abdul fibro osseous lessions (2).pptx

Fibro-Osseous Lesions Of
The Jaws
DEPARTMENT OF ORAL MEDICINE AND RADIOLOGY
SRI VENKATESHWARAA DENTAL COLLEGE
Dr. Abdul Khader
Senior Lecturer, OMR

• Introduction
• Definition
• Fibrous dysplasia
• Cherubism
• Paget’s Disease
• Ossifying Fibroma
• Juvenile Ossifying Fibroma
• Cemento-ossifying fibroma
• Cementoblastoma, Osteoblastoma, Osteoid osteoma
• CGCG
• Anerysmal Bone Cyst
• Osteochondroma
• Hyperparathyroidsm
• Conclusion
Contents:

INTRODUCTION
The term refers to a diverse process in which the normal architecture
of bone is replaced by fibrous tissue containing varying amount of
foci of mineralization. These group of lesions are known to
encompass common characteristics that include common clinical,
radiographic and microscopic features.
Bahl S, Sandhu S , Gupta M. Benign Fibro‐osseous Lesions Of Jaws‐ A Review. International
Dental Journal Of Student’s Research. 2012;1(2):56-68

INTRODUCTION
Histologically , these group of FOL are characterised by the
replacement of normal bone by fibrous connective tissue matrix.
The fibrous tissue displays variable features like varying degree of
mineralization in the form of woven bone or cementum like
basophilic structures which are indistinguishable from cementicles
Bahl S, Sandhu S , Gupta M. Benign Fibro‐osseous Lesions Of Jaws‐ A Review. International
Dental Journal Of Student’s Research. 2012;1(2):56-68

DEFINITION:
• Waldron described fibro osseous lesions as a group of
pathological changes with in the jaw bones in which normal
bone is replaced by fibrous tissue ,with or with out
calcification .
• Goaz & White Fibro osseous lesions are a group of
conditions that replace normal bone with benign fibrous
tissue containing variable amount of mineralization.
Waldron CA. Fibro-osseous lesions of the jaws. J Oral Maxillofac Surg. 1985 Apr;43(4):249-62.

DEFINITION:
Benign mesenchymal skeletal tumors in which mineralized
tissue, blood vessels and giant cells in varying proportions
replace normal bone.
Papadaki ME, Troulis MJ, Kaban LB. Advances in diagnosis and management of fibro-
osseous lesions.
Oral and maxillofacial surgery clinics of North America. 2005 Nov 30;17(4):415-34.

CLASSIFICATION
SYSTEMS:
• Charles Waldron Classification Of The Fibro-Osseous Lesions Of The Jaws
(1985)
• WHO Classification (1992)
• Waldron Modified Classification Of Fibro-Osseous Lesions Of Jaws (1993)
• Brannon & Fowler Classification (2001)
• WHO Classification Of Fibro-Osseous Lesions Of Jaws (2005)
• Paul M. Speight & Roman Carlos Classification (2006)
• Eversole Classification (2008)
Eversole R, Su L, ElMofty S. Benign fibro-osseous lesions of the craniofacial complex. A review. Head Neck
Pathol. 2008 Sep;2(3):177-202

Charles Waldron Classification Of The
Fibro- osseous Lesions Of The Jaws
(1985)
1. Fibrous Dysplasia
a. Monostotic
b. Polyostotic
2. Fibro-Osseous (Cemental) Lesions Presumably Arising In The Periodontal
Ligament
a. Periapical Cemental Dysplasia
b. Localized Fibro-Osseous-Cemental Lesions (Probably Reactive In Nature)
c. Florid Cement-Osseous Dysplasia (Gigantiform Cementoma)
d. Ossifying & Cemenifying Fibroma
3. Fibro-Osseous Neoplasms Of Uncertain Or Detectable Relationship ToThose
Arising In The Periodontal Ligament (Category II)
a. Cemetoblastoma, Osteoblastoma & Osteoid Osteoma
b. Juvenile Active Ossifying Fibroma & Other So Called Aggressive, Active Ossifying
/Cementifying Fibromas.

Classification system proposed by
Brannon and Fowler(2001)
I. Fibrous dysplasia
A. Monostotic
B. Craniofacial
C. Polyostotic
D. McCune-Albright syndrome (POLYOSTOTIC + ENDOCRINOPATHY)
II. Ossifying fibroma and juvenile ossifying fibroma
III. Osseous dysplasia
A. Periapical
B. Focal
C. Florid
D. Familial gigantiform cementoma
Eversole R, Su L, ElMofty S. Benign fibro-osseous lesions of the craniofacial complex. A review.
Head Neck Pathol. 2008 Sep;2(3):177-202

WHO Classification Of Fibro-Osseous
Lesions Of Jaws (2005)
1) Ossifying Fibroma (OF)
2) Fibrous Dysplasia
3) Osseous Dysplasia
a. Periapical Osseous Dysplasia
b. Focal Osseous Dysplasia
c. Florid Osseous Dysplasia
d. Familial Gigantiform Cementoma
4) Central Giant Cell Granuloma
5) Cherubism
6) Aneurismal Bone Cyst
7) Solitary Bone Cyst
Eversole R, Su L, ElMofty S. Benign fibro-osseous lesions of the craniofacial complex. A review. Head
Neck Pathol. 2008 Sep;2(3):177-202

(RECENT) Eversole Classification, 2008
I. Bone dysplasias
a. Fibrous dysplasia
i. Monostotic
ii. Polyostotic
iii.Polyostotic with endocrinopathy (McCune-
Albright)
b. Osteitis deformans
c. Pagetoid heritable bone dysplasias of childhood
d. Segmental odontomaxillary dysplasia
II. Cemento-osseous dysplasias
a. Focal cemento-osseous dysplasia
b. Florid cemento-osseous dysplasia
Eversole R, Su L, ElMofty S. Benign fibro-osseous lesions of the craniofacial complex. A review. Head
Neck Pathol. 2008 Sep;2(3):177-202

(RECENT) Eversole Classification, 2008
III. Inflammatory/reactive processes
a. Focal sclerosing osteomyelitis
b. Diffuse sclerosing osteomyelitis
c. Proliferative periostitis
IV.Metabolic Disease: hyperparathyroidism
V.Neoplastic lesions (Ossifying fibromas)
a. Ossifying fibroma NOS
b. Hyperparathyroidism jaw lesion syndrome
c. Juvenile ossifying fibroma
i. Trabecular type
ii. Psammomatoid type
d.Gigantiform cementomas
Eversole R, Su L, ElMofty S. Benign fibro-osseous lesions of the craniofacial complex. A review.
Head Neck Pathol. 2008 Sep;2(3):177-202

FIBROUS DYSPLASIA
• Term coined by Louis Lichenstein in 1938
• First described by Von Recklinghausen in 1891
Ricalde P,Magliocca KR, Lee JS. Craniofacial fibrous dysplasia. Oral and maxillofacial surgery clinics of
North America. 2012 Aug 31;24(3):427-41.

• Also known as:
i. Fibrocystic disease
ii. Osteitis fibrosa localista
iii. Focal osteitis fibrosa
iv. Fibro-osteodystrophy
FIBROUS DYSPLASIA

• Fibrous dysplasia (FD) is a nonheritable, genetic disorder
characterized by the replacement of normal bone by immature,
haphazardly distributed bony and fibrous tissues.
• The resultant fibro-osseous bone is more elastic and structurally
weaker than the original bone.
• The HALLMARK of the disease is a solitary focal, or generalized
multifocal inability of bone forming tissue to produce mature
lamellar bone, and an arrest at the level of woven bone
FIBROUS DYSPLASIA

• The cause of this disorder is a gene mutation that prevents the
differentiation of cells within the osteoblastic lineage.
• Slow –growing lesion
• Median age of onset: 9.5 years
• Cause painless swelling of
affected bone
FIBROUS DYSPLASIA

CLASSIFICATION - FIBROUS DYSPLASIA
• First classification
Monoostotic
Polyostotic
a) Jaffe’s type
b) Albright type
• Second classification( acc to STEWART)
Monoostotic
Polyostotic
Albright syndrome
Monomelic ( Involvement of bone of one extremity)
Ricalde P,Magliocca KR, Lee JS. Craniofacial fibrous dysplasia. Oral and maxillofacial surgery
clinics of North America. 2012 Aug 31;24(3):427-41.

Pathogenesis of fibrous dysplasia
(molecular basis)
• G protein consist of 3 subunits G alpha, G beta and G gamma located to inner surface
of cell membrane.
• Alpha subunit is also bound to
GDP(inactive G protein) or
GTP( active G protein).

• G protein family includes five types on basis of 5 different alpha subunits which
are as follows :
Gs ( stimulatory of adenyl cyclase)
Gi (inhibitory of adenyl cyclase)
Gq (activates phospholipase)
Gt (tranducins 1 and 2)
21

Cascade of event that results in transmission of signal:
Binding of ligand to G-protein coupled receptor
Dissociation of alpha subunit from Gbeta Ggamma
and replacement of linked to Galpha GDP by GTP
Activation of adenyl cyclase by binding to active alpha
subunit
Formation of cAMPfrom ATP.cAMPis secondary
messanger that activates intracellular proteins.

• Eventually alpha subunit unwind from adenyl cyclase and link again to GβGγ,
G protein is rendered
which is caused by hydrolysis of GTP to GDP i.e
inactive and ready to act again and repeat
cycle.
Schematic representation of the effects of Gsa mutation on adenylate cyclase
activity

Pathogenesis of fibrous dysplasia
So, overproduction of cAMP has 3 effects:
1. Hyperfunction of endocrine organs
2. Increased proliferation of melanocytes
3. Effect on differentiation of osteoblasts
thus leading to fibrous dysplasia

If the mutation occurs during early embryologic life
MULTIPLE BONE LESIONS, CUTANEOUS PIGMENTATION AND ENDOCRINE DISTURBANCES
(McCune Albright syndrome)
If the mutation occurs during later stages
MULTIPLE BONE LESIONS( POLYOSTOTIC)
If the mutation occurs during postnatallife
Affects single bone( MONOSTOTIC)
monostotic type of mutation takes place after birth, while the polyostotic type takes place during
the late stage of embryo development.

Clinical Features
• Following 4 patterns of disease are recognized :
1. Monostotic form (70-80%)
2. Polyostotic form (20-30%)
3. Craniofacial form
4. Cherubism

Monostotic fibrous dysplasia
• Equal gender distribution
Most common area involved is maxillary premolar-molar region.
• Occur in children and younger age group <10 years
• 6 times more common than polyostotic
 Leisons of maxilla extend locally to involve maxillary sinus,
zygomatic process, floor of orbit, skull base producing marked
•CRANIOFACIAL FORM
1. Ribs(28%)
2. Femur(23%)
3. Tibia
4. Craniofacial form (10-25%)
5. Humerus

Radiographic findings in monostotic
fibrous dysplasia
• 3 basic patterns may be seen:
 In one type, the lesion is generally a small unilocular radiolucency or somewhat larger
multilocular radiolucency both with well circumscibed border containing network of fine
trabeculae.

fibrous dysplasia
 In second type, the pattern is similar except that increased trabeculation rendersthe
lesion more opaque and typically mottled inappearance.

fibrous dysplasia
 Third type is a quite opaque type with many delicate trabeculae giving a ground glass or
peau d' orange appearance to the lesion. It is not well circumscribed and blends into
the adjacent normal bone.
NOTE : In all 3 types, generally cortical bone becomes thinned but seldom this bony plate is
perforated.
In CRANIOFACIAL FORM, there is characteristic roentgenographic thickening of the base of
the skull.

Histology
 Proliferation fibroblasts in compact
stroma of interlacing collagen fibres
 Irregular trabeculae scattered
throughout leison. Some trabecuale
are typically C,S shaped, JIG-SAW
PUZZLE or has chinese letter
appearance
 The trabeculae consist of immature,
nonlamellar (woven) bone without
osteoid rims or osteoblasts.

Polyostotic fibrous dysplasia
(Mccune albright syndrome)
• Involvement of two or more bones.
• M: F 1:3
• Bony sites affected in decreasing order of
frequency : Femur, skull, tibia, humerus, ribs,
fibula, radius, ulna, mandible,vertebrae.
• Polyostotic fibrous dysplasia + cafἐ au lait
pigmentation : Jaffe- Lichtenstein
syndrome.
• Polyostotic fibrous dysplasia + cafἐ au lait
pigmentation( irregular but regular in
neurofibromatosis) + multiple
endocrinopathies : McCune Albright
Syndrome.

Polyostotic fibrous dysplasia
(Mccune albright syndrome)
irregular “coast-of-Maine” café-au-lait
spots on the thorax of a fourteen-year-old
girl with McCune-Albright syndrome
• Cutaneous pigmentation in PFD
is ipsilateral to the side of bony
lesions, a feature that
differentiates pigmentation of
this disease from that in
neurofibromatosis. The location
and shape of the spots usually
can help to distinguish between
them. The spots in McCune
Albright Syndrome have jagged
borders whereas those in
neurofibromatosis are
smooth,regular

• Frequently identified deformities include
1.Coxa vara (Coxa vara is a deformity of the hip, whereby the angle between the head
and the shaft of the femur is reduced to less than 120 degrees. Normal 120-130)
2. bowing of the tibia
3.the Harrison groove (a horizontal depression along the lower border of the thorax,
corresponding to the costal insertion of the diaphragm)

Craniofacial fibrous dysplasia
• Occurs in 10-25% of patients with monostotic form and in 50% with the polyostotic
form.
• It also occurs in an isolated craniofacial form. In the isolated variety, no
extracranial lesions are present.
• It typically presents at around 10 years of age and then progress throughout
adolescence.

Craniofacial fibrous dysplasia
• Site of involvement most commonly include the frontal, sphenoid, maxillary and
ethmoidal bones. The occipital and temporal bones are less commonly affected.
• The clinical presentation depends on the site, duration, extent and nature of the
lesion.
• It ranges from a mild local swelling with little or no pain to a gross deformity.

Diagnosis of fibrous dysplaisa
 Imaging studies including conventional radiography, CT scan
and MRI
 Nuclear scitigraphy
 Biopsy
 Molecular or mutational analysis of GNAS1 gene
 Lab studies to document endocrine disturbances

Radiographic Features
upon the stage of the
 Depends
disease.
 Early onset lesions are radiolucent
and later progressively calcify,
culminating in a “Ground Glass” or
Mottled Mixed radiolucent/
radiopaque pattern.
 Critical feature to diagnosis- FD do
not have discrete margins; rather,
the lesion blends into the
surrounding normal appearing
bone.
EARLY
ADVANCED

Ground glass pattern
Cotton wool
Orange peel

CT SCAN
Ricalde P,Magliocca KR, Lee JS. Craniofacial fibrous dysplasia. Oral and maxillofacial surgery
clinics of North America. 2012 Aug 31;24(3):427-41.

MRI

SCINTIGRAPHY
 At the initial presentation,
radionuclide bone scintigraphy is
useful to demonstrate the extent
of the disease.
 Actively forming lesions in
adolescents have greatly
increased isotope uptake.
 The isotope scan shows increased
uptake throughout life, but the
uptake becomes less intense as
the lesions mature.
A 16-year-old boy with McCuneAlbright
syndrome and involvement of virtuallyall
skeletal sites (panostotic) is shown.

Differential Diagnosis
• Hyperparathyroidism may produce a similar pattern.
However, these diseases are polyostotic; bilateral; and, unlike
fibrous dysplasia, do not cause bone expansion.
• Paget ’s disease may produce a similar pattern and may cause
expansion, but it occurs in an older age group, and when it
involves the mandible, the whole mandible is involved, unlike
the unilateral tendency of fibrous dysplasia.

Differential Diagnosis
Cemeto-ossifyng fibroma trabeculae line by osteoblasts
Osteomyelitis may result in enlargement of the jaws, but the
additional bone is generated by the periosteum; therefore the new
bone is laid down on the surface of the outer cortex, and close
examination may reveal evidence of the original cortex within the
expanded portion of the jaw. Fibrous dysplasia, in contrast, expands
the internal aspect of bone, displacing and thinning the outer cortex
so that the remaining cortex maintains its position at the outer
surface of the bone. The identification of sequestra aids in the
identification of osteomyelitis.

Treatment
• Timing of intervention is based on the symptoms manifesting
as a result of the disease.
into 4
• Recommended treatment options can be divided
categories:
1. Observation
2. Medical therapy
3. Surgical remodelling/paring procedure/sculpting
procedure
4. Radical excision and reconstruction
Radiation therapy is contraindicated, as it carries the
risk of post irradiation bone sarcoma.

1. Observation:
• Monitoring is through serial radiographs, CT scans, and clinical
examinations.
• The preferred approach monostotic fibrous dysplasia and craniofacial
fibrous dysplasia is no treatment.
• If osseous contouring surgery is desired, it is ideal to defer it until
adulthood (ages 18 to 21 years) Like cherubism, fibrous dysplasia
shows less growth and its activity is reduced as adulthood
approaches. Regrowth is most commonly seen when surgeries are
performed on patients younger than 21 years
• Special attention to cranial nerve function during monitoring of these
lesions should be exercised
• Decreased nerve function may be an indication for surgical therapy.

2. Medical treatment
Currently, no medical therapy exists for the permanent
cure of fibrous dysplasia.
1. Bisphosphonates.
2. Systemic steroids

CHERUBISM
• Also called as familial
Kau CH, Souccar NM, English JD, Kamel SG, Wong ME. The surgical and orthodontic management of
cherubism in a growing child. Journal of Cranio-Maxillofacial Surgery. 2012 Apr 30;40(3):229-33.
fibrous
disseminated juvenile fibrous
dysplasia
dysplasia,
of jaws,
familial
multilocular cystic disease of jaws, familial fibrous swelling
of jaws.
• An autosomal dominant fibro osseous lesion of jaws that
stabilizes after growth period usually leaving some facial
deformity and malocclusion.
• First described by Jones in 1933.

CHERUBISM
mandibular ascending
 Classification: Arnott 1978
• Grade I – Bilaterally involvement of
rami.
• Grade II - Involvement of both maxillary tuberosities as
well as mandibular ascending rami.
• Grade III – Involvement of the whole maxilla and mandible
except coronoid and condylar processes.
 Clinical Features:
• Early childhood at the age of 2 - 4 years.
• M : F – 2 : 1

CHERUBISM
Lesion grading
Type-I
Type-II
Type-III

• Cherubic look- child assumes a cherubic facial appearance
with upward displacement of globe and exposure of scleral
rims (eye to heaven appearance).
• Swelling firm and hard on palpation and overlying mucosa
intact and non painful.

CHERUBISM
• Numerous dental abnormalities: agenesis of second and
third molars of mandible, displacement of teeth, premature
exfoliation, transposition and rotation of teeth.
• In severe cases, tooth root resorption occurs.
• Maxillary ridge involved: V shaped palate.
smooth
 Radiographic features:
• Bilateral multilocular cystic expansion of the jaws.
• Margins are well defined, well corticated and
around most of the radiolucency.

• Floating tooth syndrome: presence of numerous unerupted
teeth and destruction of alveolar bone may displace the
teeth.
• With adulthood the cystic areas in the jaws become re-
ossified results in patchy sclerosis and gives a ground glass
appearance.

 Treatment:
• The treatment of cherubism should be based on the known
natural course of the disease and the clinical behavior of
the individual case.
• Treatment of cherubism is usually conservative and into
teenage years is devoted to trying to aid in eruption of
teeth.
• Later it is directed towards cosmetic recontouring of the
affected bones, which is carried out in 3rd decade.
Miloro M, Ghali GE, Larsen P,Waite P.Peterson's principles of oral and maxillofacial surgery;
3rd edition; volume 1; PMPH-USA;2004.

PAGET’S DISEASE
• Also called as Osteitis deformans.
• Characterized by excessive and abnormal remodeling of
bone.
• Named after Sir James Paget in 1876 who described the
clinical course of the disease.
• Etiology: Still unknown.
• Possible etiology
Rajendran R. Shafer's textbook of oral pathology. Elsevier India; 2009.
suggested are: Autosomal dominant
cause,
inheritance, viral infection, inflammatory
autoimmune connective tissue disorder.

PAGET’S DISEASE
 Clinical features:
• Prevalence increases with age, most common after 50 years
of age.
• M = F
• Clinical features are variable and depends on whichbones
are affected.
• Commonly affects pelvis and spine and may also involve
femur, fibula, tibia, bones of hand and ribs.

• Most common presenting complaint is pain which is perceived as a
dull aching pain below the soft tissues.
• Other signs and symptoms are pathologic fracture, nonspecific
headache, impaired hearing, platybasia, paresthesia, gait difficulties,
enlargement of skull.
• Involvement of facial bones is occasionally seen which gives lion like
appearance called as Leontiasis ossea.
• Simian appearance: appearance and gait like apes.

PAGET’S DISEASE
• Waddling gait: short step gait.
• Maxilla: exhibits progressive enlargement, alveolar ridge
becomes widened and palate is flattened if teeth are present
they may become loose and migrates.
• Mandible: findings are similar but less aggressive than maxilla.
• Extraction sites heal slowly and risk of excessive bleeding from
extraction site.
• Osteogenic sarcoma may develop in patients with paget’s
disease- poor prognosis

PAGET’S DISEASE
 Radiographic features:
• Paget’s diseases has three radiographic stages:
 An early radiolucent resorptive stage.
 A granular or ground glass appearing second stage.
 A denser, more radiopaque appositional late stage creating
a cotton wool appearance.
• The trabeculae are altered in number and shape, most
often they increase in number but initially they decreases.
White SC, Pharoah MJ. Oral radiology: principles and interpretation. Elsevier Health Sciences;
2014 May 1.

• The overall density of the jaws may decrease or increase
depending upon the number of trabeculae.
• The isolated lesion in the skull referred to as osteoporosis
circumscripta.
• Dental changes: hypercementosis of roots, loss of lamina
dura, obliteration of PDL space and resorption of roots
White SC, Pharoah MJ. Oral radiology: principles and interpretation. Elsevier Health Sciences;
2014 May 1.

 Laboratory findings:
• Elevated serum alkaline phosphatase levels.
Normal value in adult : 1.5 – 5.0 (Bodansky units)
In Paget’s disease : 50 – 250 (Bodansky units)
• Elevated urinary hydroxyproline levels- reflects increased
osteoclastic activity and bone resorption.
• Urinary N-telopeptide (NTX) and alpha-C telopeptide (CTX)
have emerged recently as sensitive biochemical markers of
bone resorption.- Increased

 Histopathologic features:
• 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
• Characteristic picture of Paget’s disease is presence of
hematoxyphilic reversal lines. These lines indicate the junction
between resorptive & formative phases of the bone and results in
a “jigsaw puzzle” or “mosaic bone” appearance
PAGET’S DISEASE

• The marrow is replaced by fibrous connective tissue.
• Few cases show multiple small acellular bony masses that
fuse as the disease progresses.

 Treatment:
• Medical treatment consists of use of Calcitonin or
bisphosphonates to inhibit bone resorption. Calcitonin can be
taken either by nasal spray or subcutaneously and
bisphosphonates are taken orally or by intravenously.
• Surgical management is directed towards cosmetic and/or
functional recontouring of bones.
• Causes of death in patients with paget’s disease are left heart
failure and osteosarcomas.
• Sarcomatous changes has been reported in 5-15% patients with
paget’s disease.
Miloro M, Ghali GE, Larsen P,Waite P.Peterson's principles of oral and maxillofacialsurgery;

OSSIFYING FIBROMA
(CEMENTO- OSSIFYING FIBROMA)
• A well-demarcated, encapsulated, expansile intraosseous
lesion of the jaws composed of cellular fibrous tissue
containing interconnecting bony trabeculae lined by
osteblasts with spherical calcifications and irregular,
randomly oriented bony structures.
• Etiology is unknown
• 3 types: Cementifying – More of cementum
Ossifying - More of bone
Cemento-ossifying – Admixture of both

• Slow growing benign neoplastic lesion
• More often in jaws especially mandible in
90% of cases
• Site: Molar > Premolar >Incisors >Canine
region
• More common in women(5:1) in 20s or
40s but can be found in younger & older
men.
• Asymptomatic
• Can be ulcerated by occlusion when
achieves larger size
OSSIFYING FIBROMA
(CEMENTO- OSSIFYING FIBROMA)

Well defined unilocular radiolucency, mixed radiolucent
radiopaque,and radiopaque lesions.
Cortical expansion without perforation

Treatment & Prognosis
• Circumscribed nature of the ossifying fibroma generally
permits enucleation with ease.
• It shells out from the surrounding bone.
• Grown large lesions can be surgically resected and bone
grafting done.
• Very good prognosis, and no evidence of malignant
transformation till date.

JUVENILE OSSIFYING FIBROMA
• Trabecular form
– Diagnosed initially in younger patients.
– The mean age of trabecular juvenile ossifying fibromas is
approximately 11 years
• Psammomatoid – At 22 yrs of age.
– Appears outside the jaws, with over 70% arising in the supraorbital,
ethmoid and frontal bones and paranasal sinuses.

Clinical Features






In early to late childhood
Maxilla more often than mandible
In Maxilla : Canine fossa & zygomatic arch
Singular, rapid-growing, painless swelling Overgrowth
of tissue that occurs centrally in the jaws May
involve impacted or unerupted teeth
 Increased level of serum alkaline phosphatase


Severe maloccusion
Nasal obstruction, epistaxis, exophthalmous and rarely intracranial
extension.

 Unilocular or multilocular radiolucency with well defined borders.
Radiolucent or mixed radiolucent and radiopaque appearance
(ground glass)
Predominantly soft tissue consistency with varying internal
calcifications.
 Lamina dura is usually obscured and the cortical plates thinned

Treatment and Prognosis
• Management and prognosis are uncertain.
• Smaller lesions - complete local excision or thorough curettage
appears adequate.
• Rapidly growing lesions - wider resection may be required and
adjuvant Interferon alpha therapy for 1 yr.
• Recurrence rates - 30% to 58%
• Malignant transformation has not been documented.

CEMENTO OSSEOUS DYSPLASIA
• Cemento-osseous dysplasia occurs in the tooth bearing areas of the
jaws and is probably the most common fibro-osseous lesion
encountered in clinical practice
• Histopathologic features share many similarities with fibrous dysplasia
and ossifying fibroma, so correct diagnosis can be problematic
• Etiology: mesenchymal stem cells
• Arises in close approximation to the PDL and exhibits histopathologic
similarities with the PDL, and some investigators have suggested these
lesions are of PDL origin.

Clinical Type Periapical COD Focal COD Florid COD
Clinical Features •In periapical region
of mand. anterior
teeth with non-
inflammed pulps.
• Size always <1cm
• Asymptomatic
• More common
•Size less than 1.5
cm
•Associated with
vital teeth or
edentulous areas
• Asymptomatic
• Extreme variant
•Occurs in bilateral
fashion
• Asymptomatic
•Cortical expansion
can be there
•Non-neoplastic,
self limited growth
Site •Mand. anterior
teeth
• In post. mandible • Mand.>Maxilla
•May involve all 4
quadrants
Sexual Predilection •Middle aged black
women
•4th – 5th decade,
White women
• Adult black women
Associated
pathologies
•Idiopathic bone
cavity
•Idiopathic bone
cavity
• Osteomyelitis
D.D •Pulpal periapical
pathologies
•OF(Easily comes
out in big pieces)
• Osteomyelitis
• Paget’s Dis.
Treatment • No , only follow up •Biopsy and follow
up
•Reqd. if OM
develops.

Focal Cemento-osseous Dysplasia
Periapical Cemental Dysplasia

Florid Cemento-osseous Dysplasia
With Simple Bone Cysts
With Osteomyelitis

CEMENTOBLASTOMA, OSTEOBLASTOMAAND
OSTEOID OSTEOMA
• Osteoblastoma and Osteoid osteoma are recognized
neoplasms in the extragnathic skeleton
• Can be differentiated only on their clinical and radiologic
characteristics
• Cementoblastoma:
A benign, well-circumscribed neoplasm of cementum-like
tissue growing in continuity with the apical cemental layer of
a molar or premolar that produce expansion of cortical plates
and pain.

CEMENTOBLASTOMA
Clinical Features
1. usually 2nd or third decade,
2. usually before age 25
3. caucasian males most often
4. mandible in first premolar to molar region
5. pain, swelling, and expansion of the cortical plates
6. continuous with root, which resorbed

CEMENTOLASTOMA
1. radiopaque mass confluent with the roots of the associated tooth
2. surrounded by radiolucent line
3. loss of normal PDL area and root outline
4. root resorption of the apical third

OSTEOBLASTOMA
• Well-demarcated, rounded intraosseous swellings, each with an
active cellular central nidus surrounded by a wide zone of
osteoid, with pain upon palpation.
• Slight posterior mandibular predilection
• Slight male predominance
• Painful or tender
• Size: 2-12cm

 Well circumscribed round solitary lesion expansile
 Mixed radiolucent radiopaque lesion not surrounded by sclerotic bone
OSTEOBLASTOMA

OSTEOBLASTOMA
Treatment
 local excision or curettage
 A large surgical enbloc removal for large lesions
Prognosis
 Good
 May recur
 Transformation in to osteosarcoma

OSTEOID OSTEOMA
• Benign neoplasm of bone that arises from osteoblasts with similar
clinical, radiographic, and histopathologic features of other two
entities.
Clinical Features:
– mostly before age 25
– more often in males
– Swelling 1-2 cm
– dull or aching pain (relieves with aspirin). Pain due to
intralesional prostaglandins level.
– more in long bone and infrequent in jaws

Radiographic
Features
Sclerotic bone surrounding a radiolucent core
Peripheral radiopacity well demarcated
Treatment
local excision or curettage
Prognosis
Good
Few chances of recurrence

CENTRAL GIANT CELL GRANULOMA
• Central Giant Cell Granuloma (CGCG), first described by Jaffe
(1953)
• Benign lesion accounting for approximately 7% of all benign
tumours of the jaws (Tosco et al., 2009).
• The site most frequently involved is the
anterior part of mandible
• Females under 30 years of age.
• True biologic nature of the lesion is not
known.

• Clinical features :
• Aymptomatic slow growing swelling to
a tender aggressive lesion that cause
local bone lysis, root resorption or
tooth displacement
• CGCGs are classified into aggressive
and nonaggressive lesions based on
their biological behaviour, assessed by
the presence of pain, rapid growth,
perforation of the cortex, and a
tendency to recurrence

• Histologically
• CGCG shows an intraosseous lesion consisting of fibro-cellular
tissue.
• It contains multiple foci of haemorrhage, aggregations of
multinucleated giant cells, and occasional trabeculae of
woven bone.
• The origin of this lesion is unknown but it is assumed to be
triggered by trauma or inflammation.
• Radiologically
– Multilocular or less frequently unilocular Radiolucency
– Margins : Well Demarcated / Scalloped border
– Expansion and thining of cortices is noted

Treatment
• The conventional treatment curettage.
• Non-surgical methods
– Systemic administration of calcitonin
– intra-lesional corticosteroids (introduced by
Jacoway et al.)
– administration of a-interferon
• En-bloc resection is the treatment which
provides the lowest recurrence rate and has
been suggested as the treatment of choice for
locally aggressive CGCGs.
Miloro M, Ghali GE, Larsen P,Waite P.Peterson's principles of oral and maxillofacial
surgery;

ANUERYSMAL BONE CYST
• Aneurysmal bone cyst (ABC) has been recognized since 1893 when
it was described as an ossifying hematoma by Van Arsdale
• Jaffe and Lichtenstein were the first to recognize ABC as an
intraosseous, osteolytic lesion, chiefly affecting the metaphyseal
region of long bones and vertebrae.
• Bernier and Bhaskar described the first case of ABC in the jaws in
1958
• ABC is a benign cystic lesion of bone, composed of bloodfilled
spaces separated by connective tissue septa containing fibroblasts,
osteoclast type giant cells and reactive woven bone

• It accounts for 1.5% of the nonodontogenic, nonepithelial
cysts of the mandible.
• Mandible > Maxilla (3:1)
• Body > Ramus >Angle.
• Age >20yrs M=F
• The ABC of the jaw is a psuedocyst lacking epitheliallining.
• It consists of 5% of all the craniofacial lesions
• Most common in those regions of the skeleton where there is
both a relatively high venous and marrow content.

Conventional /Vascular Solid Mixed
95% (5%) demonstrates features of
both the vascular and
solid types.
rapidly growing
expansive
destructive
lesion
A small asymptomatic
lesion
may be a transitory phase
of the lesion because
sudden activation or rapid
enlargement of stable
lesions ha been reported
Causes cortical perforation first noticed as
and soft tissue invasion. radiolucency on a routine
radiograph or as a small
swelling.
Miloro M, Ghali GE,
Larsen P,
Waite P. Peterson's principles
of
oral and maxillofacial surgery;

 Hernandez et al. classified ABC as primary and secondary.
a)Primary :-1) Congenital 2) Acquired and could originate from
preexisting A V malformations.
 The congenital type is seen in children and young adults with no
history of trauma, whereas the acquired type is found in adults with a
history of trauma.
 b)Secondary : associated with degeneration of preexisting lesions
such as a cyst, tumor or fibrosseous lesion. The two lesions could exist
independently.

• The radiological features of ABC
• Bone is expanded
• Appears cystic resembling a
honeycomb or soap bubble and is
eccentrically ballooned.
• There may be destruction or perforation
of the cortex
• It may appear radiolucent, radiopaque
or mixed.

Treatment
• The treatment modalities are percutaneous
sclerotherapy, diagnostic and therapeutic
embolization, curettage, block resection and
reconstruction, radiotherapy and systemic calcitonin
therapy.
• Self healing cases have also been reported
• Several authors recommend immediate
reconstruction of the defect with autogenous grafts
in cases of esthetic deformity, high risk of fractures
and loss of mandibular continuity.
• Simple curettage recurrence rates varying from 21 to
50%.
• Motamedi et al stated initial resection is not necessary
and have not noted any recurrences following surgical
curettage of mandibular lesions.

OSTEOCHONDROMA
• Osteochondroma or osteocartilaginous
exostosis is characterized by a cartilage-
capped osseous projection protruding
from the surface of the affected bone.
• Although incidence in the general
population is reported as 1%, it may
increase up to 10% with local irradiation
induced osseous changes and up to 23%
with total body irradiation.
• It occurs in adolescence or young
childhood, with 80% of cases being in first
2 decades of life.
• M:F =1:1

• It is considered the most common tumor of the axial skeleton,
comprising 35.8% of benign tumors
• The usual location -distal metaphysis of the femur or the proximal
metaphysis of the tibia
• Various theories of etiopathogenesis have been proposed. However,
most accepted is the Lichtenstein theory, which says that the
periosteum has the potential to develop osteoblasts and chondroblasts
and that osteochondroma develops by metaplastic change in the
periosteum. What triggers this metaplastic change is not known
• Majority of osteochondromas in the craniofacial region occur in
mandibular areas such as the condylar process, coronoid process and
symphysis
Miloro M, Ghali GE, Larsen P,Waite P.Peterson's
principles of oral and maxillofacial surgery; 3rd edition;
volume 1; PMPH-USA; 2004.

• Osteochondromas arising from the jaw may
present as an asympotomatic bony hard
swelling
• If present in the condylar region may produce
– Unilateral open bite
– Chin deviation
– Facial asymmetry
• R/F
– Sessile /pedunculated lesion
– Continuous with the adjacent cortex and
medullary spaces
– Well defined radio-opacity
Miloro M, Ghali GE, Larsen P,Waite P.Peterson's principles of oral and
maxillofacial surgery; 3rd edition; volume 1; PMPH-USA; 2004.
OSTEOCHONDROMA

Treatment and Prognosis
• Conservative approach /
Surgical Excision
• Recurrence rarely reported
Miloro M, Ghali GE, Larsen P,Waite P.Peterson's principles
of oral and maxillofacial surgery; 3rd edition; volume 1;
PMPH-USA; 2004.

CONCLUSION
Despite recent advances in the understanding of the natural
history and molecular abnormalities, many questions remain
surrounding the progression and management of Fibro-osseous
lesions. In the absence of comorbidities such as GH excess or
secondary disorders, the expected behaviour of FOL is slow
growing and without functional consequence.

In order to optimize patient care, understanding of the
pathophysiologic mechanisms contributing to the various
phenotypes of these condition, as well as the predictors of the
different behaviours of FO lesions, must be improved. The
importance of long-term follow-up of patients with FOL cannot
be overstated because spontaneous recovery is unlikely, and the
course of disease can be unpredictable.
CONCLUSION

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