GOOD MORNING

ONE AND ALL

FIBRO-OSEOUS DISEASES AND BENIGN
NON ODONTOGENIC TUMORS OF JAW

MODERATOR : DR. KIRAN HY

PRESENTER : DR. JOMI
PORINCHU
 Introduction
Classification
Fibro-osseous lesions
Benign non-odontogenic tumors
References
Introduction
 BENIGN TUMORS OF JAW

ODONTOGENIC NONODONTOGENIC
Fibro-osseous tumors
ODONTOGENIC TUMORS Ossifying fibroma
EPITHELIAL TUMORS Juvenile ossifying fibroma
Ameloblastoma Langerhans cell disease
Calcifying epithelial odontogenic tumor Chronic localized
Adenomatoid odontogenic tumor Chronic disseminated
Squamous odontogenic tumor Acute disseminated
MESENCHYMAL TUMORS Lesions containing multinucleated giant cells
Odontogenic fibroma Central giant cell granuloma
Cementoblastoma Giant cell tumor
Odontogenic myxoma Hyperparathyroidism
Cementifying fibroma Cherubism
MIXED EPITHELIAL AND Aneurysmal bone cyst
MESENCHYMAL Neurogenic tumors
TUMORS Schwannoma
Odontoma Neurofibroma
Ameloblastic fibroma Osteoid osteoma and osteoblastoma
Ameloblastic fibro-odontoma Osteoma
M. ANTHONY POGREL, BRIAN L. SCHMIDT,
Chondroma
CHAD G. ROBERTSON Desmoplastic fibroma
 FIBRO-OSSEOUS LESIONS
DEFINITION-
The term fibro-osseous lesion
(FOL) is a generic designation of
a group of jaw disorders.

Represent diverse group of entities that are

characterized by replacement of normal bone
with a variable amounts of collagenous
connective-tissue matrix containing new bone
and/or cementum-like materials.
 Classification
Charles A Waldron(1993)

1. Fibrous dysplasia

2. Cemento-osseous dysplasia (Reactive lesion in tooth bearing

lesion)
Periapical cemento-osseous dysplasia
Focal cemento-osseous dysplasia
Florid cemento-osseous dysplasia

3. Fibro-osseous neoplasm :
cementifying /ossifying/ cemento-ossifying fibroma
 Classification
WHO(2005)
FIBROUS DYSPLASIA
MONO OSTOTIC
POLY OSTOTIC
CRANIOFACIAL
CEMENTO-OSSEOUS DYSPLASIA
PERIAPICAL
FOCAL
FLORID
FAMILIAL GIGANTIFORM CEMENTOMA
CEMENTO-OSSIFYING FIBROMA
CONVENTIONAL
JUVENILE AGGRESSIVE
TRAUMATIC BONE CYST AND ANEURYSMAL BONE CYST
 FIBRO-OSSEOUS LESIONS OF CRANIOFACIAL
COMPLEX
I. Bone dysplasias
a. Fibrous dysplasia
i. Monostotic
ii. Polyostotic
iii. Polyostotic with endocrinopathy (McCune-Albright)
iv Osteofibrous dysplasiaa
b. Osteitis deformans
c. Pagetoid heritable bone dysplasias of childhood
d. Segmental odontomaxillary dysplasia
II. Cemento-osseous dysplasias
a. Focal cemento-osseous dysplasia
b. Florid cemento-osseous dysplasia
III. Inflammatory/reactive processes
a. Focal sclerosing osteomyelitis
b. Diffuse sclerosing osteomyelitis
c. Proliferative periostitis
IV. Metabolic Disease: hyperparathyroidism
V. Neoplastic lesions (Ossifying fibromas)
a. Ossifying fibroma NOS
b. Hyperparathyroidism jaw lesion syndrome
c. Juvenile ossifying fibroma
i. Trabecular type
ii. Psammomatoid type
d. Gigantiform cementomas
BONE DYSPLASIAS
 Fibrous Dysplasia

Benign dysplastic process of altered osteogenesis

Pathogenesis
Gs-alpha protein activation
Proliferative signal to dysplastic cells
Release of cytokines Osteoclast congregation
Bone resorption & proliferation of dysplastic tissue
 Fibrous Dysplasia
Classification:
Type of tissues (According to Ian T. Jackson, Henry G. Bone,
Hemen Jaju)
i. Sclerotic
ii. Fibro-osseous
i. Vascular
ii. Cystic
iii. Fibrovascular
Clinical
i. Monostotic
ii. Polyostotic
iii. Polyostotic with endocrinopathy (McCune-Albright)
iv. Cherubism
 Fibrous Dysplasia

Clinical Features
Age at initial diagnosis 3 -15 yrs
No sex/racial predeliction
Asymptomatic phase
Malignant transformation increasing pain and enlarging soft tissue
mass.
Fibrous Dysplasia
Fibrous Dysplasia
 Fibrous Dysplasia
Associated syndromes-

1. McCune Albright Syndrome

Polyostotic FD
Caf-au-lait spots
Endocrinal disturbances

2. Jaffe-Liechtenstein Syndrome - Polyostotic FD

Cutaneous pigmentation

3. Mazabraud Syndrome - Polyostotic FD

Soft tissue myxoma
Fibrous Dysplasia
Fibrous dysplasia Radiographic Features
 Fibrous dysplasia
Radiographic Features
 Fibrous Dysplasia - Treatment

MEDICAL- (J BONE & JOINT SURG. 2005)

(CHAPURLET, J BONE MINER
RES.2006)

Aminobisphosphonate (Pamidronate)

Dose -
IV infusion 60mg( children- 1mg/ kg) over 4 hrs
( Series of 3 doses at 1 wk interval repeated at
6months)

Calcium (500-1500mg/day)
Vit. D (800-1200 IU/day)
 Fibrous Dysplasia - Treatment
RESULTS

1. Decreased bone pain

2. Decreased biochemical markers of bone
turnover
3. Radiograph filling of lytic lesion & cortical
thickening

DRAWBACKS

1. No convincing evidence of benefit in children

& adolescents.
2. Not the cure dont affect mutated
osteoblasts.
 Fibrous Dysplasia - Treatment

SURGICAL

LOCALIZED INVOLVEMENT

VESTIBULAR APPROACH

HEMICORONAL / BICORONAL APPROACH

CRANIOTOMY

RECONTOURING AESTHETICS & FUNCTION

 SURGICAL TREATMENT PROTOCOL BASED ON
LOCATION OF LESION
(Chen & Noordhoff , Plastic Recon.Surg.1990

ZONE-1 ZONE-2 ZONE-3 ZONE-4a ZONE-4b

Most Hair covered Difficult/ Maxillary Mandible
evident cranium - Dangerous alveolar
parts on Occipital areas bone
face- Temporal Pterygoid
Frontal (Lat. Cranial Sphenoid
Nasal base) (Central
Orbit cranial
Zygoma base)
Ethmoid
Maxilla(upp
er

Radical Conservativ Observation Conservativ Conservativ

excision & e or radical Surgery if e excision & e excision &
reconstructi excision symptomati recontouring recontouring
on (optional) c
Orbital involvement more early & aggressive
treatment
 Pagets Disease
Excessive and abnormal remodelling of bone
Bone hypertrophy, cortical expansion, abnormal bone structure
Bone pain, bone deformity and skeletal fragility
Bones weak, vascularised, enlarged, deformed.

Etiology:
UNKOWN
?? Genetic Increased incidence among relatives
J Cell Biochem.2004 Nov 1;93(4):688-96.
Viral Infection
JOURNAL OF BONE AND MINERAL RESEARCH. Volume 16, Number 8, 2001
Inflammatory
Autoimmune, Connective tissue, Vascular disorders
 Pagets Disease Clinical Features
Recognised most commonly after 50yrs age rarely below
20yrs
No sex predeliction
Most individuals asymptomatic incidental finding during
unrelated radiological or biochemical investigation

Skeletal deformity
Bowing of legs
Skull, jaws and clavicles deformed
Bone pain
Pagets Disease Clinical Features
Pagets Disease Clinical Features
Pagets Disease Radiographic features
 Pagets Disease Lab investigation
JOURNAL OF BONE AND MINERAL RESEARCH, Volume
16, Number 8, 2001
Tests reflecting bone matrix resorption
Second morning urine sample for urinary
hydroxyproline/creatinine
Urinary and serum deoxypyridinoline,
N-telopeptide, and C-telopeptide

Formation parameters
Serum alkaline phophatase levels reliable in absence of pregnancy or
liver disease
Bone specific alkaline phospatase (cost ineffective)
Serum osteocalcin (product of osteoblast)
Pagets Disease Management
JOURNAL OF BONE AND MINERAL RESEARCH, Volume
16, Number 8, 2001
CEMENTO-OSSEOUS
DYSPLASIA
 Cemento-osseous Dysplasia
Cemento-osseous dysplasia occurs in the tooth bearing areas
of the jaws and is probably the most common fibro-osseous
lesion encountered in clinical practice

Pathologic features similarities with fibrous dysplasia and

ossifying fibroma, correct diagnosis can be problematic

Etiology
Abnormal reaction of injured bone to low grade or chronic
injury Robinson HBC. Osseous dysplasia: reaction of bone to injury.J Oral
Surg1956;14:314.
Extraligamentary bone remodelling triggered by local
factors and hormone imbalance

 Cemento-osseous Dysplasias
(Osseous Dysplasia)
Arises in close approximation to the PDL.

Similarities present to PDL

PDL origin proposed.

Three types have been described:

1. Focal
2. Periapical &
3. Florid
 Focal cemento-osseous dysplasia

Exhibits single site of involvement,

90% of cases occur in females, mean age of 38yrs, and

mainly in whites.

Occur in any area of the jaws, but the posterior mandible is

the predominant site,

Most lesions are smaller than 1.5 cm in diameter

 Focal Cemento-osseous Dysplasia
-Radiographically
Completely radiolucent to densely radiopaque with a thin
peripheral radiolucent rim

Lesion tends to be well defined

Occur in dentulous and edentulous areas, many examples noted

in extraction sites.
 Periapical cemento osseous dysplasia

Asymptomatic diffuse periapical radiolucency & radiopaque

areas, primarily of the anterior mandible, in which cemento-
osseous tissue replaces the normal architecture of bone

Multiple cementoma
Periapical fibrous dysplasia
Periapical osteofibrosis
Localised fibro osteoma
 Periapical cemento osseous dysplasia
Clinical Features
Predilection for female patients (ranging from 10:1 to 14:1), 70%
of cases affect blacks.
Ages of 30 and 50 & never diagnosed below 20yrs of age,

Teeth associated are almost invariably vital,

 Periapical cemento osseous dysplasia
Radiologically
Circumscribed areas of radiolucency involving the apical
area of a tooth,
Cannot be differentiated radiographicaly from a periapical
granuloma or periapical cyst,
Serial radiographic studies reveal that the lesions tend to
"mature" over time to create a mixed radiolucent and
radiopaque appearance
 Florid cemento osseous dysplasia

1st described by Melrose et al, 1976

Diffuse asymptomatic, radiopaque & radiolucent intraosseous

areas of cemento-osseous tissue that involve one or both arches

Only 3 cases reported in India

 Florid cemento osseous dysplasia

Age: 40 years
Clinically rarely mild expansion
10% cases are exposed to oral flora

Radiograph:
Clouds/Cotton balls
Do not involve inferior border of
mandible
Do not occur in rami
 Florid cemento osseous dysplasia

Florid osseous dysplasia: diffuse sclerotic masses are found in all four
jaw quadrants. In the mandible, the lesions are situated mainly above
the mandibular canal.
 Cemento-osseous Dysplasia
Treatment
Asymptomatic patient
Reinforce oral hygiene

No biopsy necessary if diagnosed clinically and

radiographicaly
Usually self limiting

Follow up with radiographs every 1- 2 years

Cemento-osseous Dysplasia
Treatment

Symptomatic patient
Symptoms suggest chronic osteomyelitis
Antibiotics may be indicated
Saucerization of dead bone may speed healing
FIBRO-OSSEOUS
NEOPLASIA
 Familial gigantiform Cementoma
Autosomal dominant trait
Racial predilection- African blacks
Young age
Rapidly expansile lesions in anterior mandible
Histologic features large fused masses with heavy infiltrate
of inflammatory cells
 Cementifying fibroma / cemento- ossifying
fibroma
A well-demarcated, encapsulated, expansile intraosseous
lesion of the jaws composed of cellular fibrous tissue
containing spherical calcifications and irregular, randomly
oriented bony structures.

Etiology is unknown

Tissue of origin is bone,

Cementifying fibroma Clinical Features

slow growing neoplastic

lesion
more often in mandible
asymptomatic
more common in
children and young adults.
 Cementifying fibroma
Radiographic Features

Well defined radiolucency, mixed radiolucent radiopaque,

and radiopaque.

Cortical expansion without perforation

 Cementifying fibroma
Treatment & Prognosis;
Circumscribed nature of the ossifying fibroma generally
permits enucleation with ease.
Grown large lesions can be surgically resected and bone
grafting done.
Very good prognosis, and no evidence of malignant
transformation till date.
 Juvenile Ossifying Fibroma

(1) Trabecular and

(2) Psammomatoid,
the trabecular form is diagnosed initially in younger
patients. The mean age of trabecular juvenile ossifying
fibromas is approximately 11 years,
psammomatoid appears outside of the jaws, with
over 70% arising in the orbital and frontal bones and
paranasal sinuses.
 Juvenile Ossifying Fibroma
Clinical Features
early to late childhood
maxilla more often than mandible
singular, slow-growing, painless swelling
overgrowth of tissue that occurs centrally in the jaws
may involve impacted or unerupted teeth
increased level of serum alkaline phosphatase
severe maloccusion
aggressive form:
symptomatic if traumatized
Ulcerated
maxilla lesion may interfere with sight and breathing
Juvenile Ossifying Fibroma
Radiographic Features:
radiolucent or mixed radiolucent and
radiopaque appearance (ground glass),

lamina dura is usually obscured and the cortical

plates thinned
 Juvenile Ossifying Fibroma
Treatment and Prognosis:
management and prognosis are uncertain.
smaller lesions, complete local excision or thorough
curettage appears adequate,
rapidly growing lesions, wider resection may be required
recurrence rates of 30% to 58%
Malignant transformation has not been documented.
BENIGN NON
ODONTOGENIC TUMORS
Langerhans Cell
 Probable Pathogenesis of
LCH
Immunologic stimulation of this
normal antigen presenting cell may
continue in an uncontrolled manner
and this results in proliferation and
accumulation of these
Ladisch S: Langerhans cellsCurr opinions
cell histiocytosis.
Hematol 5:54-58, 1998
 Langerhans Cell Disease
Formerly known as histiocytosis
X and before that as three
separate diseases:
Eosinophilic granuloma
Hand-Schller-Christian
disease
Letterer-Siwe disease

Clinical manifestations range

from solitary or multiple bone
lesions to disseminated
visceral, skin, and bone lesions
 Three forms exist:
Chronic localized,
eosinophilic granuloma,
solitary or multiple bone
lesions
Chronic disseminated
Hand-Schller-Christian
disease
associated with a clinical triad
of lytic bone lesions,
exophthalmos, and diabetes
insipidus.
Acute disseminated,
Letterer-Siwe disease,
affects infants and is
multisystem in nature,
affecting the skin, bones, and
internal organs, especially the
lungs and liver.
Unifocal Disease
Single system disease
Most commonly bone
Older children and good
prognosis
Multifocal Single system disease
Multiple sites of involvement in
single organ
Bone
Young children
Intermediate prognosis
Multifocal multisystem disease
Multiple sites in more than one
organ system
Bone , skin, liver, spleen,
lymph nodes.
Children younger than 2 yrs
and infants , poor prognosis
 Langerhans Cell Disease
Radiographically, jaw lesions appear as well-defined,
punched-out radiolucencies, may also be ill defined, with or
without sclerosis
Lesions often involve the alveolar bone, producing the classic
appearance of floating teeth
 Langerhans Cell Disease
Diagnosis
Diagnosis of Langerhans cells disease is confirmed using
immunohistochemical studies.
Langerhans cells stain positive for S-100 protein and CD1a
antigen.
In addition, Langerhans cells contain unique, rod-shaped
cytoplasmic structures known as Birbeck granules, seen on
electron microscopy
 Langerhans Cell Disease
Management
Less accessible lesions may be treated with low-dose radiation
therapy.
Accessible bone lesions are treated with aggressive local
curettage or resection with 5-mm margins.
Recurrent lesions after surgery with radiotherapy 550 to 600
cGy
Intralesional steroids have also been employed with some
success.

With widespread or visceral involvement, chemotherapy is

often used.
Acute disseminated Langerhans cell disease follows a rapidly
progressive course and is treated with chemotherapy.
LESIONS CONTAINING
MULTINUCLEATED GIANT
CELLS
 Lesions Containing
Multinucleated Giant Cells

Lesions in this group are similar, if not identical, histologically,

and they usually cannot be distinguished from one another solely
on the basis of light microscopy.

Clinical history, physical and radiographical examination, and

serum biochemistry - used to differentiate these lesions
 Central Giant Cell Granuloma
Is a benign proliferation of fibroblasts and multinucleated
giant cells
No longer considered to be reparative, and if left untreated the
lesion will progress
It may be an inflammatory lesion, a reactive lesion, a
neoplasm, or an endocrine lesion
 Central Giant Cell Granuloma
The proliferating cell in this lesion is the fibroblast, which is
thought to produce cytokines, resulting in the recruitment of
monocytes, which subsequently transform into multinucleated
giant cells

Immunohistochemistry has shown the giant cells to be

osteoclasts.
 Central Giant Cell Granuloma
Clinical Features
Most often found in children and young adults
Females are affected twice as frequently as males
Lesions most often occurs anterior to the first permanent molar
teeth
Mandible is affected three times more frequently than
maxilla, and lesion may be seen to cross the midline
Produces painless expansion of the affected jaw; may
infrequently produce pain
Central Giant Cell Granuloma
Radiological features
 Central Giant Cell Granuloma
Management
Surgical curettage has been the treatment of choice.

Intralesional corticosteroid injections.

Subcutaneous calcitonin injections.

Alpha-interferon given by subcutaneous injection has also

been advocated.

Kaban LB, Troulis MJ, Ebb D et al: Antiangiogenic therapy wit

giant cell lesions of the jaws, J Oral Maxillofac Surg 2002
 Giant Cell Tumor
Normally found in long bones

Aggressive lesion believed to be

variant low-grade osteosarcoma.

Histologically, similar to central giant

cell granuloma.

Recurrence rate significant compared

to central giant cell granulomas

Resection advocated by some

Hyperparathyroidism
 Hyperparathyroidism
Clinical features

assically affects skeleton, kidneys, and GI tract

Triad of complaints: bones, stones, and abdominal gr
 Hyperparathyroidism
Radiological features
 Histologically identical to central giant cell
granulomas.

Serum calcium and PTH levels important for in

giant cell lesions to exclude hyperparathyroidism.

If a diagnosis of hyperparathyroidism is
confirmed, treatment must be aimed at the cause
and the lesions will usually resolve without any
further treatment.
 Aneurysmal Bone Cyst
Etiology and pathogenesis of the
lesion remains unknown,

Controversy remains over whether

the lesion occurs as a primary entity
or results from the development of a
dilated vascular bed in a preexisting
intrabony lesion.
Aneurysmal Bone Cyst
Features
 Aneurysmal Bone Cyst
Management
Some authors feel aneurysmal bone cysts are
associated with a relatively high recurrence rate,
yet curettage remains the treatment of choice

At the time of surgery lesional tissue appears like

a blood-soaked sponge
significant hemorrhage is usually not
encountered
NEUROGENIC TUMORS
 Schwannoma

Commonly occurs in the soft tissues of the head and

neck, as well as the flexor surfaces of upper and
lower extremities.
Intraosseous lesions are rare; however, the mandible
is the most common site of occurrence.
most common in young adults.
Bony lesions may be asymptomatic or produce
expansion, pain, paresthesia, tooth mobility, and
tooth displacement.
 Schwannoma
Features

Histologically, this is an encapsulated spindle cell

tumor that consists of variable amounts of two
types of tissue, Antoni A and Antoni B
Antoni A tissue consists of Verocay bodies
Antoni B tissue consists of spindle cells
randomly arranged within a loose, myxomatous
stroma
 Schwannoma
Management
Intraosseous schwannomas can be treated by
enucleation and curettage.

When the lesion arises from an identifiable nerve

such as the inferior alveolar nerve, it can be
excised from the nerve while preserving the
integrity of the nerve.

Recurrences are rare.

 Neurofibroma

Two types exist:

neurofibromatosis type 1 (von Recklinghausens
disease of skin)
neurofibromatosis type 2
 Neurofibroma
Management
Recommended treatment of solitary lesions
following biopsy is localized excision.
Lesions are often vascular, and extensive
blood loss has been reported from surgical
management of mandibular lesions; thus some
authors have advocated mandibular resection.
Number of neurofibromas that can occur with
neurofibromatosis type 1 makes complete
surgical therapy impractical.
In these cases surgery is reserved for lesions
that are large and symptomatic or
compromise function, or both.
OSTEOID OSTEOMA AND
OSTEOBLASTOMA
Osteoid Osteoma and Osteoblastoma

Occur in the second decade,

with 85% to 90% occurring
before 30 years of age.
2:1 male predilection exists.
Osteoid osteoma is less than
2 cm in diameter, occurring
most frequently in the femur,
tibia, and phalanges
Rarely occurs in the jaws
Classically presents with
nocturnal pain that is
alleviated by aspirin
 Osteoid Osteoma and Osteoblastoma
Osteoblastoma is greater than 2 cm in diameter,
occurring most frequently in the vertebrae and long
bones of the extremities
Craniofacial skeleton is the site of involvement in 15%
Mandible is affected more frequently than the maxilla
Posterior tooth-bearing portion is most often involved
Clinically, it often develops relatively rapidly, producing
swelling and pain
In contrast to osteoid osteomas, the pain is not typically
nocturnal and it does not respond as well to aspirin
 Osteoid Osteoma and Osteoblastoma
Features

Histologically
Irregular trabeculae of osteoid and immature
bone are seen within a cellular fibrovascular
stroma
Osteoid trabeculae, which exhibit varying degrees
of calcification, are surrounded by prominent
 Osteoid Osteoma and Osteoblastoma
Management

Treatment is generally confined to conservative

surgical excision either with curettage or local
excision.
Reports have been made of some lesions
regressing after incomplete excision or biopsy.
Recurrences are rare but have been reported and
may necessitate more aggressive treatment such
as en bloc resection.
Rare examples of malignant transformation have
 Osteoma

Benign tumors composed of mature

compact or cancellous bone
Osteomas may arise in the paranasal
sinuses, skull bones, and facial bones
including the maxilla and mandible.
Most commonly develop in young
adults
 Osteoma
Types
Osteomas may arise from the surface of
bone(periosteal osteoma), or
May be located in the medullary bone
(endosteal osteoma)

Periosteal osteomas most often present as

slow growing, painless, discrete bony masses
Endosteal osteomas are usually
asymptomatic and noted on routine
radiographs
 Osteoma
Features

Two histological variants exist

One variant consists of normal appearing,
dense, compact bone with sparse marrow tissue
Other form consists of lamellar trabeculae of
cancellous bone with fibrofatty marrow
 Gardner syndrome
Osteomas in association with
Gardner syndrome are frequently
seen at the mandibular angles, as
well as other facial bones and long
bones.
Development of osteomas precedes
other manifestations of the
syndrome.
Most clinically important aspect of
the syndrome is the high rate of
malignant transformation of bowel
polyps into invasive adenocarcinoma.
Malignant transformation rate is 50%
by age 30.
As a result, patients with an
established diagnosis of Gardner
syndrome typically undergo a
prophylactic colectomy.
 Gardner syndrome
Management
Osteomas are diagnosed and treated by local
excision.

Recurrences are rare.

Small, asymptomatic cases may be followed

clinically and radiographically.

Patients with multiple osteomas should undergo

investigation for Gardner syndrome.
 Chondroma
Most often occur in the nasal septum
and anterior maxilla.
Also been reported in the mandibular
condyle, coronoid process, body, and
symphysis.
Chondromas typically present as
painless, slowly progressive swelling
Usually appear before 50 years of age
No sex predilection
Radiographically, appear as a
unilocular or multilocular
radiolucency, which may have
internal foci of calcification
 Chondroma
Management
Considering the rarity with which chondromas
occur in the craniofacial complex, the difficulty in
differentiating between a chondroma and a low-
grade chondrosarcoma, and the aggressive nature
of chondrosarcomas, one should question the
diagnosis of a benign chondroma in the jaws.

To avoid the potential risk of undertreating a

malignancy, some authors consider chondromas
of the jaws as potentially malignant and manage
them accordingly
 Desmoplastic Fibroma
Etiology and pathogenesis
unknown
-genetic, endocrine, and traumatic
factors have been suggested.
Lesion usually occurs in children
and young adults, with most cases
before 30 years of age.
Most commonly occurs in the long
bones but may occasionally affect
the jaws. (posterior mandible is the
area most frequently involved)
Patients most often present with a
painless, slow-growing, firm
swelling of the affected jaw.
 Desmoplastic Fibroma
Features
Radiographically, the lesion produces a radiolucency,
which may be unilocular or multilocular.
Margins may be well defined or poorly defined.
Cortical perforation and root resorption may be seen.

Microscopically, the lesion is composed of interlacing

bundles and whorled aggregates of densely collagenous
tissue with spindled and elongated fibroblasts.
 Desmoplastic Fibroma
Management
Recurrence rates following conservative surgical
treatment such as curettage and local excision are
high, while lesions treated by resection or wide
excision do not tend to recur. Bohm P, Krober S, Greschniok A
et al: Desmoplastic fibroma of the bone. A report of two patients, review of
the literature, and therapeutic implications, Cancer 78(5):1011-1023, 1996.

Thus despite a benign histology, the desmoplastic

fibroma should be treated aggressively.

Radiation and chemotherapy have been recommended

for lesions involving vital structures and those located
in areas where resection would be debilitating.
 References
Journal of Oral and Maxillofacial Surgery, Volume 43, Issue 4,
April 1985, Pages 249-262 ,Charles A. Waldron
Peter Ward Booth, Stephen A. Schendel, Jarg-Erich Hausamen.
Maxillofacial Surgery. 2ED. Vol I & II
Michael Miloro. Petersons principles of oral and maxillofacial
surgery 2nd Ed.
R. Rajendran, B Sivapathasundharam. Shafers textbook of oral
pathology. 5th Ed.
Robert D. Marciani. Oral and maxillofacial surgery. 2 nd ED. Vol II
Neville, Damm, Allen, Bouquot.Oral and maxillofacial
pathology. 2nd ED.
Neville BM, DD Douglas, HW Dean. Colour atlas of Clinical Oral
Pathology. 2nd ED.
Text Book of Oral Medicine- Burkitt
Individual article references as mentioned in slides
Images from various internet sources
THANK YOU