Journal of Medicine, Radiology, Pathology & Surgery (2015), 1, 37

REVIEW ARTICLE

Molecular etiopathogenesis of ameloblastoma current

concepts revisited
P. Spandana1, S. Shylaja1, M. S. Muni Sekhar1, A. Krishna2, S. N. Bhavani1, Yukti Raj1
1

Department of Oral and Maxillofacial Pathology, SVS Institute of Dental Sciences, Mahabubnagar, Telangana, India, 2Departement of Dental Anatomy and Oral
Biology, College of Dentistry, Al Jouf University, Sakaka, Al Jouf, Kingdom of Soudi Arabia

Keywords
Ameloblastin, ameloblastoma, matrix
metalloproteinase, molecular and genetic
alterations, signaling molecules
Correspondence
Dr.S. Shylaja, SVS Institute of Dental
Sciences, Mahabubnagar, Telangana, India.
Phone: +91-9441023999, Email: eswardental@
rediffmail.com

Abstract
The ameloblastoma (AB) is a true neoplasm of enamel organ type tissue which does not
undergo dierentiation to the point of enamel formation. AB is locally invasive and recurs
despite adequate surgical removal. It is of varied origin, although the stimulus initiating
the process is unknown. The study of molecular and genetic alterations associated with
the development and progression of the AB will help to predict the course of the tumor
and lead to the development of new therapeutic concepts for their management. An
attempt has been made at compiling about molecular pathogenesis of AB.

Received 02 January 2015;

Accepted 05 February 2015
doi: 10.15713/ins.jmrps.8

Introduction
Ameloblastoma (AB) is the second most common benign
epithelial odontogenic tumor. ABs are clinically classified into
solid/multicystic, unicystic, desmoplastic, and peripheral types,
and based upon the pattern of arrangement of tumor cells they
may be divided into follicular, plexiform, acanthomatous, granular,
basal cell types, etc.[1] AB histologically resembles the epithelial
odontogenic apparatus, such as enamel organ and dental lamina, in
some respects; however, the detailed mechanism of oncogenesis,
cytodierentiation, and tumor progression remains unknown.
This review focuses on molecular and genetic alterations that
occur in AB which are helpful for better treatment and prognosis.

subfamily G member 2 [ABCG2]) in ameloblastic tumors and

in tooth germs. Positive expression of CD133 and Bmi-1 was
observed in odontogenic epithelial cells adjacent to basement
membrane in tooth germs, ABs, and metastasizing ABs, and
most of the neoplastic cells in clear cell odontogenic carcinomas
and ameloblastic carcinomas showed reactivity for CD133 and
Bmi-1. When compared to the tooth germs and ABs, malignant
ameloblastic tumors showed significantly increased expression
of CD133. ABCG2 was expressed in some ameloblastic tumors
but not found in tooth germs. Malignant ameloblastic tumors
showed significantly stronger expression of ABCG2 than that
in tooth germs. They suggested that stem cell-related molecules
might have role in cell dierentiation, oncogenesis, and
malignant potential of odontogenic epithelium.[4]

Clonality
Most odontogenic tumors are monoclonal in nature.[2] An
initial mutation/molecular alteration is the first event in the
development of the tumor. However, the sequence of events
remains unknown.[3]
Stem Cell Related Molecules
Kumamoto et al., (2010) analyzed the expression of stem cell
related molecules (Bmi-1, CD133, and ATP-binding cassette
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Cell Adhesion Molecules

Leocata et al., (2007) conducted a study in intraosseous ABs
and it was found that syndecan-1 (SDC1) expression by tumor
epithelial cells and subsequent shifting to stromal cells and
extracellular martix, which might be the reason for the local
invasiveness of some intraosseous AB subtypes.[5] BolognaMolina et al. (2008) found reduced expression of SDC1
in solid ameloblastoma (SA) and correlated with its more
aggressive biological behavior when compared to unicystic
3

Etiopathogenesis of ameloblastoma

ameloblastoma (UA).[6] Al-Otaibi et al., (2013) studied SDC-1

immunoreactivity in the stromal cells of AB, keratocystic
odontogenic tumor (KCOT), and dentigerous cysts and it
was suggested that the SDC-1 expression by the tumor stroma
is considered to be associated with poor prognosis of the
lesions.[7]
Heikinheimo et al., (1991) stated that there is an
association between the stronger labeling of 51 integrin
in the neoplastic cells of ABs and greater migration capacity
of these cells because of increased fibronectin expression in
stromal cells.[8] Later, Souza Andrade et al., (2007) studied the
role of 51 integrin in AB, adenomatoid odontogenic tumor
(AOT), and proposed that the mechanism of tumor invasion
might be because of 51 integrin binding to fibronectin
which in turn increases the secretion and expression of
metalloproteinases.[9]
Gonzalez-Alva et al. (2010) suggested role of podoplanin
which is a well-established lymphocytic specific marker, reported
to be associated with tumor induced platelet aggregation and
tumor metastasis and also with tumor invasiveness.[10]
Ribeiro et al., (2011) studied expression of metallothionein
(MT) in AB and calcifying epithelial odontogenic tumor
(CEOT) and found significantly higher expression in ABs
suggesting its role in acting as reservoir of zinc for important
proteases related to AB, such as matrix metalloproteinases
(MMP), and also their pro-mitotic and anti-apoptotic
features in the tumor.[11] Johann et al., (2014) found an
increased expression of MT in SA and they correlated it
with the clinical behavior (local invasion and high rate of
recurrence).[12]
Ameloblastin and Other Enamel Matrix Proteins
Expression of ameloblastin, sheathlin, and enamelin proteins
were not found in AB, suggesting that ameloblasts have not
attained functional maturation in tumor cells. However, Snead
(1992) found that amelogenin transcribed only by dierentiated
ameloblasts, was expressed by AB epithelial cells. Toyosawa et al.,
(2000) reported potential mutations in ameloblast transcript
although these mutations may not be primarily related to the
development of AB.[3]
Perdigao et al., (2004) also found an association of mutation
in amleoblastin gene in epithelial odontogenic tumors. The exact
mechanism of tumor formation in mutant mice is unclear but
due to deficiency of ameloblastin there may be deregulation of
ameloblast dierentiation which might be the likely cause of the
tumor.[3]
Molecules Involved In Cell Cycle Proliferation
Ki-67

Florescu et al., (2012) in their study observed an increased

expression of Ki-67 in peripheral cells of tumor islands when
compared to the central cells suggesting that the peripheral cells
4

Spandana, et al.

are more proliferative. Ki-67 indices were similar in both UA and

SA, despite some dierence in various subtypes: highest values
in the luminal UA which could be attributed to the presence
of less number of stellate reticulum-like cells when compared
to other subtypes, and consequently, most of the cells counted
corresponded to basal, and parabasal layers which are more
prone to be positive.[13]
Proliferating nuclear cell antigen (PCNA)

PCNA expression is more in UA compared to SA. Funaoka et al.

found higher PCNA labeling index for follicular AB than that
of plexiform ameloblastoma. Ueno et al., (1989) and Reichart
et al., (1995) also stated that the high expression of PCNA in
follicular AB can explain its increased potential of recurrence,
but Salehinejad et al., (2011) found the highest mean Index of
positivity for PCNA in acanthomatous AB.[14] The possibility
of malignant transformation in recurrent cases of AB can be
determined by PCNA values. There was an increase in the
expression from UA to follicular AB to plexiform AB and
with maximum positivity seen in ameloblastic carcinoma,
which may be correlated with biological behavior of the
tumor. Li et al., and Shear et al., stated that Ki-67, PCNA are
the markers for recurrence and aggressive behavior of the
tumors.[15]
Cyclin D1

Nuclear and cytoplasmic expression of cyclin D1 was

predominantly seen in both peripheral cells as well as cells of
stellate reticulum-like tissue suggesting their role in proliferation
in peripheral cells and dierentiation in central cells.[16]
Telomerase

Telomerase activity is associated with the proliferative potential

of AB cells. Expression of c-Myc protein similar to telomerase
reverse transcriptase (TERT) suggested that c-Myc might
induce the telomerase activity in ABs.[17] High expression of
human telomerase RNA and hTERT was closely related to the
clinical behavior of AB and regulated by p53.[18]
Growth factors

Increased epidermal growth factor receptor levels in AB

when compared to radicular cyst suggested their role in
tumorigenesis. Hepatocyte growth factor and c-Met show
increased expression in ameloblastic carcinoma and clear
cell odontogenic carcinoma implying their association with
the malignant potential of epithelial odontogenic tumors.
Immunohistochemical evaluation of fibroblast growth
factor (FGF)-1 and -2, showed similar staining in AB and
normal dental follicles, where as intense reactivity seen in the
cytoplasm of cultured AB epithelial cells. Ameloblast-like cells
and the cells of stellate reticulum-like tissue presented high
expression of FGF-1, whereas FGF-2 was seen in basement
membrane implying their distinct roles. Further studies are
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Etiopathogenesis of ameloblastoma

needed to confirm their role.[19] Platelet-derived growth factor

(PDGF) AA isoform and its receptor PDGF- receptor levels
were more in malignant ameloblastic tumors when compared
to non-metastasizing AB. PDGF ligand and receptor system
might participate in malignant transformation of odontogenic
epithelium.[20]
Apoptotic Markers
Kumamoto et al., (1999 and 2004) found expression of bcl2 family proteins, bcl-2 and bcl-x, and inhibitor of apoptosis
protein (IAP) family proteins, survivin, and XIAP in neoplastic
cells neighboring the basement membrane suggesting their role
in suppression of apoptosis in those cells. Later in 2005 it was
observed that the expression of apoptotic protease-activating
factor-1, cytochrome-c, apoptosis-inducing factor, and capsase-9
in tooth germ and ABs and it was suggested that apoptotic
cell death of normal and neoplastic odontogenic epithelium
is by mitochondria mediated apoptotic pathway. Increased
apoptotic cell death in keratinizing cells in acanthomatous
AB, granular cells in granular cell AB variants and neoplastic
cells of ameloblastic carcinoma was found suggesting their
role in cytodierentiation and malignant transformation of
odontogenic epithelium.[3]
Luo et al., (2006) studied the expression of the Fas/FasL and
concluded that it might have a role in the disposal of terminally
dierentiated or degenerative tumor cells in ABs. Many studies
conducted on apoptosis demonstrated that anti-apoptotic
proteins (bcl-2) and cell proliferation markers (Ki-67) were
expressed in the peripheral basal cell layers of ABs, which might
be the reason for their progression.[21]
Tumor Suppressor Genes
p53

Aberration of p14ARF-MDM2-p53 cascade strongly correlates

with neoplastic transformation. Kumamoto et al., (2004)
found an elevated expression of p14ARF, MDM2, p53 in
benign and malignant ABs and suggested that the alteration of
p14ARF-MDM2-p53 cascade leads to oncogenesis or malignant
transformation of odontogenic epithelium and that it is also
associated with tissue structuring and cytodierentiation of
ABs. However, mutations in the exons 5-8 in 10 samples were
not observed and concluded that mutations of p53 might play a
minor role in the neoplastic change of odontogenic epithelium.
Kitkumthorn et al., (2010) evaluated the association of p53
codon 72 polymorphism with AB and found that the Arg allele of
p53 gene codon 72 might increase susceptibility, and p53 may be
important in the pathogenesis of AB.[22]
Rb

Kumamoto et al., (2006) demonstrated increased expression

of retinoblastoma (Rb) and phosphorylated Rb in AB than in
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Spandana, et al.

tooth germs which might have a role in cell proliferation and

dierentiation of odontogenic epithelium. However, another
study by Lim and Ahn et al., (2006) using DNA microarray and
reverse polymerase chain reaction (more sensitive compared to
IHC) revealed downregulation of Rb1 in AB in comparison with
dentigerous cyst.[3]
PTEN

Scheper et al., (2008) found decreased expression of PTEN

in AB compared to dental follicles and elucidated the role of
PTENAKT mTOR pathway in pathogenesis and aggressiveness
of AB.[3]
MMPs

Ribeiro et al., (2009) evaluated the expression of MMP-1, -2,

and -9 in AB and AOT and suggested that MMPs are related
to growth and progression of tumors and particularly in AB, its
aggressive behavior may be due to active participation of the
stromal cells and their products (MMPs).[23]
Shen et al., (2010) studied immunohistochemical expression
of osteonectin/secreted protein acidic and rich in cysteine
(SPARC) and MMP-1, -2, and -9 in 23 cases of AB and found an
association between the SPARC and MMP-9 in AB to regulate
tumor invasion. MMP-2, -9 degrade type IV collagen component
of the basement membrane.[24] Hence, lesions with an intense
expression of MMPs show more invasive behavior.
Osteoclastic Markers
Abdelsayed et al., (2004) found an increased expression of
parathyroid hormone-related protein (PTHrP) in AB and
suggested that it has role in local bone resorption and also
provided an explanation for infiltrative growth and destructive
behavior of AB.[3]
Kumamoto et al., (2004) analyzed the expression of osteoclast
dierentiation factor/receptor activator of nuclear factorB
ligand (RANKL) and osteoclastogenesis inhibitory factor/
osteoprotegerin, PTHrP in AB and tooth germs and observed that
these factors regulate bone metabolism and dynamics in tooth as
well as in prognosis of AB and also found their involvement in
tumor cell dierentiation and tumor structuring in AB. Sandra
et al., (2005) found that the RANKL, tumor necrosis factor-
secreted by AB cells could induce the osteoclastogenesis, which
in turn provide space for it to expand.[3]
Other Signaling Molecules
The PTCH1 gene encodes a receptor for Sonic Hedgehog
(SHH). SHH regulates growth and determines the shape of the
tooth, but its signaling is not essential for the dierentiation of
ameloblasts or odontoblasts.[25]
Kumamoto et al., (2004) found lower expression of SHH
in stromal cells compared with the mesenchymal cells in tooth
germ. Zang et al., (2006) found strong cytoplasmic expression of
5

Etiopathogenesis of ameloblastoma

SHH in cellular components of the neoplastic tissues, mainly in

the peripheral or cuboidal cells and suggested that they regulate
the proliferation of tumor epithelial cells.[25]
Gao et al., (1997) conducted an immunohistochemical
study in 20 cases of AB to determine the expression of bone
morphogenic protein (BMP). Although positive expression
was seen in the ameloblasts of the tooth germs in the controls,
none of the tumor samples showed expression for BMP. As no
detectable levels of BMP found in immature tumor cells, and
the identification of such proteins might be influenced by the
degree of dierentiation of the odontogenic epithelium, present
in ABs (Gao et al., 1997). Conversely, another investigation
(Kumamoto and Ooya, 2006) revealed expression of BMP2, -4 and -7, BMPRI and BMPRII in AB samples. In all types
of AB tested, BMPs and their receptors were identified.
Immunostaining for these molecules was observed in neoplastic
cells neighboring the basement membrane of the tumors,
suggesting their role in the cytodierentiation of neoplastic
odontogenic epithelium. In addition, in keratinizing cells of
acanthomatous AB there was a strong reactivity for BMP-7
which suggests its association with cell death of neoplastic
odontogenic epithelium.[25]
An aberrant Wnt pathway was suggested to occur in
oncogenesis. -catenin molecule was found in the cytoplasm and
membrane of most neoplastic cells of ABs, and it was thought to
be associated with signal transduction and cell-cell adhesion in
the neoplastic odontogenic epithelium. Kumamoto and Ooya,
(2005) found nuclear -catenin expression in some ABs, but it
was not identified in tooth germ.[25]
Alaeddini et al., (2008) studied expression of calretinin in 55
odontogenic tumors including AB, AOT, CEOT, ameloblastic
fibroma, and odontogenic myxoma; it was expressed only
in ABs. Another study by Sireesha et al., (2010) in KCOT,
dentigerous cyst and AB, revealed that only cells of stellate
reticulum-like tissue of SA and UA expressed calretinin. Thus,
calretinin can be considered as the specific IHC marker
for neoplastic ameloblastic epithelium which is expressed
only in SA and UA and not in any other odontogenic cysts/
tumors. Furthermore, it can be used as a diagnostic marker to
dierentiate UA from other cystic lesions.[26]

Spandana, et al.

Marker
Expression in AB
ABCG2,
Increased
CD-133, Bmi-1

Suggestive of
Oncogenesis
Cell differentiation
Malignant potential

Syndecan-1

Decreased

Aggressiveness
Invasiveness

51 integrin

Increased

Invasiveness

Podoplanin

Increased

Invasiveness through
collective cell migration

MT

Increased

Invasiveness
High recurrence

Ki-67

Increased in peripheral
cells

Aggressiveness

PCNA

Unicystic ameloblastoma Recurrence

Follicular ameloblastoma Aggressiveness
Plexiform ameloblastoma
Ameloblastic carcinoma

Cyclin D1

Increased

HGF and c-Met Increased

Malignant transformation

Anti-apoptotic
(bcl-2, bcl-x)

Peripheral cells

Cytodifferentiation
Malignant transformation

Fas, FasL

Central cells in
Acanthomatous
and Granular cell
ameloblastoma

Cytodifferentiation

p14ARF, MDM2, Increased

p53

Neoplastic
transformation

Rb

Increased

Cell proliferation and

differentiation

PTEN

Increased

Aggressiveness

MMP-1,-2,-9

Increased

Aggressiveness
Invasiveness

PTHrP

Increased

Infiltrative growth and

destructive behavior

RANKL, TNF- Increased

Osteoclastogenesis tumor
expansion

PTCH1

Increased

Proliferation of
odontogenic epithelium

BMP-2,-4,-7

Increased

Cytodifferentiation
apoptotic cell death

-catenin

Increased

Cell migration

Conclusion
The development and progression of AB are aected by
alterations of many kinds of genes and molecules. Further
molecular studies, including genomic and proteomicbased profiling, are required to clarify the etiology and
pathogenesis of AB. A better understanding of underlying
molecular mechanisms will help to predict the course of AB and
lead to the development of new therapeutic applications such
as molecular-targeted treatment and patient-tailored therapy.

Invasiveness
Aggressiveness
Poor prognosis
Lymph node metastasis

ABCG2: ATP-binding cassette subfamily G member 2, PCNA: Proliferating

nuclear cell antigen, HGF: Hepatocyte growth factor, Rb: Retinoblastoma,
PTEN: Phosphatase and tensin, PTHrP: Parathyroid hormone-related
protein, RANKL: Receptor activator of nuclear factorB ligand,
TNF-:Tumor necrosis factor-alpha, BMP: Bone morphogenic protein,
MT: Metallothenin

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Etiopathogenesis of ameloblastoma

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How to cite this article: Spandana P, Shylaja S, Sekhar MS,

Krishna A, Bhavani SN, Raj Y. Molecular etiopathogenesis

of ameloblastoma current concepts revisited. J Med Radiol
Pathol Surg 2015;1:3-7.