FOL

1. DR.SHOBHA.B
FIBRO-OSSEOUS
LESIONS OF THE JAW

2. Contents
Introduction
Classifications
Common fibro osseous Lesions
• Fibrous dysplasia
• Cemento osseous dysplasia
• Ossifying fibroma
Gaint cell lesions
Inflammatory/Reactive lesions
conclusion

3. INTRODUCTION
• Fibro-osseous lesions (FOL) are diverse group of
processes characterized by replacement of normal bone
by fibrous tissue containing newly formed mineralized
product.
• Developmental
• Reactive
• Dysplastic
• Neoplastic
• These lesions are characterized microscopically by
fibrous stroma containing various combinations of bone
& cementum-like material but differ clinical &
radiographic presentation & behavior.

4. • FOL in the maxillofacial region is commonly applied to
• cemento-ossifying dysplasia (COD),
• fibrous dysplasia (FD) and
• cemento-ossifying fibroma (COF) and their subtypes.
• Regardless of subtype, all BFOLs demonstrate
replacement of normal bone by fibrous connective
tissue with an admixture of mineralized product,
including osteoid, mature bone, and/or cementum-like
calcifications.

5. Importance of Specific Diagnosis
The histopathology of all FOL is identical,
although they range widely in clinical
behavior.
More specific diagnosis is important because the
treatment of these pathoses varies from
none surgical recontouring complete
removal.
Dr.Haris PS/OMR 5

6. Waldron classification
• I. Fibrous dysplasia
• A. Monostotic
• B. Craniofacial
• C. Polyostotic
• D. McCune-Albright syndrome
• II. Fibro osseous neoplasms,-
• Ossifying fibroma
• Cementifing fibromas
• Cemento ossifying fibromas
• juvenile ossifying fibroma
• III. Reactive lesions /Osseous dysplasia
• A. Periapical
• B. Focal
• C. Florid
• D. Familial gigantiform cementoma

7. FOL of medullary bone origin
1. FD
2. Fibro osteoma
3. Cherubism
4. Juvenile OF
5. Giant cell tumor
6. ABC
7. Jaw lesions in
hyperparathyroidism
8. Paget’s disease
Dr.Haris PS/OMR 7
FOL of PDL
origin
1. Periapical
cemental
dysplasia
2. Florid osseous
dysplasia
3. CF
4. OF
5. COF

8. WHO CLASSIFICATION
1.Fibrous dysplasia
2.Reactive lesions arising in tooth bearing area,
presumably from the periodontal ligament
periapiacal cemento-osseous dysplasia
focal cemento-osseous dysplasia
florid cemento-osseous dysplasia
3. Fibrosseous neoplasms such as cemento-ossifying
fibroma
4.Traumatic bone cyst and aneurysmal bone cyst

9. Modified WHO classification
(Speight and Carlos)
Fibrous dysplasia
Monostotic
Polyostotic
Craniofacial
Dr.Haris PS/OMR 9
Osseous dysplasias
PCOD
Focal COD
Florid COD
Familial gigantiform
cementoma
Ossifying fibromas
Conventional ossifying fibroma
Juvenile trabecular (WHO type) OF
Juvenile psammomatoid OF

10. • Classification by NEVILLE-2002
• Fibrous dysplasia
• Cemento-osseous dysplasia
a. Periapical cemento-osseous
dysplasia.
b. Focal cemento-osseous dysplasia.
c. Florid cemento-osseous dysplasia.
• Ossifying fibroma

11. Classification of benign fibro-osseous
lesions
I. Bone dysplasias
a. Fibrous dysplasia
i. Monostotic
ii. Polyostotic
iii. Polyostotic with endocrinopathy
(McCune-Albright)
iv Osteofibrous dysplasia
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
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
c. Gigantiform cementomas
Head and Neck Pathol (2008) 2:177–202

12. FIBROUS DYSPLASIA
Definition:
• FD is a benign, nonneoplastic intramedullary cellular
proliferation of fibroblasts, with formation of irregular trabeculae
of bone or ovoid calcifications, that shows indistinct,
nonencapsulated borders.
• Results from localized change in the normal bone metabolism
,that results in replacement of all component of cancellous bone
by fibrous tissue containing varying amount of abnormal
appearing bone.

13. CLASSIFICATION OF FIBROUS DYSPLASIA
1. Monostotic FD
2. Polyostotic FD ( Jaffe’s form)
3. Polyostotic FD with endocrinopathy(McCune-
Albright form)
4. Craniofacial FD
5. Monomelic form
6. Subclinical fd

14. Etiology
1. Developmental-
• Somatic mutation during embryogenesis.
• Post zygotic mutation of GNAS1(Guanine
nucleotide binding protein, α-stimulating activity 1)
gene .
• There is an increase in IL-6-induced osteoclastic bone
resorption.
• There is a gain of function mutation which occurs in
undifferentiated stem cells of osteoblasts, melanocytes
& endocrine cells.
• The progeny of the mutated cell will carry the mutation
and express the mutated gene.

15. • The clinical expression depends on
1. the size of the cell mass and
2. Time when the mutation occured.
a) If mutation occurs in early embryonic life, it results in
multiple bone lesions, cutaneous pigmentation & endocrine
disturbances (Mc-Cune-Albright syndrome).
b) If it occurs in later stages of normal skeletal formation, it
results in multiple bone lesions [polyostotic (Jaffe type)].
c) If it occurs during postnatal life, confined to one bone,
results in FD of a single bone (monostotic fibrous
dysplasia).
• other causes
1. Endocrinal disturbances
2. Genetic
3. Local trauma or infection may accentuate the condition.

16. Clinical Features
• Monostotic fibrous dysplasia
• Age -second decade.
• Sex-No sex predilection
• Site-Limited to single bone.
• Commonly affect long bones followed by Jaws
• most commonly involves maxilla.premolar and molar region.
• FD is almost always a unilateral disease,
• lesions rarely cross the midline,
• It is enlarging deformity of alveolar bone involving buccal
and lingual corticle plates.
• Painless swelling – most common feature.
• Slow growth, become static with skeletal growth completion
Dr.Haris PS/OMR 16

17. Polyostotic FD
• McCune – Albright syndrome
• Female predilection
• May present with facial asymmetry
• With café au lait pigmentations - The skin spots often are
unilateral and ipsilateral to the FD lesions. Café au lait spots
- Margin typically irregular (Coastline of Maine
• Involves long bones and jaw bones.
• multiple endocrinopathies – adenomas of various
endocrine glands including the pituitary gland, Cushing
syndrome, acromegaly, benign ovarian cysts, linear
epidermal nevi, and neonatal cholestasis.
hyperthyroidism
• sexual precocity,
17

18. McCune – Albright syndrome

19. • o/m -Asymptomatic, slow progressive growth
• Cortical expansion
• Delayed tooth eruption
• bone lesions – Pathologic fractures
• Mazabraud syndrome -- sporadic disease
that is characterized primarily by
polyostotic FD and intramuscular myxomas.

20. • Jaffe – Lichtenstein syndrome
• Found in children of <10 yrs of age.
• Involvement of two or more bones other than
craniofacial bones.
• Pigmented lesion on the skin-café au lait spot.
• Becomes static when the growth stops.
• Causes facial assymetry ,with expansion of the
jaw bones.
• Disturbed eruption pattern of the teeth &loss of
its support.

21. Craniofacial fibrous dysplasia
• Peculiar form affecting skull bones
• Not restricted to single bone, but confined to single
anatomic site.
• Primarily affect maxilla later involving zygoma,
frontonasal bones and base of skull , sphenoid.
• Symptoms-malocclusion, facial deformity,
• anosmia, deafness, blindness
Dr.Haris PS/OMR 21

22. • Radiologic methods include
1. panoramic and plain films,
2. computed tomography(CT),
3. magnetic resonance imaging (MRI), and
4. whole-body bone scintigraphy.

23. Radiological feature
Early Lesion-
• Radiolucent with ill
defined borders.
• Blend with the
surrounding bone
• Margins surrounding
the lesion is wider
,giving granular
appearance
• Defect is often
unilocular,
• occasionally bony septa
may be present

24. • Mixed radiolucent-
radiopaque
• Depends upon stage of
maturity,distribution of
fibrous and osseous tissue
• New bone takes the form of
small radio opacity of poor
density appear granular as
they enlarge.
• Variation more pranounced
in mandible
• Homogenous and more
radio opaque in maxilla and
base of skull.

25. Mixed radiolucent-radiopaque
(Obisesan et al classification of radiographic appearance of
fibrous dysplasia)
• Orange peel appearance
• Thumb print
• Diffuse sclerotic type
• Cyst like type
• Pagetoid
• Chalky type

26. Orange peel or stippled appearance

27. Thumb print like pattern
Ground glass
pattern

28. Mixed R/L & R/O Hyperostotic with
Granular pattern

29. • Mature radio opaque
lesion
• Bone is prominent
• Have varied appearance
• Loss of lamina dura of
involved teeth,
• pdl space appears
narrow
• Trabeculae are shorter,
thinner,
• More numerous, and
irregularly aligned

30. Effect on surrounding
structures
• Small lesions are entirely
contained in the bone
• Thinning of cortex
• Loss of lamina dura
• Displacement of teeth
• Interference with normal
eruption
• Superior displacement –
unique to FD. This is due to
the epicenter of the lesion
being below the canal
• In maxilla may expand into
the antrum,displacing the
cortical boundry occupying
whole of the antrum.starts
from lateral border and lst
section is most postero
superior portion Dr.Haris PS/OMR 30

31. Cranio facial form
• Marked radio density
encroaching orbit and
antral cavity.
• Effected bones are
thickened at the base of
skull giving granular
appearance
• Nasal septum is
thickened dense and
curved ,gross caricature
of letter ‘S’

32. Differential Diagnosis
• Osteolytic stage-
• Central gaint cell granuloma
• Traumatic bone cyst
• ABC
• Periapical cyst
• Chronic osteomyelitis
• Squamous cell carcinoma
• Metastatic tumor

33. • Mottled stage
• Pcod
• Pegets disase
• Cf and of
• Chronic osteomyelitis
• Osteo sarcomas
• Chondro sarcomas
• Mature stage
• Pagets disease .
• Gaint cell lesion of hyper parathyroidism

34. CT
• To define extent of involvement of cranial
base.
• 34 – 513 HU
• Heterogeneous pattern of CT densities
associated with scattered or confluent islands
of bone formation
Dr.Haris PS/OMR 34

35. NUCLEAR MEDICINE
• Increased uptake of
Technetium Tc 99m
methylene
diphosphonate (MDP)
shows osteoblastic
activity

36. Histopathologic features
• Fibrillar CT with irregular osseous trabeculae
• Chinese letter pattern.
• No osteoblastic rimming
• Polarizing lenses, the trabeculae show a woven bone
pattern
• Shows increased Osteoclastic activity

37. LAB STUDIES
• Serum alkaline phosphatase levels = increased .
• Serum calcium, phosphate, and vitamin D levels = N
• Thyroid function tests, including triiodothyronine (T3),
thyroxine (T4), and thyroid-stimulating hormone (TSH)
levels, are performed to exclude hyperthyroidism.
• Pituitary gonadotropins and Sex hormone levels are assessed.

38. Management and Prognosis
• Small lesions can be resected entirely
• Most lesion stabilize with skeletal maturation
• Surgical recontouring after skeletal maturation
• Osteosarcoma-when received radiation.
• Complete surgical resection is recommended for
patients with rapidly expanding FD.
• Long-term clinical and radiographic follow-up is
recommended for any patient with FD.
Dr.Haris PS/OMR 38

39. COMPLICATIONS
1) Fracture
2) Deformity
3) Malignant transformation .
4) Formation of aneurysmal bone cysts
5) Osteomyelitits

40. CEMENTO-OSSEOUS DYSPLASIAS (COD)
cementoma
• The most common of all the FOLs
• COD occurs in the tooth-bearing areas of the jaws.
• Correct diagnosis is critical for appropriate
management as the pathologic features share many
similarities with fibrous dysplasia and ossifying
fibroma.
• Occurs in close approximation to the periodontal
ligament.
• Periodontal ligamental origin or may be due to a defect
in extraligamentary bone remodeling that may be
triggered by local factors and possibly correlated to an
underlying hormonal imbalance.

41. Melrose Classification
I ) Non-hereditary
1) periapiacal cemento-osseous dysplasia (PCOD)
2) focal cemento-osseous dysplasia (FCOD)
3) florid cemento-osseous dysplasia (FOD)
II) Heriditary
1) Familial gigantiform Cementoma
Cemento-Osseous Dysplasia (COD)

42. Periapical cemento-osseous dysplasias
• DEFINITION: Localized change in the
normal metabolism that results in the
replacement of components of normal
cancellous bone with fibrous tissue &
cementum like material, abnormal bone or a
mixture of the two.
• It occurs at the apices of lower anterior teeth.

43. Clinical Features
• age: middle age, 39 yrs.
• sex: female
• site: mandibular anterior teeth.
• Asymptomatic , if lesion is close to mental
foramen pain and paresthesia.
• Resembles periapical abscess.but the involved
teeth is vital .
• Usually smaller in size <1 cm ,but can enlarge
causing notable expansion.

44. Radiographic Features
Location
• Apices of mandibular anterior teeth,
• epicenter at the apical 3rd of the root.
• Multiple & bilateral
• Shape and Borders
• Well defined,radiolucent border
• Round, oval or irregular in shape
• surrounded by sclerotic bone.

45. 3 stages
1) Osteoporotic stage &Osteolytic stage
2) Cementoblastic stage
3) Mature stage

46. • PERRPERY&SHAPE:
• Welldefined
• round/oval
• INTERNAL STRUCTURE:
Early mixed mature
SURROUNDING STUCTURES:
loss of Lamina dura
large lesions –
expansion of jaw

47. Osteoporotic &
osteolytic stage
• Cementoblastic
stage

48. Mature stage
• Well defined radio
opacity
• Usually bordered by
radiolucent capsule
separating it from
adjacent bone
• Margins -Well defined
to poorly defined .
• Discontinuous lamina
dura .

49. Differential diagnosis
• Osteoporotic & osteolytic stage
• Periapical lesions
• Tbc
• Cementifying and ossifying fibroma.
• Cementoblatoma

50. Cementoblastic stage
• Odontome
• Calcifying crown,
• fibrous dysplasia
• Cementifying and
ossifying fibroma.
• Cementoblatoma
Mature stage
• Hypercementosis
• condensing ostites,
• idiopathic osteosclerosis
• pagets disease.
• Cementoblatoma

51. Focal cemento-osseous dysplasia (FCOD)
• Clinical features
• Exhibits single site of involvement.
• mean age is 38years.
• Female : Male = 8 : 1
• occur in any areas of the jaws, posterior mandible is
predominant site.
• asymptomatic and is detected usually in a routine
radiographic examination.
• Solitary lesions
• Most lesions are smaller than 1.5 cm in diameter.
• no cortical expansion

52. • Radiographic appearance
• completely radiolucent -- densely radiopaque
• with a thin peripheral radiolucent rim.
• The lesion is well defined, with irregular borders.
• Occurs in dentulous and edentulous areas,
• usually noted in extracted sites.
• Occasionally, an apparently focal lesion may
represent an early stage in the transition to
multifocal involvement.

53. Management
• Observe for life time
• Surgical enucleation of the lesion.
• Replace the missing tooth

54. Florid osseous Dysplasia
• Appear as a widespread form of periapical cemental
dysplasia.
• Normal cancellous bone is replaced with dense,
acellular, cemento-osseous tissue in a background of
fibrous connective tissue.
• Called FOD when lesions are present in three or
more quadrants
• Age -middle –elderly aged .
• Female predilection
• restricted to jaw bones only.

55. • Involves anterior as well as posterior region of
the jaws.
• Have a tendency for bilateral and symmetric
involvement and may be seen as extensive
lesions in all four posterior quad rants.
• Both dentulous and edentulous areas may be
affected, and involvement appears to be
unrelated to the presence or absence of teeth
• Asymtomatic & Occasional painfull.

56. • Appears with multifocal involvement.
• Large lesions may expand the cortices
• May be associated with simple bone cysts
• Lesions with SBC’s may produce a dull pain
• May become infected as surrounding bone resorbs.
• Pressure from a denture may cause perforation of the
overlying mucosa, exposing the lesion to the oral
environment.
• Alveolar sinus tract may be seen with exposed bone.
• The result may be osteomyelitis
• Cortical plates expansion may be seen

57. Radiographic Features
• Initially, the lesions are predominantly
radiolucent but with time become mixed, then
predominantly radiopaque with only a thin
peripheral radiolucent rim.
• Some times lesion can become almost totally
radiopaque and blend with the adjacent
normal- appearing bone.
• Contains nodular opacities.

58. • Location
• Often bilateral
• Found only in tooth-bearing areas
• Often present in both jaws
• More common in mandible
• Shape and Borders
• – Irregularly shaped
• – Well-defined, with a sclerotic border
• – Soft tissue capsule may disappear in long-
standing lesions

59. • Internal Architecture
• – Varies from mixed to completely opaque
• – Opacities may have a cotton wool appearance
• – Some lesions may have a large central lucent area.
• This may represent a simple bone cyst.
• SBC’s may enlarge over time
• Effect on adjacent structures
• May displace the inferior alveolar canal inferiorly, or
• the floor of the maxillary sinus superiorly

60. DD
• Pagets disease
• Osteopetrosis
• Chronic sclerosing osteomylities
• Treatment
• No treatment ,regular check up

61. Familial gigaintiform cementoma
Included in florid cemento-osseous dysplasia now .
• Pedigrees of this familial form have passed generations : expression is
varied
• some patients exhibit multiple opacities with little or no tendency for
expansion
• Some are multiple and massive.
• Most lesions arise in the tooth-bearing regions of the mandible and
maxilla
• Their growth eventually slows or ceases.
• Treatment -Surgical enucleation / excision
• Tooth with resorbed root = Extraction
• Recurrent & Massive lesions need resection

62. OSSIFYING FIBROMA
OF is a benign neoplasm arising in craniofacial
bones,composed of proliferating fibroblasts with
osseous products that include bone and ovoid
calcifications; the lesion is well demarcated from
adjacent bone.
Behaviorally, these lesions are proliferative, and may
exhibit slow growth, continue to grow steadily, or
show highly accelerated growth.

63. CLASSIFICATION
• Ossifying fibroma
– Ossifying form
– Cementifying forms
– Aggressive (juvenile) form
• Multiple ossifying fibromas
OMSF clinics of NA VOL 9 Nov 1997
term ‘‘cementifying fibroma & ossifying fibroma’’
was reduced to ossifying fibroma in the new WHO
classification in 2005

64. • Ossifying fibroma is a true neoplasm with a significant growth
potential & are relatively rare.
• The origin of OF is thought to be the periodontal membrane.
• The tumor is limited to the tooth bearing areas of maxilla &
mandible.
• The neoplastic cells elaborate bone & cementum & hence
thought to arise from progenitor cells (capable of dual
differentiation) of periodontal ligament or odontogenic.
• The cementum-like material present in ossifying fibromas is
considered as a variation of bone (Neville)
• Ossifying fibroma and cementifying fibroma are now
considered to be the two extremes of the same spectrum;
because both frequently contain both bone and cementum-like
tissue; these lesions are now called cemento-ossifying fibroma
(COF). *WHO

65. CLINICAL FEATURES
• 3 & 4 decades of life
• Female predilection
• limited to the bones of the craniofacial complex
• Mandible is affected more often than the maxilla
• Lesion typically involving areas inferior to premolar
& molar and superior to inferior alveolar nerve canal .
• In maxilla canine fossa and zygomatic arch region
• Whereas in the other cranial and facial bones the
periorbital, frontal, ethmoid, sphenoid, and temporal
bones are tumor sites.

66. • COF presents clinically as painless expansion of the jaw.
• Small lesions are discovered in routine radiographs.
• Larger lesions causes facial symmetry.
• Pain & parasthesia are rarely seen.
• Nasal obstruction, headache, bone pain,
• Proptosis are reported by patients with periorbital and
juxta sinonasal lesions.
• rhinorrhea and epiphoria,
• epistaxis and hemoptysis.
• Death is a rare occurrence secondary to
intracranial extension.

67. Radiographic Features
• Well-defined
• have a thin lucent rim around lesion.
represents a soft tissue capsule,
• Variable mixed lucent/opaque
• May have flocculent (snowflakes) or wispy Pattern
– Tumor-like behavior
– Concentric growth and expansion
– Displaces teeth
– Expands and thins cortices
– May fill entire maxillary sinus, but retains bony
cortex around lesion

68. • Radiolucent- enlarges concentrically
• A thin radiolucent line representing fibrous
capsule which is a separated from the
surrounding bone
• Hyperostotic borders may separate the lesion.
• Mixed lesion –appearance of radio opaque
foci
• Appearance of wipsy and flocculant pattern

69. • Mature lesion-completely radio opaque
• Grows concentrically with in medullary bone with
outward expansion equal in all direction
• It causes displacement of teeth and inferior alveolar
nerve canal
• Expansion of the outer cortical plates ,may be displaced
but remain intact.
• Missing lamina dura &resorption of the teeth
• In maxilla it has unique growth pattern,there is
desolution of neighboring bone without displacing by
pressure.

70. Differental diagnosis
• Early lesion-
• pcod
• Ameloblatomas
• AOT
• residual cyst ,
• primodial cyst
• Mixed lesion-
• Ceoc,ceot
• Pcod
• Pagets disease
• Fibrous dysplasia
• Osteoblastoma
• Osteoid osteoma
• Osteo sarcoma
• Mature lesion
• Hyper cementosis
• Condensing ostites
• Idiopathic osteosclerosis

71. Histopathology
• Consist of fibrous tissue that exhibits varying degrees
of cellularity and contains mineralized material.
• Trabeculae of bone and droplets of cementum-like
material can be seen forming within a background of
cellular fibrous connective tissue.
• Trabeculae of osteoid and bone are basophilic and
poorly cellular spherules that resemble cementum .
• In polarized light cementum-like material shows
characteristically QUILTED pattern.

72. Treatment and Prognosis
• The circumscribed nature of the ossifying fibroma
generally permits enucleation of the tumor with
relative ease.
• Untreated tumors of massive size may require
surgical (enbloc) resection and bone grafting.
• prognosis is very good.
• Recurrence after removal of the tumor is rare.
• No evidence of COFs undergoing malignant
change.

73. JUVENILE OSSIFYING
FIBROMA
• The juvenile ossifying fibroma (JOF) is a relatively rare
controversial lesion & also is a actively growing lesion.
• Also known as
• “Aggressive ossifying fibroma or
• Active ossifying fibroma” (Neville et al, 2002).
• Well demarcated from surrounding bone, which is
composed of cell-rich fibrous tissue containing bundles of
cellular osteoid & bone trabeculae with out osteoblastic
rimming.
• Two accepted patterns of juvenile ossifying fibroma:
• (I) Trabecular and
• (2) Psammomatoid. Neville

74. Clinical Features
• Age of trabecular JOF - 11 years & for the
psammomatoid - 22years.
• No sexual predilection in either form
• Both patterns occur in either jaw but reveal a maxillary
predominance.
• Initially discovered upon routine radiographic
examination.
• Cortical expansion may result in clinically detectable
facial enlargement.
• The psammomatoid variant frequently appears outside
of the jaws, with over 70% arising in the orbital and
frontal bones and paranasal sinuses.

75. • With persistent growth, lesions arising in the
paranasal sinuses penetrate the orbital, nasal, and
cranial cavities.
• Nasal obstruction, exophthalmos or proptosis
maybe seen.
• Rarely, temporary or permanent blindness occurs.
• Intracranial extension has been discovered in
some cases & convulsions due to meningitis led
to death in a reported case.

76. • Neoplasms grow slowly & are well-circumscribed
• lack continuity with the adjacent normal bone.
• have circumscribed radiolucencies & in some cases contain
central radiopacities.
• Those present within air sinus may appear radiopaque and
often create a clouding that maybe confused with sinusitis.
• Age at diagnosis varies from less than 6 months to over 70
years of age.
• Both patterns reveal similar radiographic features & growth
patterns, the trabecular form is diagnosed initially in
younger patients.
• Both patterns are typically nonencapsulated but well
demarcated from the surrounding bone

77. Treatment and Prognosis
• Uncertain, as some tumors grow slowly &
progressively & other demonstrate rapid
enlargement.
• Aggressive tumors are seen in infants & young
children.
• Smaller lesions are completely excised.
• Rapidly growing requires wider resection.
• 30-58% reoccurs.
• Malignant transformations has not been reported.

78. Giant Cell Lesions
• Central Giant Cell Granuloma
• Aneurysmal Bone Cysts
• Cherubism
• Brown Tumor of Hyperparathyroidism
Osteodystrophy
• Pagets Disease

79. Cherubism
• Def:- Is a rare, inherited, developental
abnormality that causes bilateral enlargement
of jaws, giving a child a cherubic facial
appearance.
• Formerly called “Familial Fibrous Dysplasia”,
although it is not fibrous dysplasia
• gene responsible for cherubism – chromosome
4p16.

80. Classification
• Grade-1-tends to be bilateral and symmetrical
Present primarily in the ramus of the mandible.
• Grade-2-ramus and body are involved
resulting in congenital missing of 3rd molar
and some times 2nd molar.
• Grade-3-effects maxilla and mandible entirely
and resulting in considerable facial deformity.

81. • Grade-1-lesion of mandible without signs of root
resorption
• Grade-2-maxilla & mandible without signs of root
resorption
• Grade-3- aggressive lesion of mandible with root
resorption
• Grade-4 - maxilla & mandible with root resorption
• Grade-5-rare massively growing aggressive and
deforming juvenile cases that involve maxilla &
mandible &may include coronoid processes &
condyles .
Oral Maxillofacial Surg Clin N Am 17 (2005)
415 – 434

82. Clinical features
• age- 2-6yrs.
• site- mandible.
• Characterized by painless bilateral swelling of the posterior
mandible.enlargement of of submandibular lymph nodes.
• bilateral enlargement of maxilla slowly follows.
• Epicenter always in the posterior aspect of the jaws ramus of the
mandible or the tuberosity.
• Child assumes a chubby ,cherubic facial appearance with
involvment of orbital floor and upward displacement of globe and
exposure of sclera rim.
• EYES RAISED TO HEAVEN.
• Difficulty in speech deglutition mastication and limited jaw
movements.

83. • Swelling is nontender ,firm and hard with intact
overlying mucosa.
• Alveolar process appears wide.
• Actual palate reduced to narrow fissure
• Displaces deciduous teeth.resulting in irregular
spacing premature loss .
• Rapid increase in the size of the lesion up to 7-8
yrs later lesion becomes static .
• Active cases serum alkaline phosphatase levels
are raised.

84. Radiographic Features
• Location
• Bilateral, multilocular lesions, well defined periphery
• May affect maxilla as well as mandible
• Epicenter is in the ramus or maxillary tuberosity area
Shape and Border
• Well-demarcated
• May have corticated borders
Internal architecture
multilocular appearance
• Granular Lesions get filled in with granular bone after the active phase ends
• Thin trabeculae or septae.
Effects on adjacent structures
• Expands cortices of the mandible
• Maxillary lesions may expand into the maxillary sinus
• Teeth are displaced anteriorly as lesions expan

85. • D/D:-
• Central giant cell granuloma
• Fibrous dysplasia.
• Central hemangioma
• Gaint cell lesion of hyper thyroidism
• Odentogenic myxoma
• Multiple dentigerous cyst
• Management:- Surgical procedures
• Orthodontic treatment.

86. Central Giant Cell Granuloma
• Def- Is thought to be a reactive lesion to unknown
stimulus & not a neoplastic lesion.
• C/F- adolescents & young adults Seen in 2 or 3 rd
decade
• location- mandible
• Painless swelling.
• Involved area tender on palpation.
• Presents as a painless swelling on routine examination
• Usually slow growing; rapidly-growing lesions may
resemble malignancy.
• Overlying mucosa purple in colour.

87. Radiographic Features
Location
• 2:1 Mandible to maxilla
• Usually anterior to first molar in mandible
• Usually anterior to canine in maxilla
Mandibular lesion occasionally crosses the Midline
Borders
Mandibular lesions are well-defined, but non-corticated
Maxillary lesions usually have ill-defined borders.
This may give the radiographic appearance of a malignancy
Internal Architecture
• Usually completely radiolucent
• May have subtle granular pattern or septae that are difficult to distinguish.
• Proper viewing conditions are imperative .

88. • Effects on adjacent structures
• May displace or resorb teeth
• Effaces lamina dura of adjacent teeth
• Expands cortices unevenly
• Differential Diagnoses
• Cysts
• Radicular
• OKC
• Primordial
• Residual
• Ameloblastoma
• Odontogenic myxoma

89. Aneurysmal Bone Cyst
• A reactive lesion of bone
• Resembles CGCG due to the histologic presence of
giant cells
• ABC’s may develop in association with other primary
lesions such as
1. fibrous dysplasia,
2. central hemangioma,
3. giant cell granuloma and
4. osteosarcoma.
• Occurs in individuals <30 yrs, mostly females
• Mandible to maxilla 3:2, molar region > anterior region

90. Radiographic features
• Well defined periphery,
circular
• Multilocular and septate
resembling central giant
cell granuloma (CGCG)
• Extreme expansion of
outer cortical plates
• ABCs can displace and
resorb teeth
• A hemorrhagic aspirate
favors the diagnosis of
ABC

91. Hyperparathyroidism
• primary and secondary hyperparathyroidism
(HPT) = Craniofacial bone lesions + benign
fibroosseous lesions + renal osteodystrophy .
• thickening of diploe
• Marked facial deformity
• massive maxillomandibular enlargement
• protrusion of the anterior teeth and wide
diastemas.

92. • In the early stages of renal osteodystrophy, the jaws and
facial bones will exhibit a loss of normal trabeculation
• replaced by a nonexpansile diffuse ground glass
opacification
• hyperparathyroidism-jaw tumor syndrome-
1. familial parathyroid adenomas
2. ossifying fibroma of the jaws,
3. renal cysts and
4. Wilms tumors.

93. Paget’s Disease of Bone Osteitis
Deformans
• Def- Is condition of a abnormal resorption &
apposition of osseous tissue in one or more bones.
• Abnormal resorption and deposition of bone
• May involve many bones, although it is not
generalized
• Initially, osteoclastic activity creates bone cavities
• Later, new bone is deposited in an abnormal pattern

94. • Clinical feature - later middle age & old age.
• female predilection.
• Effect on jaws- enlargement
• Effect on teeth- separation & movement
• Effect on denture- tight or poorly fit.
• Slow healing of extraction sites is common
Increased incidence of osteomyelitis

95. • Approximately 10% of patients with polyostotic Paget’s
Disease of Bone develop osteosarcoma
• Kidney stones are common
• Skull bones may enlarge 3-4 times their normal
thickness
• Outer cortex may remain the same or slightly thinned
• Bone scans reveal the activity of the lesion ( increased
uptake)
• Extreme elevation of serum alkaline phosphatase
levels aid in the diagnosis

96. • ƒ
Location
• Found most commonly in pelvis, femur, skull, and vertebrae
• Involvement of the jaws is uncommon
• Maxilla to mandible 2:1
• Usually bilateral, but one side may have greater involvement
• ƒ
Internal Architecture
• Three stages (which overlap)
• 1. Radiolucent stage representing osteoclastic activity
• 2. Granular appearing stage resembling Fibrous Dysplasia
• 3. Denser, later stage (cotton wool appearance)– Linear trabecular pattern
• ƒ
Effects on adjacent structures
• Affected bones are enlarged
• Cortices may be thinned
• Sinus floor is usually involved in maxillary lesions
• Associated teeth may develop hypercementosis

97. • Management- Calcitonin - Sodium etidronate
• Surgery- to correct bony deformities

98. Inflammatory/Reactive Processes
• Most infections of the jaws are odontogenic in origin.
• Both pyogenic and anaerobic bacteria are usually responsible for
acute, subacute or chronic osteomyelitis
(streptococci,bacteroides, actinomycetes).
• These infections are caused by anaerobic organisms of low virulence
and histologic evidence of an inflammatory response in bone
marrow is typically absent.
• The host response to these low grade infections is reactive
osteogenesis and imaging patterns show diffuse homogeneous
opacification.
• Reactive proliferation of the periosteum is also a
frequent accompaniment.
• Low grade infections may occur within the craniofacial bones,
usually the mandible, and initiate osteoblastic rather than
osteoclastic activity.

99. Focal Sclerosing Osteomyelitis
(Condensing Osteitis)
• The mildest and most self-limited form of sclerosing
osteomyeliti
• Is encountered in the posterior mandible at the apices of
molar teeth
• The condition is extremely rare in the maxilla.
• characterized by an asymptomatic, nonexpansile periapical
lesion associated with non vital tooth.

100. • . In the early stage of the infection,
radiolucency is seen at the apex, simulating
a dentalabscess, granuloma or cyst .
• DD-
• focal osteosclerosis or bone scar
• focal cemento-osseous

101. Diffuse Sclerosing Osteomyelitis
• DSO is usually caused by gram negative anaerobic bacteria of low
virulence.
• The source of infection may be odontogenic with a grossly carious
tooth overlying the region;
• Dull episodic pain that may last for weeks only to subside and
later become symptomatic again.
• Presents with cortical osseous expansion
• Is characterized by a unilateral diffuse ground glass
opacification without defined boundaries, of the mandibular
body.
Differential diagnosis
• Fibrous dysplasia and
• florid cemento-osseous dysplasia

102. Proliferative Periostitis
• low grade infectious progress of DSO involves the
• periosteum neo-osteogenesis periosteal layer
becomes redundant ‘‘onion skinning’’ phenomenon.
• It is the periosteal reaction that accounts for the clinically
evident cortical expansion.
• DSO is managed by eliminating any odontogenic sources of
infection by either extraction or root canal therapy.

103. Conclusion
• FOLs of the jaws comprise a controversial group of pathologic
conditions that causes difficulty in classification, pathogenesis
& treatment.
• Modifications are almost certain to be needed as experience
accumulates.
• In conclusion, a suggestion is made that a classification based
on origin & pathogenesis may be helpful in understanding
FOLs as well as diagnosis & choice of treatment.
• that analysis of histopathologic characteristics must be made
in reference to clinical & radiographic findings.