Bone Diseases in Jaws: Fibrous Dysplasia, Paget's Disease, Cherubism and More

Diseases Bone
manifested in jaws
INDIAN DENTAL ACADEMY
Leader in continuing Dental Education
www.indiandentalacademy.com

1. FIBROUS DYSPLASIA
2. OSTEITIS DEFORMANS (PAGET’S DISEASE)
3. CHERUBISM
4. CLEIDOCRANIAL DYSPLASIA
5. OSTEOPETROSIS
6. CEMENTO OSSEOUS DYSPLASIA
7. CEMENTO OSSIFYING FIBROMA
8. ACHONDROPLASIA
INDEX

FIBROUS DYSPLASIA
•It is a fibo-osseous lesion in which normal medullary bone is
gradually replaced by an abnormal fibrous C.T. proliferation.
•The mesenchymal tissue contains various amounts of osteoid &
osseous material that presumably arises through metaplasia.
Etiology:
•Unknown
•Many workers believe ---
--it is a non-neoplastic, hamartomatous growth
resulting from deranged mesenchymal cell activity
--another hypothesis suggests that it is an abnormal
reaction of bone to a localized traumatic episode

FIBROUS DYSPLASIA
Clinical features:Clinical features:
--Seen early in lifeSeen early in life
-It can affect single bone or several to many bones.-It can affect single bone or several to many bones.
M O N O S T O T I C F D
- a f f e c t in g s in g le b o n e
J a f f e -L ic h t e n s t e in t y p e
- m u lt ip le b o n e le s io n s
- s k in p ig m e n t a tio n ( c a f e a u la it m a c u le s )
M c C u n e - A lb r ig h t s t y p e
- m u lt ip le b o n e le s io n s
- s k in p ig m e n t a tio n ( c a f e a u la it m a c u le s )
- v a r o iu s t y p e s o f e n d o c r in e d is o r d e rs
P O L Y O S T O T I C F D
- a f f e c t in g m a n y b o n e s
F I B R O U S D Y S P L A S IA

MONOSTOTIC F.D.
•It is much more common than Polyostotic type (80% of cases)
•Jaws are most commonly affected sites
•1st
or 2nd
decade of life
•M = F
•Slow growing, painless swelling of the affected area (usually
unilateral)
•Teeth involved in the lesion usually remain firm but may be
displaced by bony mass
• Although the mand lesions are truly Monostotic, maxillary
lesions often involve adjacent bones such as zygoma, sphenoid,
occiput & are not strictly monostotic.
Termed as -- Craniofacial fibrous dysplasia
FIBROUS DYSPLASIA

POLYOSTOTIC F.D.
•1st
or 2nd
decade of life (early in life)
• It is less common than Monostotic type (20% of cases)
•Clinical picture is dominated by symptoms related to long bone
lesions. Jaws are less commonly affected.
•deformity, bowing or thickening of long bones is evident
•Pathological fractures with resulting pain & deformity is very
common
•Leg length discrepancy is noted as a result of involvement of upper
portion of femur (Hockey stick deformity)
• Café au lait (Coffee in milk) macules are pale brown well defined
pigmentation with irregular outline, generally unilateral.
--present on neck, trunk, thigh & also on oral mucosa.
FIBROUS DYSPLASIA

FIBROUS DYSPLASIA
McCune-Albrights syndrome
•Sexual precocity is the most common endocrine manifestation
•Menstrual bleeding may occur during the first few months of life
•Breast development may be seen in the first few years of life
•Variety of other endocrine disturbances are seen -related to
pituitary, thyroid, parathyroid etc….

FIBROUS DYSPLASIA
Intra-oral appearance of the bony swelling which has remained
virtually unchanged after five years (Next slide)

Five years later
FIBROUS DYSPLASIA

FIBROUS DYSPLASIA

FIBROUS DYSPLASIA
Radiography:
•Margins of the lesion are poorly defined
-- lesion appears to blend into surrounding normal bone
without evidence of circumscribed border
•Lesions may be radiolucent or densely radiopaque
•Characteristic X-ray picture – radiopacity of numerous poorly
calcified bony trabeculae imparting a“Ground glass appearance”
or “Orange peel appearance”
•Skull X-ray – max sinus is radiopaque
-- base of the skull shows increased density
(involved bones are sphenoid, roof of
orbit frontal bones & occiput)

Histopath:
•Typical microscopic feature of FD shows irregularly shaped
trabeculae of immature (woven) bone in a cellular, loosely arranged
fibrous stroma.
•Lesional bone fuses directly to normal bone at the periphery of the
lesion, so that NO capsule or line of demarcation is present
•Bony trabeculae often assume curvilinear shapes, which have been
described as “CHINESE LETTER” arrangement.
(₣ ₤ ₪ ŧ Ħ ¥ コゴ )
•Bony trabeculae are considered to arise by metaplasia & are not
surrounded by osteoblasts.
•Jaw lesions might undergo maturation but long bone lesions do not
show any maturation even in older aged individuals
FIBROUS DYSPLASIA

FIBROUS DYSPLASIA
Treatment:
•Difficult
•Cosmetic reshaping after certain age (after the growth has stopped)
•Radiation therapy is CONTRAINDICATED, as it carries the risk of
development of post-radiation Osteosarcoma

PAGET’S DISEASE
(Osteitis Deformans)
PD is characterized by abnormal & anarchic resorption &
deposition of bone, resulting in distortion & weakening of the
affected bones
Disease principally affects older individuals (rarely below 40 yrs of
age)
Etiology:
•Unknown
•Inflammatory, genetic & endocrine factors may be contributing
agents
•Slow virus infection has received considerable attention (unproven)
Slow virus-is one which produces a disease with a prolonged incubation
period. www.indiandentalacademy.com

Clinical features:
•Most cases are polyostotic
•M>>F (2:1)
•Geographic variation is seen
[Britain>>USA, Africa & Asia very rare] {W>>B}
•Relatively asymptomatic, but severe bone pain is a common
complaint
•Pelvis, skull & femur are the most commonly affected bones
•Jaw involvement is seen in about 10% - 15% of cases
•Max >> mand
•Bones affected by PD becomes thickened, enlarged & weakened
•Skull involvement leads to increase in circumference of head
PAGET’S DISEASE

C/F:
•The bones are weakened -- Due to which bowing deformity is
present ---- this gives a “Simian Stance” (Monkey-like)
•The alveolar ridge tend to become grossly enlarged (symmetrically).
•In severe cases lip closure is difficult or impossible
•Dentulous patients C/O : spacing of teeth
•Edentulous patients C/O: non-fitting dentures (as the jaw is enlarging)
PAGET’S DISEASE
•In extreme cases of jaw enlargement “Leontasis Ossea” (Lion-like)
facial deformity is seen
•Neurological complications, such as deafness or visual
disturbances may result from bony encroachment on cranial nerves

PAGET’S DISEASE

Radiography:
•Depends on the stage of the disease (osteoclastic & osteoblastic)
•Early stages reveal a decreased radiodensity– slight radiolucecy with
alteration in trabecular pattern
•In early stages – skull might show large circumscribed areas of
radiolucency (osteoporosis circumscripta)
PAGET’S DISEASE
•During later stages of (osteoblastic) disease there is haphazardly
formed patchy areas of radio-opacities (bone formation) – giving it a
“Cotton wool” appearance
•Dental changes : -- hypercementosis of roots,
loss of lamina dura,
obliteration of PDL space &
resorption of roots

Lab findings:
•Important information is provided
•Serum Calcium & Phosphate levels are within normal limits
•Serum Alkaline phosphatase levels are markedly elevated
Normal value in adult: 1.5 – 5.0 (Bodansky units)
In Paget’s disease : 50 – 250 (Bodansky units)
PAGET’S DISEASE
Other units for measuring Alkaline phosphatase
•King-Armstrong – Normal value = 5 -10 units
•Phenol units -- Normal value = 1.0 – 3.5 units

Histopath:
•Depends on the stage of the disease (osteoclastic or osteoblastic)
•In the active resorptive stages, numerous Osteoclasts surround the
bone trabeculae
•Simultaneously, osteoblastic activity is seen with formation of
osteoid rims around bone trabeculae
•The marrow is replaced by fibrous C.T.
•Characteristic picture of PD is presence of basophilic reversal lines.
These lines indicate the junction between resorptive & formative
phases of the bone and results in a “jigsaw puzzle” or “mosaic bone”
appearance
•Few cases show multiple small acellular bony masses that fuse as
the disease progresses.
PAGET’S DISEASE

Treatment:
•No treatment is required for mild cases
•Use of parathyroid hormone antagonist, such as calcitonin or
biophosphonates can reduce bone turnover
•Dental: - difficulty in extraction is encountered (hypercementosis)
- edentulous patients may require periodic new & larger
dentures
PAGET’S DISEASE
Complications:
• Development of malignant tumor, usually an osteosarcoma is
reported.
• Other neurological complications.

CLEIDOCRANIAL DYSPLASIA
(Marie & Sainton’s syndrome)
•It is a disease of unknown etiology which is often but not always
hereditary.
•The disease shows an autosomal dominant inheritance pattern.
•Chiefly involved bones are skull & clavicles,
although a wide variety of anomalies may be found in other
bones.

Clinical features:
•Short stature & have large heads
•Pronounced frontal & parietal bossing with underdeveloped or
narrow paranasal sinuses is evident.
•Ocular hypertelorism is frequently present.
•In the skull the fontanels often remain open or at least exhibit
delayed closing.
•Sutures also may remain open & wormian bones are common.
•Mid-facial skeleton tends to be hypoplastic, and this combined with
normal mandibular growth results in a relative prognathism.
•Patients neck is long, the shoulders are narrow & show marked
drooping.

•Patients show an unusual mobility of their shoulders because of the
absence or hypoplasia of the clavicles. (in some instances patient
approximates the shoulders in front of chest)
•A disease known as Pycnodysostosis (Maroteaux-Lamy syndrome)
has all features of CD, but in addition to this
-- bones are dense & fragile
-- partial agenesis of the phalanges of hand & feet
(these features are absent in CC dysplasia)

Oral manifestation:
•High, narrow, arched palate. Sometimes cleft palate is present
•Maxilla is underdeveloped
•Mandibular prognathism is seen
•Prolonged retention of deciduous teeth & subsequent delayed
eruption of permanent teeth
•Numerous unerupted supernumerary teeth are present
•The roots of the teeth are often short & thinner than usual & may be
deformed
•Absence or decreased amount of cementum is seen.

Histopath:
•Absence or lack of secondary cementum.
Treatment:
•No specific treatment
•Care of the oral conditions is important

CHERUBISM
(Familial FD of Jaws; Hereditary FD of Jaws)
•Cherubism is a rare developmental disease involving jaws
•Cherub meaning plump-cheeked little angels
•Autosomal dominant pattern of inheritance
Clinical features:
•Occur in children ( mean age – 7yrs) but can be noticed as early
as 1 yr of age. Milder cases may not be detected until the patients
reaches 10-12 yrs of age.
•A painless bilateral expansion of the posterior mandible is the
most common early manifestation.
•Lesion tend to involve ascending ramus & body of the mandible.

•The bilateral bony expansion imparts a “chubby” facial appearance
•Extensive maxillary involvement causes stretching of the skin of the
upper face to expose the sclerae. This results in an “eye upturned to
heaven” appearance
•Extensive bone involvement causes a marked widening & distortion
of alveoli.
•All 4 quadrants may be simultaneously involved.
•Palatal vault may be obliterated.
•Premature exfoliation of deciduous teeth may occur as early as 3 yrs
of age.
•Developing teeth are often displaced & fail to erupt & may be
malformed
•Lymphadenopathy- Submand & Upper cervical
CHERUBISM

Lab findings:
•Serum Alkaline phosphatase levels may be elevated
•Whereas serum Calcium & Phosphate levels are within normal
limits
CHERUBISM

CHERUBISM

Radiographic findings:
•Multilocular expansile bilateral radiolucencies (rarely Unilocular)
•The borders are distinct & divided by bony trabeculae giving a
“Soap Bubble” appearance
•Unerupted teeth are often displaced & appear to be floating in the
cyst-like spaces www.indiandentalacademy.com

Histopath:
•Stroma is loosely arranged
•Consists of vascular fibrous tissue containing variable numbers of
multinucleated Giant cells
•The Giant cells tend to be small & are usually focally aggregated
•In few cases perivascular eosinophilic cuff-like deposits are evident
•Foci of extravasated blood are commonly present
•In long standing cases (resolving lesions) the tissue becomes more
fibrous, the number of Giant cells decreases & new bone formation is
seen.
CHERUBISM

Histology of cherubism is similar to giant cell granulomas.
*** the association between Cherubism & Noonan-like
syndrome have been reported; but they are two separate
diseases
CHERUBISM
Treatment:
•Usually self limiting & regressive
•Cosmetic surgery for improving esthetics & function

OSTEOPETROSIS
(Marble Bone Disease; Albers-Schönberg Disease)
•Osteopetrosis is a rare hereditary skeletal disorder characterized
by a marked increase in the bone density resulting from a defect in
bone remodeling.

OSTEOPETROSIS
Clinical features:
Infantile:
Initial signs are normocytic anemia & hepato-splenomegaly
resulting from compensatory extramedullary hematopoiesis
Increased susceptibility to infection is common
Facial deformity develops in many of the children
-- broad face; hypertelorism; snub nose; frontal bossing
Skull : failure of resorption & remodeling of skull bones
produces narrowing of the various foramina (blindness, deafness
&facial paralysis
Dental : Tooth eruption is delayed,
Osteomyelitis is common complication of
extraction

Adult:
Detected at a later age than the infantile type
Asymptomatic in early life & progressively involves more bones
It is not life threatening
NO- anemia, hepato-slenomegaly, blindness, deafness
Dental : Fracture & Osteomyelitis are common complications of
extraction
OSTEOPETROSIS

OSTEOPETROSIS
Radiography:
•Increase in skeletal density with defects in the metaphyseal
remodeling
•Distinction between cancellous & cortical bone is lost

OSTEOPETROSIS

OSTEOPETROSIS
Histopath:
•Number of osteoclasts is increased, but their function to resorb
bone is altered.
•Osteoclasts appear atypical.
• defective resorption combined with continued bone formation
& endochondral ossification is seen.
•Several patterns of abnormal endosteal bone formation have
been described:
# tortuous lamellar trabeculae replacing the cancellous
portion of the bone
# globular amorphous bone deposition in marrow spaces
# osteophytic bone formation

Treatment:
•No specific treatment
•Both the adult and childhood forms of osteopetrosis may benefit from
Actimmune injections. Actimmune (interferon gamma-1b) delays the
progression of osteopetrosis because it causes an increase in bone
resorption (breakdown of old bone tissue) and in red blood cell
production.
•Bone marrow transplant is the only complete cure available. Bone
marrow transplant has many risks, but if it is successful it saves the life of
a child who would otherwise die from complications of the disorder.
•Other treatments include nutrition, prednisone (helps improve the blood
cell count), and physical and occupational therapy.
OSTEOPETROSIS

CEMENTO OSSEOUS DYSPLASIAS
Periapical cemental dysplasia
Florid osseous dysplasia
They are seperated on the basis of
extent of involvement of jaws.
Now,
Periapical cemental dysplasia :-
Replacement of normal cancellous bone
with fibrous tissue and cementum-like material,
abnormal bone or a mixture of the two.
By definition the lesion is located
near the apex of a tooth.

Clinical Features
PCD is a common bone dysplasia that
typically occurs in middle age
More often in females than in males.
Teeth are vital, and usually has no history of pain or
sensitivity.
It is a incidental finding during a periapical or panoramic
radiographic examination made for other purposes.
The lesions can become quite large, causing
a notable expansion of the alveolar process,
and may
continue to
enlarge slowly.
Early stage Mixed stage

Radiographic Features
Lies at the apex of a tooth commonly in mandibular anterior
teeth, although any tooth can be involved.
The lesion is multiple and bilateral, but occasionally a solitary
If the involved teeth have been extracted, this lesion can still
develop and in these cases the term cemental dysplasia may be
more appropriate.
Lesion is well defined with radiolucent border, surrounded by
a band of sclerotic bone.
The lesion may be irregularly shaped or may have an overall
round or oval shape centered over the apex of the tooth.

In the early stage - radiolucency at the apex, continuous with
the periodontal ligament with loss of the lamina dura.
In the mixed stage - radiopaque tissue appears in the
radiolucent structure. (round, oval, or irregular shape
composed of cementum or abnormal bone k/as cementicles).
Mature stage - Totally radiopaque with a thin radiolucent
margin can be seen at the periphery because this lesion matures
from the center outward in most of the cases this radiolucent
margin is not apparent, which makes the
differential diagnosis more difficult.
Rarely root resorption and bone expansion.
Mature stage

D/D :-
 Periapical rarefying osteitis.
 Cementoblastoma.
 Odontomas.
 Cemento-ossifying fibroma.
Treatment is not required.

FLORID OSSEOUS DYSPLASIA :-
Florid osseous dysplasia (FOD) is a widespread form of PCD.
 The lesion has a poor vascular supply, a condition that likely
contributes to its susceptibility to infection.
Clinical features similar to PCD
Occasionally low-grade, intermittent, poorly localized pain in
the affected bone, especially when a simple bone cyst has
developed within the lesion.
If the lesions become secondarily infected, features of
osteomyelitis may develop, including mucosal ulceration,
fistulous tracts with suppuration, and pain.

Radiographic Features
Lesions are bilateral and present in both jaws.
When they are present in only one jaw, the mandible is
the more common location.
The epicenter is apical to the teeth, within the alveolar
process and usually posterior to the cuspid.
Lesions are well defined and has a sclerotic border that
can vary in width, very similar to PCD.

The soft tissue capsule may not be apparent in mature
lesions.

Density of the internal structure can vary from an equal
mixture of radiolucent and radiopaque regions to almost
complete radiopacity.
 Some radiolucent regions, which usually represent the
development of a simple bone cyst.
These cysts may enlarge with time, even beyond the boundary
of the lesion into the surrounding normal bone, or may fill in
with abnormal dysplastic cementoosseous tissue.
Can displace the inferior alveolar nerve canal in an inferior
direction and the floor of the antrum in a superior direction and
can cause enlargement of the alveolar bone by displacement of
the buccal and lingual cortical plates.

D/D :-
Paget's disease
Chronic sclerosing osteomyelitis.
Treatment
No treatment is required.
Maintenance of good oral hygiene to prevent secondary
infection.

ACHONDROPLASIA
•It is a hereditary condition that is transmitted as an autosomal
dominant characteristic
•Disease begins in utero & may actually be diagnosed before
parturition
•80% are stillborn

Clinical features:
Person is Dwarf (1.4 mtrs) with short & thick muscular
extremities.
Brachycephalic skull & bowed legs are seen
Short hands & stubby fingers
Lumbar lordosis with prominent buttocks & protruding abdomen
Many joints show limited movement, because of which the
elbows cannot be straightened
They are of Normal intelligence
They have unusual strength & agility (some adopt the
occupation of professional wrestlers)
ACHONDROPLASIA

Oral manifestations:
Maxilla is retruded because of restriction of growth of the base
of the skull
This may produce relative mandibular prognathism
Difference in jaw sizes – causes malocclusion
Dentition is usually normal (sometimes teeth have altered shape)
ACHONDROPLASIA
Radiographic features:
Except for the retrusion of the maxilla & malocclusion, there
are no changes in the jaw bones
Long bones are short, thick & mild clubbing may be seen
Bones at the base of the skull fuse

ACHONDROPLASIA
Retruded maxilla

ACHONDROPLASIA
Hsitopath:
Basic defect appears as a retardation or even aplasia of the zone
of calcification of endochondral growth
Cartilage columns fail to calcify and are not replaced by bone
Treatment:
No treatment

DOWN SYNDROME
(Trisomy 21 syndrome; Mongolism)
•DS is a disease associated with subnormal mentality in which an
extremely wide variety of anomalies & functional disorders may
occur (cranial & facial deformities)
Etiology:
•Many factors like --- advanced maternal age& uterine & placental
abnormalities, have been regarded as causes of the disease, Recent
concept: chromosomal abnormality

Three forms of DS:
1. One in which there is a typical trisomy 21 with 47
chromosomes (95% cases)
2. Another is a translocation type, in which there appears to be 46
chromosomes, although the extra-chromosomal material of no
21 is translocated to another chromosome (3% cases)
3. Another results from chromosomal mosaicism (2% cases)
DOWN SYNDROME

Clinical features:
•Flat face, large anterior fontanel, open sutures, small slanting eyes
with epicanthal folds, eye defects (refractive errors, nystagmus,
cataracts etc..); open mouth with frequent prognathism, sexual
underdevelopment, cardiac abnormalities & hypermobility of the
joints, Congenital heart diseases is commonly seen.
•Oral manifestations:
- hypoplasia of maxilla, sphenoid bones, ribs & pelvic bones
- macroglossia with protrusion of tongue, fissured tongue,
open mouth, frequent mouth breathing causes drying & cracking of
lips, palatal width is decreased & bifid uvula & cleft palate are seen
- teeth :
delayed eruption of permanent dentition, dental caries, microdontia,
enamel hypocalcification is seen, severe PDL destruction is seen
DOWN SYNDROME

TREACHER COLLINS SYNDROME
(Mandibulo-facial syndrome)
•TCS is primarily affects structures developing from 1st
branchial
arch, but also involves 2nd
arch to a minor degree
Etiology:
•TCS is transmitted by an autosomal dominant mode of inheritance
•Incidence : between 0.5 – 10 cases in 10,000 births

Clinical features:
• various degree of hypoplasia of max, mand, zygomatic process of
temporal bone, external & middle ear
•Notched or colobomas of the lower eyelid,
•Lower eye-lashes are absent
•Malformation of external ear
•Hair growth is Tongue-shaped in the region of pre-auricular area
(known as “Hair-lick”)
•Macrostomia, high palate, cleft palate & malocclusion of teeth
•Facial clefts & skeletal deformities are seen in few individuals
•Characteristic appearance are described as being “Bird like” or “Fish-
like”

Treatment:
•None
Radiography:
•Underdeveloped or complete agenesis of malar bones and
also mandible are seen
•Clefting may be seen
•Paranasal sinuses are grossly underdeveloped

MARFAN’S SYNDROME
(Marfan-Achard syndrome)
•Is a heritable disorder of connective tissue, characterized by
abnormalities of the skeletal, cardiovascular, & ocular systems
Etiology:
•MS is transmitted by an autosomal dominant mode of inheritance
•Incidence : between 0.5 – 1 case in 10,000 births
•The Marfan gene is believed to produce a change in one of the
proteins that provides strenght to a component of C.T. (probably collagen)

Clinical features:
• tall, slender stature with relatively long legs & arms, large hands
with long fingers, & loose joints
•The arms, legs & digits are disproportionately long compared with
patients trunk
•Chest deformities include a protrusion or indentation of breast bone.
•Various degree of scoliosis is present
•Face appears long & narrow
•Oral finding: narrow, high-arched palate & dental crowding
•Cardiac : Mitral valve disease,
•Ocular : dislocation of lens (ectopia lentis); myopia
MARFAN’S SYNDROME
Treatment:
•Annual medical examination & treatment of cardiac & ocular defects

PIERRE ROBIN SYNDROME
(Robin anomalad)
•It is a isolated defect (non-genetic)
Etiology:
•Incidence : between 5.3 – 22 case in 100,000 births
•Fetal malposition & interposition of the tongue between the palatal
shelves- is considered the etiology of palatal deformity
• Evidence suggests that primary defect may be due to metabolic
growth disturbances of the max & mand.

Clinical features:
•Severe micrognathia & mandibular hypoplasia
•“U” shaped cleft palate is common. (speech & feeding difficulty)
•Glossoptosis is seen (due to retropositioning of genioglossus muscle
because of retrognathic mandible)
•Airway obstruction (particularly in supine position)

Treatment:
•Multiple surgical therapy.
Micrognathia

REFERENCES
White and pharoah. Oral radiology principles and
interpretation. Diseases of bone manifested in jaws.
485-515. 5th
edition. Mosby publication.
Neville and Damm. Oral and maxillofacial pathology.
Bone pathology. Pp-533. 2nd
edition. Saunders
publication.

Shafer and levy. Oral pathology. Diseases of bone and
joints. Pp-674. 4th
edition. Elsevier publication.
Wood and Goaz. Differential diagnosis of oral and
maxillofacial lesions. Bony lesions. 5th
editon. Mosby
publication.
N. H. Sherman, V. M. Rao. Fibrous dysplasia of the
facial bones and mandible. Skeletal Radiology. 1982;
(8)2: 141-143.

Victor Perez Teixeira, Rogério Aparecido Dedivitis.
CHERUBISM: CASE REPORT AND LITERATURE
REVIEW. Rev. de Clín. Pesq. Odontol. 2004;(1)1,
Nilton Alves , Reinaldo de Oliveira. Cleidocranial
Dysplasia - A Case Report. Int. J. Morphol.
2008,26(4):1065-1068.
Saadettin Dağistan, Ümmühan Tozoğlu. Florid
cemento-osseous dysplasia: A case report. Med Oral
Patol Oral Cir Bucal 2007;12:E348-50.

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