definitions, lesions in detail

1. FIBRO-OSSEOUS LESIONS
DR. Ratna . Samudrawar
III YEAR PG
DEPARTMENT OF ORAL MEDICINE & RADIOLOGY
RCDSR, BHILAI

2. CONTENTS:
• Introduction
• Definitions
• Classifications
• Fibrous dysplasia
• Cherubism
• Ossifying fibroma
• Juvenile ossifying fibroma
• Cemento-osseous dysplasia
• Central giant cell granuloma
• Aneurysmal bone cyst
• Radiological differential diagnosis of fibroosseous lesions
• Conclusion
• references

3. INTRODUCTION:
• All fibro-osseous lesions are characterized by replacement of
normal bone by fibrous tissue containing a newly formed
mineralized product. The designation fibro-osseous lesion is
not a specific diagnosis and describes only a process.
• Fibro-osseous lesions of the jaws include developmental
(hamartomatous) lesions, reactive or dysplastic processes, and
neoplasms. From a clinical stand point, the fibro-osseous
lesions may vary from the extensive, and cosmetically or
functionally disturbing lesions detected only during a routine
radiographic examination.

4. DEFINITION:
• Waldron in 1970 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 .
• Fibro osseous lesions are a group of conditions that replace
normal bone with benign fibrous tissue containing variable
amount of mineralization.

5. • Fibro – osseous lesion may be non neoplastic or neoplastic &
of odontogenic or non odontogenic origin.
• Regardless of the subtype, all fibro-osseous lesions
demonstrate replacement of normal bone by fibrous
connective tissue with an admixture of the mineralized
product including osteoid, mature bone, and/or cementum
like calcifications.

6. Classification :
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

7. 3. Fibro-Osseous Neoplasms Of Uncertain Or Detectable
Relationship To Those 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.

8. Working Classification Of Fibro-Osseous Lesions By Mico M. Malek
(1987)
In 1987 from the viewpoint of diagnostic pathologist, a working
classification of fibro-osseous lesions was given by Mico M. Malek
which is as follows
1. Developmental Disorders
A. Fibrous Cortical Defects (Non Ossifying Fibroma)
B. Fibrous Dysplasia
2. Reactive Reparative Lesions
A. Traumatic Periosteitis
B. Periosteitis Ossificans
C. Osseous Keloid
D. Periapical Cemental Dysplasia & Florid Cemento-Osseous
Dysplasia
E. Sclerosing Osteomyelitis (Focal & Diffuse Type)
F. Osteitis Deformans

9. 3. Fibromatosis
A. Desmoplastic Fibroma (Intraosseous Fibromatosis)
4. Neoplasms
A. Tooth Bearing Areas Only
i. Cementoblastoma
ii. Periodontoma
1. Central
2. Peripheral
B. All Cranio-Facial Bones (Including Tooth Bearing Areas)
i. Osteoma
1. Trabecular
2. Compact
ii. Osteoid Osteoma
iii. Psammous Desmo-Osteoblastoma
iv. Trabecular Desmo-Osteoblastoma

10. Peiter J. Slootweg & Hellmuth Muller (1990)
• In 1990 Peiter. J. Slootweg & Hellmuth Muller gave a classification
that laid emphasis primarily on the histopathological features, and
they underscore that this classification requires inclusion of
adjacent normal bone to make diagnosis. However in the absence
of this, the clinical & radiological features have to be taken in to
consideration.
Group I: Fibrous Dysplasia
Group II: Juvenile Ossifying Fibroma
Group III: Ossifying Fibroma
Group IV: Periapical Cemental Dysplasia & Florid Osseous Dysplasia

11. WHO Classification (1992)
• But the identification of identical cementum like tissues in
lesions in extra-gnathic sites suggested that this tissues may
be a merely normal variant of bone, and that dental
cementum itself is a specialized form of “bundle-bone”.
• Therefore, in the second edition of the who’s classification in
1992, three of the “cemental” lesion were transferred to the
“neoplasm and other tumors related to bone “group, leaving
the benign cementoblastoma as the sole true neoplasm of
dental cementum.

12. • This second edition of the WHO Histological Typing of
odontogenic tumors in 1992 recognized them as the group of
cement-osseous dysplasia which included “florid cement-
osseous dysplasia” that form with “Periapical cemental
dysplasia” & “other cemento-osseous dysplasia”
1. Osteogenic Neoplasms
a. A.Cemento-Ossifying Fibroma (Cementifying Fibroma,
Ossifying Fibroma)

13. 2. Non-Neoplastic Bone Lesions
a. Fiberous Dysplasia Of Jaws
b. Cemento-Osseous Dysplasia
I. Periapical Cemental Dysplasia (Periapical Fiberous Dysplasia),
II. Florid Cemento-Osseous Dysplasia (Gigantiform Cementoma,
Familial Multiple Cementomas)
III. Other Cemento-Osseous Dysplasia
c. Cherubism (Familial Multilocular Cystic Disease Of The Jaws)
d. Central Giant Cell Granuloma
e. Aneurismal Bone Cyst
f. Solitary Bone Cyst (Traumatic, Simple, Hemorrhagic Bone Cyst)

14. Waldron Modified Classification Of Fibro-Osseous Lesions Of
Jaws (1993)
• Later on, to overcome the demerits of his own classification,
Waldron reviewed the subject of benign fibro-osseous lesions
of jaws (BFOL) in 1993 and suggested a modification of his
earlier classification.
1. Fibrous Dysplasia
2. Cement-Osseous Dysplasia
a. Periapical Cement-Osseous Dysplasia
b. Focal Cement-Osseous Dysplasia
c. Florid Cement-Osseous Dysplasia
3. Fibro-Osseous Neoplasm
a. Cementifying Fibroma, Ossifying Fibroma, Cement-Ossifying
Fibroma

15. Brannon & Fowler Classification (2001)
• In 2001, Brannon & Fowler gave another classification which
was quite different from that of Waldron & WHO
classification. this was done to include more number of
lesions which were also showing features like FOL:
1. Osseous Dysplasia (OD) (Reactive)
a. Nonhereditary
i. Periapical
ii. Focal
iii. Florid
b. Hereditary (Developmental)
i. Familial Gigantiform Cementoma
2.Fibro-Osseous Neoplasm
a. Ossifying Fibroma (OF)
b. “Juvenile”, “Active” or “Aggresive” Varients of OF

16. 3. Fibrous Dysplasia
a. Polyostotic FD
b. Monostotic FD
c. Craniofacial FD
4. Giant Cell Lesions
a. Central Giant Cell Granuloma
b. Aneurismal Bone Cyst
c. Cherubism
5. Miscellaneous Benign Fibro-Osseous Lesions
a. Cementoblastoma
b. Tori/Exostoses
c. Osteoma

17. WHO Classification Of Fibro-Osseous Lesions Of Jaws (2005)
• In the latest WHO’s classification of odontogenic tumors in
2005, COD has been therefore called osseous dysplasias (Barnes
Et Al.).
• Because the discussions during these last decades about whether
cementum-like tissues is present, it has been decided to give up
the term of “cement”.
• The core of this classification is the concept of a spectrum of
clinicopathological entities in which the diagnosis can only be
made on the basis of a full consideration of clinical, histological
and radiological features.
1) Ossifying Fibroma (OF)
2) Fibrous Dysplasia

18. 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

19. Paul M. Speight & Roman Carlos Classification (2006)
• In 2006, Paul M. Speight & Roman Carlos gave a classification
based on new WHO classification & also from Waldron,
Slootweg, Brannon and Fowler and El-Mofty.
• A number of workers have tried to clarify the classification of
these lesions and although that may not have agreed on an
exact terminology, a concept has emerged which has
culminated in the latest WHO classification.
• Although the terminology is still problematic, this new
classification concentrated on the histopathological features that
may guide the working surgical pathologist towards a diagnosis.
• 1. Fibrous Dysplasia
a. Monostotic FD
b. Polyostotic FD
c. Craniofacial FD

20. 2. Osseous Dysplasia
a. Periapical Osseous Dysplasia
b. Focal Osseous Dysplasia
c. Florid Osseous Dysplasia
d. Familial Gigantiform Cementoma
3. Ossifying Fibroma
a. Conventional Ossifying Fibroma
b. Juvenile Trabecular Ossifying Fibroma
c. Juvenile Psammomatoid Ossifying Fibroma

21. Eversole 2008 Classification :
• Further, a much more comprehensive classification has been
suggested by Eversole et al in 2008 and this suggests that the
classification of these disease is likely to evolve still further.
• This classification includes neoplasm, developmental dysplastic
lesions and inflammatory/reactive processes.
• The basis of this classification is that definitive diagnosis can rarely
be rendered on the basis of histopathological features alone rather;
procurement of a final diagnosis is usually dependent upon
assessment of microscopic, clinical and imaging features together.
Classification of Benign Fibro-Osseous Lesions of the Craniofacial
Complex:
1.Bone dysplasias
a. Fibrous dyspla
i. Monostotic
ii. Polyostotic

22. iii. Polyostotic with endocrinopathy (McCune-Albright)
iv Osteofibrous dysplasia
b. Osteitis deformans
c. Pagetoid heritable bone dysplasias of childhood
d. Segmental odontomaxillary dysplasia
2. Cemento-osseous dysplasias
a. Focal cemento-osseous dysplasia
b. Florid cemento-osseous dysplasia
3.Inflammatory/reactive processes
a. Focal sclerosing osteomyelitis
b. Diffuse sclerosing osteomyelitis
c. Proliferative periostitis

23. 4. Metabolic Disease: hyperparathyroidism
5. Neoplastic lesions (Ossifying fibromas)
a. Ossifying fibroma
b. Hyperparathyroidism jaw lesion syndrome
c. Juvenile ossifying fibroma
i. Trabecular type
ii. Psammomatoid type

24. FIBROUS DYSPLASIA (FD): (‘fibrocystic disease’, ‘osteitis
fibrosa localisata’,‘focal osteitis fibrosa’ and ‘fibro-
osteodystrophy’
• The term FD was first suggested by Lichtenstein in 1939.
• FD is a benign fibro-osseous disease frequently affecting the
jaw bones and represents about 5% of all benign bone tumors.
• It is postulated to occur as a result of a developmental failure
in the remodeling of primitive bone to mature lamellar bone
leaving a mass of immature isolated trabeculae enmeshed in
dysplastic fibrous tissue that undergo turn over constantly but
never (or very, very slowly) complete the remodeling process.
• In addition, the immature matrix does not mineralize
normally.

25. Pathophysiology :
• Fibrous dysplasia (FD) is a benign dysplastic disease with a
well-known genetic basis.
• FD is a condition that results from a mutation in (Guanine
nucleotide binding protein alpha stimulating activity
polypeptide 1 (GNAS 1) gene.
• The clinical severity of the condition depends upon the time of
GNAS 1 mutation occurrence during fetal or postnatal life.

26. • If mutation occurs during the early embryonic life, the
osteoblast, melanocyte and endocrine cells carry the mutation
and express the mutated gene in form of multiple bone
lesions, cutaneous pigmentation and endocrine disturbances
(McCune Albright syndrome).
• Mutations in the alpha subunit of a G stimulatory protein
lead to constitutive activation of adenylyl cyclase, resulting in
a persistent elevation of cyclic adenosine monophosphate
(cAMP) and stimulation of endocrine receptors.

27. • The increase in cAMP as a result of the genetic mutation has
several so-called downstream effects .
• The constitutive elevation in cAMP level caused by Gsα
mutations results in abnormal expression of several target
genes such as c-fos, c-jun, interleukin-6 (IL-6) which contain
cAMP-responsive elements in their promoter which in turn
affects.
• The transcription and expression of several down stream genes
and therefore leads to osteoblast recruitment and function
disturbance in dysplastic bone lesions.

28. • Increased number of osteoclasts and bone resorption
observed in fibrous dysplasia have been attributed to IL-6 .
• In a study accomplished by Candeliere et al., bone marrow
spaces of FD-affected bones were shown to contain high
levels of c-fos, while healthy subjects bones or uninvolved
bones of FD patients showed no c-fos expression.
• Intracellular c- AMP raises in bone marrow osteo-progenitor
cells of FD-affected bones, leading to cell proliferation
together with differentiation defects.

30. • FD is classified by Waldron as being monostotic when it
affects a single bone or, less commonly, polyostotic when it
involves multiple bones concomitantly.
• Two apparently separate types of polyostotic FD are
described:
1. FD involving a variable number of bones although most of
the skeleton is normal, accompanied by pigmented lesions of
the skin or cafe-au-lait spots (Jaffe- lichtenstein type).
2. An even more severe porous dysplasia involving nearly all
bones in the skeleton and accompanied by pigmented
lesionsof the skin, and in addition, endocrine disturbances of
varying types (McCune Albright syndrome).

31. • According to shafer’s text book of oral pathology –
Apart from the above mentioned types of FD –
• Craniofacial form and cherubism were also included.
C/F
• FD is diagnosis before the age of 30 years .
• Equally distributed in both the gender.
• Monostotic forms at least 6 times more common than
polyostotic form.

32. a) Monostotic FD
• Monostotic presentation is more frequent, and lesions enlarge
in proportion to skeletal growth accounting for 80-85% of
cases of FD.
• This is seen with approximately equal frequency in males and
females in their first or second decades of life.
• It is usually insidious in onset and manifests clinically as a
slow growing, painless expansion of the involved bone
monostotic FD commonly occurs in the rib (24%), femur
(17%), tibia (13%), mandible (12%), and maxilla (12%).
• In the skull, it commonly involves the ethmoid, sphenoid,
frontal, and temporal bones in decreasing order, respectively.

33. • The clinical term “leontiasis ossea” has often been applied to
cases of FD which affects the maxilla or facial bones and give
the patient a leonine appearance.

34. • Maxillary involvement, specifically posterior maxilla is more
common than mandibular.

35. • There may be some malalignment, tipping or displacement of
the teeth due to the progressive expansile nature of the lesion
and tenderness may develop.
• The mucosa is almost invariably intact over the lesion.
Radiological features:
The radiographic appearances of FD of jaws is extremely
variable
Three basic patterns are seen
• Type 1- the lesion is generally a rather small unilocular
radiolucency or a somewhat larger multilocular radiolucency,
both with a rather well-circumscribed border and containing
a network of fine bony trabeculae.

36. Type one Type two
Second type - the pattern
is similar except that
increased trabeculation
renders the lesion more
opaque and typically
mottled in appearance.
Type 1- the lesion is small
unilocular radiolucency
with well-circumscribed
border

37. Type three - peau d’orange’ / orange peel appearance
Third type of quite
opaque with many
delicate trabeculae
gives a ‘groundglass’
or ‘peau d’orange’
appearance to the
lesion.

38. • The abnormal trabeculae usually are shorter, thinner,
irregularly shaped, and more numerous than normal
trabeculae.
• This creates a radiopaque pattern that can vary; it may have a
granular appearance-
 "ground-glass" appearance, resembling the small fragments of
a shattered windshield,
 a pattern resembling the surface of an orange “peau d'orange,

39. Monostotic maxillary fibrous dysplasia, (b) CT showing extensive
maxillary involvement, (c) PNS Radiograph showing maxillary sinus
obliteration. The CT showed thickening of the frontal and parietal regions with
deposition of bone on the inner aspect, at the expense of the cranial contents b-
c. The frontal area showed thinning and perforation with loss of the anterior wall
of the frontal sinus.
Craniofacial fibrous dysplasia: Surgery and literature review, menon .S etal. Annals of maxillofacial
surgery. 2013;3(1):66-71

40. (a) An orthopantomogram of case 1 revealing groundglass appearance in the
left mandible and having a fusiform shape. (b) A mandibular right lateral
cross-sectional occlusal radiograph of case 2 showing ground-glass
appearance. (c) An intraoral periapical radiograph of case 2 showing ground-
glass appearance and dilacerations of the roots. (d) An orthopantomogram of
case 3 revealing ground-glass appearance in the right premolar -- molar
region

41. (a) Mandibular right lateral cross-sectional occlusal radiograph of case 10
revealing orange peel appearance. (b) Orthopantomogram of case 10 revealing
orange peel appearance with a cystic variety. (c) Orthopantomogram of case 11
revealing cotton wool appearance in the mandible and maxilla involving the
craniofacial complex. (d) Mandibular left lateral cross-sectional occlusal
radiograph of case 13 showing sunray appearance

42. Orthopantomogram of case 12 revealing sacromatous transformation in the
mandible and maxilla involving the craniofacial complex. (b) Axial computed
tomography of case 13 showing sun spicule pattern. (c) Maxillary left lateral
cross-sectional occlusal radiograph of case 14 revealing thumb print
appearance in the molar region

43. Histologic Features:
• The lesion is essentially a fibrous one
made up of proliferating fibroblasts in
a compact stroma of interlacing
collagen fibers Irregular trabeculae of
bone are scattered throughout the
lesion with no definite pattern of
arrangement.
• Characteristically, some of these
trabeculae are C-shaped/Chinese
character-shaped.
• These trabeculae are usually coarse
woven bone but may be lamellar,
although not as well organized as
normal lamellar bone.

44. POLYOSTOTIC FIBROUS DYSPLASIA
• Approximately 20–30% of fibrous dysplasias are polyostotic.
Polyostotic fibrous dysplasia more frequently involves the
skull and facial bones, pelvis, spine, and shoulder girdle.
• The disease apparently has a distinct tendency to occur in
women with a male: female ratio of 1:3
• Two-thirds of patients are symptomatic before they are 10
years of age.

45. • The sites of involvement are the femur, tibia, pelvis, ribs, skull
and facial bones, upper extremities, lumbar spine, clavicle,
and cervical spine in decreasing order of frequency.
• The dysplasia may be unilateral or bilateral

46. • Although the polyostotic variety tends to occur in a unilateral
distribution, involvement is asymmetric and generalized
when disease is bilateral
• The initial symptom is pain in the involved limb associated
with a limp(stiff), spontaneous fracture, or both.
• In one series, pathologic fracture was present in 85% of
polyostotic fibrous dysplasias.

47. • Leg-length discrepancy of varying degrees occurs in about
70% of patients due to involvement of upper portion of femur
-Hockey-stick deformity
• The structural integrity of the bone is weakened, and the
weight-bearing bones become bowed. The curvature of the
femoral neck and proximal shaft of the femur markedly
increase causing a Shepherd’s crook deformity, which is a
characteristic sign of the disease

48. • Philip (1997) polyostotic type of FD is divided in to three
subtypes:
• Craniofacial FD – in which only the bones of craniofacial
complex are affected including the mandible and maxilla.
• Lichtenstein and jaffe type of FD – in which multiple bones of
the skeleton with café au lait pigmentation.
• Albright syndrome type of FD – has a traid of severe
polyostotic FD, café au lait pigmentation and various
endocrinopathies.

49. Craniofacial form.
• This pattern of the disease occurs in 10– 25% of patients with
the 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.
Sites of involvement most commonly include the frontal,
sphenoid, maxillary, and ethmoidal bones.
• The occipital and temporal bones are less commonly affected.

50. • Hyper telorism, cranial asymmetry, facial deformity, visual
impairment, exophthalmos, and blindness may occurbecause
of involvement of orbital and periorbital bones.
• Involvement of the sphenoid wing and temporal bones may
result in vestibular dysfunction, tinnitus, and hearing loss.
• When the cribriform plate is involved, hyposmia (reduced
ability to smell) or anosmia may result.

51. CT images of fibrous dysplasia. A. Coronal section shows craniofacial
type of fibrous dysplasia with involvement 1. frontal, temporal, 2.
zygomatic, 3. maxilla, and 4. mandible. B. Another coronal section shows
maxillofacial type with involvement of 1. maxilla and 2. zygomatic bone

52. Lichtenstein and jaffe type of FD:
• In which multiple bones of the skeleton with café au lait
(coffee with milk) pigmentation.
• The hyperpigmentation tends to be on same side and on the
skin overlying the lesions of FD.
• The hyperpigmented macules are well defined
and have irregular borders.
• The color can be medium to dark brown.

53. McCune-Albright syndrome:
• McCune-Albright syndrome (MAS) is classically defined by
the clinical triad of fibrous dysplasia of bone (FD), café-au-lait
skin spots, and precocious puberty (PP).
• In addition to PP (vaginal bleeding or spotting and
development of breast tissue in girls, testicular and penile
enlargement and precocious sexual behavior in boys), other
hyperfunctioning endocrinopathies may be involved
including hyperthyroidism, growth hormone excess, Cushing
syndrome, and renal phosphate wasting.

54. • Therefore, a more clinically relevant definition of MAS,
broader than the original triad of FD + PP + café-au-lait is:
MAS =FD + at least one of the typical hyperfunctioning
endocrinopathies and/or café-au-lait spots, with almost any
combination possible.
Epidemiology
• MAS is a rare disease and reliable data of prevalence are not
available (the estimated prevalence ranges between
1/100,000 and 1/1,000,000).

55. Pathophysiology:
• McCune-Albright syndrome has been shown to be due to a
postzygotic activating mutation of the GS alpha gene in the
affected tissues. The GS alpha subunit is the component of the
G-protein complex, which couples hormone receptors to
adenylate cyclase (the intracellular second messenger) in a
submembrane site.
• It then mediates the cellular effects of hormone binding.

56. Clinical Features.
Precocious puberty associated with the
• condition is gonadotrophin-independent.
• Among the endocrine disturbances described in association
with Albright syndrome are:
 Hyperthyroidism
 Acromegaly
 Gonadotrophin—McCune-Albright syndrome
 Hyperprolactinemia
 Cushing syndrome
 Hyperparathyroidism
 Hypophosphatemic rickets.

57. • The pigmented macules or café-au-lait spots are related to
increased amounts of melanin in the basal cells of the
epidermis.
• They tend to be arranged in a linear or segmental pattern
near the midline of the body, usually overlying the lower
lumbar spine, sacrum, buttocks, upper back, neck, and
shoulders.

58. • Similar lesions may occur on the lips and oral mucosa.
Pigmentation may occur at birth, and precede the
development of skeletal and endocrine abnormalities.

59. Café-au-lait skin pigmentation. A
typical lesion on the
face, chest, and arm of a 5-year-
old girl with McCune-Albright
syndrome which demonstrates
jagged "coast of
Maine" borders, and the
tendency for the lesions to both
respect the midline and follow
the developmental lines of
Blashko.

60. Malignancies in MAS
• While malignancies associated with MAS are distinctly rare
occurrences.
• This occurs in probably less than 1% of the cases of FD/MAS.
• While some have suggested that sarcomatous transformation
of skeletal lesions may occur more commonly in patients with
Mazabraud's syndrome (benign intramuscular myxomas in
association with long standing FD)

61. Radiographic features:
• In general, lesions in the long bones have a "lytic" appearance.
• The lesions usually arise in the medullary cavity and expand
outward replacing normal bone, which results in thinning of
the cortex .
• It is usually the metaphysis and/or the diaphysis that are
involved, with sparing of the epiphysis

62. The appearance of FD may vary
from entirely lytic (probably due to
cystic degeneration) to entirely
sclerotic.
On the left images of a patient with
polyostotic fibrous dysplasia, with
lucent lesions in the proximal and
mid-diaphyseal femur, and lesion
with groundglass density and
calcifications in the fibula
The lesion may be surrounded by a layer
of thick, sclerotic reactive bone ( rind
sign )

63. Anteroposterior radiograph of the
hip of a twenty-two-year-old man
who presented with a two-year
history of hip pain. The radiograph
demonstrates a fatigue fracture of
the femoral neck with the
characteristic “parrot’s beak”
deformity.

64. •a wispy arrangement “cotton wool”, or an amorphous, dense
pattern
•Occassionally,organization of the abnormal trabeculae into a
swirling pattern similar to a fingerprint

65. DIFFERENT APPEARENCES IN FD (ACC TO HM WORTH)
• Thumb print appearance: it occurs at the lower margin of the
jaw as if, when it was soft the imprint has been made,
squashing out a portion of the bone, causing it to protrude.
• This picture is pathognomic of fibrous dysplasia.
Part of a panoramic radiograph showing
the ‘‘thumb print’’ pattern of the lesion in
the mandible. Note that the inferior dental
canal has been displaced inferiorly
Fibrous dysplasia—a 13-year retrospective radiographic
analysis in a south Indian population. DMFR 2011

66. • Over a localized area the cortex is lost and the site there is
smooth and curved projection downward of the inferior
margin of the bone, the convexity downward.
• The appearance resembles thumbprint, as if the bone had
been soft and pressed upon by the thumb.
• Ribbon like cortex: when present next to thumb print stamps
the diagnosis of FD.
• Stippled appearance of the bone: pathognomic orange peel
appearance:

67. FINGERPRINT PATTERN
GROUND GLASS PATTERN
COTTON WOOL PATTERN
ORANGE PEEL PATERN

68. EFFECTS TO SURROUNDING STRUCTURE:
• If small- no effect (subclinical variety)
• Expansion of bone with maintanence of thinned cortex
• May expand into antrum
• Bone surrounding the teeth may get affected without
affecting the dentition.
• Lamina dura may get disappear.
• PDL space become narrow
• Has unique ability to displace IAN canal to superior direction.

69. OTHER RADIOLOGICAL FEATURES :
• Cyst like
• Peau d’ orange
• Finger print pattern
• Cotton ball pattern in adult monostotic fibrous dysplasia
• Sclerotic
• Smoky & cloudy appearance( Waldron & Giansanti)
• Chalky appearance
• Whorled
• Diffuse sclerosis (Obisesan & coworkers)

70. • Obisesan et al classified the lesions of fibrous dysplasia
radiographically into 6 types.
• ‘Peau d’ orange’ or orange peel—in this type, there are
alternating areas of granular density and lucency giving a
radiographic appearance resembling the ring of orange.
• Whorled plaque like type—in this type, the matrix of the well
circumscribed lesion is composed of plaques of amorphous
material of intermediate radiodensity, which on close
examination are seen to be arranged in whorled onion peel
appearance.
• Diffuse sclerotic type—the lesions of this show as
homogeneous dense area, which gradually merges with the
normal bone.

71. • Cyst like type—in this type, the lesions are radiolucent. It is
unilocular or multilocular, more often multilocular with well
defined margins.
• Pagetoid type—in this type of lesions, the affected area of
bone markedly expands and shows alternating areas of
radiopacities and lucency, as those seen in Paget’s disease of
bone.
• Chalky type—it manifests itself as a well circumscribed lesion
consisting of an amorphous dense radiopaque material.
Text book of oral medicine – anil ghom 2/e

72. RADIOLOGICAL FINDINGS IN CRANIOFACIAL REGION :
• Cortical plate expansion
• Tooth root displacement
• Lamina dura is obscured, because this bone is changed into the
abnormal bone pattern.
• Thinned cortical plates
• Inferior alveolar canal is displaced superiorly and laterally,
which helps to distinguish from ossifying fibroma.
• Skull lesions – bulging of outer table
• Typical sclerotic density in the base of the skull.

73. SKULL LESIONS :
• Wilner has classified into three types-
• Lytic
• Mixed (localized, regional, diffuse)
• Sclerotic.
LONG BONES :
• Femur – Shepherd’s crook or Hockey stick deformity
• Long bones – Candle flame appearance
• Iliac lesions – Smudged appearance.

74. BONE SCAN :
• Technetium diphosphonate – increased uptake of radionuclide.
• Described as “Hot”.
• Increased uptake is seen in ground glass & cystic appearing lesions
and bowed bones.
COMPUTED TOMOGRAPHY :
• Shows typical ground glass appearance
• To assess fluid-fluid levels
• To assess full thickness cortical destruction.

75. MAGNETIC RESONANCE IMAGING :
• Best tool to assess intraosseous extent.
• To define the internal architecture.
• Typical abnormal dark gray marrow signal of fibrous tissue
on T1 weighted images changes on T2 weighted images.
• On T2 – increase intensity is in cystic areas or fractures & less
in calcified area

76. Laboratory investigations:
• Serum alkaline phosphatase levels .
• 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.
• There are no consistent significant changes in the serum
calcium or phosphorus, although the serum alkaline
phosphatase level is sometimes elevated.
• Premature secretion of pituitary follicle-stimulating
hormone has been reported, as well as moderately elevated
basal metabolic rate.

77. COMPLICATIONS
1) Fracture
2) Deformity
3) Malignant transformation occurs in fewer than
0.5% - 1% of cases.
4) Formation of aneurysmal bone cysts
5) Osteomyelitits

78. D/D:
1. Ossifying fibroma
2. Neurofibromatosis : Cutaneous pigmentation in polyostotic
fibrous dysplasia is ipsilateral to the side of bony lesions, a
feature that differentiates this disease from pigmentation in
neurofibromatosis.
3. Chronic sclerosing osteomyelitis
4. Pagets disease: serum alkaline phosphate levels are elevated
5. Osteosarcoma: Cortical bone destruction, Invasion into
surrounding structures

79. Features Fibrous dysplasia Ossifying fibroma
Margins Not demarcated Well demarcated
Shape Fusiform Spherical or elongated
Cortices Replaced by disease Expanded –present or
partially present
Medullary pattern Homogenous Heterogenous

80. Management:
• Surgical—surgical removal of the lesion should be
carried out.
• Osseous contouring—it is necessary for correcting the
deformity for esthetics or pre-esthetic purposes.

81. CHERUBISM
(Familial fibrous dysplasia of jaws, disseminated juvenile fibrous
dysplasia, familial multilocular cystic disease of jaws, familial
fibrous swelling of jaws)
• First described by Jones in 1933.
• An autosomal dominant fibro-osseous lesion of the jaws
involving more than one quadrant that stabilizes after the
growth period, usually leaving some facial deformity and
malocclusion.
• Affects the jaws of children bilaterally and symmetrically,
usually producing the cherubic look

82. • According to the WHO classification, cherubism belongs to a
group of non-neoplastic bone lesions affecting only the jaws.
It is a rare, benign condition with autosomal dominant
inheritance.
• Lesion remits after puberty.
Genetic basis –
The locus for the cherubism gene in 4p16. Ueki etal detected
point muations causing amino acid substitutions in the SH3-
binding protein SH3BP2.

83. C/F
• Affected children are normal at birth and are without
clinically or radiographically evident disease until 14 months
to 3 years of age.
• At that time, symmetric enlargement of the jaws begins.
• Typically, the earlier the lesion appears, the more rapidly it
progresses

84. • The self-limited bone growth usually begins to slow down
when the patient reaches five years of age, and stops by the
age of 12–15 years.
• Respiratory obstruction and impairment of vision and
hearing.
• The lesions, which are firm to palpation and nontender, most
commonly involve the molar to coronoid regions, the
condyles always being spared, and are often associated with
cervicaL lymphadenopathy
• Profound swelling of maxilla, may results in streching of skin
of cheeks, which depresses the lower eyelids giving ‘eye
raised to heaven apperance’

86. Oral manifestations:
• When maxilla is involved, the palate assumes V shape.
• Agenesis of the second and third molars of the mandible,
displacement of the teeth, premature exfoliation of the
primary teeth, delayed eruption of the permanent teeth, and
transpositions and rotation of the teeth.
• In severe cases, tooth resorption occurs.
• In few cases cherubism has been described as being
associated with other diseases and conditions such as
Noonan’s syndrome, gingival fibromatosis, psychomotor
retardation, and obstructive sleep apnea

87. . Facial appearance of the patient showing symmetrical swelling of
the mandibular angles. B, Intraoral image showing thickening of
the alveolar processes, with partial obliteration of the palatal vault
Peñarrocha et al. Cherubism. J Oral Maxillofac Surg 2006.

88. Arnott’s grading system
• grade I: by involvement of both mandibular ascending rami,
• grade II: involvement of both maxillary tuberosities as well as
the mandibular ascending rami, and
• grade III: McCune- Albright syndrome involvement of the
whole maxilla and mandible except the coronoid process and
condyles.

89. • In order to over come the limitations of arnott’s classification
system, kalantar Motamedi developed a different
classification system which addresses both the involvement
and aggressive behaviour of the disease.
Grade- I : lesions of mandible without signs of root resorption.
Grade –II: lesions of mandible and maxilla without signs of root
resorption.

90. Grade – III : aggressive lesions of mandible with signs of root
resorption
Grade – IV: lesions involving mandible and maxilla with signs
of root resorption.
Grade – V : massively growing , aggressive and extensively
deforming juvenile cases involving the maxilla and the
mandible and which may include the coronoid process and
condyles

91. R/F
• Characterized by bilateral multilocular cystic expansion of
the jaws.
• Early lesions occur in the posterior body of the mandible and
the ascending rami.
• Maxillary lesions may occur at the same time but escape
early radiographic detection because of overlap of the sinus
and nasal cavities.
• Displacement of the inferior alveolar canal.

92. The presence of numerous unerupted teeth and the destruction
of the alveolar bone may displace the teeth, producing a
radiographic appearance referred to as floating tooth syndrome

93. • With adulthood, the cystic areas in the jaws become re-
ossified, which results in irregular patchy sclerosis. There is a
classic (but nonspecific) ground glass appearance because of
the small, tightly compressed trabecular pattern.
• Location. - This lesion is bilateral and often affects both jaws.
• When it is present in only one jaw, the mandible is the most
common location.

94. • The epicenter is always in the posterior aspect of the jaws, in the
ramus of the mandible, or the tuberosity of the maxilla
• The lesion grows in an anterior direction and in severe cases can
extend almost to the midline.
• Periphery - The periphery usually is well defined and in some
instances corticated.

95. Internal structure.
• The internal structure resembles that of CGCG, with fine,
granular bone and wispy trabeculae forming a prominent
multilocular pattern.
Effects on surrounding structures.
• Expansion of the cortical boundaries of the maxilla and
mandible by cherubism can result in severe enlargement of
the jaws.

96. • Maxillary lesions enlarge into the maxillary sinuses.
• Because the epicenter is in the posterior aspect of the jaws,
the teeth are displaced in an anterior direction.
• The degree of displacement can be severe, and with some
lesions the tooth buds are destroyed

97. Histological features:
• Numerous multinucleated giant cells
• Various spindle shaped fibroblasts
• Numerous small vessels are present, and the capillaries
exhibit large endothelial cells and perivascular cuffing.

98. D/D
• Giant cell granuloma of jaws – usually unilateral , affects 20-
40 years of age .
• Osteoclastoma – occurs rarely in jaws unlike cherubism
• Aneurysmal bone cyst – may also exihibit giant cells but its
main feature is a cavity lined with tissue other than
endothelium.
• Fibrous dysplasia- mostly 2 or 3 decade of life. elevated level
of serum alkaline phospatasae , histopathology shows chinese
characters with proliferating stroma.
• Hyperparathyroidism- rarely affects jaws. Serum
concentration of calcium and PTH can help in distinguishing

99. Treatment :
• The condition is selflimiting and generally regresses by
puberty.
• Surgery to correct the jaw deformities of cherubism .

100. OSSIFYING FIBROMA (cementifying fibroma; cemento-
ossifying fibroma)
Introduction :
• OF is most common fibroosseous neoplasm of the jaw.
• It is bone producing , slowly growing asymptomatic, well
demarcated, bening lesion common in maxilla and mandible.
• The tumor is defined as demarcated and occasionally
capsulated consisting of fibrous tissue containing variable
amounts of mineralized material resembling bone or
cementum or both.

101. • The term OF is used if the predominant component is bone .
• Cementifying fibroma is used when the predominat
component is cementum- like spherical calcifications .
• The lesions characterised by presence of bone and cementum
are refferred as cemento – ossifying fibroma.
Etiology –
OF occuring in jaws seems to arise from periodontal membrane
which contains pluripotential cells capable of forming
cementum, bone and fibrous tisssue.

102. C/F
• There is a definite female predilection.
• Seen in third and fourth decade of life.
• OF predominantly affects the craniofacial bone and rarely
involves the long bones.
• Mandible is involved more than maxilla.
• Mandibular premolar and molar area is the most common
site.
• The lesion appears as hard , localized and slow growing ,
painless mass that may displace adjacent structures and cause
root resorption.

103. R/F
• The lesion appears to be well defined.
• Initially lesions are radiolucent representing an osteolytic
image followed by gradual transformation into a mixed
lesion and eventually becoming radioopaque.
• The periodontal ligament space of the involved teeth is clearly
seen unlike FD.
Eversole et al described 2 basic patterns –
• Unilocular radiolucency with /without radiopaque foci
• A multilocular radiolucency.
• The unilocular pattern is more common.
• Expansion of cortical plates are common finding.
• Lamina dura of involved teeth usually missing, teeth
displacement and root resorption may be seen

104. Well-delimited mixed
radiographic image
causing displacement of
the involved teeth
Ossifying Fibroma of the Jaws: A Clinicopathological Case Series Study,
andrade M, Braz. Dent. J. 2013;24(6).
OF shows a well-demarcated mixed radiolucent and
radiopaque image as observed in all cases from this series,
which were well-circumscribed and separated from the
cortical bone.

105. H/F
• It shows fibrous and osseous tissue with former tissue
predominating . The fibrous stroma is highly cellular with
spindle shaped fibroblastic cells arranged in whorls .
• Osteoblastic rimming along the trabeculae are seen.
• The spherules of cementum like material often demonstrates
peripheral brush borders that blend into the adjacent
connective tissue.

106. • D/D
• In fact,the differential diagnosis depends on the radiographic
features of the lesion.
• In OF, it appears as a radiolucent image, odontogenic cysts,
ameloblastoma, central giant cell lesions and idiopathic bone
cavity.
• For mixed lesions, osteoblastoma, calcifying cystic odontogenic
tumor and calcifying epithelial odontogenic tumor should be
considered in the differential diagnosis.
• Finally, for radiopaque OF, complex odontoma and idiopathic
osteosclerosis are the main differential diagnoses.

107. • OF may also resemble a cementoblastoma if it occurs around
the tooth root however, cementoblastoma is fused to the tooth
root.
• Management : excision

108. JUVENILE OSSIFYING FIBROMA- (juvenile active ossifying
fibroma Or Juvenile aggressive ossifying fibroma)
• JOF is an uncommon lesion that affects the jaw of children
under 15 years of age.
Etiology :
• JOF is considered to develop from undifferentiated cells of
periodontal ligament.
• Two histologic variants of juvenile ossifying fibroma are :
1. Trabecular
2. psammomatoid

109. C/F:
• The lesion characteristically occurs under the age of 15 years.
• The psammomatoid variant occurs exclusively in the
extragnathic craniofacial region especially in the orbit bones
and paranasal sinuses (61.6%), maxilla (19.7%) and mandible
(7%).
• In mandible ,the tumor occurs more commonly in the ramus
than in the body of the mandible
• No gender predeliction.
• Patients often present with symptoms such as exopthalmus,
bulbar displacement and proptosis when affecting the orbital
bones and paranasal sinuses.

110. • Development of aneurysmal bone cyst in psammomatoid
juvenile ossifying fibroma is commonly reported .
Trabecular variant is characterized by a progressive and
sometimes rapid aggressive growth.
• The tumor expands the affected bone, leading to facial
asymmetry.
• It occurs more commonly in maxilla as compared to
mandible

111. R/F-
• The psammomatoid variant shows well defined expansion of
affected bone having mixed radolucent, radiodense and
ground glass appearance.
• The lesion is partially or completely surrounded with thin,
corrugated margins.
• Sometime multilocular appearances may be seen
representing the small cystic spaces.

112. • The trabecular variant is expansive , well defined and
unilocular or multilocular with cortical thinning and
perforation .
• The tumor mass is radiolucent with variable calcification
induced radiopacities, occasionally demonstrating fine specks
and producing ground glass appearance.
• Increase in radiodensity may be observed over time
• Root resorption and displacement of involved teeth are also
observed.

113. pattern An expansile
growth in lower
right anterior
region with mixed
radiolucent and
radiopaque
Trabecular Juvenile Ossifying Fibroma of the Craniofacial Skeleton: Etiopathogenesis and a Case Report of
the Rare Entity, Kadam.R et al international Scientific Journali 2014;4(1):51-55.

114. H/F
• Psammomatoid juvenile ossyfing fibroma shows well
demarcated but uncapsulated lesion composed of numerous
small rounded mineralised collagenase bodies
(psammomatoid ossicles).
• Uniformly distributed within a cellular fibroblastic stroma.
Occasional shrunken cells , representing neucli of osteocytes,
are embedded within the ossicles, there is usually a collagen
outer band to these mineralised bodies.

115. • Trabacular variant – shows an uncapsulated tumor mass
infilterating into the surrounding bone and reactive bone
formation at the periphery . The tumors show a characteristic
loose structure with cell rich stroma composed of fibroblastic
spindle cells that produced little collagen.
• Anastomosing trabaculae of osteoid is seen in a pattern that
resembles pain brush strokes.

116. • Aggregates of osteoclastic giant cells are commonly present
and seen in association with the bony trabeculae and in
separate foci in the fibrous stroma.
• Management : excision
• Recurrence reported to a range of 30-50% in both the types.
• Malignant change has not been reported.

117. CEMENTO-OSSEOUS DYSPLASIA
• The jaws can be affected by several non-neoplastic
cementum-containing lesions.
• Collectively, these are referred to as cemento-osseous
dysplasias.
• In these cases, the term dysplasias are used to designate
abnormal development.
• All are presumed to be derived from the periodontal
ligament.

118. • These are classified into:
– Focal Cemento Osseous Dysplasia
– Periapical Cemental Dysplasia
– Florid Cemento Osseous Dysplasia

119. Periapical Cemental Dysplasia
Synonyms
• Cementoma, fibrocementoma, sclerosing cementoma,
periapical osteofibrosis, periapical fibrous dysplasia, and
periapical fibroosteoma.
DEFINITION: Periapical cemental dysplasia (PCD) is a localized
change in normal bone metabolism that results in the
replacement of the components of normal cancellous bone
with fibrous tissue and cementum-like material, abnormal
bone (similar to that seen in fibrous dysplasia), or a mixture
of the two.
• By definition the lesion is located near the apex of a tooth.

120. Etiopathogenesis
• Irrespective of the cause, the initial lesion of PCD is thought to
occur as a result of a proliferation of the principal fibers of the
periodontal ligament in the apical region of a tooth root.
• Thoma has described three stages in the development of this
entity.

121. • The first osteolytic stage is characterized by proliferation of
the principal fibers of the periodontal ligament, resulting in
the destruction and replacement of the contiguous bone by a
well- Circumscribed mass of fibrous connective tissue that
may or may not contain small, isolated nests of cementum
and or bone.

122. • In the second cementoblastic stage, larger islands of
cementum or bone are deposited within the fibrous stroma.
• The third mature stage is characterized by fusion of the
previously formed nests of cementum or bone, eventuating in
the formation of a calcified mass.
• It has been estimated that this calcification process may take
from 1 to 20 years or from 3 to 10 years. In some instances,
however, the lesion may remain static or even regress.

123. Clinical features
• PCD is a common bone dysplasia that typically occurs in
middle age; the mean age is 39 years.
• It occurs nine times more often in females
• Three times more often in blacks than in whites.
• The involved teeth are vital, and the patient usually has no
history of pain or sensitivity.

124. • The lesions usually come to light as an incidental finding
during a periapical or panoramic radiographic examination
made for other purposes.
• The lesions can become quite large, causing a notable
expansion of the alveolar process, and may continue to
enlarge slowly.

125. • R/ F
• Location - The epicenter of a PCD lesion usually lies at the
apex of a tooth.
• In rare cases the epicenter is slightly higher and over the
apical third of the root.
Radiolucent Stage.
Two periapical films
showing loss of lamina
dura; however, the
periodontal
membrane space can still
be seen around some of
the teeth.

126. • Predilection for the periapical bone of the mandibular
anterior teeth, although any tooth can be involved, and in
rare cases the maxillary teeth may be involved.
Examples of
periapical cemental
dysplasia in the
maxilla.
A mixed lesion.
B Mature lesions

127. • In most cases the lesion is multiple and bilateral, but
occasionally a solitary lesion arises.
• If the involved teeth have been extracted, this lesion can still
develop but the periapical location is less evident . In these
cases the term cemental dysplasia may be more appropriate.

128. • Periphery and shape. In most cases the periphery of a PCD
lesion is well defined. Often a radiolucent border of varying
width is present, surrounded by a band of sclerotic bone that
also can vary in width.

129. • The sclerotic bone represents a reaction of the immediate
surrounding bone.
• The lesion may be irregularly shaped or may have an overall
round or oval shape centered over the apex of the tooth.
• Internal Structure. The internal structure varies, depending
on the maturity of the lesion. In the early stage, normal bone
is resorbed and replaced with fibrous tissue that usually is
continuous with the periodontal ligament (causing loss of the
lamina dura).
•
• Radiographically, this appears as a radiolucency at the apex
of the involved tooth

130. • In the mixed stage, radiopaque tissue appears in the
radiolucent structure.
• This material usually is amorphous; has a round, oval, or
irregular shape; and is composed of cementum or abnormal
bone

131. • Sometimes the cementum-like material forms a swirling
pattern.
• These structures sometimes are called cementicles.

132. • In the mature stage, the internal
aspect may be totally radiopaque
without any obvious pattern.
Usually, a thin radiolucent
margin can be seen at the
periphery because this lesion
matures from the center
outward.

133. Effects on surrounding structures.
• The normal lamina dura of the teeth involved with the lesion
is lost, making the periodontal ligament space either less
apparent or giving it a wider appearance.

134. • The tooth structure usually is not affected, although in rare cases
some root resorption may occur.
• Also, occasionally hypercementosis occurs on the root of a tooth
positioned within the lesion.
• Some lesions stimulate a sclerotic bone reaction from the
surrounding bone.
• Small lesions do not cause expansion of the involved jaw.
• However, larger lesions may cause expansion of the jaw, an area
that is always bordered by a thin, intact outer cortex similar to
that seen in fibrous dysplasia.
• This lesion may elevate the .floor of the maxillary antrum.

135. Differential diagnosis
• Periapical rarefying osteitis:
 PCD cannot be differentiated from inflammatory lesions in
the early stage by radiographs alone.
 Final diagnosis rely on clinical examination and final
diagnosis.
• Benign cememtoblastoma
 In the case of a solitary mature form of PCD, the differential
diagnosis may include a benign cementoblastoma, especially
when the lesion is periapical to the mandibular first molar

136.  This tumor is usually is attached to the surface of the root,
which may be partly resorbed.
 Also, the peripheral soft tissue capsule is better defined and
there may be a unique pattern to the internal structure, such
as a radiating pattern.
 The presence or absence of clinical symptoms may help
distinguish PCD from benign cementoblastoma.

137. BENIGN CEMENTOBLASTOMA PCOD

138. FOCAL CEMENTOOSSEOUS DYSPLASIA
• It is a recently described entity that is thought to fall between
P.C.D. and florid osseous dysplasia in the biologic spectrum of
C.O.D.
• The term focal cementoosseous dysplasia was first suggested
by Tomich and Summerline in 1989.
• The etiology and precise pathogenesis are unknown, but it is
thought to be a reactive lesion.
Clinical features:
(1) Most common in females and a higher incidence in whites.

139. • Seen in 4th to 5th decades of life
• Seen in edentulous areas
• Lesions are typically solitary involving the bone in posterior
mandible.
• Characteristically asymptomatic and frequently discovered
during routine radiographic examination.

140. • R/F
• Most lesions are mixed radiolucent – radio opaque areas,
although the radiographic appearance may very from well
defined radiolucent lesion to a densely radio opaque area.
• Most of lesions < 1.5 cm in size
H/F
• Microscopically areas of cellular fibrous tissue containing
numerous small blood vessels, irregular trabaculae of woven
bone or cemetum like calcifications are seen .Scattered foci of
multinucleate giant cells may seen.

141. Focal cementoosseous dysplasia masquerading as a residual cyst. Bhandari
.R Contemp Clin Dent. 2012 ; 3: S60–S62.

142. • D/D
• PCD
• FCOD frequently occurs in edentulous as well as dentulous
areas, whereas PCD is always found apically to teeth
Treatment and prognosis:
• As lesions exhibits only limited potential for progressive
growth, most lesions require no additional treatment.
• Partial removal of the lesion also advocated in cases.
.

143. FLORID CEMENTO-OSSEOUS DYSPLASIA
Synonyms
• Florid cemento-osseous dysplasia, gigantiform cementoma,
familial multiple cementomas, sclerotic cemental masses,
sclerosing osteitis.
• Florid osseous dysplasia (FOD) is a widespread form of PCD.
• The term Florid cemento osseous dysplasia was first suggested
by Melrose et al in 1976.
• Normal cancellous bone is replaced with dense acellular
cemento-osseous tissue in a background of fibrous
connective tissue.

144. Etiology - is unknown
• Waldron has proposed reactive or dysplastic changes in
periodontal ligament may be a cause
• The lesion has a poor vascular supply, a condition that likely
contributes to its susceptibility to infection.
• In some cases a familial trend can be seen.

145. C/F
• Most patients with FOD are female (blacks) and middle aged
• Striking tendency for bilateral occurance often presenting
symmetry of the jaws.
• Many patients are partially or completely edentulous when
the conditions are detected.
• Occasionally patients complain of low-grade, intermittent,
poorly localized pain in the affected bone, especially when a
simple bone cyst has developed within the lesion.

146. • Extensive lesions often have an associated bony swelling.
• If the lesions become secondarily infected, features of
osteomyelitis may develop, including mucosal ulceration,
fistulous tracts with suppuration, and pain.

147. R/F
• Location. FOD lesions usually are
bilateral and present in both
jaws).
• However, when they are present
in only one jaw, the mandible is
the more common location.
• The epicenter is apical to the teeth,
within the alveolar process and
usually posterior to the cuspid.
• In the mandible, lesions occur
above the inferior alveolar canal.

148. • Periphery. The periphery
usually is well defined and has
a sclerotic border that can vary
in width, very similar to PCD.
• Soft tissue capsule may not be
present in mature lesions.

149. Internal Structure.
• The density of the internal structure can vary from an equal
mixture of radiolucent and radiopaque regions to almost
complete radiopacity.
• Some prominent radiolucent regions, which usually represent
the development of a simple bone cyst, may be present.
• These cysts may enlarge with time, even beyond the boundary
of the lesion into the surrounding normal bone, or may fill in
with abnormal dysplastic cemento-osseous tissue.

150. • The radiopaque regions can vary from small oval and
circular regions (cotton-wool appearance) to large, irregular,
amorphous areas of calcification.
• These calcified masses are similar in appearance to those seen
in mature PCD lesions.

151. Two examples of
florid osseous
dysplasia
(FOD) associated
with multiple
simple bone
cysts.

152. Effect on the sourrounding structure
• Large lesions may displace inferior alveolar nerve canal
• Floor of antrum in superior direction
• Expansion of cortices
• Hypercementosis irt involved tooth, which may fuse with the
adjacent teeth (extraction difficult)
Histopathological features:
• FCOD shows admixtures of woven bone trabaculae and
droplets of cementum like calcifications in a fibroblastic
stroma. The cementum like calcifications often fuse to form
coalescing masses.

153. D/D
PAGET’S DISEASE:
• PD also shows cotton wool appearance and hypercmentosis,
but PD affects entire bone whereas FOD is centered above the
inferior alveolar nerve canal.
• Also PD is polystotic.

154. Paget' Disease (PD) Florid Cemento-Osseous
Dysplasia (FLCOD)
Generalized changes that are
apparent throughout the jaws
Alterations confined to tooth-
bearing areas.
Maxilla preferentially affected Mandible is favored.
May cause displacement and
separation of teeth.
No effect on tooth alignments
More common in females More Common males
Accompanied by increase in
serum alkaline phosphatase levels.
Alkaline phosphatase levels are
within normal limits
Often polyostotic and frequently
involves the skull.
Disease limited to the jaw.

155. • Chronic diffuse sclerosing osteomyelitis
 Regions of cementum-like masses may appear similar to the
sequestrum seen in osteomyelitis.
 This is not to be confused with a situation where FOD has
become secondarily infected, resulting in osteomyelitis. The
cemental-like masses that are secondarily infected have a
wider and more profound radiolucent border
 CT imaging is essential for the diagnosis and to determine
the extent of the osteomyelitis within the FOD.

156. A, Axial CT of a case of florid osseous dysplasia (FOD); multiple
foci of cemental dysplasia are bordered by a soft tissue capsule
(white arrow) and a cemental mass has become secondarily
infected with a wider and more pronounced radiolucent border
(black arrow).
B, Axial CT image of a different casae of osteomyelitis from
secondarily infected FOD; note the break in the outer cortex where
the lesion is draining into the surrounding soft

157. CENTRAL GIANT CELL GRANULOMA
Synonyms
• Giant cell reparative granuloma, giant cell lesion, and giant
cell tumor
• Central giant cell granuloma (CGCG) is thought to be a
reactive lesion to an as-yet-unknown stimulus and not a
neoplastic lesion.
C/F
• CGCG is a common lesion in the jaws that affects mostly
adolescents and young adults; at least 60% of cases occur in
individuals younger than 20 years.

158. • The most common presenting sign of CGCG is painless
swelling.
• The overlying mucosa may have a purple color.
• Some of these lesions cause no symptoms and are found only
on routine examination.
• The lesion usually grows slowly, although it may grow
rapidly, creating the suspicion of a malignancy.

159. • Depending on clinical and radiographic features, central
giant cell granuloma can be classified into two types.
• The first type of lesion is non-aggressive, slow growing, does
not show root resorption or cortical perforation, and often
shows new bone formation.
• The second type is an aggressive type which grows quickly,
shows pain, cortical perforation, and root resorption.

160. R/F
• Location- Lesions develop in the mandible twice as often as in
the maxilla.
• In the first two decades there is a tendency for the epicenter
of the lesion to be anterior to the first molar in the mandible
and anterior to the cuspid in the maxilla.
• However, in older individuals this lesion can occur in greater
frequency in the posterior aspect of the jaws

161. • Periphery.- Because this grows relatively slowly, it usually
produces a well-defined radiographic margin in the
mandible.
• In most cases the periphery shows no evidence of cortication.
• Lesions in the maxilla may have ill-defined, almost
malignant-appearing borders.

162. • Internal Structure. Some CGCG lesions show no evidence of
internal structure, especially small lesions.
• Other cases have a subtle granular pattern of calcification.
• granular bone is organized into ill-defined, wispy septa
• If present, these granular septa are characteristic of this lesion.
especially if they emanate at right angles from the periphery of the
lesion.
• In some instances the septa are better defined and divide the
internal aspect into compartments, creating a multilocular
appearance.

163. Effects on Surrounding Structures.
• Giant cell granulomas often displace and resorb teeth with
irregular outline.
• 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.

164. Histologic Features.
• Central giant cell granuloma is made up of a loose fibrillar
connective tissue stroma with many interspersed
proliferating fibroblasts and small capillaries.
• The collagen fibers are not usually collected into bundles;
however, groups of fibers will often present a whorled
appearance.
• Multinucleated giant cells are prominent throughout the
connective tissue, but not necessarily abundant.

165. • In addition, there are usually numerous foci of old
extravasated blood and associated hemosiderin pigment,
some of it phagocytized by macrophages. Foci of new
trabeculae of osteoid or bone also are often seen, particularly
around the periphery of the lesion.

166. Treatment and Prognosis.
• The treatment of the giant cell granuloma is curettage or
surgical excision.
• The lesions so treated almost invariably fill in with new bone
and heal with no difficulty.
• Occasional lesions recur, but this is seldom sufficient cause
for more radical procedures. X-ray radiation is
contraindicated.

167. • Interim intralesional steroids definitely helped to prevent the
progression of this lesion and avoided extensive bony
destruction.( MOA-It has been shown that osteoclast-like
multinucleated giant cells decrease their lysosomal protease
extracellular production, which mediates bone resorption, in
the presence of steroids.
An Unusual Presentation of a Central Giant Cell Granuloma and Initial Treatment
with Intralesional Steroids– A Case Report and Review of the Literature. Richard M
Graham et alJ Oral Health Comm Dent 2008;2(3):65-69

168. • Successful examples of the use of intralesional steroids are as
follows: In Kurtz’s case; 12 injections of intralesional
Triamcinalone Acetonide were given, in total, for a 15cm
lesion, 150mg each for at least 6 of these, which resulted in
complete re-ossification of the area affected by a central
giant cell granulomas.
• In addition, Carlos et al. have reported 4 cases of central giant
cell granulomas, which were treated successfully in the same
way (the average dose was 25mg of Triamcinalone Acetonide
for the paediatric patients).
• Khafif et al.’s case of a central giant cell granuloma of the
maxilla was successfully treated with intralesional
corticosteroids; there was no lesion recurrence and the defect
calcified (average dose of 40mg Triamcinalone Acetonide +
0.5% Bupivacaine weekly for 6 weeks).

169. Aneurysmal Bone Cyst
• Aneurysmal bone cyst (ABC) has been recognized since 1893
when it was described as an ossifying hematoma by Van
Arsdale.
• An aneurysmal bone cyst (ABC) usually is considered to be a
reactive lesion of bone rather than a cyst or true neoplasm.
• It represent an exaggerated proliferative response of vascular
tissue in bone.

170. • The cause of this strange process in bone is unknown but several
examples apparently arose after a fracture.
• It is similar to and probably related to other reactive non-
neoplastic processes, including giant cell reparative granuloma
of the jaws, traumatic reactions in periosteum and bone and even
florid heterotopic ossification.
• Aneurysmal bone cyst may arise denovo in bone; that is, a
definite preexisting lesion cannot be demonstrated in the tissue.
• Rarely malignant tumors of bone contain such benign areas as
well. Obviously, recognition of an underlying process is
important.

171. C/F
• Fifty percent of ABCs arise in the long bones and 20% in the
vertebral column.
• It accounts for 1.5% of the nonodontogenic, nonepithelial
cysts of the mandible
• Younger than 30 years.
• predilection for females.
• It is found more frequently in the mandible than the maxilla
(3:1) with preponderance for the body, ramus and angle of
the mandible.
• An ABC in the jaw usually manifests as a fairly rapid bony
swelling .
• Pain is an occasional complaint, and the involved area may
be tender on palpation

172. R/F
• Location - The mandible is involved more often than the
maxilla (ratio of 3 : 2), and the molar and ramus regions are
more involved than the anterior region
• Periphery and Shape. The periphery usually is well defined,
and the shape is circular or “ hydraulic. ”
Aneurysmal bone cyst of the mandible: A case report and review of literature,
parvathi deviJ Oral Maxillofac Pathol; 15(1): 105–108.

173. • Often the internal aspect
has a multilocular
appearance.
• The septa bear a striking
resemblance to the
wispy, illdefined septa
seen in giant cell
granulomas.
• Another similar finding
is septa positioned at
right angles to the outer
expanded border.

174. Effects on Surrounding Structures.:
• After an ABC becomes large, expansion of the outer cortical
plates and root reeorption may be seen.
Histologic Features.
• The aneurysmal bone cyst consists of a fibrous connective
tissue stroma containing many cavernous or sinusoidal
blood-filled spaces. These spaces may or may not show
thrombosis.

175. • Young fibroblasts are numerous in the connective tissue
stroma, as well as multinucleated giant cells with a patchy
distribution similar to that in the giant cell granuloma.
• But in the latter lesion the cavernous spaces are not found.
Varying amounts of hemosiderin are present and, invariably,
new osteoid and bone formation

176. D/D
• The multilocular appearance of ABCs most resembles that of
giant cell granulomas; in fact, the radiographic appearance of
the two lesions may be identical.
• However, ABCs may expand to a greater degree, and they are
more common in the posterior parts of the mandible.

177. • Ameloblastoma may be considered, but this lesion usually
occurs in an older age group.
• ABCs may show a similarity to cherubism, which has giant
cell – like features, but cherubism is a multifocal bilateral
disease.
• Hemorrhagic aspirate is seen in abc
Treatment
• Surgical curettement or excision is the treatment of choice,

178. Differential diagnosis of fibro-osseous lesions
Radiolucent lesions-
• Unicystic radiolucency with sclerotic margin-
• Cyst- radiolucency will be smooth, thin and sharply defined.
Tooth will be vital and aspiration shows positive response.
• Unilocular radiolucency without sclerotic margin with ill
defined margins should be differentiated with malignancies.
• Root resorption will also be seen in all malignant lesions.
Multilocular radiolucent lesion
• Locules of trabeculae might be few in number and of poor
density like central giant cell granuloma or it may be coarse
and thick resembling like ameloblastoma

179. Mixed radiolucent and radioopaque lesions-
 Periapical cement osseous dysplasia
 Malignant metastatic lesions like osteogenic sarcoma and
osteoblastic carcinoma
 Fibrous dysplasia
 Condensing osteitis
 Cement-ossifying fibroma
 Periapical cement osseous dysplasia- radiolucent lesion
surrounds the apex of the tooth, with either sclerotic margin
or opaque masses within the lucent lesion. Tooth will be vital,
absence of pain, no expansion of cortices

180. • Malignant metaststic lesions like osteogenic sarcoma and
osteoblastic carcinoma appears as mixed radiolucent –
radioopaque lesions but they are usually irregular and ill
defined along with root resorption which is not seen in fibro-
osseous lesions.
• Odontoma- it is usually located above the crown of an
unerupted tooth and seldom it is found in the apical region .
these are more radioopaque compared to fibroosseous lesions.

181. • Fibrous dysplasia- common in maxilla, seen in 1st and 2nd
decade of life. Has equal predilection for both male and
female. Jaw expansion is seen which is of fusiform type. there
is no line of demarcation between normal bone and defective
bone.
• Condensing osteitis- clinically pain, inflammation, drainage,
tenderness on palpation and regional lymphadenitis will be
present.
• Cement-ossifying fibroma- predilection for premolars and
molars. Seen under 30 years . Attains size of 2 to 4 cm,
produces discernible expansion.

182. • Mixed radiolucencies and radioopacities not necessarily
contacting teeth
 Fibrous dysplasia
 Chronic osteomyelitis
 Cement-ossifying fibroma
 Pagets disease
 Chondrosarcoma
• Radio-opaque lesions-
 Fibrous dysplasia
 Focal sclerosing osteomyelitis
 Diffuse sclerosing osteomyelitis
 Focal cement-osseous dysplasia.

183. Conclusion :
The Fibro-osseus lesions of the jaws comprise a diverse,
interesting, and challenging group of conditions that pose
difficulties in classification and treatment. Common to all is the
replacement of normal bone by a tissue composed of collagen
fibers and fibroblasts that contain varying amounts of
mineralized substance, which may be bony or cementum-like in
appearance.
A definitive diagnosis of a Fibro-osseus lesion requires
correlation of the histologic features with the clinical,
radiographic, and intraoperative findings.
Despite the advances in the understanding of these conditions,
fibro-osseous lesions continue to present problems in
classification, diagnosis, and management due to multiple
histological and radiographic similarities.

184. References :
• A textbook of oral pathology: shafer, hine and levy: 5th edition
• Burket’s oral medicine: 11th edition
• Differential diagnosis of oral lesions: wood and goaz: 3rd edition .
• Oral pathology .Regezi & scuibba.4th edition.
• Oral & maxillofacial pathology. Neville 2nd edition
• Oral radiology, principles and interpretation, 4th edition, white and
pharoah.
• Current concepts review fibrous dysplasia pathophysiology, evaluation,
and treatment mathew r etal. The journal of bone and joint surgery 2005
• The radiological versatility of fibrous dysplasia: An 8-year retrospective
radiographic analysis in a north Indian population ,praksah.R
etal, journal of dentistry 2014; 5(3):139-145.
• Peñarrocha et al. Cherubism. J Oral Maxillofac Surg 2006.

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Gulati A J Clin Exp Dent. 2011;3(4):e297-302.
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2016; Vol, 2 No 1:1-10.
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literature Devi PJ Oral Maxillofac Pathol. 2011;15(1): 105–108.
• An Unusual Presentation of a Central Giant Cell Granuloma and Initial
Treatment with Intralesional Steroids– A Case Report and Review of the
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2008;2(3):65-69