Ameloblastoma is a true neoplasm originating from the enamel organ, classified by clinical and histological types, with a notable prevalence in the mandible and a mean diagnosis age of 30-39 years. The tumor displays varying growth patterns and can have high recurrence rates, with management strategies ranging from enucleation to more aggressive surgical interventions. Malignant variants, including ameloblastic carcinoma, present significant challenges due to their aggressive nature and potential for metastasis, primarily to the lungs and cervical lymph nodes.
Ameloblastoma is a benign neoplasm of dental origin, previously known as adamantinoma, characterized by non-differentiated enamel organ-like tissues.
Ameloblastoma arises from dental organ remnants and is classified into solid/multicystic, unicystic, and peripheral types based on behavior, location, and histology.
Typically seen in individuals aged 10-90, with an average age of 30-39. Characterized by slow growth and potential for bone erosion, often occurs in the mandible.
Desmoplastic ameloblastoma resembles a mixed lesion, while differential diagnoses include odontogenic keratocyst, myxoma, and radicular cyst.
Common histological variations include plexiform, acanthomatous, granular, desmoplastic, and basal cell patterns, each with distinct characteristics.
Represents 10%-46% of intraosseous cases. Asymptomatic in younger patients, often resembling dentigerous cysts radiographically.
Occurs in 1%-10% of cases, primarily affects middle-aged individuals. Histopathologically similar to intraosseous forms with varying recurrence rates.
Poor prognosis for malignant cases, with metastases primarily affecting lungs and cervical lymph nodes. Histopathological features indicate malignancy.
Key references include textbooks on oral pathology and relevant online resources.
INTRODUCTION
Is atrue neoplasm of enamel organ type
tissue which does not undergo differentiation
to point of enamel formation
Robinson described tumor as usually
unicentric, nonfunctional, intermittent in
growth, anatomically benign and clinically
persistent.
3.
Previously calledadamantinoma –
malassez in 1885
Since this term implied the formation of hard
tissue, and no such material was present in
this lesion, it was replaced with term
ameloblastoma suggested by churchill in
1934
4.
ORIGIN
Cell restsof dental organ, either remnants of dental lamina or remnants
of hertwig’s sheath
Epithelium of odontogenic cysts (dentigerous cysts and odontoma)
Enamel organ
Basal cell of surface epithelium of jaws
Heterotopic epithelium of pituitary gland
Reduced enamel epithelium
5.
PATHOGENESIS
• Low proliferationrate (ki67)
• Over expression of
antiapoptotic proteins (bcl-2,
bclxl)
Cell cycle
related
factors
• Overexpression of interface
protein (fibrinoge growth factor)
• Overexpression of matrix
metallo groth factor proteinase)
Interface
factors
6.
CLASSIFICATION
Based onclinical types
1. Conventional solid or multicystic (about 86%
of all cases)
2. Unicystic (about 13% of all cases)
3. Peripheral (extraosseous) (about 1% of all
cases)
Based onloaction
Intraosseous/ central
Extraosseous/ peripheral
9.
Based onhistological classification
1.Follicular pattern and its variant
granular
acanthomatous
basal cell variant
2. plexiform pattern
3. unicystic ameloblastoma
luminal
intraluminal
mucosal
10.
CONVENTIONAL SOLID ORMULTICYSTIC
INTRAOSSEOUS AMELOBLASTOMA
CLINICAL FEATURES
• Age- 10-90 years
• Average age of diagnosis
30-39 years
• No sex predilection
• Race: more common in blacks
than in white race.
• Site- Mandible (molar-angle-ramus area three
times more commonly than premolar and anterior
region combined)
11.
CLINICAL PRESENTATION
Slowgrowing,
painless, bony hard
swelling
Facial asymmetry
Large lesions- mobile
teeth, pain and
paraesthesia
Locally invasive
Infiltrate medullary
spaces causing
erosion of cortical
bone
12.
RADIOGRAPHIC FEATURES
multilocularradiolucent lesion
“soap bubble” appearance (when the
radiolucent loculations are large) or as
being “honeycombed”(when the
loculations are small)
Compartmented appearrances with
septa of bone extending into
radiolucent tumor mass
Buccal and lingual cortical expansion
Resorption of the roots of teeth
adjacent to the tumor is common
The margins of these radiolucent
lesions, however, often show irregular
scalloping
16.
DESMOPLASTIC AMELOBLASTOMA
occurin the anterior regions
of the jaws particularly the
maxilla
resembles a fibro-osseous
lesion because of its mixed
radiolucent and radiopaque
appearance
mixed radiographic
appearance is due to
osseous metaplasia within
the dense fi brous septa that
characterize the lesion, not
because the tumor itself is
producing a mineralized
product
17.
DIFFERENTIAL DIAGNOSIS
Odontogenickeratocyst- displaced thinning
of cortical bone and associated with
unerupted tooth
Myxoma- condyle involved- spontaneous
fracture
Odontogenic myxoma- soap bubble
appearance, multiple loculayion
Radicular cyst – associated with apex of
tooth
VICKER AND GORLINCRITERIA FOR
AMELOBLASTOMA
Hyperchromatism of basal cell nuclei.
Palisading of basal cell with polarization of
nuclei away from basement membrane (
reverse polarity)
Cytoplasmic vacuolization of basal call
20.
FOLLICULAR PATTERN
Mostcommon
Islands of epithelium resemble enamel organ
epithelium in a mature fibrous connective tissue
stroma
epithelial nests consist of a core of loosely arranged
angular cells resembling the stellate reticulum of an
enamel organ
A single layer of tall columnar ameloblast-like cells
surrounds this central core. The nuclei of these cells
are located at the opposite pole to the basement
membrane (reversed polarity). In other areas, the
peripheral cells may be more cuboidal and resemble
basal cells.
Cyst formation is common
23.
PLEXIFORM PATTERN
consistsof long, anastomosing cords or larger
sheets of odontogenic epithelium.
The cords or sheets of epithelium are bounded
by columnar or cuboidal ameloblast-like cells
surrounding more loosely arranged epithelial
cells.
The supporting stroma tends to be loosely
arranged and vascular.
Cyst formation is relatively uncommon
When it occurs, it is more often associated with
stromal degeneration rather than cystic change
within the epithelium
26.
ACANTHOMATOUS PATTERN
Whenextensive squamous metaplasia, often
associated with keratin formation, occurs in
the central portions of the epithelial islands of
a follicular ameloblastoma, the term
acanthomatous ameloblastoma
may be confused with squamous cell
carcinoma or squamous odontogenic
29.
GRANULAR CELL PATTERN
Transformation of groups of lesional epithelial cells to
granular cells.
cells have abundant cytoplasm filled with eosinophilic
granules that resemble lysosomes ultrastructurally and
histochemically.
Lysosomal aggreration caused by
• dysfunction of either a lysosomal enzyme or
• lysosome associated protein involved in enzyme
activation, enzyme targeting or lysosomal biogenesis
• Increased apoptotic cell death by neighbouring neoplastic
cells
Aggressive lesion and marked recurrence
32.
DESMOPLASTIC PATTERN
smallislands and cords of odontogenic epithelium in a
densely collagenizedstroma.
Immunohistochemical studies have shown increased
production of the cytokine known as transforming growth
factor-b (TGF-β) in association with this lesion,
suggesting that this may be responsible for the
desmoplasia.
Peripheral columnar ameloblast-like cells are
inconspicuous about the epithelial islands
Dense collagenous stroma that may appear hyalinized
and hypocellular
Epithelium squeezed and fragmented by dense stroma
Grow in thin strand and cords of epithelium stretched out
in kite tail like appearance
35.
BASAL CELL PATTERN
Least common type
composed of nests of uniform basaloid cells,
and they histopathologically are very similar
to basal cell carcinoma of the skin.
No stellate reticulum is present in the central
portions of the nests.
The peripheral cells about the nests tend to
be cuboidal rather than columnar
37.
HYBRID AMELOBLASTOMA
Extremelyunusual
Desmoplastic varient with areas of classical
follicular/plexiform varient
Some cases- tumor cells with granular
transformation along with areas of follicular
and plexiform ameloblastoma while some
show basaloid changes
38.
HEMANGIOMATOUS AMELOBLASTOMA
Lesscommon
Connective tissue stoma with many blood
filled spaces or large endothelial lined
capillaries
Theories
Hamartomatous malformation
trauma
Separate neoplasm or collision tumor
39.
PITUITARY AMELOBLASTOMA
Neoplasminvolving central nervous system
Common- childhood and adolescence
Origin- unobliterated portions of fetal
craniopharyngeal duct, derived from Rathke’s
pouch and epithelial remnants of this duct
are common on adult
40.
ADAMANTINOMA OF LONGBONES
Superficial microscopic resemblance to
ameloblastoma of jaws
Sites
tibia(common)
ulna, femur, fibula
TREATMENT AND PROGNOSIS
simple enucleation
curettage to en bloc resection
Recurrence rates of 50% to 90%
43.
UNICYSTIC AMELOBLASTOMA
10%to 46% of all intraosseous ameloblastomas
Origin
1. de novo as a neoplasm or
2. neoplastic transformation of nonneoplastic cyst
epithelium
Criteria for diagnosis
Demonstration of single( often macro) cystic sac
Odontogenic(ameloblastomatous) epithelium present
usually in focal area
44.
CLINICAL FEATURES
youngerpatients
mandible, posterior regions
Asymptomatic
large lesions may cause a painless swelling
of the jaws.
45.
RADIOGRAPHIC FEATURES
circumscribedradiolucency
that surrounds the crown of
an unerupted mandibular
third molar clinically
resembling a dentigerous
cyst.
sharply defined radiolucent
areas and are usually
considered to be a
primordial, radicular, or
residual cyst, depending
onthe relationship of the
lesion to teeth in the area.
LUMINAL UNICYSTIC AMELOBLASTOMA
tumor is confined to the
luminal surface of the cyst
fibrous cyst wall with a lining
that consists totally or partially
of ameloblastic epithelium
basal layer of columnar or
cuboidal cells with
hyperchromatic nuclei that
show reverse polarity and
basilar cytoplasmic
vacuolization
Overlying epithelial cells are
loosely cohesive and resemble
stellate reticulum
50.
INTRALUMINAL UNICYSTIC AMELOBLASTOMA
one or more nodules of
ameloblastoma project
from the cystic lining into
the lumen of the cyst
Nodules may be relatively
small or largely fill the
cystic lumen
plexiform unicystic
ameloblastomas- nodule
of tumor that projects into
the lumen demonstrates
an edematous, plexiform
pattern
PERIPHERAL (EXTRAOSSEOUS)
AMELOBLASTOMA
Uncommon
1% to 10% of all ameloblastomas.
arises from rests of dental lamina beneath
the oral mucosa or from the basal epithelial
cells of the surface epithelium.
Histopathologically same features as the
intraosseous form of the tumor.
56.
CLINICAL FEATURES
middle-agedpersons
(average 52 years)
Sites- posterior gingival
and alveolar mucosa,
common in mandibular
than in maxillary areas.
painless,
nonulcerated
sessile or pedunculated
57.
HISTOPATHOLOGIC FEATURES
islandsof ameloblastic
epithelium that occupy the
lamina propria underneath the
surface epithelium
Plexiform or follicular patterns
are the most common
Connection of the tumor with
the basal layer of the surface
epithelium is seen in about
50% of cases
58.
TREATMENT AND PROGNOSIS
respond well to local surgical excision
local recurrence has been noted in 15% to
20% of cases
59.
MALIGNANT AMELOBLASTOMA AND
AMELOBLASTICCARCINOMA
malignant ameloblastoma
a tumor that shows the histopathologic
features of ameloblastoma, both in the primary
tumor and in the metastatic deposits
ameloblastic carcinoma
an ameloblastoma that has cytologic
features of malignancy in the primary tumor,in a
recurrence, or in any metastatic deposit
60.
CLINICAL AND RADIOGRAPHIC
FEATURES
age - 4 to 75 years (mean age,
30 years)
Metastases from
ameloblastomas are most
often found in the lungs-
aspiration or implant
metastases
Cervical lymph nodes are the
second most common site for
metastasis of an
ameloblastoma
Ameloblastic carcinomas are
often more aggressive
lesions,with ill-defi ned margins
and cortical destruction
61.
HISTOPATHOLOGIC FEATURES
primaryjaw tumor and the
metastatic deposits show
features that of ameloblastomas
with a completely benign local
course
addition to cytologic features of
malignancy
• increased nuclear-to-
cytoplasmic ratio,
• nuclear hyperchromatism,
• presence of mitoses
• Necrosis in tumor islands
areas of dystrophic calcification
may be present.
62.
TREATMENT AND PROGNOSIS
Prognosis poor
50% of the patients with
documented metastases
and long-term follow-up
have died of their disease
Ameloblastic carcinoma
have demonstrated a
uniformly aggressive
clinical course, with
perforation of the cortical
plates of the jaw and
extension of the tumor into
adjacent soft tissues.
63.
REFERENCES
Text bookof oral pathology- Shafer 8th
edition.
Text book of oral & maxillofacial pathology-
Neville 3rd edition.
https://www.researchgate.net/figure/209389225
_fig10_Fig-10-Types-of-growth-in-Unicystic-
Ameloblastoma-1-Luminal-2-Intraluminal-3
https://www.facebook.com/hackdentistry