This document provides information on fibro-osseous lesions. It begins with definitions and classifications of fibro-osseous lesions. It then focuses on fibrous dysplasia, the most common fibro-osseous lesion. Fibrous dysplasia is a skeletal developmental anomaly caused by a mutation that results in abnormal bone formation. It can be monostotic, affecting a single bone, or polyostotic, affecting multiple bones. Radiographs show poorly defined lesions blending into normal bone with abnormal trabeculae. Histologically, there is replacement of bone by proliferating fibrous tissue and irregular bony trabeculae.

1. FIBRO OSSEOUS LESIONS
DAVIS NADAKKAVUKARAN

2. Contents
• Introduction
• Classifications of fibro-osseous lesions
• Fibro-osseous lesions in detail (etiology,
clinical features, radiographic features,
histopathology, investigations, differential
diagnosis and management )
• Conclusion
• Referencess

3. Introduction

4. Definition By - IAOMP
Fibro-osseous lesions of the jaws are a group of bone disorders where there is a
replacement of normal bone by tissue comprising collagen fibres and
fibroblasts, containing varying amounts of mineralized substance which may be
osseous or cementum-like in appearance. The lesions are essentially benign.
Frankly malignant lesions (e.g. osteosarcoma) showing osteoid/ cementoid are
not included in this category.
Definition by WHO, 2005
 A collection of non- neoplastic intra osseous lesions that replace normal bone
and consists of a cellular fibrous connective tissue within which nonfunctional
osseous structures forms.

5. CHARLES.A.WALDRON (1985)
1.Fibrous dysplasia
a.monostotic
b.polyostotic
2.Fibro osseous lesions of PDL origin
a. ossifying fibroma
b. cementomas
i) periapical cemental dysplasia
ii) benign cementoblastoma
iii) cementifying fibroma
iv) gigantiform cementoma
c. fibro cemento osseous of reactive
origin
d. juvenile active ossifying fibroma
3. Fibro osseous lesions of medullary
origin
a. Familial/genetic origin – Cherubism
b. Tumors
i) cementoblastoma
ii) osteoid osteoma
iii) osteoblastoma
iv) osteoid fibroma
c. unknown origin
i) pagets disease
ii) aneurysmal bone cyst
iii) few giant cell lesions
iv) brown tumors of hyper –
-parathyroidism

6. IAOMP ( Indian Association of Oral & Maxillofacial Pathologist )
CLASSIFICATION
• Developmental/Hereditary
Cherubism
Gigantiform cementoma (Florid
osseous dysplasia)
• Reactive/Reparative
Traumatic periosteitis
Garre's osteomyelitis
Sclerosing osteomyelitis (focal and
diffuse)
Central giant cell granuloma
Osseous keloid
Periapical cemental dysplasia
Aneurysmal bone cyst
• Neoplastic
Osteoma
Osteoid osteoma
Osteoblastoma
Ossifying fibroma
(periodontoma, fibro-osteoma)
Juvenile ossifying fibroma
(aggressive periodontoma)
• Metabolic
Brown tumor
• Idiopathic
Fibrous dysplasia
Pagets disease of bone
• Solitary bone cyst

7. Based on WHO 2005 , WALDRON 1993, NEVILLE et al 1995

8. FIBROUS DYSPLASIA
Definition:
Skeletal developmental anomaly of the bone forming mesenchyme
that manifests as a defect in osteoblastic differentiation and
maturation .
History
• First described by von Recklinghausen in 1891
• Elaborated by Lichtenstein in 1938 and by Lichtenstein and Jaffe in
1942

9. Types
1. Monostotic
2. Polyostotic
- Polyostotic with pigmentation….(Jaffe)
- Polyostotic with pigmentation & endocrine
dysfunctions
(Mc-cune Albright).
- Cranio facial fibrous dysplasia

10. Etiopathogenesis
• Abnormal bone reaction to a localized traumatic episode
• Altered bone expression in response to altered endocrine disturbance
• The disease is caused by a post zygotic somatic mutation of GNAS1(guanine
nucleotide-binding protein, a-stimulating activity polypeptide 1) gene (chromosome
20) that codes for a type of intracellular signaling protein called Gsα.
• Mutated Cells with the Gsα have high cAMP level that result in abnormalities
in osteoblast differentiation .
• These cells produce the osteoclast activating proteins (unscheduled bone
resorption) that, in turn, trigger bone formation out of order. There is also an
increase in IL-6- induced osteoclastic bone resorption.
• Normal medullary bone is replaced by abnormal fibrous connective tissue
proliferation.
• osseous matrix that presumably arises through metaplasia and consists only of woven
bone.
• Arrest of bone development in woven bone stage with failure to mature to lamellar bone.

11. Monostoticfibrous dysplasia
• Common in children and young adults.
• M = F , or mild female predom.
• Diagnosed - 2ND decade of life.
• Limited to a single bone - 70% to 80% of all cases.
• Any bone of skeleton, lower limbs & jaws are most commonly affected, than
ribs and cranial bones.
• Less amount of bone deformity present.
• Growth stops at the end of puberty and may again get aggravated at pregnancy.
• Associated with pain and pathologic fractures

12. • Maxilla > mandible. 2:1 , posterior , bilateral
• Mandibular lesions are truly monostotic.
• Maxillary lesions not strictly monostotic- not well circumscribed -zygoma,
sphenoid, orbit and even base of skull and occiput and sinus .
• Painless , slow growing swelling . Bulging of labial and buccal plate , lower
border of mandible . Bulging of canine fossa or extreme prominence of
zygomatic process.
• Overlying mucosa is always intact .
• Malignment, tipping or displacement of teeth. Associated with pain and
pathologic fractures

13. • First recognized case by Weil in 1922
• More common in First decade of life.
• Females more affected.
• 75% of skeletal bones
• Involvement of two or more bones. A relatively uncommon condition. account
for 20-30 % of all cases, has a aggressive nature deformity.
• Unilateral or bilateral Lesion occurs in bone of limb (particularly lower).
• Seen in femur, tibia, pelvis, ribs, skull and facial bones, upper extremity, lumbar
spine, clavicle, cervical spine.
• When upper limb are affected, there may be one or more skull lesions as well.
Polyostotic fibrous dysplasia
• Symptoms related to long bone lesions…pathologic # ,bowing ,
thickening, leg length discrepancy ( hockey stick deformity)

14. Fairbank et al
– 1/3rd of cases without cutaneous pigmentation.
– 2/3rd of cases with cutaneous pigmentation.
Cutaneous pigmentation in 50%, usually ipsilateral to bone lesion.
• Oral picture – facial asymmetry , disturbed eruption pattern, deformed bony
tissue.
• Two variants known
Polyostotic FD + Café au lait pigmentation - Jaffe-lichtenstein syndrome
Polyostotic FD + Café au lait pigmentation+ Multiple endocrinopathies - Mc
Cune Albright syndrome.

15. Jaffe-Lichtenstein syndrome
• Polyostotic fibrous dysplasia involving variable
number of bone although most of the skeleton
normal when seen with café au lait (coffee with
milk) pigmentation.
• The café au lait pigmentation consists of well-
defined, generally unilateral tan macules on the
trunk and thighs.
• These pigmented lesions may be congenital, and
intra oral pigmented macules also may be present.
• The margins of the café au lait spots are typically
very irregular. like a coast line of Maine

16. McCune-Albright syndrome
• Fuller albright in 1937.
• Due to postzygotic acitivating mutation of GS-alpha gene
• Almost exclusively affects female
• Severe Polyostotic fibrous dysplasia nearly involving all bones in skeleton
accompanied by café au lait pigmentation and multiple endocrinopathies,
such as precocious puberty, acromegaly, hyperthyroidism,
hypophosphatemic rickets., accel skeletal growth .
• Patient may have hepatic, cardiac and GI dysfunction
• Mazabraud’s Syndrome – association with intra muscular myxomas

17. Cranio-facial fibrous dysplasia
• Occurs in 10-25% with monostotic form and in 50% of patient with polyostotic
form….may also occur as a separate entity
• Sites include – frontal, sphenoid, maxillary and ethmoid. The occipital and
temporal bones are less commonly effected
• Hypertelorism, cranial asymmetry, facial deformity, visual impairments,
exopthalmus, blindness – orbit and periorbital bone.
• Vestibular dysfunction, tinnitis and hearing loss – sphenoid wing and temporal
bone.
• Hyposmia and anosmia – cribrifoirm plate

18. Radiographic features
Location
• 2:1 maxilla to mandible ratio
• More frequent in posterior
• Lesions are usually unilateral
Shape and Borders
• Usually poorly defined, with the lesion gradually blending into
the normal trabecular Pattern- hallmark

19. Internal Architecture
Worth 1963
Radiolucent
• Oval RL 2-5 cm in dia – thin ill defined borders
• As the lesion matures dysplastic bone trabaculae increase in number and
size. The radiolucent appearance changes to smoky mottled radio opacity.
• Unicystic RL with sclerotic margins – thin / wide , granular
• Unicystic RL with out sclerotic margins - Punched out / ill defined
• Multilocular – few , wispy OR coarse , thick -
Mature
Homogeneous dense sclerotic area

20. Radiographic appearances may simulate Terms .
• Ground glass- new bone takes form of very small opacities of poor density
• Orange peel - alternating areas of granular densities
• Thumb print- mandible , vertical deapth of mand is increased , inferior border is
ribbon like , smooth down ward curve of inf border , as if soft bone has been
pressed by thumb
• Pagetoid type – Marked expansion , alternate areas of RO & RL
• Cotton wool
• Worm like - peculiar pattern ( WORTH 1963) D D
Appearance due to replacement of fibrous tissue by trabeculae of approximately
equal size.
The lesion may contain a central lucent area that is analogous to a simple bone
cyst
Mixed

21. Cotton wool apperance

22. Striking apperance

23. Effects on adjacent structures
• Small lesions are entirely contained in the bone
• Skull and facial bones – frontal bone commonly involved with oblitration of
sphenoidal , maxillary & frontal sinus, single or multiple, symmetrical or
asymmetrical , radiolucent or sclerotic.
• Max-mand present with mixed radiopaque and radiolucent pattern with
displacement of the teeth and distortion of the nasal cavity.
• Expansion & thinning of cortical plate in buccal & distal aspect , bulging of
lower border - with no perforation, no root resorption, root displacement .
• Superior & lateral displacement of the inferior alveolar canal maybe seen .- dd

24. Histopathological features
• Histologically FD reveals presence of highly cellular fibroblastic stroma &
proliferating fibrous connective tissue that replaces the normal bone.
• Multiple, coarse, irregular bony trabaculae are distributed within the
fibrous tissue.
• The bone trabaculae are delicate and are not connected to one another.
They resemble curvilinear shapes resembling Chinese script writing.

25. Lab findings
• No significant changes in the total serum calcium
• Serum alkaline phosphatase mildly increased
• Elevated level of pitutary follicle-stimulating hormone
• Elevated BMR

26. Differential diagnosis
• Chondrosarcoma
• Osteosarcoma
• Pagets disease
• Cemento ossifying fibroma
• Traumatic bone cyst
• Browns tumor
Chronic osteomyelitis

27. Malignant transformation
• Common in skull and facial bones in monostotic and femoral bone in
polyostotic
• 0.4-1% Malignant transformation has been reported
• Osteosarcoma, chondrosarcoma, fibrosarcoma, liposarcoma

28. Treatment
• Conservative and primarily to prevent deformity
• Correct any underlying endocrinopathies
• Vitamin D and Bisphosphonate therapy (after ephysial closure)
• Surical management – curretage and replacement of bone defect with
autograft or allograft
• Cosmetic correction by bone shaving
• The regrowth is more common in younger patients, surgical intervention
should be delayed for as long as possible.
• Radiation therapy for fibrous dysplasia is contraindicated because it
carries the risk for development of postirradiation bone sarcoma.

29. Management:
•
• Surgical management includes contour excision or enbloc resection
with or without grafting.
• Contour excision :- patients with quiescent and non-aggressive
lesions that have observed no growth over at least 1 year.
• Contour resection :-aesthetic deformities or functional problems
like paresthesia, trismus, proptosis, pain.
• Enbloc resection is reserved in patients with aggressive lesions that
may compress nerves, airway or in cases with recurrence.
• Bisphosphonates – IV – pamidronate – for 3 days every 3 – 4
months.
• - oral – aldendronate.

30. PAGET’S DISEASE
Synonyms: Osteitis deformans
Paget’s disease of bone is characterized by excessive osteoclastic bone
resorption in a focal area that is accompanied by an increased osteoblastic
bone deposition. This abnormal resorption and deposition of bone results in
weakened and distorted architecture of bone.
History: Was first described by Sir James Paget in 1877
Rhodes B and Jawad ASM suggested it as a disorder in bone turnover
Etiology: The cause of Paget's disease is unknown, but inflammatory, genetic, viral
and endocrine factors may be contributing agents

31. Progression of disease
SCLEROTIC PHASE
INTERMEDIATE PHASE
LYTIC PHASE

32. Clinical features
• Affects people over 40 years of age with a male
predilection.
• Common sites involved are the bones of the axial skeleton
spine, pelvis, sacrum, femur and the skull.
• Bone pain perceived as a dull constant aching pain, deep
below the soft
tissues. It may persist or exacerbate during nights.
The involved bones become warm to touch because of
increased vascularity.
• Softened base at the base of the skull may lead to platybasia, the descent of the
cranium on to the cervical spine.

33. Investigations :
- Elevated serum alkaline phosphatase levels.
- Thyroid function tests: including
triiodothyronine (T3), thyroxine (T4),
and thyroid- stimulating hormone (TSH)
levels
- Pituitary gonadotropins and gonadosteroids

34. Oral manifestations:
Maxilla is more commonly affected. The
involved jaw will be enlarged.
Enlarged maxilla will cause widening of the
alveolar ridge and flattening of the palatal
vault.
If teeth are present, they may become loose and
migrate, producing some spacing.

35. Radiographic features
• An early radiolucent resorptive stage
• A granular or ground-glass-appearing second
stage characterised by irregular areas of patchy
osteosclerosis with radiolucency and radiopacity.
• A denser, more radiopaque appositional late
stage when the trabeculae may be organized into
rounded, radiopaque patches of abnormal bone,
creating a cotton-wool appearance.

36. Radiographic features
Effects on surrounding structures:
• Prominent pagetoid skull bones may swell to
three or four times their normal thickness. In
enlarged jaws the outer cortex may be
thinned but remains intact.
• The lamina dura may become less evident.
Often hypercementosis develops on a few or
most of the teeth in the involved jaw.

37. Investigations
• Serum alkaline phosphatase may show very
high values.
• Urinary excretion of the deoxypyridinolone
and N-telopeptide of type 1 collagen are
elevated.
• Alpha- type 1C –telopeptide fragments are
sensitive markers of bone resorption

38. Management
• When symptomatic, bone pain is noted most frequently and often may be
controlled by aspirin or other analgesics. Use of parathyroid hormone
antagonists, such as calcitonin and bisphosphonates, can reduce bone
turnover and improve the biochemical abnormalities.
Commonly prescribed drugs and dosages:
• Calcitonin (Miacalcin injection), Calcitonin-salmon (Calcimar) 200 U per
mL; 100 U subcutaneously or intramuscularly once daily for six to 18
months.
• Alendronate (Fosamax) 40 mg orally once a day for six months.
• Tiludronate (Skelid)400 mg daily for three months.
• Risedronate (Actonel) 30 mg daily for two months.
• Etidronate (Didronel) 5 mg per kg per day

39. Developmental Fibro-osseous
Lesions

40. Gigantiform Cementoma
Is a uncommon hereditary disorder of gnathic bone that ultimately
leads to the formation of massive sclerotic masses of disorganized
mineralized
material.
History:
• It was first described by Norberg in 1930
• In 1971, WHO classified gigantiform cementoma in the category of
cemental lesions.
Etiology: Autosomal dominant disorder that
demonstrates high penetrance and variable
expressivity. Both familial and sporadic occurrence
has been reported.

41. Clinical features:
• The lesions are usually seen in younger age with no sexual
predilection.
• They typically present as a slow growing, multifocal/
multiquadrant, and expansile lesions involving both the
jaws.
• The characteristic clinical manifestation is of a maxillary
and mandibular swelling with associated facial deformity.
Tooth impaction, malposition, and malocclusion of the
involved dentition were also reported.
If not treated, the osseous enlargement eventually ceases
during the fifth decade.

42. Radiographic features: Multiple, circumscribed,
expansile, mixed
radiolucent-radiopaque lesions that usually cross
the midlines of the jaws.
With further maturation, the lesions become
predominantly radiopaque but often maintain a
thin radiolucent rim
Management: Extensive resection of the altered bone
and reconstruction of the facial skeleton and
associated soft tissues have been recommended

43. Complications
• Chronic osteomyelitis – Shafer 1957
• Traumatic bone cyst – obstruction to drainage
of interstitial fluid due to fibro osseous
proliferation
Precautions
• Avoid use of tissue borne prosthesis / trauma
to alv ridge
• Avoid exposure of cemental mass – biopsy/
elective extraction

44. Cherubism
Synonyms: Familial fibrous dysplasia of the jaws, disseminated
juvenile fibrous dysplasia, familial multilocular cystic disease of the
jaws,
familial fibrous swelling of the jaws, bilateral giant cell tumour.
History:
• First described by Jones in 1933.
• The name cherubism was applied to this condition because the
facial
appearance is similar to that of the plump-cheeked little angels
(cherubs)
depicted in Renaissance paintings.
Etiology: Inherited as an autosomal dominant trait
with high penetrance but variable expressivity. The
locus for the cherubism gene is 4p 16.

45. Clinical features
• It affects children in the age range of 2 - 5 years.
• The cherub like facies arises from bilateral involvement
of the posterior mandible that produces angelic
chubby cheeks. In addition, there is an "eyes upturned
to heaven" appearance that is due to a wide rim of
exposed sclerae noted below the iris.
• The jaw lesions are usually painless, symmetric, and
have florid maxillary involvement. The lesions which
are firm to palpation and nontender, most commonly
involve the molar to coronoid regions.

46. Clinical features
On occasion, affected patients also reveal marked cervical lymphadenopathy.
The mandibular lesions typically appear as a pain less, bilateral expansion of
the posterior mandible that tends to involve the angles and ascending rami.
The clinical alterations typically progress until puberty, then stabilize and
slowly regress
Noonan’s syndrome – Cherubism, gingival fibromatosis, a lesion in the
humerus,, psychomotor retardation, orbital involvement and obstructive
sleep apnoea.

47. Grading system:
Arnott in 1978 suggested grading system for the
lesions of cherubism
• Grade I: Involvement of both mandibular
ascending rami.
• Grade II: Involvement of both maxillary
tuberosities as well as the mandibular ascending
rami.
• Grade III: Massive involvement of the whole
maxilla and mandible except the coronoid
process and condyles.Oral manifestations:
Extensive bone involvement causes a marked widening and distortion of the
alveolar ridges. These
enlargements may cause agenesis of the second and third molars of the
mandible, tooth displacement,
premature exfoliation of the primary teeth, delayed eruption of the
permanent teeth, transpositions and

50. Radiographic features:
• Location: This lesion causes bilateral multilocular
cystic expansion of the jaws. The epicenter is
always in the posterior aspect of the jaws, in the
ramus of the mandible, or the tuberosity of the
maxilla.
• Periphery: The periphery usually is well defined.
• Internal structure: The internal structure consists
fine, granular ,wispy trabeculae forming a
prominent multilocular pattern.

51. Effects on surrounding structures: Jaw expansion in maxillary lesions may
extend into the maxillary sinuses. Because the epicenter is in the posterior
aspect of the jaws, the teeth are displaced in an anterior direction.
Numerous unerupted teeth &destruction of the alveolar bone may displace the
teeth, producing floating tooth syndrome. With adulthood, the cystic areas in
the jaws become re-ossified, which results in irregular patchy sclerosis.

52. Management
The condition is self limiting and generally
regresses by puberty. After skeletal growth
has stopped, conservative surgical procedures,
if required, may be done for cosmetic
problems. Surgery also may be required to
uncover displaced teeth, and orthodontic
treatment may be needed

53. • Cherubism is expected to regress spontaneously,
operative treatment may not be necessary.
• Management in most of the cases consists of
longitudinal observation.
• Surgical intervention include severe esthetic or
functional problems, such as airway obstruction.
• Surgical contouring during growth – rapid
regrowth, malignancies, few favorable results.
• Radiation therapy is contraindicated.

54. Reactive/ reparative
fibro-osseous lesions

55. Central giant cell granuloma
Synonyms: Giant cell granuloma, giant cell tumour
In 1953 Jaffe introduced the term giant cell reparative granuloma

56. Clinical features
• Most cases arise in those less than 30 years of
age with female predominance.
• Approximately 70% arise in the mandible.
Lesions are more common in the anterior
portions of the jaws, and mandibular lesions
frequently cross the midline.- Nonaggressive lesions exhibit few or no
symptoms, demonstrate
slow growth, and do not show cortical
perforation or root resorption
of teeth involved in the lesion.
- Aggressive lesions are characterized by pain,

57. Radiographic features
Effects on surrounding structures:
Giant cell granulomas often displace and resorb teeth. The lamina dura
of teeth within the lesion usually is missing. The inferior alveolar canal
may be displaced in an inferior direction. This lesion has a strong
propensity to expand the cortical boundaries of the mandible and
maxilla.

58. Management:
• Curettage and surgical excision.
• In patients with aggressive tumors, the role of
corticosteroids, calcitonin, and interferon alfa
is being investigated as an alternative to
surgery.
• Intralesional triamcinolone injections were
also employed successfully.

59. Osseous dysplasias (OD)
• Benign fibro osseous lesions of the jaws closely associated
with the apices of teeth and containing amorphous spherical
calcifications thought to resemble an aberrant form of
cementum: lesions are usually without signs and symptoms.
WHO,2005

60. Introduction
• Cemental lesion , Represent a single disease process
• Classified byWHO 1971
Origin
• Because cemento-osseous dysplasia arises in close approximation to the
periodontal ligament and exhibits histopathologic similarities with the
structure, some investigators have suggested these lesions arer eactive lesion
derived from odontogenic cells in the periodontal ligament.
• Only occurs in jaws – Pdl
• Others believe cemento-osseous dysplasia represents a defect in
extraligamentary bone remodeling that may be triggered by local factors and
possibly correlated to an underlying hormonal imbalance.

61. Classification ( clinical radiologic )
WALDRON
• 1. Periapical COD
• 2. Focal COD
• 3. Florid COD
R.J MELROSE
NON HERIDITARY
• PCOD
• FCOD
• FLOD
HERIDITARY
• Familial gigantiform
cementomas

62. Periapical cemento-osseous dysplasia
• WHO DEFINITION, 2005
“ A non neoplastic lesion affecting the periapical tissues of one or
more teeth and with histologic features similar to those of
cementossifying fibroma group but with out a sharply defined
margin.”
• Also known as cementoma, fibrocementoma, sclerosing
cementoma, periapical osteofibrosis, or periapical fibro osteoma.

63. PERIAPICAL CEMENTO-OSSEOUS DYSPLASIA
• F > M (10:1 )
• Approximately 70% of cases affect blacks.
• Age - 30 to 50 years, never under 20 years.
• Predominantly - periapical region of the anterior mandible.
• Asymptomatic - discovered when radiographs are taken for other purposes.
• Teeth - vital and seldom have restorations.
• Duration – 6-10 yrs

64. Radiographic feature
Location
• Apices of mandibular anterior teeth
• Multiple or solitary
Shape and Borders
• Commonly - Round, oval, rarely - irregular shape
• May have a sclerotic border
Internal Architecture
• Varies from lucent to mixed density to opaque as the lesion matures
• With time, adjacent lesions often fuse to form a linear pattern of radiolucency
that envelopes the apices of several teeth.
• The periodontal ligament is intact, and fusion to the tooth is not seen.
• Individual lesions seldom exceed 1.0 cm in diameter.
• Each lesion is self-limiting and does not typically expand the cortex.

65. • Acc toTHOMA - 3 stages of development
1. Osteolytic / Radiolucent
0.5-1cm R L lesions, spreads laterally as it enlarges
-well demarcated sclerotic rim – thick, irregular, diffused
- loss of lamina dura at root apex
2. Cementoblastic/ Mixed
Target appearance- prominent RL area + radiodense cemental
mass at centre .
- sclerotic rim – active lysis of host bone
3. Mature inactive/ Radiopaque
Dense mass uniformly radiopaque, - 1.5 cm
, smooth margins .

66. Effects on adjacent structures
• May resorb the lamina dura of adjacent teeth
• Root resorption is rare
• Occasionally, large lesions may cause expansion of the jaws
• Edentulous- Arises De novo/ Present before extraction
- only lesion to produce a a cresent RO mass
• Association with Traumatic Cyst ( L & L )

67. • Called as – gigantiform cementoma , Chronic sclerosing
osteomyelitis , sclerotic cemental mass , multiple exostosis .
• 1st defined – Bhaskar & Curight 1968
• Term – Waldron 1985
• Acc to L & L – FLOD is simply a more advanced stage of PCOD
in people predisposed to its development .
FLORIDCEMENTO-OSSEOUSDYSPLASIA

68. Clinical Features
• Sex - F > M ( 33: 1 ) , ( Middle aged black women)
• Age – 5 th decade
• Site – Mand > max , Multile teeth, three or more quadrants.
• Marked tendency for bilateral and often quite symmetric involvement
• Asymptomatic - radiographs are taken for some other purpose.
• Symptomatic –- dull pain , swelling ,ulcer , pale yellow sequestration -
because of alveolar atrophy under denture , extraction , biopsy - infection –
osteomtelitis . (hypovascular and prone to necrosis with minimal
provocation.)
• Large lesions may expand the cortices
• Tendency – Traumatic bone cyst

69. Radiographic feature
Matured & generalised manefestation of PCOD
Location
• Often bilateral, ant & post , dentulous & edentulous
• Often present in both jaws- Alveolar processes
• More common in mandible- vertical ramus & inferior cortex of mandible
spared
Shape and Borders
• Irregularly, Well-defined sclerotic border
• Soft tissue capsule may disappear in longstanding inactive lesions
Internal Architecture
• Varies from mixed opaque/lucent to completely opaque
• Opacities may have a cotton wool appearance / ground glass

70. • Management:
• Asymptomatic patient, the best
management consists of regular recall
examinations with prophylaxis and
reinforcement of good home hygiene care
to control periodontal disease and prevent
tooth loss.
• Symptomatic - Surgical removal of the
exposed cemental masses.

71. FOCAL CEMENTO-OSSEOUS DYSPLASIA
• Until the mid-1980s. misdiagnosed as a variant of ossifying fibroma.
• Summerlin & tomich 1989
• Females. ( 8 : 1 )
• Predilection for the third to sixth decades. Mean age of 38.
• Higher percentage in whites.
• Site : Single site of involvement., vital teeth
Posterior mandible > maxilla > ant mand ( canine )
• Typically asymptomatic and is detected only on a radiographic examination.
• Most lesions are smaller than 1.5 - 2 cm in diameter, no expansion
• R /G – same phases of PCOD – post variant

72. OSSIFYING FIBROMA
(CEMENTIFYING FIBROMA; CEMENTO-OSSIFYING FIBROMA,)
• A benign osteogenic, well demarcated neoplasm composed of calcified
material and a fibroblastic stroma, which may be very cellular
• Montgomery 1st described jaw lesions of such type- 1927
Makek 1983- Benign periodontoma
 Its a true neoplasm with a significant growth potential. In reality true
ossifying fibroma are relatively rare.
• Although lesion contain variety of minearalized structure but the same
progenitor cell produces the different materials.

73.  It has been suggested that the origin of these tumors is odontogenic or
from periodontal ligament, but microscopically identical neoplasms
with cementum -like differentiation also have been reported in the
orbital, frontal, ethmoid, sphenoid, and temporal bones
• Today, many authorities prefer to designate the cementum-like material
present in ossifying fibromas as a variation of bone.
• VARIOUS TERMS HAVE BEEN USED FROM TIME TO TIME…
• When bone predominates in a particular lesion – Ossifying fibroma.
• Curved/linear trabeculae or spheroidal (psammoma) like calcifications –
Cementifying fibroma
• When both of bone & cementum – Cement-ossifying fibroma.
• The WHO classification in 1992 has grouped cementifying fibroma and
ossifying fibroma under a single designation as cemento-ossifying fibroma.

74. Peripheral - Clinical Feature
• Common in children, age range 5 – 25yr with peak incidence at 13yr, with
the mean age was 29 years
• M:F = 2:1, max=mand, ant. to molar common site
• Well defined focal mass on the gingiva with a sessile or pedunculated base.
• Color same as normal mucosa or may be bit more reddened
• Most commonly appears to originate from interdental pappila
Radiographic features
• No apparent underlying bone involvement
• In rare cases superficial bone erosion may be seen

75. Central – Clinical features
• Epidemiology unclear as was confused with COD
• Wide age range (3rd & 4th decades)
• Female predilection, ( 5 : 1 )
• Whites > blacks
• JAW : Mandible ( PM, molar ) > maxilla, orbit, frontal, ethmoidal .
• Small lesions – asymptomatic and are detected only on radiographic
examination.
• Larger tumors -painless swelling of the involved bone, expansion
• obvious facial asymmetry
• Pain and paresthesia are rarely associated with an ossifying fibroma.

76. Radiographic features
Location
• Most common in the mandible, cementoid, multiple
• Inferior to the premolars and superior to the mandibular canal
• In maxilla – solitary – osteoid , cemento osteoid , canine fossa or the
zygomatic process of the maxilla
Borders and shape
• Well-defined unilocular
• May have a thin lucent rim around lesion. This represents a soft tissue capsule,
which may help to differentiate COF from Fibrous Dysplasia
• Sclerotic rim – regular , diffused – 3mm
• 3 different radio features..
1. a well defined lesion with a sclerotic border…..45%
2. a defined lesion without a sclerotic border………. 40%
3.a lesion with ill defined borders…. 15%.

77. Radiographic features
Internal Architecture
• Variable mixed lucent/opaque- 3 stages
• Variable patterns, similar to Fibrous Dysplasia
• May have flocculent (snowflakes) or wispy pattern
• “ Coiled worm “ - DD from thumb print of FD
Effect on adjacent structure
• Tumor like behavior
centrifugal growth – circular and expansion & thinning Cortical plates , Displaces
the teeth, resorbs roots
• May fill max sinus but retains the thin cortex around it
• characteristic downward bowing of the inferior cortex of the mandible. ,
parallel to the margin of tumour mass above .

78. Histopathology
The calcified component is present which is
usually a combination of bony trabeculae &
strongly basophilic cementum like structures
with variable osteoblastic rimming.
• Osteoclast like giant cells & sinusoid blood
space may be present.
• Characteristically encapsulated lesions
consists of highly cellular fibrous tissue in
which bone formation occurs.

79. STRIKING FEATURES
• .

80. Treatment and Prognosis
• The circumscribed nature of the ossifying fibroma generally permits
enucleation of the tumor with relative ease.
• Some examples, however, which have grown large and destroyed
considerable bone, may necessitate surgical resection and bone
grafting.
• Prognosis is very good
• Recurrence after removal of the tumor is rarely encountered.
• No evidence of malignant change.

81. JUVENILE OSSIFYING FIBROMA
(JUVENILE ACTIVE OSSIFYING FIBROMA; JUVENILE AGGRESSIVE OSSIFYING FIBROMA)
• It’s a controverial lesion Distinguished from
the larger group of ossifying fibromas on
the basis of the age, most common sites,
and clinical behavior.
• Two different neoplasms have been
reported.
1) trabecular
2) psammomatoid.
The two forms demonstrate different
histopathologic and clinical features.

82. Clinical features
• M = F in both the forms
• Age 6month- 70 years
• Trabecular pattern diagnosed initially in younger patient mean
11years
• Maxilla more common
• Cortical expansion in facial deformity may be seen
• Psammomatoid mean 22 years
• Psammomatoid variant occurs commonly outside the jaw – orbit,
frontal bone and paranasal sinuses

84. • Complications secondary due to impingement on neighboring
structures. With persistent growth, lesions arising in the paranasal
sinuses penetrate the orbital, nasal, and cranial cavities.
• Nasal obstruction, exophthalmos, or proptosis may be seen.
• Intracranial extension has been discovered in neoplasms arising
adjacent to the cribriform plates.
• Because of circumscribed nature of the lesion frontal lobe is elevated
without ant neurological symptoms

85. HISTOLOGICAL FEATURES

86. Treatment & Prognosis
• Many tumors demonstrate slow but progressive growth, some
juvenile ossifying fibromas demonstrate rapid enlargement.
• Aggressive in infant and young children
• For smaller lesions, complete local excision or thorough curettage
appears adequate.
• For some rapidly growing lesions, wider resection may be required.
• In contrast to the negligible recurrence rate seen in the common
types of ossifying fibromas, recurrence rates of 30% to 58% have been
reported for juvenile ossifying fibromas.
• Malignant transformation has not been documented.

87. Conclusion
• A number of other disease processes involving the jaws may be
clinically, radiographically and or histologically confused with
conventional fibro-osseous lesions of the jaw.
• It is also often difficult to distinguish between benign and
malignant.
• One must rely upon all observations that can be gathered,
paying particular attention to symptomatology, duration and
rate of enlargement, and roentgenographic appearance, as well
as to the histology when the biopsy is attained.

88. REFERENCES
• Diagnostinc imaging of jaws – L & L
• Text book of oral pathology – Shafers
• Text of oral & maxillofacial pathology – Neivell
• Text book of maxillofacial pathoogy marx stern