Diseases of bone and its oral aspects

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.

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 BONE
 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

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

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. OSTEOPETROSIS
3. OSTEOGENESIS IMPERFECTA
4. CLEIODOCRANIAL DYSPLASIA.

CHERUBISM
Rare 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 “CChheerruubb” 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 = females
Site predilection:
Mostly bilateral involvement
Mandible 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 IMPERFECTA
Most 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 ame nts, 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 FEATURES
The 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
Osteopetrosis
Fetal rickets
Turner syndrome
Pagets disease
Marfan syndrome &
Ehlers-Danlos syndrome.
Some times in normal infants.

Additional signs & symptoms
Deafness- 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.

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.
Kyphoscoliosis
Easy bruising
Short 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 features
Hallmarks of OI includes:
Osteopenia
Bowing
Angulation
Deformity of long bones
Multiple 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 DYSPLASIA
Bone 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 a ns 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.

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 OSTEOPETROSIS
CLINCAL 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 Osteopetrosis
Affected 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 OSTEOPETROSIS
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 seen
10% 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 adult
osteopetrosis  Facial deformity (broad face,
Common orofacial
findings in infantile
osteopetrosis
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.

Age incidence: Middle aged
individuals
Sex incidence: Male to female
ratio is 2:1
Site 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.

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 DISEASE
The 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.

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”.

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.

Other lesions with multifocal,
multilocular radiolucency are
- Cemento-osseous dysplasia
- Hyperparathyroidism
- Cherubism
- Multiple myeloma

Central giant cell granuloma
Aneurysmal bone cyst
Traumatic 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.

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.

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

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 CYST
Primarily 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.

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 teeth
Migration of teeth
Root resorption
Pain is often present.
Paresthesia is present
If 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.

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 jaws
Jaw lesions are mostly seen in ramus and angle region
Affected 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.

Age incidence: Young individuals
10-20 yrs
Sex 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 DYSPLASIA
Condition 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 DYSPLASIA
Age incidence: 1st or 2nd decade of life.
Sex incidence: equal
Site 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.

Clinically, FD must be differentiated from
1. Ossifying fibroma
2.Paget’s disease.
Though, its radiographic appearance is typical, it
must be distinguished from
1. Hyperparathyroidism.
2.Paget’s disease (early stage).

POLYOSTOTIC FIBROUS DYSPLASIA
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

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 DYSPLASIAS
Commonest 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 dysplasia
2.Focal cemento-osseous dysplasia
3.Florid cemento-osseous dysplasia

PERIAPICAL CEMENTO-OSSEOUS DYSPLASIA
It a reasonably well-defined clinical-radiologic entity
Age incidence: 30 – 50 years
Sex incidence: marked female predilection
(female : male ratio is 14 : 1)
Racial predilection: Predominantly blacks
Site 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.

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.

Age incidence: 2nd and 3rd decades.
Sex incidence: predominantly females.
Racial predilection: 90% cases in black women.
Site predilection:
Mostly bilaterally symmetrical
Either 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.

In early stages when the lesion is radiolucent,
1. Nevoid basal cell carcinoma syndrome.
2.Cherubism
3.Multiple myeloma
4.Brown’s tumor of hyperparathyroidism.
In later stages when lesion is mixed,
1. Odontoma
2.Ossifying fibroma
3.Ameloblastic fibro-odontoma
4.COC
5.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.

Age incidence: 3rd and 4th decades.
Sex incidence: Female to male ratio in
5 : 1
Site 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.

Most often lesions are well
defined, unilocular.
Some lesions may be mixed
depending on the amount of
calcified material present in the
tumor.
Large lesion may produce root
divergence and root resorption.

Fibrous dysplasia
Osteoblastoma and osteoid osteoma
cementoblastoma
Focal sclerosing osteomyelitis.
Cemento-osseous dysplasia.

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 FIBROMA
Uncommon 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.

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
depending on amount of
calcified material present
within the tumor.
Lesion may be well
demarcated or may show
invasion into surrounding
bone.

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%.

OSTEOMYELITIS
Refers 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 osteomyelitis
2.Chronic osteomyelitis
3. Diffuse sclerosing osteomyelitis
4.Condensing osteitis (Focal sclerosing
osteomyelitis)
5.Osteomyelitis with proliferative periostitis (Garre’s
osteomyelitis).
6.Alveolar osteitis (Dry socket)

PREDISPOSING FACTORS: -
1. After odontogenic infections
2.Trauma to jaws
3.Presence of ANUG
4.Chronic systemic diseases
5.Immunocompromised states
6.Tobacco and alcohol abuse
7.Diabetes mellitus
8.Exanthematous fevers
9.Malignancy
10.Malnutrition

ACUTE OSTEOMYELITIS
Acute osteomyelitis occurs when acute
inflammation spreads through medullary spaces of
bone.
Age incidence: Any age
Sex incidence: Strong male predilection
Site 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.

-
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 OSTEOMYELITIS
It can arise either de novo from the onset or as a
continuation of acute osteomyelitis, if it is not
resolved quickly.
Age incidence: Any age
Sex incidence: Strong male predilection
Site 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 OSTEOMYELITIS
Characterized 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.

Age incidence: Almost exclusively in adults.
Sex incidence: Nil
Site predilection: Primarily in mandible
Signs & 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.

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.

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.

This lesion must be distinguished
from
1.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.

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).

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 trauma
2.Estrogens
3.Bacterial toxins
4.Inadequate irrigation of surgery
site
5.Tobacco abuse.

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.

OSTEOMA
Benign 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

Age incidence: Young adults.
Sex incidence: Nil
Site 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.

-
Endosteal osteomas appear as
radiopaque sclerotic masses.
Periosteal osteomas may
appear as uniform ‘opaque
mass or sclerotic periphery
with central trabecular
pattern.

Exostoses
Osteoblastoma and osteoid
osteoma:
Odontomes
Focal sclerosing osteomyelitis.

.
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 SYNDROME
Multiple osteomas
Multiple intestinal polypoid lesions
Multiple 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)

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.

- Osteoblastoma
- Fibrous dysplasia
- Ossifying fibroma

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

CHONDROMA
Benign 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.

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.

CHONDROSARCOMA
Malignant 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.

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.

Usually seen as poorly defined
radiolucency with variable
amounts of radiopaque foci
(caused by calcification of
cartilage matrix).
If tumor penetrates cortex –
sunburst appearance.

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.

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 SARCOMA
Primary 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.

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.

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

Age incidence: Older age persons
Sex incidence: Nil
Site 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.

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.

BIBLIOGRAPHY Shafer 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.

Diseases of bone and its oral aspects

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