AMELOBLASTOMA

INTRODUCTION

• HISTORY
• PATHOGENESIS
• CLASSIFICATION
• CLINICAL FEATURES
• RADIOGRAPHIC FEATURES
• HISTOPATHOLOGY
• INVESTIGATIONS
• TREATMENT
• DIFFERNTIAL DIAGNOSIS
• PROGNOSIS
• REFRENCES
 TUMOUR-DEFINITION

• A TUMOUR OR NEOPLASM IS DEFINED AS AN

ABNORMAL MASS OF TISSUE , THE GROWTH OF
WHICH IS UNCONTROLLED & UNCOORDINATED WITH
THAT OF NORMAL TISSUE & PERSIST IN THE SAME
EXCESSIVE MANNER EVEN AFTER THE CESSATION OF
STIMULUS THAT EVOKED THE CHANGE.- R.A. WILLI
• BASED ON ORIGIN
• • ODONTOGENIC
• NON ODONTOGENIC
• BASED ON ITS NATURE
• • BENIGN
• MALIGNANT
• A. BENIGN
• 1)ODONTOGENIC EPITHELIUM WITHOUT ODONTOGENIC MESENCHYME
• AMELOBLASTOMA
• SQUAMOUS ODONTOGENIC TUMOR
• CALCIFYING EPITHELIAL ODONTOGENIC TUMOR
• ADENOMATOID ODONTOGENIC TUMOR
• 2)ODONTOGENIC EPITHELIUM WITH ODONTOGENIC ECTOMESENCHYME WITH OR WITHOUT HARD
TISSUE FORMATION
• AMELOBLASTIC FIBROMA
• AMELOBLASTIC FIBRO-DENTINOMA
• AMELOBLASTIC FIBRO ODONTOMA
• ODONTOAMELOBLASTOMA
• CALCIFYING ODONTOGENIC CYST COMPLEX ODONTOMA
• COMPOUND ODONTOMA
• 3.ODONTOGENIC ECTOMESENCHYME WITH OR WITHOUT INCLUDED ODONTOGENIC EPITHELIUM
• 1. ODONTOGENIC FIBROMA
• 2. MYXOMA
3. CEMENTOBLASTOMA
• B. MALIGNANT
1. ODONTOGENIC CARCINOMA
• 1. MALIGNANT AMELOBLASTOMA
2. PRIMARY INTRA-OSSEOUS CARCINOMA
• 3.CLEAR CELL ODONTOGENIC CARCINOMA
• 4.GHOST CELL ODONTOGENIC CARCINOMA
• 2.ODONTOGENIC SARCOMAS
•  AMELOBASTIC FIBROSARCOMA
•  AMELOBASTIC FIBRO-DENTINOSARCOMA
 AMELOBLASTOMA
• “USUALLY UNICENTRIC, NONFUNCTIONAL, INTERMITTE
NT IN GROWTH ,ANATOMICALLY BENIGN AND CLINICALLY
PERSISTENT”
• - ROBINSON
• • TRUE NEOPLASM OF ENAMEL ORGAN TYPE TISSUE
• SECOND MOST COMMON ODONTOGENIC NEOPLASM
 HISTORY

• ORIGINATED FROM EARLY ENGLISH WORD ‘AMEL’ MEANING

‘ENAMEL’ AND GREEK WORD ‘BLASTOS’ MEANING ‘GERM’
•  IT WAS RECOGNISED BY CUSACK IN 1827
•  NAMED AS ADAMANTINOMA BY LOUIS CHARLES MALASSEZ
BECAUSE OF ITS HISTOLOGICAL SIMILARITY WITH
ADAMANTINOMA OF LONG BONES
•  COINED AS AMELOBLASTOMA BY CHURCHILL AND IVEY IN 1934
•  FIRST DETAILED DESCRIPTION GIVEN BY FALKSON IN 1879
 CLINICAL CLASSIFICATION

• CENTRAL (INTRAOSSEOUS)
1. CONVENTIONAL/ MULTICYSTIC/SOLID (MOST COMMON)
• 2. UNICYSTIC
3. PERIPHERAL (EXTRAOSSEOUS)
4. PITUITARY AMELOBLASTOMA
5. MALIGNANT AMELOBLASTOMA
• BASED ON HISTOLOGICAL TYPE
• FOLLICULAR AMELOBLASTOMA
• PLEXIFORM AMELOBLASTOMA
• ACANTHOMATOUS AMELOBLASTOMA
• GRANULAR CELL AMELOBLASTOMA
• BASAL CELL TYPE OF AMELOBLASTOMA
 ETIOLOGY
• TRAUMATIC EPISODES:
• EXTRACTION,
• CYSTECTOMY,
• FRACTURES
• INFECTIONS
• DIETARY DEFICIENCY:
• VITAMIN D DEFICIENCY,
• LACK OF PROTEIN INTAKE
 PATHOGENESIS
• AMELOBLASTOMA IS BELIEVED TO BE DERIVED FROM
• A) CELL REST OF ENAMEL ORGAN, EITHER REMNANTS OF DENTAL
LAMINA OR HERTWIG’S SHEATH, THE EPITHELIAL REST OF
MALASSEZ.
• B) EPITHELIUM OF ODONTOGENIC CYSTS, PARTICULARLY THE
DENTIGEROUS CYST & ODONTOMAS.
• C) DISTURBANCE TO DEVELOPING ENAMEL ORGAN.
• D) BASAL CELLS OF THE SURFACE EPITHELIUM OF THE JAWS.
• E) HETEROPIC EPITHELIUM IN OTHER PARTS OF BODY ESPECIALLY
THE PITUITARY GLAND.
 CLINICAL FEATURES
• AGE: 20-50 YEARS
• SEX: NO SIGNIFICANT SEX
• PREDILECTION
• RACE: MORE COMMON IN BLACKS THAN IN WHITE RACE.
• SITE: MANDIBLE > MAXILLA(MORE THAN 80% MANDIBLE)
•  WITH IN MANDIBLE MOLAR RAMUS AREA IS AFFECTED THREE
TIMES MORE COMMONLY THAN PREMOLARS & ANTERIORS.
• SIZE: SMALL AS 1CM TO LARGE AS 16 CM SPREAD: LOCAL INVASION
• CAUSES EXPANSION OF BONE THAN DESTRUCTION.
• • INFILTRATES CANCELLOUS BONE BUT NEVER CORTICAL
• BONE
 MURAL AMELOBLASTOMA:
• AMELOBLASTOMA FROM DENTIGEROUS CYST
• MAXILLARY AMELOBLASTOMA:
• COMMON IN TUBEROSITY.
• MORE DANGEROUS AS
1. IT MAY CAUSE NASAL OBSTURCTION
• 2. PROPTOSIS OF EYE
3. DAMAGEVITALSTRUCTURES
4. INVOLVECRANIALBASE
 SIGNS AND SYMPTOMS
• IT STARTS AS A SLOW GROWING , PAINLESS, HARD, NON
TENDER, OVOID SWELLING WHICH OFTEN ENLARGES IN SIZE
AS IT CAUSES LITTLE DISCOMFORT IN EARLY STAGE.
• FACIAL ASSYMETRY
• MOBILTY OF TEETH AND EXFOLIATION
• PAIN OR PARESTHESIA IF IMPINGES ON NERVE
 DENTAL FEATURES MAY INCLUDE
• MAY BE ASSOCIATED WITH UNERUPTED TEETH.
• • AND CAUSES MOBILE TEETH,
• EXFOLIATION OF TEETH,
• ROOT RESORPTION,
• • ILL FITTING DENTURES,
• MALOCCLUSIONS,
• ULCERATIONS,
• NASAL OBSTRUCTIONS AND
• INABILITY TO OCCLUDE
 IN THE ABSENCE OF TREATMENT,
• • IT MAY BE EXTREMELY DISFIGURING ,FUNGATING AND ULCERATIVE
LIKE CARCINOMA
• KEEPS ON ENLARGING AND CAUSE “EGG SHELL CRACKLING’’&
FLUCTUATION
• PALPATION ELICIT HARD SENSATION OR CREPITUS.
• NOT ENCAPSULATED
• INVADES SURROUNDING TISSUES
• BONE DESTRUCTION IS A COMMON FINDING BY INVASION TO BONE
MARROW
• ROOT RESORPTION IS CAUSED
 VICKER’S AND GORLIN’S CRITERIA
HISTOLOGY
• 1.TALL COLUMNAR CELL
• 2.HYPERCHROMATIC NUCLEUS
• 3.PALISADED NUCLEI
4.REVERSE POLARITY OF NUCLEI
• 5.SUBNUCLEAR VACUOLE FORMATION
• 6 HISTOLOGIC SUBTYPES
 FOLLICULAR AMELOBLASTOMA
 PLEXIFORM AMELOBLASTOMA
• ACANTHOMATOUS AMELOBLASTOMA
•  GRANULAR AMELOBLASTOMA
•  BASAL CELL TYPE OF AMELOBLASTOMA
• DESMOPLASTIC AMELOBLASTOMA
 FOLLICULAR AMELOBLASTOMA
• SMALL DISCRETE ISLANDS OF TUMOUR CELLS.
• *PERIPHERAL LAYER OF CUBOIDAL OR COLUMNAR CELLS.
• *NUCLEI WELL POLARIZED.
• *RESEMBLES AMELOBLAST.
• *CYST FORMATION IS RELATIVELY COMMON.
• *STELLATE RETICULUM LIKE CELLS PROMINENT ENCLOSED
BY COLUMNAR OR CUBOIDAL CELLS
 PLEXIFORM AMELOBLASTOMSA
• AMELOBLAST LIKE CELLS ARRANGED IN IRREGULAR MASSES.
•  NETWORKS OF INTERCONNECTING STRANDS OF CELLS.
•  EACH STRANDS BOUNDED BY LAYER OF COLUMNAR CELLS.
•  IN B/W THESE PRESENT STELLATE RETICULUM LIKE TISSUES
LESS PROMINENT COMPARED TO FOLLICULAR
AMELOBLASTOMA.
•  AREAS OF CYSTIC DEGENERATION IS COMMON.
 ACANTHOMATOUS AMELOBLASTOMA
• CELLS OCCUPYING THE POSITION OF STELLATE RETICULUM
UNDERGO SQUAMOUS METAPLASIA
• SOMETIMES WITH KERATIN FORMATION IN THE CENTRAL
PORTION OF TUMOR ISLANDS
• USUALLY OCCURS IN FOLLICULAR TYPE
• SOMETIMES KERATIN PEARLS MAY BE OBSERVE
 GRANULAR CELL AMELOBLASTOMA
• MARKED TRANSFORMATION OF CYTOPLASM,USUALLY OF
STELLATE RETICULUM LIKE CELLS BECOME
COARSE,GRANULAR,EOSINOPHILIC APPEARANCE
• INCLUDE PERIPHERAL COLUMNAR OR CUBOIDAL CELLS
• HYPERCHROMATISM
• REVERSE POLARITY
 BASAL CELL AMELOBLASTOMA

• BEAR RESEMBLANCE TO BASAL CELL CARCINOMA OF SKIN

• • RAREST HISTOLOGIC SUBTYPE
• • HYPERCHROMATIC ,LESS COLUMNAR,ARRANGED IN SHEETS WITHOUT
PERIPHERAL PALISADING
 DESMOPLASTIC AMELOBLASTOMA
• FOUND IN A DENSE COLLAGEN STROMA THAT IS HYPOCELLULAR AND HYALINIZED
• GROW IN THIN STRANDS AND CORDS OF EPITHELIUM
• • EPITHELIAL PROLIFERATION SEEMS TO BE COMPRESSED AND FRAGMENTED BY
HYALINISED STROM
 UNICYSTIC AMELOBLASTOMA

• SINGLE CYSTIC CAVITY SHOWING AMELOBLASTOMATOUS DIFFERENTIATION

• AGE: THE PATIENTS ARE YOUNGER THAN THOSE WITH THE SOLID/MULTICYSTIC
FORM IE AROUND 20 YRS
• SEX PREDILECTION: EQUAL
• LOCATION: 90 % OCCUR IN THE MANDIBLE USUALLY IN THE POSTERIOR
REGION
• TYPICALLY SURROUNDS THE CROWN OF UNERUPTED MANDIBULAR THIRD
MOLAR AND RESEMBLES DENTIGEROUS CYST
 HISTOLOGY
• CLASSIFICATION
• LUMINAL TYPE: THE TUMOR IS CONFINED TO THE LUMINAL SURFACE OF THE
CYST BY FIBROUS CONNECTIVE TISSUE PARTIALLY OR TOTALLY
• INTRALUMINAL: THE TUMOR NODULES PROJECTS FROM THE CYSTIC LINING
• MURAL: THE TUMOR INFILTRATES THE FIBROUS CYSTIC WALL.(HIGH
RECURRENCE RATE)
 RADIOGRAPHIC FEATURES

• PRESENT A UNILOCULAROR MULTILOCULAR RADIOLUCENCY IN DIFF

FORMS AND SHAPES
• 50%MULTILOCULAR,2% PERIPHERAL AND 6% UNICYSTIC LESIONS
• • MULTILOCULARRADIOLUCENCY WITH COMPARTMENTALISED
APPEARANCE DUE TO BONY SEPTA (HONEY COMB OR SOAP BUBBLE
APPEARANCE)
• • ROOTRESORPTIONANDTOOTH DISPLACEMENT
• SMALL / LARGE UNILOCULAR OR MULTILOCULAR LESION MAY SHOW
UNERUPTED TOOTH
• • BUCCOLINGUAL CORTICAL EXPANSION( HOLLOWING OUT)
 UNICYSTIC TYPE
•

WELL DEFINED RADIOLUCENT LESION WITH

• MINIMAL PERIPHERAL SCLEROTIC BORDER
• MIMICS DENTIGEROUS CYST
• ASSOCIATED WITH IMPACTED 3RD MOLAR
• IN ADV STAGE THINNING OF CORTICAL BONE SEEN
MAXILLARY LESIONS INVOLVE MAXILLARY SINUS AND MAKE IT MORE
OPACIFIED APPEARANCE
• • CT SCAN AND 3D RECONSTRUCTIONS
 PERIPHERAL AMELOBLASTOMA
• RARE TYPE
DEVELOPS IN SOFTTISSUE OF GINGIVA AND MUCOSA
• NON INVASIVE
• CLINICAL FEATURES
*YOUNGER INDIVIDUALS
*MANDIBLE>MAXILLA
*IN PREMOLAR REGION
*APPERAS AS A NODULE ON THE GINGIVA/ MUCOSA *SIZE 3MM-
2CM
 PITUITARY AMELOBLASTOMA
• CRANIOPHARYNGIOMA/RATHKE’S POUCH TUMOR.
• NEOPLASM INVOLVING CNS.
• GROWS AS A PSEUDO ENCAPSULATED MASS IN THE SUPRASELLAR
AREA AND DESTROYS PITUITARY GLAND.
• CLINICALFEATURES-
• ENDOCRINE DISTURBANCES,DROWSINESS& EVEN TOXIC
SYMPTOMS.
 MALIGNANT AMELOBLASTOMA

• MALIGNANT TRANSFORMATION OF AMELOBLASTOMA

• RARE LESION
• ALMOST EXCLUSIVELY IN MANDIBLE
• MEAN AGE: 28-32 YRS
• COMMON SITES FOR METASTASIS;
LUNGS,SPLEEN,KIDNEY,ILEUM
 INVESTIGATIONS

• RADIOGRAPHS
• • BIOPSY
• CT
• MRI
• • ULTRASOUND
 TREATMENT OPTIONS INCLUDE

• A) RADICAL & CONSERVATIVE SURGICAL EXCISION.

• B) EN BLOC RESECTION
• C) SEGMENTAL RESECTION
• D) CURETTAGE
• E) CHEMICAL & ELECTROCAUTERY
• F) CHEMOTHERAPY
• G) RADIATION.
 SIMPLE EXCISION/ENUCLEATION

• IN CASE OF PERIPHERAL AMELOBLASTOMA,SIMPLE EXCISION OF THE LESION IS

PERFORMED
 ENUCLEATION&CURETTAGE
• IN PERIPHERAL AMELOBLASTOMA, SIMPLE EXCISION IS PERFORMED
• MEANS REMOVAL OF THE TUMOR BY SCRAPING IT FROM THE
• SURROUNDING NORMAL TISSUE.
• CURETTAGE GIVEN A CURE RATE OF ONLY 10%
• 60-90% OF RECURRENCE RATE COMPLICATIONS OF CURETTAGE
• SEEDING INTO LUNGS
• MALIGNANTTRANSFORMATION
• FAILURE OF CURETTAGE IS PROBABLY RELATED TO THE FACT THAT THE NEST OF
TUMOR CELLS EXTEND BEYOND CLINICAL & RADIOGRAPHIC MARGINS OF THE
LESION.
• THEREFORE IMPOSSIBLE TO ERADICATE THE LESION BY SCRAPING PROCEDURE.
 EN BLOC RESECTION
• MEANS REMOVAL OF SEGMENT OF THE MAXILLA / MANDIBLE UP TO
& INCLUDING HEMI SECTION OR MORE.
• INCLUDES HEMIMAXILLECTOMY&HEMIMANDIBULECTOMY.
• MOST COMMONLY USED TREATMENT.
• LEAST CHANCE OF RECURRENCE.
• IT IS NOTED THAT THE LESION MOST LIKELY TO RECUR AFTER
SEGMENTAL RESECTION ARE THOSE OVER 5CM.
 CHEMOTHERAPY
• MAY BE SENSITIVE TO PLATINUM AGENTS
• MAY HAVE ROLE IN IMPROVEMENT IN NON SURGICAL
• PATIENTS
• EG; CYCLOPHOSPHAMIDE,CISPLATIN,VINBLASTINE,METHOTR
EXATE ETC
 SEGMENTAL RESECTION
• DESICCATION / ELECTRO COAGULATION OF THE LESION
INCLUDING VARIOUS AMOUNT OF SURROUNDING NORMAL
TISSUES.
•  NOT BEEN COMMONLY USED AS PRIMARY MODE OF THERAPY.
•  MUCH MORE EFFECTIVE THERAPY THAN CURETTAGE.
 50% RECURRENCE RATE.
•  BECAUSE OF POOR RESULTS –NOT BEEN USED AS A SOLE
METHOD OF TREATMENT.
 ELECTROCAUTERY
• DESSICATION ELECTROCAUTERY OF THE LESION NCLUDING
VARIOUS AMOUNT OF SURROUNDING NORMAL TISSUES.
• NOT BEEN COMMONLY USED AS PRIMARY MODE OF THERAPY.
MUCH MORE EFFECTIVE THERAPY THAN CURETTAGE.
50% RECURRENCE RATE.
• BECAUSE OF POOR RESULTS –NOT BEEN USED AS A SOLE METHOD
OF TREATMENT.
 RADIATION THERAPY

• AMELOBLASTOMA IS GENERALLY RADIORESISTANT

• • POST OPERATIVELY IN PTS WITH GROSS/MICROSCOPIC RESIDUAL DISEASE
• • RECURRENT DISEASE
• PTS WHO ARE POOR CANDIDATES OF SURGERY
 POST OPERATIVE MANAGEMENT
rehabilitation with obturator in maxilla
RECONSTRUCTION WITH GRAFT
Reconstruction with titanium plates and screws
 PROGNOSIS

• SIMPLE CURETTAGE- 90% RECURRENCE RATE.

• AMELOBLASTOMA OF MAXILLA – MORE AGGRESSIVE – POOR PROGNOSIS
 DIFFERENTIAL DIAGNOSIS
• AMELOBLASTIC FIBROMA
• ODONTOGENIC MYXOMA
• CENTRAL GIANT CELL GRANULOMA
• DENTIGEROUS CYST
• OKC
 CONCLUSION

• IN THE EVENT OF RECURRENCE A SECOND SURGERY MAY BE SUCCESSFUL.

• PATIENT COMPLIANCE AND FOLLOW UP ARE IMPORTANT.
• CT IS AN EXCELLENT IMAGING MODALITY TO CHARACTERIZETHE LESION
AND KNOW THE EXTENT OF TUMOR INVASION.
• HISTOPATHOLOGY IS MANDATORY TO CONFIRM DIAGNOSIS.
• TREATMENT OF AMELOBLASTOMA DEPENDS ON EXTENTOF
INFILTRATION . A WELL CONTAINED LESION IS EXCISEDWITH WIDE
MARGINS ,EN BLIC RESECTION IS DONE FOR AN EXTENSIVE LESION .
• GOOD RESULTS CAN BE ACHIEVED IN THE TREATMENT OF
AMELOBLASTOMA IN CHILDREN USING CONSERVATIVE SURGERY
 REFRENCES

• DANIEL.M.LASKIN – ORAL & MAXILLOFACIAL SURGERY- VOLUME 2

• SHAFER’S TEXTBOOK OF ORAL PATHOLOGY- 7TH EDITION