3. INTRODUCTION
• “THE TERM FIBRO-OSSEOUS LESION (FOL) IS A GENERIC DESIGNATION
OF A GROUP OF JAW DISORDERS” CHARACTERIZED BY THE
REPLACEMENT OF BONE BY A BENIGN CONNECTIVE TISSUE MATRIX.
• THIS MATRIX DISPLAYS VARYING DEGREES OF MINERALIZATION IN THE
FORM OF WOVEN BONE OR OF CEMENTUM-LIKE ROUND ACELLULAR
INTENSELY BASOPHILIC STRUCTURES.
4. • DIAGNOSIS OF THESE LESIONS BASED ON HISTOLOGIC APPEARANCE
ALONE HAS CONSIDERABLE LIMITATIONS.
• BENIGN FIBRO-OSSEOUS LESIONS (BFOL) OF THE JAW, FACIAL AND
SKULL BONES ARE A VARIANT GROUP OF INTRAOSSEOUS DISEASE
PROCESSES THAT SHARE MICROSCOPIC FEATURES, WHEREAS SOME
ARE DIAGNOSABLE HISTOLOGICALLY.
• MOST REQUIRE A COMBINED ASSESSMENT OF CLINICAL,
MICROSCOPIC AND RADIOLOGIC FEATURES.
5. • CHARLES WALDRON WROTE “IN ABSENCE OF GOOD CLINICAL AND
RADIOLOGIC INFORMATION A PATHOLOGIST CAN ONLY STATE THAT A
GIVEN BIOPSY IS CONSISTENT WITH A FOL. WITH ADEQUATE CLINICAL
AND RADIOLOGIC INFORMATION MOST LESIONS CAN BE ASSIGNED
WITH REASONABLE CERTAINTY INTO ONE OF SEVERAL CATEGORIES”.
6. CLASSIFICATION
WHO CLASSIFICATION OF FIBROOSSEOUS LESIONS OF JAWS (2005)
1) OSSIFYING FIBROMA (OF)
2) FIBROUS DYSPLASIA
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
7. PAUL M. SPEIGHT & ROMAN CARLOS CLASSIFICATION (2006)
1. FIBROUS DYSPLASIA
A. MONOSTOTIC FD
B. POLYOSTOTIC FD
C. CRANIOFACIAL FD
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
8. • IT WAS FIRST REPORTED IN 1921 BY FRANGHENHEIM.
• THE WORLD HEALTH ORGANIZATION (WHO) IN 1971 CLASSIFIED OSSIFYING
FIBROMA AS A TYPE OF CEMENTIFYING FIBROMA.
• ACCORDING TO THE 1992 WORLD HEALTH ORGANIZATION
(WHO)CLASSIFICATION, COF IS A "DEMARCATED OR RARELY ENCAPSULATED
NEOPLASM CONSISTING OF FIBROUS TISSUE CONTAINING VARYING AMOUNTS
OF MINERALIZED MATERIAL RESEMBLING BONE AN/OR CEMENTUM."
OSSIFYING FIBROMA (OF)
9. ETIOLOGY
1. ORIGIN: CLOSE PROXIMITY TO THE PERIODONTAL LIGAMENT HAS LED TO A
PRESUMPTION THAT COFS ORIGINATE IN THE PERIODONTAL LIGAMENT
WITH THE POTENTIAL FOR BOTH OSSEOUS AND CEMENTAL
DIFFERENTIATION.
2. PROBABLY THEY ARISE FROM THE MULTIPOTENT MESENCHYMAL BLAST
CELLS PRESENT IN THE PERIODONTAL MEMBRANE AND HAVE A CAPACITY
TO PRODUCE CEMENTUM, ALVEOLAR BONE AND FIBROUS TISSUE.
3. RECENTLY MUTATIONS IN THE TUMOR SUPRESSOR GENE HRPT2 WERE
IDENTIFIED.
10. OF IS FURTHER DIVIDED INTO SUBTYPES:
CONVENTIONAL AND
JUVENILE (JOF) :
TRABECULAR (JTOF)
PSAMMOMATOID (JPOF)
11. CLINICAL FEATURES
• AGE: 3RD AND 4TH DECADES → MEAN AGE OF 32 YRS
• SEX: FEMALE PREDILECTION
• SITE: MANDIBLE ˃MAXILLA. MAINLY ARISES IN THE TOOTH BEARING AREAS.
• MOST COMMON SITES : MANDIBULAR PREMOLAR AND MOLAR AREAS.
• ASYMPTOMATIC AND EXPANSILE LESION
• PAIN AND PARESTHESIA ARE RARELY ASSOCIATED.
• SMALL LESIONS → DETECTED ONLY ON RADIOGRAPHIC EXAMINATION.
• LARGER TUMORS → PAINLESS SWELLING OF THE INVOLVED BONE → FACIAL
ASYMMETRY.
• GROWTH RATE IS UNPREDICTABLE AND MAY BE SLOW AND STEADY OR RAPID
12. RADIOGRAPHIC FEATURES
• EVERSOLE ET AL FOUND 2 MAJOR PATTERNS
1. WELL-DEFINED UNILOCULAR, ROUND, OR OVAL
STRUCTURES.
2. LARGER TUMORS →MULTILOCULAR RADIOGRAPHIC
APPEARANCE.
• ACCORDING TO MACFRONALD-JANKOWSKI'
INITIAL RADIOLUCENT
PROGRESSIVELY RADIOPAQUE
INDIVIDUAL RADIOPACITIES COALESCE
13. GROSS PATHOLOGY
• CUT SURFACE → WHITISH YELLOW,
• CONSISTENCY → VARIES WITH THE AMOUNT OF
CALCIFIED MATERIAL.
• WELL CIRCUMSCRIBED
• RELATIVELY SMALL LESIONS OFTEN EXCISED
COMPLETE WITH SOME SURROUNDING NORMAL
BONE.
14. HISTOPATHOLOGIC FEATURES
• SU ET AL FOUND THREE HISTOLOGIC SUBTYPES:
1. EQUAL AMOUNT OF CALCIFIED MATERIAL AND FIBROBLASTIC STROMA.
• CALCIFIED STRUCTURES → BOTH SEPARATE AND RETIFORM BONY TRABECULAE
WITH A PROMINENT OSTEOBLASTIC RIM AND OCCASIONAL OSTEOCLASTS. ROUNDED
OR LOBULATED CEMENTUM- LIKE BODIES MAY BE SCATTERED THROUGHOUT THE
LESION
• CONNECTIVE TISSUE → SHEETS OF SPINDLE-SHAPED, FIBROBLASTIC, OR STELLATE
CELLS WITH FOCAL AREAS OF STORIFORM PATTERN
2. LEAST COMMON SUBTYPE → CHARACTERIZED BY PREDOMINANTLY STORIFORM
CELLULARITY IN THE STROMA CONTAINING SCANT SEPARATE OSTEOID OR BONY
TRABECULAE, OFTEN WITHOUT OSTEOBLASTIC RIMMING.
3. COMBINATION OF THE FIRST TWO, WHICH ARE EACH SEEN IN DIFFERENT AREAS OF
LARGE LESIONS.
15. • SPHERULES OF CEMENTUM-LIKE MATERIAL → PERIPHERAL ‘BRUSH BORDERS’. THAT
BLEND INTO THE ADJACENT CONNECTIVE TISSUE → PARTICULAR ARRANGEMENT OF
EXTRINSIC COLLAGEN FIBER BUNDLES OF ACELLULAR CEMENTUM.
• FEATURE IN DISTINGUISHING OF FROM FD:
COF IS A SHARPLY DEMARCATED LESION. THE HARD TISSUES OF THE TUMOR DO
NOT FUSE WITH THE SURROUNDING BONE, EXCEPT OCCASIONALLY IN LIMITED
AREAS
PATTERN OF MINERALIZATION VARIES FROM PLACE TO PLACE WITHIN THE LESION,
WHEREAS IN FIBROUS DYSPLASIA, THE PATTERN TENDS TO BE UNIFORM
THROUGHOUT THE LESION
18. TREATMENT AND PROGNOSIS
• UNCOMPLICATED JAW CASES → SIMPLE ENUCLEATION/CURETTAGE.
• AGGRESSIVE LESIONS → MORE EXTENSIVE SURGICAL RESECTION.
• PROGNOSIS → VERY GOOD
• RECURRENCE →RARELY ENCOUNTERED
19. JUVENILE OSSIFYING FIBROMA
(ACTIVE OSSIFYING FIBROMA OR AGGRESSIVE OSSIFYING
FIBROMA)
• AN ACTIVELY GROWING LESION CONSISTING OF A CELL RICH FIBROUS
STROMA, CONTAINING BANDS OF CELLULAR OSTEOID WITHOUT
OSTEOBLASTIC RIMMING TOGETHER WITH TRABECULAE OF MORE TYPICAL
WOVEN BONE.
• SMALL FOCI OF GIANT CELLS MAY ALSO BE PRESENT, AND IN SOME PARTS
THERE MAY BE ABUNDANT OSTEOCLASTS RELATED TO THE WOVEN BONE.
• USUALLY NO FIBROUS CAPSULE CAN BE DEMONSTRATED,
• WELL DEMARCATED FROM THE SURROUNDING BONE.
• 2 PATTERNS:
1. PSAMMOMATOID AND
2. TRABECULAR- JUVENILE OSSIFYING FIBROMA
20. PSAMMOMATOID FIBROMA
• FIRST REPORTED BY BENJAMINS, IN 1938.
• THE TERM WAS COINED BY GOGL, IN 1949
• JOHNSON ET AL, IN 1952 COINED THE TERM JUVENILE ACTIVE OF → “CELLULAR
MASS WHICH GENERATES INNUMERABLE SMALL UNIFORM-SIZED OSTEOID
BODIES.”
• REPORTED MORE FREQUENTLY IN THE LITERATURE
21. ETIOLOGY
• OVERPRODUCTION OF THE MYXOFIBROUS CELLULAR STROMA NORMALLY
INVOLVED IN THE GROWTH OF THE SEPTA IN THE PARANASAL SINUSES AS
THEY ENLARGE AND PNEUMATIZE.
• THESE STROMAL CELLS SECRETE HYALINE MATERIAL THAT OSSIFIES AND
CONNECTIVE TISSUE MUCIN THAT INITIATES THE CYSTIC AREAS (SARODE,
SARODE ET AL. 2011).
22. CLINICAL FEATURES
PSAMMOMATOID JUVENILE OSSIFYING FIBROMA (PJOF)
• MEAN AGE: 22 YEARS
• SEX: MALE˃ FEMALE
• SITE: 75% → DEVELOP IN THE ORBIT, PARANASAL SINUSES AND CALVARIA
WHEREAS ONLY ABOUT 25% OF ALL CASES INVOLVE THE MAXILLA OR
MANDIBLE.
• MAXILLARY PREDOMINANCE.
23. TRABECULAR JUVENILE OSSIFYING FIBROMA (TJOF)
• AGE: MEAN AGE; 11 YEARS
• SEX: MALE˃ FEMALE.
• SITE: 95% OF THE DOCUMENTED CASES OF TJOF HAVE DEVELOPED WITHIN
THE JAW BONES.
• MAXILLARY PREDOMINANCE.
• IN MOST INSTANCES, THE NEOPLASMS GROW SLOWLY, ARE WELL -
CIRCUMSCRIBED AND LACK CONTINUITY WITH THE ADJACENT NORMAL BONE
24. COMPLICATIONS
• DUE TO IMPINGEMENT ON NEIGHBORING STRUCTURES.
• WITH PERSISTENT GROWTH, LESIONS ARISING IN THE
PARANASAL SINUSES PENETRATE THE ORBITAL, NASAL
AND CRANIAL CAVITIES.
NASAL OBSTRUCTION,
EXOPHTHALMOS, .
INTRACRANIAL EXTENSION → MENINGITIS
25. RADIOGRAPHIC FEATURES
• BOTH TUMORS →`WELL-DEMARCATED, UNILOCULAR OR MULTILOCULAR
RADIOLUCENCIES WITH A VARIABLE AMOUNT OF RADIOPACITY, USUALLY
MANIFESTING AS FINE SPECKS OR AS GROUND-GLASS OPACIFICATION.
• MANY TUMORS ARE INITIALLY DISCOVERED UPON ROUTINE RADIOGRAPHIC
EXAMINATION, CORTICAL EXPANSION MAY RESULT IN CLINICALLY DETECTABLE
FACIAL ENLARGEMENT.
• CIRCUMSCRIBED RADIOLUCENCIES BUT IN SOME CASES, CENTRAL
RADIOPACITIES CAN BE SEEN.
• MAXILLARY TUMORS → OFTEN FILL AND OBLITERATE THE MAXILLARY SINUS,
• MANDIBULAR TUMORS → USUALLY INVOLVE THE RAMUS AND ANGLE.
27. GROSS PATHOLOGY
• CONSISTENCY → FIRM TO HARD
• COLOR → TAN-WHITE, GRAYISH-WHITE OR
GRAYISH-BROWN
• WELL DEMARCATED FROM THE SURROUNDING
BONE, THOUGH NOT ENCAPSULATED.
• ALSO DISPLAYS LARGE CYSTIC AREAS
28. HISTOPATHOLOGIC FEATURES
• NONENCAPSULATED BUT WELL DEMARCATED FROM THE SURROUNDING
BONE.
• CELLULAR FIBROUS CONNECTIVE TISSUE → EXHIBITS AREAS THAT ARE
LOOSE AND OTHER ZONES THAT ARE SO CELLULAR THAT THE CYTOPLASM
OF INDIVIDUAL CELLS IS HARD TO DISCERN BECAUSE OF NUCLEAR
CROWDING.
• MYXOMATOUS FOCI ARE NOT RARE AND OFTEN ARE ASSOCIATED WITH
PSEUDOCYSTIC DEGENERATION.
• MITOTIC FIGURES CAN BE FOUND BUT ARE NOT NUMEROUS.
• AREAS OF HEMORRHAGE AND SMALL CLUSTERS OF MULTI NUCLEATED
GIANT CELLS ARE USUALLY SEEN.
30. PSAMMOMATOID PATTERN FORMS
• CONCENTRIC LAMELLATED AND SPHERICAL
OSSICLES THAT VARY IN SHAPE AND TYPICALLY
HAVE BASOPHILIC CENTERS WITH PERIPHERAL
EOSINOPHILIC OSTEOID.
• A PERIPHERAL BRUSH BORDER BLENDING INTO
THE SURROUNDING STROMA IS NOTED IN MANY
OF THE OSSICLCS. OCCASIONALLY. INDIVIDUAL
OSSICLES UNDERGO REMODELING AND FORM
CRESCENTIC SHAPES.
32. TREATMENT AND PROGNOSIS
• SMALLER LESIONS → COMPLETE LOCAL EXCISION OR THOROUGH
CURETTAGE.
• RAPIDLY GROWING LESIONS → WIDER RESECTION MAY BE REQUIRED.
• RECURRENCE RATES → 30% TO 58%
• MALIGNANT TRANSFORMATION HAS NOT BEEN DOCUMENTED.
33. FIBROUS DYSPLASIA
• A BENIGN, SELF-LIMITING, BUT NONENCAPSULATED LESION
OCCURRING MAINLY IN YOUNG SUBJECTS, USUALLY IN THE MAXILLA,
AND SHOWING REPLACEMENT OF THE NORMAL BONE BY A CELLULAR
FIBROUS TISSUE CONTAINING ISLANDS OR TRABECULAE OF
METAPLASTIC BONE.
• FIRST REPORTED BY VON RECKLINGHAUSEN IN 1891
• THE TERM FIBROUS DYSPLASIA WAS FIRST MENTIONED BY
LICHTENSTEIN IN 1938.
35. • THE ETIOLOGY HAS BEEN LINKED WITH A MUTATION IN THE GNAS1 GENE
LOCATED AT CHROMOSOME 20q13.2
GNAS1 (GUANINE NUCLEOTIDE BINDING PROTEIN) GENE ENCODES A G -
PROTEIN
MUTATION RESULTS IN THE CONTINUOUS ACTIVATION OF THE G - PROTEIN
OVERPRODUCTION OF cAMP IN AFFECTED TISSUES.
HYPERFUNCTION OF CELLS AND ORGANS
36. • OSTEOBLASTS, MELANOCYTES, AND ENDOCRINE
CELLS THAT REPRESENT THE PROGENY OF THAT
MUTATED CELL CARRIES THAT MUTATION AND
EXPRESS THE MUTATED GENE.
• THE CLINICAL PRESENTATION OF MULTIPLE BONE
LESIONS, CUTANEOUS PIGMENTATION, AND
ENDOCRINE DISTURBANCES WOULD RESULT.
UNDIFFERENTIATED STEM
CELLS → EARLY
EMBRYOLOGIC LIFE
• PROGENY OF THE MUTATED CELL WILL DISPERSE
• MULTIPLE BONE LESIONS OF FIBROUS
DYSPLASIA.
MUTATION OCCURS
DURING THIS LATER
PERIOD
• PROGENY OF MUTATED CELL ARE CONFINED TO
ONE SITE,
• MONOSTOTIC FIBROUS DYSPLASIA
MUTATION OCCURS
DURING POSTNATAL LIFE
40. MONOSTOTIC FIBROUS DYSPLASIA
• WHEN THE DISEASE IS LIMITED TO A
SINGLE BONE, IT IS TERMED
MONOSTOTIC FIBROUS DYSPLASIA.
• ACCOUNTS FOR ABOUT 80% TO 85%
OF ALL CASES
• THE CLINICAL TERM "LEONTIASIS
OSSEA" → A LEONINE APPEARANCE
41. CLINICAL FEATURES
• M:F= 1:1
• SWELLING INVOLVES BUCCAL AND
LABIAL PLATE AND SELDOM THE LINGUAL
PLATE
• PAINLESS AND SLOW GROWTH
• OCCURS IN RIB (28%) > FEMUR (23%) >
TIBIA > CRANIOFACIAL BONES (10-25%) >
HUMERUS.
43. POLYOSTOTIC FIBROUS DYSPLASIA
• 1ST RECOGNIZED BY WEIL IN 1922
• INVOLVEMENT OF TWO OR MORE BONES.
• A RELATIVELY UNCOMMON CONDITION.
• THE NUMBER OF INVOLVED BONES VARIES FROM A FEW TO 75% OF THE ENTIRE
SKELETON.
• AFFECTS MULTIPLE BONES LIKE JAWS, FEMUR, TIBIA, PELVIS, RIBS, SKULL,
CLAVICLE AND FACIAL BONES
2 TYPES:
1. JAFFE'S LICHTENSTEIN SYNDROME
2. McCUNE ALBRIGHT'S SYNDROME
44. JAFFE'S LICHTENSTEIN SYNDROME
• FD INVOLVING A VARIABLE NUMBER OF BONES, ACCOMPANIED BY PIGMENTED
LESIONS OF THE SKIN OR "CAFE-AU-LAIT" SPOTS OF THIN LIGHT BROWN
COLOR.
• IT IS MILD AND NON- PROGRESSIVE FORM.
• OCCURS IN ABOUT 50% OF THE CASES.
CAFÉ AU LAIT SPOTS:
• FLAT, PIGMENTED BIRTHMARKS
• CAUSED BY A COLLECTION OF PIGMENT-PRODUCING MELANOCYTES IN THE
EPIDERMIS OF THE SKIN.
45. McCUNE-ALBRIGHT SYNDROME
• FULLER ALBRIGHT FIRST DESCRIBED THIS SYNDROME IN 1937.
• MCCUNE ALBRIGHT SYNDROME IS DEFINED AS THE ASSOCIATION OF
POLYOSTOTIC FIBROUS DYSPLASIA,
PRECOCIOUS PUBERTY,
CAFЀ-AU-LAIT SPOTS, AND
OTHER ENDOCRINOPATHIES DUE TO HYPERACTIVITY OF VARIOUS ENDOCRINE
GLANDS.
46. Mc CUNE ALBRIGHT SYNDROME NEUROFIBROMATOSIS
NEVER CROSS MIDLINE CROSS THE MIDLINE
IRREGULAR BORDERS SMOOTH BORDERS
COAST OF MAINE COAST OF CALIFORNIA
47.
48. CLINICAL FEATURES
• 20-30 % CASES OF FD.
• IT MOST COMMONLY OCCURS IN CHILDHOOD.
• AGE: MEDIAN AGE OF ONSET OF SYMPTOMS IS 8-10
YEARS,
• STRUCTURAL INTEGRITY OF THE BONE IS
WEAKENED
• WEIGHT BEARING BONES BECOME BOWED
• THE CURVATURE OF THE FEMORAL NECK AND
PROXIMAL SHAFT OF THE FEMUR MARKEDLY
INCREASE CAUSING A 'SHEPHERD CROOK
DEFORMITY', WHICH IS A CHARACTERISTIC SIGN OF
THE DISEASE.
• COMPLICATION: SPONTANEOUS FRACTURES
49. ORAL MANIFESTATIONS OF FIBROUS DYSPLASIA
MALALIGNMENT
TIPPING
DISPLACEMENT
DELAYED ERUPTION
INTACT OVER LESION
50. MAZABRAUD'S SYNDROME
• RARE DISEASE CAUSED DUE TO ASSOCIATION OF FD AND INTRAMUSCULAR
MYXOMA.
• PATIENTS WITH SOFT TISSUE MYXOMAS SHOULD BE THOROUGHLY EXAMINED
FOR FD AS GREATER RISK OF SARCOMATOUS TRANSFORMATION IN FD WITH
MAZABRAUD'S SYNDROME.
• THERAPEUTIC IRRADIATION EXPOSURE.
• FEMALES MAY HAVE A GREATER RISK FOR BREAST CANCER, PROBABLY DUE
TO THEIR PROLONGED EXPOSURE TO ELEVATED ESTROGEN LEVELS.
• ETIOLOGY: UNDERLYING GS ALPHA GENE MUTATION
52. CRANIOFACIAL FIBROUS DYSPLASIA
• NOT RESTRICTED TO A SINGLE BONE, BUT MAY BE CONFINED TO A SINGLE
ANATOMICAL SITE.
• PRIMARILY THE MAXILLA
• MAY ALSO CROSS SUTURES INTO THE SPHENOID, ZYGOMA, FRONTONASAL
BONES AND BASE OF THE SKULL.
• DOES NOT MEET THE PRECISE CRITERIA FOR THE MONOSTOTIC OR
POLYOSTOTIC FORMS AND HAS BEEN TERMED CRANIOFACIAL FIBROUS
DYSPLASIA.
53. CLINICAL FEATURES
• 10-25% OF PATIENTS WITH THE MONOSTOTIC
FORM
• 50% WITH THE POLYOSTOTIC FORM.
• OCCURS DURING 1ST AND 2ND DECADES.
• COMMON SITES OF INVOLVEMENT ARE FRONTAL,
SPHENOID, MAXILLARY AND ETHMOID BONES.
54. INVOLVEMENT OF ORBITAL AND PERIORBITAL
BONES
HEADACHE
HYPERTELORISM,
CRANIAL ASYMMETRY,
FACIAL DEFORMITY,
VISUAL IMPAIRMENT,
EXOPTHALMOS AND BLINDNESS.
INVOLVEMENTOF ETHMOID BONE OR FRONTAL BONE
:
A NARROWING AND DISPLACEMENT OF THE
ORBITAL CAVITY.
INVOLVEMENTOF NASAL AND PARANASAL CAVITIES:
55. RADIOGRAPHIC FEATURES
• OFTEN MORE RADIODENSE → HIGHER PROPORTIONS OF
BONE.
• MARGINS OF EXTRA-GNATHIC FD APPEAR WELL DEFINED
WHEREAS THEY ARE POORLY-DEFINED IN THE JAWS.
• ‘ORANGE PEEL PATTERN’ WHICH CONSISTS OF AREAS OF
ALTERNATING GRANULAR DENSITY AND RADIOLUCENCY.
• TOOTH DISPLACEMENT AND LOSS OF LAMINA DURA IS
NOTED IN PATIENTS WITH LESIONS INVOLVING THE TEETH.
56. GROSS PATHOLOGY/ MACROSCOPY
• CONSISTENCY →VARIABLE, SOFT TO VERY HARD.
• COLOR→ GRAYISH WHITE TISSUE
• GRITTY TEXTURE WHEN CUT WITH A SCALPEL.
• DEFORMITY OF THE AFFECTED BONE IS OBSERVED
57. HISTOPATHOLOGIC FEATURES OF FIBROUS DYSPLASIA
• NO DISTINGUISHING HISTOLOGICAL FEATURES BETWEEN THE THREE TYPES OF
FIBROUS DYSPLASIA.
• VARY WITH THE DURATION OF DISEASE AND STAGE OF DEVELOPMENT.
• FD REPLACES NORMAL BONE WITH A CELLULAR, FIBROUS TISSUE CONTAINING
IRREGULARLY SHAPED BONY TRABECULAE.
• THE TRABECULAE CONSIST OF IMMATURE, NON LAMELLAR (WOVEN) BONE
WITHOUT OSTEOID RIMS OR OSTEOBLASTS.
• EARLY OF FD → CHARACTERIZED BY A FIBROBLASTIC TISSUE WHICH IS RICHLY
CELLULAR, OFTEN REVEALING A WHORLED PATTERN WITH LITTLE BONE.
• "CHINESE CHARACTER TRABECULAE".
• AFFECTED BONE USUALLY FUSES WITH THE ADJACENT NONAFFECTED BONE,
WHETHER CORTICAL OR CANCELLOUS
58. • AS FD PROGRESSES, THE AMOUNT OF LAMELLAR TRABECULAE INCREASES.
THESE TRABECULAE ARE SLENDER AND TEND TO RUN PARALLEL TO EACH
OTHER. THEY LIE VERY CIOSE TOGETHER IN A MODERATELY CELLULAR
FIBROUS STROMA. THE TERM OSSEOUS KELOID HAS SOMETIMES BEEN USED
FOR THIS TYPE OF LESION.
• MONOSTOTIC FD OF THE JAWS MAY EXHIBIT VARYING AMOUNTS OF
SPHERICAL, AMORPHOUS CALCIFICATIONS AND CURVED/ LINEAR, ROUND,
CALCIFIED TRABECULAE WHICH TEND TO FORM CONGLOMERATE
STRUCTURES. THESE ARE CONSIDERED BY SOME RESEARCHERS TO BE
MORE REPRESENTATIVE OF CEMENTUM THAN BONE.
• A CHARACTERISTIC FEATURE OF FIBROUS DYSPLASIA THAT MAY HELP
DISTINGUISH IT FROM OSSIFYING FIBROMA IS THAT THE LESIONAL BONE
MERGES IMPERCEPTIBLY WITH ADJACENT CANCELLOUS BONE OR WITH THE
OVERLYING CORTEX.
59. Early of FD → characterized by a fibroblastic tissue which Is richly cellular, often revealing a whorled
pattern with little bone.
"Chinese character trabeculae".
60. • LAMELLAR BONE IS ARRANGED IN
PARALLEL ARRAYS.
• STROMA IS TYPICALLY MODERATELY
CELLULAR WITH SPARSE COLLAGEN
LESIONAL BONE MERGES
IMPERCEPTIBLY WITH ADJACENT
CANCELLOUS BONE OR WITH THE
OVERLYING CORTEX
61. LABORATORY FINDINGS
• ↑ SERUM ALKALINE PHOSPHATASE LEVEL
• PREMATURE SECRETION OF PITUITARY FOLLICLE STIMULATING HORMONE HAS
BEEN REPORTED
• ↑ BASAL METABOLIC RATE.
63. MALIGNANT TRANSFORMATION
• RARE
• RANGES FROM 0.5% (IN MONOSTOTIC DISEASE) TO 4% IN ALBRIGHT'S
SYNDROME.
• THE FIRST DOCUMENTED CASE WAS REPORTED BY COLEY AND STEWART IN
1945.
• MOST COMMON OF THE MALIGNANCIES → OSTEOSARCOMA, FOLLOWED BY
FIBROSARCOMA AND CHONDROSARCOMA.
• MOST MALIGNANT NEOPLASMS DEVELOP IN PATIENTS WHO PREVIOUSLY HAVE
UNDERGONE RADIATION THERAPY TO THE AFFECTED AREA.
64. TREATMENT AND PROGNOSIS
• SMALLER LESIONS → SURGICALLY RESECTED IN THEIR ENTIRETY WITHOUT TOO
MUCH DIFFICULTY,
• LARGE LESIONS → COSMETIC DEFORMITY → SURGICAL RECONTOURING
• IN MANY CASES, THE DISEASE TENDS TO STABILIZE AND ESSENTIALLY STOPS
ENLARGING WHEN SKELETAL MATURATION IS REACHED.
• 25% AND 50% OF PATIENTS SHOW SOME REGROWTH AFTER SURGICAL SHAVE-
DOWN.
• SURGICAL INTERVENTION SHOULD BE DELAYED FOR AS LONG AS POSSIBLE.
• RADIATION THERAPY IS CONTRAINDICATED IN FD BECAUSE IT CARRIES THE RISK
FOR DEVELOPMENT OF POST IRRADIATION BONE SARCOMA
65.
66. CEMENTO- OSSEOUS DYSPLASIA
• CEMENTO-OSSEOUS DYSPLASIA (COD) ARE BFOLS OF THE JAWS CLOSELY
ASSOCIATED WITH THE APICES OF TEETH AND CONTAINING AMORPHOUS
SPHERICAL CALCIFICATIONS WHICH MAKES THEM RESEMBLE AN ABERRANT
FORM OF CEMENTUM.
• IN COD, THE TERM DYSPLASIA REFERS TO THE ABNORMAL DEVELOPMENT AND
DISORDERED PRODUCTION OF BONE AND CEMENTUM-LIKE TISSUE.
• MOST COMMON FIBRO-OSSEOUS LESION ENCOUNTERED IN CLINICAL
PRACTICE.
67. CEMENTO-OSSEOUS DYSPLASIA CAN BE CLASSIFIED INTO 2 GROUPS:
NON HEREDITARY
PERIAPICAL
FOCAL
FLORID
HEREDITARY
FAMILIAL GIGANTIFORM CEMENTOMA.
68. ETIOLOGY
THE ETIOLOGY AND PATHOGENESIS OF COD ARE UNKNOWN.
PERIODONTAL LIGAMENT ORIGIN.
EXTRALIGAMENTARY BONE REMODELING MAY BE TRIGGERED BY LOCAL
FACTORS AND POSSIBLY CORRELATED TO AN UNDERLYING HORMONAL
IMBALANCE
69. PERIAPICAL CEMENTO-OSSEOUS DYSPLASIA
(SYNONYMS: OSSEOUS DYSPLASIA, CEMENTAL DYSPLASIA,
CEMENTOMAS)
• PREDOMINANTLY INVOLVES THE PERIAPICAL REGION OF THE ANTERIOR
MANDIBLE.
• SOLITARY LESIONS OR MULTIPLE FOCI ARE PRESENT MORE FREQUENTLY.
• MARKED PREDILECTION FOR FEMALE PATIENTS (RANGING FROM 10:1 TO 14:1)
• APPROXIMATELY 70% OF CASES AFFECT BLACKS.
• AGE: 30 AND 50 YEARS.
• SITE: MANDIBULAR PERIAPICAL AREA IS THE MOST COMMON SITE OF
APPEARANCE.
70. THE KEY POINTS FOR THIS DISEASE DIAGNOSIS, ACCORDING TO BRANNON &
FOWLER ARE:
PREDILECTION FOR MID-AGE BLACK WOMEN;
ONE OR MORE CIRCUMSCRIBED LESIONS → PERIAPICAL AREA OF VITAL
TEETH;
PAINLESS NON-EXPANSIVE LESION LOCATED USUALLY AT MANDIBLE’S
ANTERIOR AREA;
RADIOGRAPHIC CHARACTERISTICS CAN BE RADIOLUCENCY OF MIXED
DENSITY (RADIOLUCENT WITH OPACITIES), OR OPAQUE WITH A NARROW
RADIOLUCENT MARGIN;
CELLULAR FIBROUS STROMA WITH LAMELLAR OSSEOUS TISSUE AND/OR OVAL
CALCIFICATIONS.
72. • CLASSICALLY, THE HISTOLOGIC FEATURES HAVE THREE STAGES AND ARE
CORRELATED WITH THE RADIOGRAPIC FINDINGS
STAGE1: RADIOLUCENT (OSTEOLYTIC STAGE) - UNENCAPSULATED, CELLULAR,
FIBROUS CONNECTIVE TISSUE WITH NUMEROUS SMALL-CALIBER BLOOD
VESSELS.
STAGE2: RADIOLUCENT/ RADIOPAQUE (CEMENTOBLASTIC STAGE) – VARIABLE
AMOUNTS OF WOVEN TRABECULAR BONE AND/OR SPHERULES OF CEMENTUM
LIKE TISSUE.
STAGE3: RADIOPAQUE (MATURE STAGE) - COALESCENCE OF THE BONE AND/OR
CEMENTUM LIKE TISSUE
73. FOCAL CEMENTO - OSSEOUS DYSPLASIA
• EXHIBITS SINGLE SITE OF INVOLVEMENT.
• ACCORDING TO WALDRON "LOCALIZED FIBRO-OSSEOUS CEMENTAL LESIONS
PRESUMABLY REACTIVE IN NATURE.”
• SEX: 90% IN FEMALES HAVING MALE : FEMALE OF 1: 8, WHITES > BLACKS
• AGE: THIRD TO SIXTH DECADES WITH AN APPROXIMATE MEAN AGE OF 38
YEARS
• SITE: TOOTH-BEARING AREAS OF THE POSTERIOR JAWS
PREVIOUS EXTRACTIONS
• ASYMPTOMATIC, PAINLESS AND FREQUENTLY NONEXPANSILE.
74.
75. FLORID CEMENTO-OSSEOUS DYSPLASIA (FCOD)
• MULTIFOCAL INVOLVEMENT NOT LIMITED TO THE ANTERIOR MANDIBLE.
• PREDOMINANTLY INVOLVES BLACK WOMEN
• MARKED PREDILECTION FOR MIDDLE AGED TO THE ELDERLY.
• MARKED TENDENCY FOR BILATERAL AND OFTEN QUITE SYMMETRIC
INVOLVEMENT.
• NOT UNUSUAL TO ENCOUNTER EXTENSIVE LESIONS IN ALL FOUR POSTERIOR
QUADRANTS.
• USUALLY ASYMPTOMATIC,
• SOMETIMES ALVEOLAR SINUS MAY BE PRESENT.
76.
77. HISTOPATHOLOGIC FEATURES
• ALL THREE PATTERNS DEMONSTRATE SIMILAR HISTOPATHOLOGIC FEATURES.
• FRAGMENTS OF CELLULAR MESENCHYMAL TISSUE COMPOSED OF SPINDLE-SHAPED
FIBROBLASTS AND COLLAGEN FIBERS WITH NUMEROUS SMALL BLOOD VESSELS.
• FREE HEMORRHAGE IS TYPICALLY NOTED INTERSPERSED THROUGH OUT THE
LESION.
• WITHIN THIS FIBROUS CONNECTIVE TISSUE BACKGROUND IS A MIXTURE OF WOVEN
BONE, LAMELLAR BONE, AND CEMENTUM LIKE PARTICLES.
• AS THE LESIONS MATURE AND BECOME MORE SCLEROTIC. THE RATIO OF FIBROUS
CONNECTIVE TISSUE TO MINERALIZED MATERIAL DECREASES.
• WITH MATURATION, THE BONE TRABECULAE BECOME THICK CURVILINEAR
STRUCTURES THAT HAVE BEEN SAID TO RESEMBLE THE SHAPE OF GINGER ROOTS.
• WITH PROGRESSION TO THE FINAL RADIOPAQUE STAGE, INDIVIDUAL TRABECULAE
FUSE AND FORM LOBULAR MASSES COMPOSED OF SHEETS OR FUSED GLOBULES OF
RELATIVELY ACELLULAR AND DISORGANIZED CEMENTOOSSEOUS MATERIAL
78. ct stroma containing spindle-shaped fibroblasts and
collagen fibers with numerous small blood vessels, free
hemorrhage .
curvilinear structures
80. TREATMENT AND PROGNOSIS
• SCLEROSIS → HYPOVASCULAR → PRONE TO NECROSIS
• SEQUESTRATION → OCCURS SLOWLY → HEALING.
• ASYMPTOMATIC PATIENT → REGULAR RECALL EXAMINATIONS WITH
PROPHYLAXIS.
• BIOPSY OR ELECTIVE EXTRACTION OF TEETH SHOULD BE AVOIDED.
• SAUCERIZATION OF DEAD BONE MAY SPEED HEALING.
81. FAMILIAL GIGANTIFORM CEMENTOMA
• FIRST DESCRIBED BY AGAZZI AND BELLONI IN 1953
• WHO DEFINES IT AS “A MASS OF DENSE, HIGHLY CALCIFIED PARTLY OR
ALMOST CELLULAR CEMENTUM OFTEN OCCURRING SIMULTANEOUSLY IN A
NUMBER OF DIFFERENT LOCALISATIONS IN THE JAW.”
• RARE AUTOSOMAL BENIGN DENTAL TUMOR
• UNKNOWN ETIOPATHOGENESIS
82. CLINICAL FEATURES
• NO SEXUAL PREDILECTION
• COMMON IN AFRICAN BLACKS
• PREVALENCE: FIRST DECADE; USUALLY CEASES
DURING 5TH DECADE
• MULTI FOCAL INVOLVEMENT OF BOTH THE MAXILLA
AND MANDIBLE → FACIAL DEFORMITY
• IMPACTION, MALPOSITION AND MALOCCLUSION.
86. CENTRAL GIANT CELL GRANULOMA
• WHO DEFINES IT AS "AN INTRAOSSEOUS LESION CONSISTING OF MORE OR
LESS FIBROUS TISSUE CONTAINING MULTIPLE FOCI OF HEMORRHAGE,
AGGREGATIONS OF MULTINUCLEATED GIANT CELLS, AND SOMETIMES
TRABECULAE OF WOVEN BONE FORMING WITHIN THE SEPTA OF MORE
MATURE FIBROUS TISSUE THAT MAY TRAVERSE THE LESION.“
• FIRST INTRODUCED BY JAFFE IN 1953
• LESS THAN 7% OF ALL JAW LESIONS
87. PATHOGENESIS
• GIANT CELL REMAINS THE MOST PROMINENT FEATURE
• SPINDLE CELL FIBROBLAST RECRUITS MONOCYTES FROM THE VASCULAR SYSTEM AND INDUCES
THEM TO DIFFERENTIATE INTO OSTEOCLASTIC GIANT CELLS THROUGH RELEASE OF CYTOKINES.
• ORIGIN- MESENCHYME OF MARROW AND AN EPIGENETIC EVENT
88. OTHER THEORIES………
CGCG IS A VASCULAR PROLIFERATIVE LESION, → ANGIOGENESIS UNDER THE
INFLUENCE OF THE TUMOR CELLS IS REQUIRED FOR TUMOUR GROWTH,
INVASION, AND DESTRUCTION OF LOCAL TISSUE.
MUTATIONS IN THE GENE SH3BP2
LOCAL FACTOR : TRAUMAS AND VASCULAR DAMAGE, WHICH PRODUCE
INTRAMEDULLARY HEMORRHAGE AND INTRAOSSEOUS REPLACEMENT
FIBROSIS.
89. CLINICAL FEATURES
• AGE: YOUNG PATIENTS LESS THAN 30 YEARS
• SEX: FEMALE˃ MALE
• SITE: MANDIBLE ˃ MAXILLA, ANTERIOR PORTION OF THE JAW NOT COMMONLY
CROSS THE MIDLINE.
• PAINFUL OR PAINLESS RED TO PURPLISH BLUE NODULE LOCATED ON THE GUMS
OR EDENTULOUS ALVEOLAR REGION
92. HISTOPATHOLOGIC FEATURES
• LOOSE FIBRILLAR CONNECTIVE TISSUE STROMA WITH MANY INTERSPERSED
PROLIFERATING FIBROBLASTS ANS SMALL CAPILLARIES.
• PRESENCE OF FEW TO MANY MULTINUCLEATED GIANT CELLS IN A BACKGROUND
OF OVOID TO SPINDLE SHAPED MESENCHYMAL CELLS.
• THERE IS EVIDENCE THAT THESE GIANT CELLS REPRESENT OSTCOCLASTS,
ALTHOUGH OTHERS SUGGEST THE CELLS MAY BE ALIGNED MORE CLOSELY WITH
MACROPHAGES.
• GIANT CELLS VARY CONSIDERABLY IN SIZE AND SHAPE AND MAY CONTAIN ONLY A
FEW OR SEVERAL DOZEN NUCLEI.
• AREAS OF ERYTHROCYTE EXTRAVASATION AND HEMOSIDERIN DEPOSITION ARE
PROMINENT
• FOCI OF OSTEOID OR NEWLY FORMED BONE ARE PRESENT
93. Numerous multinucleated giant cells within a background
of plump proliferating mesenchymal cells. Note extensive
red blood cell extravasation
spindle-shaped fibroblast-like
Aggregations of multinuclear giant cells are
distributed between the stromal cells and often
found near or evensituated inside (arrow) thin-
walled vascular channels. osteoid trabeculum can
be seen
95. TREATMENT AND PROGNOSIS
• CURETTAGE OR SURGICAL EXCISION
• IN PATIENTS WITH AGGRESSIVE TUMORS. THREE ALTERNATIVES TO SURGERY-
(I) CORTICOSTEROIDS,
(2) CALCITONIN, AND
(3) INTERFERON ALFA-2A
• RECURRENCE RATE- 11%- 50%
96. CHERUBISM
• WHO IN 1992 DEFINED IT AS “A BENIGN, SELF-LIMITING CONDITION IN WHICH
THE LESLONAL TISSUE CONSISTS OF VASCULAR FIBROUS TISSUE CONTAINING
VARYING NUMBERS OF MULTINUCLEATED GIANT CELLS ARRANGED DIFFUSELY
OR FOCALLY.”
• FIRST DESCRIBED BY JONES IN 1933
• AUTOSOMAL DOMINANT
• 100% PENETRANCE IN MALES, ONLY 50-70% PENETRANCE IN FEMALES
• NON NEOPLASTIC BONE LESIONS AFFECTING ONLY THE JAWS.
97. PATHOGENESIS
MOST ACCEPTED THEORY:
ASSOCIATION WITH AUTOSOMAL DOMINANT GENE.
MUTATION IN GENE SH3BP2 ON CHROMOSOME 4P16
OTHER POSSIBLE HYPOTHESIS (CABALLERO AND VINALS)
MESENCHYMAL ALTERATION DURING JAW DEVELOPMENT
HORMONAL FACTORS
TRAUMA
100. • SEX PREDILECTION:100% MALE PENETRANCE AND 50-70% FEMALE
PENETRANCE
• PREVALENCE: BETWEEN THE AGES OF 2 AND 5 YEARS.
• LOCATION: BILATERAL INVOLVEMENT OF THE POSTERIOR
MANDIBLE
• PAINLESS, BILATERAL, SYMMETRIC JAW ENLARGEMENT
RESULTING IN MARKED FACIAL EXPANSION
• CHARACTERISTIC “EYE TO HEAVEN” APPEARANCE.
• TOOTH DISPLACEMENT OR FAILURE OF ERUPTION, IMPAIRED
MASTICATION, SPEECH DIFFICULTIES, LOSS OF NORMAL VISION
OR HEARING
CLINICAL FEATURES
101.
102. SEX STEROID AND THE INCREASE IN PLASMA
CONCENTRATION OF ESTRADIOL AND TESTOSTERONE AT
PUBERTY
REDUCTION IN OSTEOCLAST FORMATION
103. A GRADING SYSTEM HAS BEEN PROPOSED":
GRADE 1: INVOLVEMENT OF BOTH MANDIBULAR ASCENDING RAMI
GRADE 2: INVOLVEMENT OF BOTH MANDIBULAR ASCENDING RAMI AND BOTH
MAXILLARY TUBEROSITIES
GRADE 3: MASSIVE INVOLVEMENT OF THE ENTIRE MAXILLA AND MANDIBLE
EXCEPT THE CONDYLAR PROCESSES
GRADE 4: SAME AS GRADE 3 WITH INVOLVEMENT OF THE ORBITS, CAUSING
ORBITAL COMPRESSION.
104. ORAL MANIFESTATION
• AGENESIS OF THE 2ND AND 3RD MOLAR
• DISPLACEMENT OF TEETH
• PREMATURE EXFOLIATION OF TEETH
• DELAYED ERUPTION OF PERMANENT TEETH
• TRANSPOSITION OR ROTATION OF TEETH
• NOONAN’S SYNDROME: A LESION IN THE HUMERUS, GINGIVAL FIBROMATOSIS,
PSYCHOMOTOR RETARDATION, ORBITAL INVOLVEMENT AND OBSTRUCTIVE
SLEEP APNEA
108. TREATMENT
• SELF LIMITING CONDITION, TREATMENT IS MAINLY FOR THE ESTHETIC NEEDS AND FOR
UNERUPTED TEETH.
• CURETTAGE IS THE SURGERY OF CHOICE.
• LIPOSUCTION
• RADIOTHERAPY IS CONTRAINDICATED BECAUSE OF FEAR OF RETARDATION OF JAW
GROWTH , OSTEORADIONECROSIS AND CHANCES OF MALIGNANT DEGENERATION.
• MEDICAL THERAPY LIKE CALCITONIN IS THEORETICALLY APPROPRIATE
• RECENT ADVANCEMENT → GENETIC THERAPY.
RECURRENCE RATE OF 15-20%
109. ANEURYSMAL BONE CAVITY (ANEURYSMAL BONE CYST)
• WHO DEFINED IT AS "A BENIGN INTRAOSSEOUS LESION, CHARACTERIZED BY
BLOOD-FILLED SPACES OF VARYING SIZE ASSOCIATED WITH A FIBROBLASTIC
TISSUE CONTAINING MULTINUCLEATED GIANT CELLS, OSTEOID, AND WOVEN
BONE.“
• 1ST RECOGNIZED BY JAFFE AND LICHTENSTEIN IN 1942.
• ETIOLOGY: CHROMOSOMAL INSTABILITY INVOLVING THE BAND 16q22
(PANOUTSAKOPOULOS ET AL)
110. ETIOPATHOGENESIS
1. LICHTENSTEIN IN 1950 - DUE TO ALTERED HAEMODYNAMICS.
CYST
↑ VENOUS
PRESSURE
ENGORGEMENT
OF VASCULAR
BED
RESORPTION
CT
REPLACEMENT
AND OSTEOID
FORMATION
111. 2.BERNIER AND BHASKAR
• RESEMBLES CENTRAL GIANT CELL REPARATIVE GRANULOMA OF JAWS
• BOTH LESIONS REPRESENT OVERZEALOUS ATTEMPTS OF CT TO REPLACE A
HAEMATOMA IN THE BONE MARROW
HAEMATOMA
MAINTAINS CIRCULATORY
CONNECTION WITH DAMAGED
B.V
ANEURYSMAL BONE
CYST
OBLITERATION OF
CIRCULATION
GIANT CELL
REPARATIVE
GRANULOMA
112. 3. BIESECKER ET
AL
PRIMARY BONE LESION
OSSEOUS AV
MALFORMATION
SECONDARY REACTIVE
LESION
AV FISTULA
RESORPTION OF
ADJACENT BONE
VASCULAR
CHANNELS
BOUND BY
PERIOSTEAL
BONE
GIANT CELLS AND
STROMAL CELLS
SEEN
FINALLY RESULTS IN
THE FORMATION OF
CYST CAVITY
113. 4. STRUTHERS AND
SHEAR
LOOSE FIBRILLAR CT
STROMA OF CGCG
INTERCELLULAR
OEDEMA AND
MICROCYST
FORMATION
ENLARGE AND
COALESCE…
PRESSURE
RESORPTION OF
MEDULLARY BONE
ENDOSTEAL
RESORPTION AND
BLOWOUT OF LESION
CYSTIC CAVITY IS
FORMED
114. PHASES OF PATHOGENESIS
1. OSTEOLYTIC INITIAL PHASE
2. ACTIVE GROWTH PHASE
3. MATURE PHASE OR PHASE OF STABILIZATION
4. HEALING PHASE
119. HISTOPATHOLOGIC FEATURES
• TWO TYPES ARE:
1.CONVENTIONAL(95%)
OSTEOLYTIC LESION WITH MULTINUCLEATED GIANT CELLS
VASCULAR AREAS OF VARIABLE SIZE SEPARATED BY CONNECTIVE TISSUE
BONE TRABECULAE, OSTEOID TISSUE AND HEMOSIDERIN PIGMENT
2.SOLID(5%):
SOLID MASS WITHOUT CYSTIC COMPONENT
MULTIPLE HEMORRHAGIC FOCI
PLENTY OF FIBROBLASTS, OSTEOBLASTS AND OSTEOCLASTS
122. TREATMENT AND PROGNOSIS
• CURETTAGE OR ENUCLEATION
• CRYOSURGERY
• SURGICAL DEFECT HEALS WITH 6 MONTHS – 1 YEAR.
• RECURRENCE- 8%- 60%
123. TRAUMATIC BONE CYST
• FIRST DESCRIBED BY LUCAS AND BLUM IN 1929
• LATER DESCRIBED BY RUSHTON AS “A SINGLE CYST THAT HAS NO EPITHELIAL
LINING, HAS AN INTACT BONY WALL, IS FLUID FILLED, AND HAS NO EVIDENCE OF
ACUTE OR CHRONIC INFLAMMATION.”
• IT COMPRISES OF A SINGLE LESION WITHOUT AN EPITHELIAL LINING, SURROUNDED
BY BONY WALLS AND EITHER LACKING CONTENTS OR CONTAINING LIQUID AND/OR
CONNECTIVE TISSUE.
125. OTHER THEORIES
MIRRA ET AL PROPOSED THAT “A SMALL NEST OF SYNOVIUM BECOMES
TRAPPED INTRAOSSEOUSLY DURING FETAL OR EARLY INFANT DEVELOPMENT
AND THAT THIS TISSUE MAY RETAIN SOME SECRETORY FUNCTION, RESULTING
IN THE DEVELOPMENT OF A CYST.”
LOW-GRADE INFECTION ,
CYSTIC DEGENERATION OF BONE TUMORS,
LOCAL ALTERATION OF BONE METABOLISM RESULTING IN OSTEOLYSIS
ISCHEMIC MARROW NECROSIS,
126. CLINICAL FEATRURES
• VAST MAJORITY INVOLVES THE LONG BONES.
• AGE: 10-20 YEARS
• SEX: MALE ˃ FEMALE
• SITE: MANDIBLE ˃ MAXILLA
• OCCASIONALLY BILATERAL
• ASYMPTOMATIC
• SOMETIMES PAIN AND PARESTHESIA PRESENT
128. HISTOLOGIC FEATURES
• THE WALLS OF THE DEFECT MAY BE LINED BY A THIN
BAND OF VASCULAR FIBROUS CONNECTIVE TISSUE OR
DEMONSTRATE A THICKENED MYXOFIBROMATOUS
PROLIFERATION THAT OFTEN IS INTERMIXED WITH
TRABECULAE OF CELLULAR AND REACTIVE BONE.
• THIS LINING MAY EXHIBIT AREAS OF VASCULARITY,
FIBRIN, ERYTHROCYTES, AND OCCASIONAL GIANT
CELLS ADJACENT TO THE BONE SURFACE.
• NO EPITHELIAL LINING.
• THE BONY SURFACE NEXT TO THE CAVITY OFTEN
SHOWS RESORPTIVE AREAS (HOWSHIP'S LACUNAE)
INDICATIVE OF PAST OSTEOCLASTIC ACTIVITY.
Bone covered by a layer of loose fibrous connective
tissue
130. TREATMENT AND PROGNOSIS
• LONG BONES OFTEN IS MORE AGGRESSIVE AND INCLUDES INTRALESIONAL
STEROID INJECTIONS OR THOROUGH SURGICAL CURETTAGE.
• ENUCLEATION OF LINING IN THE COURSE OF MANIPULATION
• RE-ESTABLISH BLEEDING
• IF THE CAVITY IS THEN CLOSED→ HEALING IN 6-12 MONTHS
• IN LARGE CAVITY → BONE CHIPS TO FILL THE CAVITIES
131. CONCLUSION
• FIBRO-OSSEOUS LESIONS ARE A POORLY DEFINED GROUP OF LESIONS
AFFECTING THE JAWS AND CRANIOFACIAL BONES.
• CLASSIFICATION AND, THEREFORE, DIAGNOSIS OF THESE LESIONS IS DIFFICULT
BECAUSE THERE IS SIGNIFICANT OVERLAP OF CLINICAL AND HISTOLOGICAL
FEATURES.
• NEW TERMINOLOGY HAS EMERGED THAT HAS CULMINATED IN THE LATEST WHO
CLASSIFICATION.
• DEFINITIVE DIAGNOSIS REQUIRES CORRELATION OF THE HISTOPATHOLOGIC
FEATURES WITH THE PATIENT’S HISTORY, CLINICAL FINDINGS,
RADIOGRAPHIC/IMAGING ANALYSIS, AND OPERATIVE FINDINGS BECAUSE OF THE
HISTOLOGIC SIMILARITIES AMONG THIS DIVERSE GROUP OF LESIONS
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Higher power view depicting a cellular mesenchymal tissue composed of spindle-shaped fibroblasts with numerous small blood vessels.
Giant cell lesion of the maxilla with clinical and
histologic features suggestive of a giant cell tumor. The giant cells
are larger with more numerous nuclei than the ones commonly
seen in giant cell granuloma.
