominantly females.Racial predilection: 90% cases in black women.Site predilection: Mostly bilaterally symmetricalEither jaw may be involved.

Signs & symptoms:Usually asymptomatic.Patients may complain

of dull pain.In some cases,

yellowish, avascular bone like material may be seen exposed to oral cavity.

Affected jaw bone may show expansion.

RADIOGRAPHIC FEATURES: -

Lesions are well defined and radiopaque, often mixed with areas of less well defined mixed radiopaque-radiolucent regions.

In some cases, single / multiple simple bone cysts may be associated with this disease.

DIFFERENTIAL DIAGNOSIS: -In early stages when the lesion is radiolucent,1. Nevoid basal cell carcinoma syndrome.2.Cherubism3.Multiple myeloma4.Brown’s tumor of hyperparathyroidism.In later stages when lesion is mixed,1. Odontoma2.Ossifying fibroma3.Ameloblastic fibro-odontoma4.COC5.CEOT

HISTOLOGICAL FEATURES: -

In early stages, lesion shows fibroblastic proliferation which may contain small areas of osteoid formation.

No evidence of inflammation.

In later stages, the lesion shows increasing deposition of bone or cementum like material.

In the final stages, the entire lesion may be composed of dense mineralized tissue.

OSSIFYING FIBROMA(Cementifying fibroma / Cemento-ossifying fibroma)

Ossifying fibroma (OF) is a well circumscribed, sometimes encapsulated neoplasm composed of fibrous tissue containing varying amounts of calcified material.

This calcified material may be bone, cementum like spheruls or a mixture of both.

It has been suggested that the origin of the tumor is odontogenic or from periodontal ligaments.

But identical tumors have been reported in orbital, frontal, ethmoid, sphenoid and temporal bone, leaving these prior theories of origin open to question.

CLINICAL FEATURES: -Age incidence: 3rd and 4th decades.Sex incidence: Female to male ratio in

5 : 1Site predilection: Mandible involved more frequently

than maxilla.Within mandible, premolar – molar

area is the commonest site affected.

Signs & symptoms:Small lesions are asymptomatic

and detected only during routine radiographic examination.

Larger lesions may cause painless expansion of involved bone.

Expansion of bone can cause facial asymmetry.

Pain and paresthesia are very rarely noted.

RADIOGRAPHIC FEATURES: Most often lesions are well

defined, unilocular.Some lesions may be mixed

radiopaque-radiolucent depending on the amount of calcified material present in the tumor.

Large lesion may produce root divergence and root resorption.

DIFFERENTIAL DIAGNOSIS: -Fibrous dysplasiaOsteoblastoma and osteoid osteomacementoblastoma Focal sclerosing osteomyelitis.Cemento-osseous dysplasia.

HISTOLOGICAL FEATURES: Most tumors are well

circumscribed masses composed of fibrous tissue and containing calcified material.

The calcified material may be in the form of irregular trabeculae of osteoid or basophilic, globular calcifications resembling cementum.

Many times both are present in the same lesion.

Mixture of woven bone and cementum-like material.

Image shows- a well circumscribed solid tumor mass.

Trabeculae of bone and droplets of cementum like material can be

seen forming within a background of cellular fibrous connective

tissue.

JUVENILE OSSIFYING FIBROMAUncommon lesion of bone.Differentiated from ossifying fibroma

on the basis of age incidence, site predilection and clinical behavior.

However, histologically the distinction from OF is not so clear.

Two patterns recognized – trabecular and psammomatoid.

CLINICAL FEATURES: -Age incidence: Patients younger than 15

years of age.Sex incidence: Equal.Site predilection:Most commonly involves orbital and frontal bones.Maxilla is involved more commonly.

Signs & symptoms:Most tumors show rapid growth.In such cases, pain and

paresthesia may be noted.Psammomatoid variant

frequently appears outside the jaws, mostly arising in the orbital and frontal bone and paranasal sinuses.

Cortical expansion and facial asymmetry is seen with jaw lesions.

Orbital and sinus involvement may cause exophthalmus, proptosis and nasal obstruction.

RADIOGRAPHIC FEATURES: -

Can be radiolucent or mixed radiopaque-radiolucent depending on amount of calcified material present within the tumor.

Lesion may be well demarcated or may show invasion into surrounding bone.

HISTOLOGICAL FEATURES: -1. TRABECULAR J.O.F:Both patterns of JOF well

circumscribed but not encapsulated.

Tumor composed of fibrocellular CT, areas of nuclear crowding, heamorage and occasional multinucleated giant cells.

Mineralized component shows irregular strands of osteoid lined by plump osteoblasts.

Jof- Trabeculae of cellular woven bone are present in a cellular fibrous stroma.

2. PSAMMOMATOID JOF: The stroma is similar to

trabecular JOF.The mineralized material is

composed of concentric, lamellated and spherical ossicles.

These ossicles vary in size and typically have basophilic centers with eosinophilic osteoid rims.

Jof- cellular fibrous connective tissue containing spherical ossicles with basophilic centers and peripheral eosinophilc rim .

Treatment For smaller lesions, complete local excision or

curettage appears adequate. Rapidly growing lesion, wider resection may be

required.Recurence rate is about 30% to 58%.

INFECTIOUS DISEASES

OSTEOMYELITISRefers to acute / chronic

inflammatory process in medullary spaces or cortical surfaces of bones.

Various patterns recognized like focal and diffuse sclerosing osteomyelitis, proliferative periostitis etc.

TYPES OF OSTEOMYELITIS: -1. Acute osteomyelitis2. Chronic osteomyelitis3. Diffuse sclerosing osteomyelitis4.Condensing osteitis (Focal sclerosing

osteomyelitis)5. Osteomyelitis with proliferative periostitis (Garre’s

osteomyelitis).6.Alveolar osteitis (Dry socket)

PREDISPOSING FACTORS: -1. After odontogenic infections2.Trauma to jaws3.Presence of ANUG4.Chronic systemic diseases5.Immunocompromised states6.Tobacco and alcohol abuse7.Diabetes mellitus8.Exanthematous fevers9.Malignancy10.Malnutrition

ACUTE OSTEOMYELITISAcute osteomyelitis occurs when acute

inflammation spreads through medullary spaces of bone.

CLINICAL FEATURES: -Age incidence: Any ageSex incidence: Strong male predilectionSite predilection: Mostly in mandible. Maxilla

involved primarily in children.

Signs & symptoms: Fever, leukocytosis,

lymphadenopathy and soft tissue swelling of affected area.

X-rays can show an ill defined radiolucency.

Occasionally, fragments of necrotic bone can be seen separating from surrounding normal bone – Sequestrum.

If sequestrum is surrounded by vital bone – Involucrum.

HISTOLOGICAL FEATURES: -

Biopsy specimen usually contains necrotic bone, showing loss of osteocytes from lacunae and bacterial colonization.

Bone periphery shows necrotic debris and infiltration with PMNL’s.

Specimen is diagnosed as sequestrum unless there is good clinico-pathologic correlation.

CHRONIC OSTEOMYELITISIt can arise either de novo from the onset or as a

continuation of acute osteomyelitis, if it is not resolved quickly.

CLINICAL FEATURES: -Age incidence: Any age Sex incidence: Strong male predilectionSite predilection: Mostly in mandible.

Signs & symptoms:Pain, swelling, purulent

discharge, sinus formation, sequestrum formation, tooth loss.

Frequent acute exacerbations may occur if infection continues for a long time.

X-rays reveal ill defined, moth eaten radiolucency often showing a central radiopacity (sequestrum).

HISTOLOGICAL FEATURES:

Biopsy material contains significant soft tissue component consisting of chronically inflamed fibrous CT filling intertrabecular areas of bone.

Scattered areas of sequestrum may also be noted.

DIFFUSE SCLEROSING OSTEOMYELITISCharacterized by pain, inflammation, varying degrees

of periosteal hyperplasia, sclerosis and radiolucency of affected bone.

Can be confused clinically and radiologically with certain other intrabony pathoses like florid cemento-osseous dysplasia or Paget's disease of bone etc.

CLINICAL FEATURES: -Age incidence: Almost exclusively in adults.Sex incidence: NilSite predilection: Primarily in mandibleSigns & symptoms:Pain and swelling are uncommon.To make a definitive diagnosis of diffuse sclerosing

osteomyelitis, microbiological cultures must be positive.

RADIOGRAPHIC FEATURES: -

Increased radiopacity around sites of chronic inflammation like periodontitis, pericoronitis, periapical pathology etc.

Sclerosis occurs more in alveolar crest regions of tooth bearing areas.

HISTOLOGICAL FEATURES: -Sclerosis and remodeling of

bone.Significant inflammation of bone

is not seen even though sclerosis occurs adjacent to inflammation.

Necrosis of sclerotic bone secondary to inflammation may occur.

In this case, necrotic bone separates and is surrounded by granulation tissue

FOCAL SCLEROSING OSTEOMYELITIS(Condensing osteitis)

This refers to a focal area of bone sclerosis associated with apices of pulpally involved (caries, deep restorations or pulp necrosis) teeth.

To be diagnosed as condensing osteitis, association with inflammation is essential, as it resembles several other intrabony pathoses.

CLINICAL FEATURES: -Occurs mostly in children

and young adults.Mostly occurs in mandibular

premolar / molar area, associated with pulpitis / pulp necrosis.

Localized, uniform zone of increased radiopacity seen adjacent to tooth apex.

No swelling / cortical expansion noted clinically.

DIFFERENTIAL DIAGNOSIS: -This lesion must be distinguished

from1.Focal cemento osseous dysplasia

– it shows a radiolucent border.2.Idiopathic osteosclerosis – here,

the lesion is separated from the tooth apex.

OSTEOMYELITIS WITH PROLIFERATIVE PERIOSTITIS

Also called Periostitis ossificans or Garrѐ’s Osteomyelitis.

It is a type of osteomyelitis associated with periosteal bone formation.

CLINICAL FEATURES: -Age incidence: Children & young

adults

Sex incidence: Nil

Site predilection: Mostly in premolar / molar regions of mandible.

Signs & symptoms:Swelling may be noted on lower border of

mandible.Pain may / may not be present.Radiographs demonstrate radiopaque laminations

roughly parallel to each other and the underlying cortical surface (onion skin appearance).

HISTOLOGICAL FEATURES: Shows parallel rows of highly

cellular, woven bone in which the individual trabeculae are oriented perpendicular to surface.

Sometimes, trabeculae are interconnected or they may be scattered, resembling fibrous dysplasia.

In between trabeculae, fibrous CT is relatively non inflamed.

ALVEOLAR OSTEITIS(Dry socket / Fibrinolytic alveolitis)

Sometimes, the blood clot at the extraction site fails to organize which eventually leads to delayed healing and causes a condition called “Dry socket”.

Research shows it is due to transformation of plasminogen to plasmin with resultant lysis of fibrin and formation of kinin (pain mediators).

PREDISPOSING FACTORS: -1.Local trauma2.Estrogens3.Bacterial toxins4.Inadequate irrigation of surgery

site5.Tobacco abuse.

CLINICAL FEATURES: -Age incidence: Between 20 – 40 years

Sex incidence: Nil

Site predilection: Posterior mandibular teeth, especially impacted third molars.

Signs & symptoms: Affected extraction site filled with a dirty gray clot,

which is lost, leaving behind a bare, bony socket (Dry socket).

Diagnosis is confirmed by probing of socket which shows an exposed and extremely sensitive bone.

Severe pain, foul smell and lymphadenopathy develop within 3 – 4 days of extraction.

OSTEOMABenign tumors composed of mature compact /

cancellous bone.Most commonly occur in craniofacial skeleton – rare

in other parts of body.Palatal and mandibular tori are not considered as

osteomas although they are histologically identical.

TYPES OF OSTEOMA: -I. Depending on location:

- Periosteal- Endosteal

II. Depending on type of bone:- Compact- Cancellous

CLINICAL FEATURES: -Age incidence: Young adults.Sex incidence: NilSite predilection: Mandible affected more commonly than maxilla.In mandible – body / condyle.Body of mandible – posterior to premolars on lingual

surface.

Signs & symptoms:1. Periosteal – slowly growing

polypoid / sessile mass, usually solitary.

2.Endosteal – usually seen in condyles, cause progressive shift in patient’s occlusion towards unaffected side. Other signs include facial pain swelling and limited mouth opening.

RADIOGRAPHIC FEATURES: -

Endosteal osteomas appear as radiopaque sclerotic masses.

Periosteal osteomas may appear as uniform ‘opaque mass or sclerotic periphery with central trabecular pattern.

DIFFERENTIAL DIAGNOSIS: -ExostosesOsteoblastoma and osteoid

osteoma:Odontomes Focal sclerosing osteomyelitis.

.HISTOLOGICAL FEATURES: - 1. Compact Osteoma:Normal appearing mature

compact bone showing minimal marrow tissue.

2. Cancellous osteoma: Trabeculae of bone and

fibrofatty marrow.Significant osteoblastic activity

may be seen

GARDNER SYNDROMEMultiple osteomas Multiple intestinal polypoid lesionsMultiple epidermoid and dermoid

cysts Multiple supernumerary teeth

OSTEOSARCOMA(Osteogenic sarcoma)

Malignancy of mesenchymal cells that have the ability to produce osteoid or immature bone.

Commonest malignancy arising within the bone along with hematopoietic neoplasms.

Majority arise from within the bone (intramedullary), some may be peripheral (juxtacortical)

CLINICAL FEATURES: -Age incidence: 3rd and 4th

decades.Sex incidence: Commoner in

males.Site predilection: Long bones and

U / L jaws.

Signs & symptoms: Swelling and pain -

commonest symptoms.Loosening of teeth,

paresthesia and nasal obstruction (in case of maxillary tumors) may also be noted.

RADIOGRAPHIC FEATURES: -

Radiographic features vary from densely sclerotic

Mixed radiopacity – radiolucency (mottled)

• To completely radiopaque• Periphery of lesions usually

indistinct and ill defined.

The characteristic “sunburst” appearance can be noted in about 25% of jaw tumors.

Produced by osteophytic bone production.

DIFFERENTIAL DIAGNOSIS: -- Osteoblastoma - Fibrous dysplasia- Ossifying fibroma

HISTOLOGICAL FEATURES: -Considerable variation seen.Essentially – osteoid production

by malignant mesenchymal cells.In addition to osteoid, chondroid

and fibrous material also seen many times.

Tumor cells may vary from spindle shaped to highly pleomorphic types.

Osteosarcomas can be classified on the basis of relative amounts of chondroid / osteoid / fibers produced by tumor into:

1. Chondroblastic

2. Fibroblastic

3. Osteoblastic

CHONDROMABenign tumors composed of mature hyaline cartilage.Common bone tumor, occurring mostly in short

bones of hands and feet.Occur very rarely in jaw bones.Jaw tumors occur usually in anterior maxilla of adult

patients.

HISTOLOGICAL FEATURES: -Very difficult to differentiate between a benign

chondroma and well differentiated, low grade chondrosarcoma.

Chondroma composed of mature hyaline cartilage.However, a diagnosis of chondroma for jaw lesion is

rarely given as most of them are malignant.

CHONDROSARCOMAMalignant tumor characterized by

cartilage formation, but not bone, by the tumor cells.

They comprise about 10% of all primary bone tumors of skeleton, but occur very rarely in the jaws.

CLINICAL FEATURES: -Age incidence: Occurs in a wide age

range. Average age incidence is 3rd

decade.Sex incidence: Slightly more in males.Site predilection: Involves maxilla and

mandible with equal frequency.

Signs & symptoms:Manifests usually as a

painless swelling.There may be separation

and loosening of teeth also.Pain is not usually a feature

of this tumor, as in case of osteosarcoma.

Maxillary tumors – nasal obstruction or epitaxis.

RADIOGRAPHIC FEATURES:Usually seen as poorly defined

radiolucency with variable amounts of radiopaque foci (caused by calcification of cartilage matrix).

If tumor penetrates cortex – sunburst appearance.

DIFFERENTIAL DIAGNOSIS: -1. Osteosarcoma (especially if tumor shows sunburst

appearance).2. Osteomyelitis.3. Periapical granuloma.4.Ewing’s sarcoma.5. Primary intraosseous carcinomas like

Mucoepidermoid carcinoma, Ameloblastic carcinoma etc.

HISTOLOGICAL FEATURES: Composed of cartilage showing

varying degrees of maturation and cellularity.

Most cases – typical lacuna formation with chondroid matrix.

Lobular growth pattern seen with centre of lobule showing greatest maturation and periphery showing immature cartilage along with a stroma of round / spindle cells.

EWING’S SARCOMAPrimary malignant tumor of bone.Histogenesis is uncertain.Comprises 6 % – 10 % of all primary bone tumors.Earlier believed to arise from endothelial cells,

hematopoietic cells or undifferentiated mesenchymal cells.

Now – possibly neuroectodermal origin.

CLINICAL FEATURES: -Age incidence: Children & adolescents.Sex incidence: more than 60% cases

occur in males.Racial incidence: Predominantly in

whites.Site predilection:Primarily affects femur and pelvic bones.Jaw tumors very rare.

Signs & symptoms:Pain and swelling are the commonest manifestations.Pain is usually intermittent and can be dull or severe.Other signs include paresthesia and tooth mobility.General signs – fever & elevated ESR (can be mistaken

for osteomyelitis).

RADIOGRAPHIC FEATURES: -

Seen as irregular, radiolucent lesion with poorly defined margins.

Cortical destruction or expansion is not usually seen.

HISTOLOGICAL FEATURES: - Composed of small round cells

with indistinct cell outlines but well defined nuclear boundary.

Tumor cells proliferate in sheets without any pattern.

Large areas of necrosis and hemorrhage also seen.

Diagnosis difficult, as it is similar to lymphomas, small cell osteosarcoma, embryonal rhabdomyosarcoma etc.

Definition: Metastasis is the transfer of disease from one organ or part to another organ or part not directly connected with it.

Pathogenesis: Disease can spread to other regions through- Hematogenous spread- Lymphatic spread- Perineural invasion

Types of metastases to jaws:- Adenocarcinomas- Carcinomas- Sarcomas

Sites of primary tumors:- Breast- Prostrate- Kidney- Lungs- Thyroid

CLINICAL FEATURES: -

Age incidence: Older age personsSex incidence: NilSite predilection: More than 80% cases of jaw

metastasis occurs in mandible.Signs & symptoms: Pain, swelling, tooth mobility.Inferior alveolar nerve involvement may cause

paresthesia and anesthesia.Occasionally, patients are asymptomatic and

diagnosis occurs only after microscopic examination after the lesion is noted on a radiograph.

RADIOGRAPHIC FEATURES: -Metastatic deposits in the jaws appear as radiolucent

defects.These defects may be either poorly defined “moth

eaten” radiolucencies or rarely, well circumscribed like a cyst.

Some carcinomas, particularly from breast and prostrate may stimulate new bone formation, resulting in a mixed radiopaque – radiolucent lesion.

HISTOLOGICAL FEATURES: -Varied presentation.Some times – metastatic deposits well differentiated

and closely resemble primary malignancy of specific site like kidney, thyroid etc.

Most commonly however, the deposits are poorly differentiated and histological study does not provide any clue to the primary site of tumor.

BIBLIOGRAPHYShafer WG, Hine MK, Levy BM. A text book of oral

pathology. 6th ed. W.B. Saunders Company. Phil, London, Toronto, 2005.

Neville BW, Damm DD, Allen CM, Bouquot JE. Oral and maxillofacial pathology. 2nd ed. WB Saunders Company. Phil, London, Toronto, 2007.

Cawson RA, Odell EW, Porter S. Cawson’s essentials of oral pathology and oral medicine, 7th Ed, Churchill Livingstone, 2002.

Regezi JA, Sciubba JJ, Jordan RCK. Oral pathology: Clinical Pathologic Correlations. 4th ed. Saunders Company, 2003.

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