benign fibro-osseous lesions of jaw

1. PRESENTED BY: Shivani Yadav
BDS 4th year

2.  Fibro-osseous lesions refer to a collection of
nonneoplastic intra-osseous lesions that replace
normal bone and consist of a cellular fibrous
connective tissue within which nonfunctional
osseous structures form.(Eversole)
 Fibro osseous lesions are a diverse group of
processes that are characterized by replacement
of normal bone by fibrous tissue containing a
newly formed mineralized product.(Neville)

3. A. Fibrous Dysplasia
B. Reactive (dysplastic) lesions arising in the tooth bearing area:
NON-HERIDITARY
 -Periapical cemento-osseous dysplasia
 -Focal cemento-osseous dysplasia
 -Florid cemento-osseous dysplasia
HEREDITARY
 -Familial gigantiform cementoma
C. Fibro – osseous neoplasms
 -Cementifying fibroma
 -Ossifying fibroma
 -Cemento-ossifying fibroma
 -Juvenile ossifying fibroma
D. Cherubism

4.  Definition: Fibrous dysplasia is an asymptomatic
regional alteration of bone in which the normal
architecture is replaced by fibrous tissue and
nonfunctional trabecule-like osseous structures;
lesions may be monostotic or polyostotic, with or
without associated endocrine disturbances.

5.  Unknown
 No hereditary influence
 Results from mutation in GNAS 1 gene(Guanine nucleotide-
binding protein, α-stimulating activity polypeptide 1).
 GNAS 1 gene encodes a G-protein
stimulates
production of cAMP.
mutation results in continuous production of G-
protein overproduction of cAMP in affected
tissues.
 This results in hyperfunction of endocrine organs, giving rise to
precocious puberty, hyperthyroidism, growth hormone and cortisol
production.
 There is increased proliferation of melanocytes resulting in large
café au lait spots.
 cAMP effect on differentiation of osteoblasts leading to fibrous
dysplasia.

6.  Monostotic fibrous dysplasia- only one bone is
involved.
 Polyostotic fibrous dysplasia- more than one bone is
involved:
- Jaffe type; fibrous dysplasia involving variable
number of bones, accompanied by pigmented lesions
of the skin or café-au-lait spots.
- Mc-Cune albright’s syndrome; this is severe form of
fibrous dysplasia involving nearly all bones in the
body, accompanied by pigmented lesions of the skin
plus endocrinal disturbance of various types.
 A craniofacial form- In which the maxilla and
adjacent bones are involved.

7. CLINICAL FEATURES
 Limited to a single bone.
 It is common than the polyostotic form
 Accounts for 70% to 80% of all cases
 Occurs most commonly at the age of 20
to 30 years.
 M:F = 1:1
 Most common sites in order of affection
are ribs, femur, tibia, maxilla and
mandible.
 In Jaw bones Maxilla > Mandible.
 Unilateral painless facial swelling or
enlarging deformity of alveolar process.
 Slow growth, become static with
skeletal growth completion
 Teeth involved are either malaligned,
tipped or displaced.

8.  Involvement of two or more bones.
 When seen with café au lait pigmentation  Jaffe-
Lichtenstein syndrome.
 Polyostotic fibrous dysplasia + café au lait
pigmentation + multiple endocrinopathies (
precocious puberty, goiter, hyperthyroidism,
acromegaly )  McCune Albright Syndrome.

9.  In children usually less than 10 years of age.
 male: female = 1:3
 May present with facial asymmetry
 Clinical features usually dominated by symptoms
related to long bone lesions – Pathologic fractures
with pain and deformity
 Leg length discrepancy due to involvement of upper
portion of femur (hockey stick deformity)
 Café au lait pigmentation – well defined, generally
unilateral tan macules on the trunk and thighs.
- May be congenital
- Oral cavity can be involved.
- Margin typically irregular (resembling map of
Coastline of Maine)

13.  Occurs in 10-25% pateint with monostotic form and
in 50% with polyostotic form
 Peculiar form affecting skull bones
 Not restricted to single bone, but confined to single
anatomic site.
 Primarily affect maxilla, but may cross sutures into
sphenoid, zygoma, frontonasal bones and base of
skull.
 Hypertelorism, cranial asymmetry, facial deformity,
visual impairment, exophthalmos, blindness,
vestibular dysfunction,tinnitus and hearing loss may
occur

14.  LOCATION: involves the maxilla almost twice as often as the mandible
Occurs more frequently in the posterior aspect.
More commonly are unilateral.
 PERIPHERY: ill defined, with a gradual blending of normal trabecular bone
into an abnormal trabecular pattern.
 INTERNAL STRUCTURES: density and trabecular pattern of fibrous
dysplasia lesions vary, more pronounced in mandible.
Early onset lesions are single or multiple, symmetrical or asymmetric
radiolucency with ill-defined borders.
Later progressively calcify and can present as a spectrum of four patterns in a
panoramic radiograph:
1. Ground glass (condensed/granular),
2. Cotton-wool pattern
3. An orange-peel pattern
4. Fingerprint pattern.
 EFFECTS ON SURROUNDING STRUCTURES: Variations in the cortical
thickness are caused by slow resorption of the endosteal surface, commonly
referred to as "endosteal scalloping.”
The periosteal surface remains smooth.

15. A series of films showing a variety of internal patterns of fibrous dysplasia.
A fingerprint pattern around the
roots of the first molar (arrow).
A granular, or ground-glass,
pattern (arrow)
A cotton-wool pattern An orange-peel pattern.

17.  Juvenile Ossifying fibroma
 Cemento-osseous dysplasia
 Paget’s disease
 Hyperparathyroidism
 Cementoma
 Cherubism
 Chronic sclerosing osteomyelitis
 Osteogenic sarcoma.
 Periapical cemental dysplasia

18.  Treatment is conservative and primarily to prevent
deformity.
 Recommended treatment options can be divided into
4 categories:
1. Observation
2. Medical therapy
3. Surgical remodelling
4. Radical excision and reconstruction
 Most lesion stabilize with skeletal maturation
 Small lesions can be resected entirely
 Surgical recontouring after skeletal maturation

19.  Cemento-osseous dysplasia occurs in the tooth-
bearing areas of the jaws.
 Most common fibro-osseous lesion encountered
in clinical practice.
 Periodontal ligament origin
 It is of three groups:
1. Focal
2. Periapical
3. Florid

20.  PCD is not a true neoplasm but a dysplastic condition in which multiple
focal areas of bone and marrow are replaced by cellular connective tissue
lesions with limited growth potential.
 The lesion attains a fixed size and later undergoes a maturation process
that culminates in the formation of multiple dense calcified (sclerotic)
intrao-sseous nodules.
CLINICAL FEATURES
 Involves periapical region of anterior mandible.
 Asymptomatic.
 Occurs in middle-aged women.
 Mean age is 39 years.
 More female predilection.
 Involved teeth are vital and
 Buccal and lingual expansion of
cortices is absent.

21.  3 radiographic features indicates stage from early
formation to maturation:
1. OSTEOLYTIC STAGE: in this early stage, lesion
are well defined radiolucencies at apex of one or
more teeth.
2. CEMENTOBLASTIC STAGE: displays similarly
sized lesions and a demarcated border with
radiolucencies containing nodular radiopaque
deposits.
3. MATURE STAGE: well defined, dense radiopacities
exhibit some nodularity. Each radiopaque nodule
has thin radiolucent zone around its periphery that
separates it from the surrounding bone and nearby
teeth.

22. Radiolucent Stage
3 stages of Periapical Cemental Dysplasia
Mixed lesion. Mature lesions (arrows).

23. Radiolucent stage
 Apical periodontal granuloma or a radicular cyst
 Primordial odontogenic cyst
 Early phase of ossifying fibroma
 Chronic osteomyelitis( If 4 to 6 anterior teeth are
involved)
Mixed stage and radiopaque stage
 Odontoma
 Chronic osteomyelitis
 Ossifying fibroma
 Osteoblastoma

24.  After a diagnosis of PCD is made, no further
treatment is necessary.
 A possible complication of biopsy in secondary
infection, which may occur in lesions that have
abundant amorphous bone formation and poor
vascularity.

25. Focal cemento-osseous dysplasia exhibits single site of involvement.
Etiology
 Unknown
 Derives histogenetically from elements of the periodontal ligament.
 Reactive lesion
Clinical Features :
 Female predominance.
 3rd – 6th decades of life.
 Mean age 38 years.
 Solitary lesions , in posterior mandible.
 Asymptomatic
 Occurs in periapical areas of teeth
with vital pulps or in regions of
extractions.
 Lesions are smaller than
1.5cm in diameter.
Curetted material consisting of multiple
small gritty and hemorrhagic fragments

26.  Most lesions appear as radiolucent – radio-opaque
areas with thin peripheral radiolucent rim.
 Lesion is well defined, borders are slightly irregular.
 In edentulous areas development of idiopathic bone
cavities, result in bony expansion of affected area.

27. OSTEOLYTIC STAGE
 periapical granuloma or cyst
 chronic osteomyelitis
MIXED AND RADIOPAQUE STAGE
 chronic sclerosing osteomyelitis,
 ossifying/cementifying fibroma,
 odontoma
 osteoblastoma.

28. • No treatment is required for FCOD
• Follow-up is required to confirm the diagnosis.
Some authors have hinted on the possibility of
transformation of FCOD into florid cemento-osseous
dysplasia and emphasized on the importance of
recall visits

29. It is widespread form of periapical osseous dysplasia.
DISEASE MECHANISM:
 Normal cancellous bone is replaced with dense,
acellular amorphous bone in a background of
fibrous connective tissue.
 The lesion has a poor vascular supply, a condition
that likely contributes to susceptibilty to infection.
 Familial trend can be seen.

30.  Multifocal lesion, affect all quadrants of
the maxilla and mandible.
 Middle-aged females . ( mean age 42
years)
 Painless non-expansile lesion often
involving two or more jaw quadrants.
 Tendency toward bilateral, symmetrical
involvement
 Asymptomatic and detected incidentally
Jaw expansion - large lesions.
 Dull pain or an alveolar sinus tract may
be present, exposing yellowish, avascular
bone to oral cavity.

31.  LOCATION: Usually bilateral and present in both jaws.
 PERIPHERY: Well defined, and has sclerotic borders
 INTERNAL STRUCTURES: 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.
The radiopaque regions can vary from small oval and circular
regions (cotton-wool appearance) to large, irregular, amorphous
areas of calcification.
 EFFECTS ON SURROUNDING STRUCTURE: can displace the
inferior alveolar nerve canal in an inferior direction, the floor of
the antrum in a superior direction and can cause enlargement of
the alveolar bone by displacement of the buccal and lingual
cortical plates.

32. Florid cemento osseous dysplasia: multiple mixed radiopaque-radiolucent
lesions in the periapical regions throughout the jaws (arrows)
Undulating expansion of the
medial cortical plate (arrow).
multiple, very mature, almost totally
radiopaque lesions in edentulous jaws.

33.  Paget’s disease.
 Chronic sclerosing osteomyelitis
 Gigantiform cementoma,
 Osteogenesis imperfecta
 Polyostotic fibrous dysplasia.

34.  Usually no treatment is necessary for FOD.
 Patients are asked to maintain a good oral
hygiene as FOD can get infected causing
secondary osteomyelitis. That is one of the
reasons why care should be done when extracting
teeth associated with the lesion to avoid
secondary infection to the underlying FOD.

35.  It is a disorder of gnathic
bone that leads to formation
of massive sclerotic masses of
disorganisnized mineralized
products.
 An autosomal dominant
variant usually involving
multiple quadrants with
variably expansile lesions.

36.  Anterior mandible.
 No sexual predilection.
 No racial predilection.
 Begins during 1st decade of life and can grow
rapidly.
 Involvement of both maxilla and mandible.
 Gnathic enlargement result in facial deformity, as
well as impaction, malposition and malocclusion
of the involved dentition.

37.  Multiple radiolucencies in periapical regions
 Expansion of affected side and develop mixed
radiolucent and radiopaque pattern.
 Further maturation, lesion become predominantly
radiopaque with thin radiolucent rim.

38.  Paget’s disease
 Chronic sclerosing osteomyelitis
 Scelerotic cemental masses
 Chronic productive osteitis
 Osseous dysplasia,
TREATMENT
Resection of altered bone with immediate or staged
reconstruction of facial skeleton and associated soft
tissues can produce acceptable functional and
aesthetic results.

39.  A true neoplasm with a significant growth potential.
 Composed of fibrous tissue that contains a variable
mixture of bony trabeculae, cementum- like
spherules, or both.
 Origin from odontogenic or periodontal ligament
 Cementum-like material present
Types
 Ossifying/ Cementifying Fibroma
 Juvenile Ossifying Fibroma
-Trabecular Juvenile Ossifying Fibroma
-Psammomatoid Juvenile Ossifying Fibroma

40.  This bone tumour consists of highly cellular, fibrous
tissue that contains varying amounts of abnormal bone or
cementum-like tissue.
 Most common form of OF occurs in maxilla and
mandible.
 Mutation in HRPT2 (hyperparathyroidism 2) gene that
encodes parafibromin protein in patient with rare
condition known as hyperparathyroidism-jaw tumor
syndrome.
 Painless with expansion of both cortices.
 Larger lesions may expand the inferior aspect of
mandible.
 Teeth are displaced superiorly ( mandibular lesion) and
inferiorly( maxillary lesion) and expand into the antrum.

42.  Location. COF appears almost exclusively in the facial bones and
most commonly in the mandible, typically inferior to the premolars
and molars and superior to the inferior alveolar canal.
 Periphery. borders are well defined.
A thin, radiolucent line, representing a fibrous capsule, may separate it
from surrounding bone.
 Internal Structure mixed radiolucent-radiopaque density with a
pattern that depends on the amount and form of the manufactured
calcified material. In the type that contains mainly abnormal bone, the
pattern may be similar to that seen in fibrous dysplasia, or a wispy
(similar to stretched tufts of cotton) or flocculent pattern (similar to
large, heavy snowflakes) may be seen.
 Effects on Surrounding Structures. growth of the lesion, which
tends to be concentric within the medullary part of the bone with
outward expansion approximately equal in all directions. This can
result in displacement of teeth or of the inferior alveolar canal and
expansion of the outer cortical plates of bone.
The lamina dura of involved teeth usually is missing, and resorption of
teeth may occur.

43. A solid, radiopaque,
cementum-like pattern
(arrow).
Various Bone Patterns Seen in Cemento-Ossifying Fibromas
A wispy trabecular
pattern (arrow)
Radiolucent pattern with
a few wispy trabeculae
(arrow).
A fibrous dysplasia,
granular-like pattern
(arrows).
A flocculent pattern with larger
tufts of bone formation (arrow).

44.  Fibrous dysplasia
 Periapical cemento-osseous dysplasia
 Giant cell granuloma,
 Calcifying odontogenic cysts
 Calcifying epithelial odontogenic( Pindborg)
tumors
 Adenomatoid odontogenic tumors.
 Osteogenic sarcoma

45.  The prognosis of COF is favourable with surgical
enucleation or resection.
 Large lesions require a detailed determination of
the extent of the lesion, which can be obtained
with CT imaging. Even if the lesion has reached
appreciable size, it usually can be separated from
the surrounding tissue and completely removed.
 Recurrence after removal is unlikely.

46.  Juvenile ossifying fibroma (JOF) appears at an early age and 79% of
the patients are diagnosed before the age of 15.
 Males and females are equally affected
 JOF originates from periodontal ligament and ranges 2% of oral
tumours in children.
 Located mainly (85%) in facial bones, in some cases (12%) in
calvarium and very seldom (3%) extracranially.
 Mandibular lesions are seen in 10% of the cases
 The tumour is well circumscribed by a tiny sclerotic shell of bone.
 It appears locally aggressive with cortical disruption and involvement
of many adjacent anatomical structures.
 Lesion has soft tissue consistency with variable amounts of internal
calcification and/or linear or irregular focal bone.
 2 clinicopathologic entities:
1. Trabecular Juvenile Ossifying Fibroma
( TrJOF)
2. Psammomatoid Juvenile Ossifying Fibroma (PsJOF)

47. Photograph of a 9 year old girl with JOF
showing unilateral swelling extending
from the right submandibular to the right
mandibular ramus and corpus region.
Photograph of mandibular ramus and
corpus region showing clear lingual
expansion of the mandible (arrow).

48.  Also known as trabecular desmo-osteoblastoma.
 Majority of patients are children and adolescents.
 Only 20% are over 15 years of age.
 M:F = 1:1
 Maxilla and mandible are dominant sites.
 Maxilla is slightly more affected.
 Progressive and sometimes rapid expansion of bone
 In maxilla, obstruction of nasal passages and
epistaxis may be present.

49.  Expansive and well
demarcated
 With cortical thinning
and perforation
 Shows varying amount
of radiolucency and
opacity depending upon
amount of calcified
tissue.
 Ground glass and
honeycomb appearance.

50.  Uncapsulated and shows
infiltration of surrounding bone
 Characteristic loose structure
 Stroma is cell rich, with
spindle or polyhedral cells,
produce little collagen
 Cellular, immature osteoid
forms strands.
 Irregular mineralization takes
place at the centre of the
strands
 Local aggregates of
osteoclastic giant cells are
invariably present in the
stroma.
Tumour shows the presence of
trabeculae of fibrillar osteoid and
woven bone (hematoxylin and eosin
stain)

51.  Clinical course is characterized by infrequent
recurrence following conservative excision.
 Complete cure could be achieved in those cases
without resorting to radical surgical intervention.
 Malignant transformation not reported

52.  JOF is characterised by the presence of small uniform
spherical ossicles that resemble psammoma bodies
 It is reported more commonly than trabecular JOF.
 16 to 33 years.
 Range of 3 months to 72 years.
 Occurs predominantly in the sinonasal and orbital bones,
and trabecular JOF predominantly affects the jaws.
 Bone expansion involves orbital or nasal bones and
sinuses.
 Orbital extension- proptosis and visual complaints
including blindness, nasal obstruction, ptosis, and
disturbances in ocular mobility.
 Aggressive behaviour and it has a very strong tendency
to recur.

53.  Round, well defined,
corticated osteolytic lesion
with a cystic appearance.
 In CT scans, appear less
dense than normal bone,
appear multiloculated
 Size range from 2 to 8 cm
 In facial skeleton a well
circumscribed expansive mass
with a thick wall of bone
density on CT scan is strongly
suggestive of psammomatoid
juvenile ossifying fibroma.

54.  On gross examination tumor is
yellowish, white and gritty.
 Histologically, multiple round
uniform small ossicles
(psammomatoid bodies)
embedded in a cellular stroma
composed of uniform, stellate,
and spindle shaped cells.
 Psammomatoid bodies are
basophilic and bear superficial
resemblance to dental
cementum, but may have an
osteoid rim.
Cellular fibrous connective
tissue containing spherical
ossicles with basophilic
centres and peripheral
eosinophilic rims

55.  Surgical excision is treatment of choice.
 Recurrence rate of >30% reported.
 No malignant change observed.

56.  Monostotic fibrous dysplasia.
 Central giant cell granuloma
 Aneurysmal bone cyst
 Osteoblastoma
 Calcifying odontogenic cyst
 Primodial cyst
 Adenomatoid odontogenic tumor

57.  It is a autosomal dominant fibro-osseous benign hereditary
condition which affects only the jaw bones and it is
characterized by “bilaterally symmetrical enlargement” of
mandible sometimes maxilla.
PATHOGENESIS
 Hereditary disease
 Inherited as an autosomal dominant trait.
 Gene for cherubism present on chromosome 4p16.3.
 It can occur as a result of:
-anomalous development of bone
-latent hyperthyroidism
-hormone dependent neoplasm
-disturbance in development of bone forming mesenchyme.

58. On the bases of severity and location of lesion and
extent to which jaws are affected.
1. Grade 1: Fibro-osseous expansion tends to be
bilateral and symmetrical. Primarily in the ramus of
mandible.
2. Grade 2 : In more severe cases the ramus and the
body of mandible are involved resulting in
congenital absence of third and occasionaly second
mandibular molar teeth. Maxillary tuberosity may
also be affected.
3. Grade 3: Lesion affect maxilla and mandible
entirely and may result in considerable facial
deformities.

59.  At birth, appearance is normal.
 Between 1 to 5 years, symmetrical,
painless, bilateral mandibular swelling with
cheek fullness give appearance of ( chubby
face)to a child.
 In extensive maxillary swelling, pressure on
floor of orbit result in upward turn of pupil,
revealing a rim of white sclera below iris (
Heavenward look/ angelic appearance)
 Expansion and widening of alveolar ridge,
flattening of palatal vault.
 Submandibular lymphadenopathy
 Premature exfoliation of decidous teeth,
rotation transposition teeth and occasionally
resorption of root, malocclusion occurs.
 Difficulty in mastication, speech and
swallowing.

60.  LOCATION: bilateral affects both jaws involving posterior
mandible ramus, tuberosity.
 PERIPHERY: well defined, corticated.
 INTERNAL STRUCTURES: fine granular bone and wispy
trabeculae forming prominent multilocular “cyst-like” pattern.
 EFFECT ON SURROUNDING STRUCTURES: Expansion of
cortical boundaries, severe enlargement of jaws.
Multiple unerupted and displaced teeth appear to be floating
within the cyst-like spaces (Floating tooth syndrome)

61.  Fibrous dysplasia
 Giant cell granuloma
 Multiple odontogenic keratocysts
 Hyperparathyroidism
 Ameloblastoma
 Odontogenic myxoma
 Nevoid basal cell carcinoma
 Aneurysmal bone cyst

62.  The lesions tend to show varying degree of
remission after puberty.
 By 4th decade facial feature approach normalcy.
 Early surgical intervention for cosmesis has
given good results.
 Some studies showed the use of calcitonin, but
still not proved.

63.  Paget ’ s disease is a skeletal disorder and essentially
a disease involving osteoclasts, resulting in abnormal
resorption and apposition of osseous tissue in one or
more bones.
 The disease may involve many bones
simultaneously, but it is not a generalized skeletal
disease.
 Initiated by an intense wave of osteoclastic activity,
with resorption of normal bone resulting in
irregularly shaped resorption cavities. After a period
of time, vigorous osteoblastic activity ensues,
forming woven bone.

64.  Later middle and old age (40 years of age) ,More in males
than female
 Affected bone is enlarged and commonly deformed,
resulting in bowing of the legs, curvature of the spine, and
enlargement of the skull.
 Irregular overgrowth of the maxilla may lead to the facial
appearance described as “leontiasis ossea,” and edentulous
patients may complain that their dentures no longer fit.
 Separation and movement of teeth may occur, causing
malocclusion.
 Bone pain is an inconsistent symptom, most often directed
toward the weight-bearing bones; facial or jaw pain is
uncommon.
 Patients may also have ill-defined neurologic pain as the
result of bone impingement on foramina and nerve canals.

66.  Location. Paget ’ s disease occurs most often in the pelvis, femur, skull,
and vertebrae and the maxilla about twice as often as the mandible.
 Internal Structure. Generally the appearance of the internal structure
depends on the developmental stage of the disease.
Paget ’s disease has three radiographic stages,:
1) An early radiolucent resorptive stage,
2) A granular or ground glass – appearing second stage,
3) A denser, more radiopaque appositional late stage.
The trabeculae are altered in number and shape.
In Early stage, trabeculae may be long and may align themselves in a
linear pattern which is more common in the mandible.
In second stage may be short, with random orientation, and may have a
granular pattern similar to that of fibrous dysplasia.
A third pattern occurs when the trabeculae may be organized into
rounded, radiopaque patches of abnormal bone, creating a cotton-wool
appearance
The overall density of the jaws may decrease or increase, depending on
the number of trabeculae.

67.  Effects on Surrounding Structures.
Enlargement of affected bone (Prominent pagetoid skull
bones may swell to three or four times their normal
thickness)
In enlarged jaws the outer cortex may be thinned but
remains intact.
Loss of lamina dura and irregular hypercementosis
Loss of normal outer cortex and the linear
alignment of trabeculae.
Exuberant irregular
hypercementosis of the roots.

68. The expansion of the
mandible and the
maintenance
of a thin outer cortical
plate.
Paget ’ s Disease
Multiple radiopaque masses in the
mandible that have
a cotton-wool appearance

69.  High elevations in serum alkaline phosphate
levels
 Normal blood calcium and phosphorus levels.
 Urinary hydroxyproline levels are markedly
elevated

70.  Early stage ( radiolucent appearance)
-Giant cell lesions of hyperparathyroidism
-Osteoporosis
-Osteomalacia
-Multiple myeloma
 Second stage ( mixed radiolucent appearance)
-Osteogenic sarcoma
-Cementifying and ossifying dysplasia
-Fibrous dysplasia
-Osteoblastic metastatic carcinoma
 Advanced stage ( purely radiopaque appearance )
-Florid osseous dysplasia
-Osteosclerosis
-Osteoma

71.  In patients with limited involvement and no symptoms,
treatment is often not required.
 Calcitonin, sodium etidronate, or biphosphonates are used
presently to relieve pain and reduces the serum alkaline
phosphatase levels and osteoclastic activity.
 Surgery may be required to correct deformities of long
bone and treat fractures.
COMPLICATIONS:
Extraction site heals slowly.
Incidence of jaw osteomyelitis is more higher.
Invasion and bone destruction, indicates presence of a
malignant neoplasm.

72.  Langerhans’ cell histiocytosis, formerly called histiocytosis X,
comprises a group of conditions that are characterized
histologically by a monoclonal proliferation of large
mononuclear cells accompanied by a prominent eosinophil
infiltrate.
 The clinical spectrum of Langerhans’ cell histiocytosis includes
 (1) Single or multiple bone lesions with no visceral involvement
(eosinophilic granuloma);
 (2) A chronic disseminated form (Hand-Schüller-Christian
disease) that includes a classic triad of skull lesions,
exophthalmos, and diabetes insipidus;
 (3) An acute disseminated form (Letterer-Siwe disease) that
affects multiple organs and has a poor prognosis.

73.  Each of these forms tends to affect patients at different
ages,
-With the eosinophilic granuloma affecting older children
and young adults,
-The chronic disseminated form affecting young
children.
-The acute disseminated form affecting infants and children
under the age of 2 years.
 Both the maxilla and the mandible may be affected ,both
with and without systemic involvement
 Bony swelling, soft tissue mass, gingivitis, pain and
ulceration

74.  It is divided into 2 types that occur in alveolar bone and that
occur intra-osseous else where in jaws.
 LOCATION: Alveolar type- Multiple
Intraosseous type- Solitary
Posterior part of mandible and ramus are more common sites.
 PERIPHERYAND SHAPE: Moderate to well defined without
cortication.
 INTERNAL STRUCTURE: Totally radiolucent.
 EFFECT ON SURROUNDING STRUCTURES :
Alveolar type show scooped-out bone destuction with loss of
lamina dura.
Intraosseous type shows periosteal new bone formation and may
destroy outer cortex.

75. A panoramic film of
multiple lesions of
Langerhans ’ cell
histiocytosis.
Note the scooped out shape
of the bone destruction in the
mandible. The floor of the
right maxillary antrum has
been destroyed.
Lateral skull films of lesions of
Langerhans ’ cell histiocytosis showing
well-defined, punched-out lesions.

76. Two periapical films of the same area of the mandible taken approximately 1 year apart
in a patient with Langerhans ’cell histiocytosis.
A, The earlier phase of the disease produces a scooped out shape (arrows) that shows
that the epicenter of the lesion is in the midroot area of the involved teeth, unlike in
periodontal disease.
B, One year later, bone destruction is extensive, resulting in loss of teeth.

77. A panoramic film showing the bone destruction that can
occur with Langerhans ’ cell histiocytosis.
The bone around many of the remaining mandibular
teeth has been destroyed, leaving the teeth apparently
unsupported

78.  ALVEOLAR TYPE
-Periodontal disease
-Squamous cell carcinoma
 INTRA-OSSEOUS LESION
-Metastatic malignant neoplasia and
-Malignant tumors from adjacent soft tissues

79.  The treatment varies, based on the clinical
presentation of the disease.
 Solitary eosinophilic granuloma may be treated by
surgical curettage.
 Low-dose radiation therapy has been used
successfully for lesions that are multiple, less
accessible, or persistent.
 The older the patient with Langerhans’ cell
histiocytosis and the less visceral involvement, the
better the prognosis.
 Langerhans’ cell histiocytosis is a life-threatening
disease in infants and very young children.

80.  Oral and maxillofacial pathology,
Neville.Damm.Allen.Bouquot 3rd Edition
 Contemporary oral and maxillofacial pathology, Sapp.
Eversole. Wysocki 2nd edition
 Oral Radiology principle and interpretations, White. Pharoah
6th edition.
 Shafer’s textbook of oral pathology 7th edition
 Textbook of dental and maxillofacial radiology, Freny R
Karjodkar 2nd edition.
 Pdf article BENIGN FIBRO‐OSSEOUS LESIONS OF
JAWS‐ A REVIEW by Rashi Bahl, Sumeet Sandhu , Mohita
Gupta.
 Pdf article Updated Classification Schemes for Fibro-Osseous
Lesions of the Oral & Maxillofacial Region: A Review by
Dr.Karan Rajpal, Dr.Raghav Agarwal, Dr.Richie Chhabra,
Dr.Maumita Bhattacharya