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Fulltext Unicystic ameloblastoma: a new entity?

Zain R

Med J Malaysia, 1986 Dec;41(4):370-3.

This article consists of two selected case reports of a recently named odontogenic tumour, unicystic ameloblastoma. The clinical and radiographic findings of the two cases mimic that of odontogenic cysts but not dentigerous cysts as in most reported, cases. Histologically, either a normal or ameloblastomatous cyst lining is evident. Other features of ameloblastoma are present within the cyst wall or as luminal nodules within the cystic space. A review of the literature indicates that this is a non-aggressive tumour with a low recurrence rate.

Matched MeSH terms: Ameloblastoma/pathology*

Premolar Cystic Ameloblastoma in a Child

Pathak S, Sonalika WG, Hs V, Tegginammani AS

J Coll Physicians Surg Pak, 2017 Jan;27(1):47-48.

PMID: 28292369 DOI: 2521

Mandibular swellings may occur as a result of many benign lesions of odontogenic or non-odontogenic origin. Ameloblastomas are benign tumours of odontogenic origin, whose importance lies in its potential to grow into enormous size with resulting bone deformity, it is a slow-growing, persistent, and locally aggressive neoplasm. The unicystic ameloblastoma (UA) represents an ameloblastoma variant, presenting as a cyst clinically and radiographically, but showing typical ameloblastomatous epithelium lining histologically. It commonly occurs in second and third decades of life and is rare in children under 12 years of age, and better response to conservative treatment. It shares many clinical and radiographic features with odontogenic cysts/tumours and/or periapical disease of endodontic origin. Reported here is an unusual case of unicystic ameloblastoma involving the crown of an unerupted mandibular first premolar in a 9-year boy in an uncommon location, which was misdiagnosed as periapical lesion of inflammatory origin clinically, and as a dentigerous cyst radiographically. This highlights the importance to routinely submit the removed surgical specimen for histopathological examination.

Matched MeSH terms: Ameloblastoma/pathology*

Desmoplastic ameloblastoma in Indians: report of five cases and review of literature

Sivapathasundharam B, Einstein A, Syed RI

Indian J Dent Res, 2007 10 17;18(4):218-21.

PMID: 17938502

In the recent World Health Organization classification of odontogenic tumours, desmoplastic ameloblastoma has been characterized as a variant of ameloblastoma, with specific clinical, radiographical, and histological features. Till date, 145 cases have been reported in Japanese, Chinese, Malaysian, Western, and African populations, with very few cases described in Indians. Here, we report five cases in the Indian population. The male to female ratio was 3:2. The mean age at diagnosis was 33.2 years. Four of the tumours were located in the maxilla, in the anterior premolar region. The lone mandibular tumour was located anteriorly, crossing the midline. Three of the tumours had a mixed radiologic appearance with poorly defined borders. Unilocular change was seen in one of them. Two tumours presented as unilocular radiolucencies with specks of radiopacities and well-circumscribed borders. Histologically, irregular odontogenic islands, with a stretched-out 'kite-tail' appearance, were seen in a dense desmoplastic stroma. The peripheral layer of the epithelial islands was made up of flattened cells and the inner core was made up of spindle-shaped and, in some instances, squamous-shaped cells. In two cases, odontogenic epithelium in the form of follicles, typical of solid/multicystic ameloblastoma, was seen and these were typed as 'hybrid' variants. All the cases were treated by resection.

Matched MeSH terms: Ameloblastoma/pathology

Desmoplastic variant of ameloblastoma in Malaysians

Ng KH, Siar CH

Br J Oral Maxillofac Surg, 1993 Oct;31(5):299-303.

PMID: 8218083

Seventeen cases are reported of desmoplastic variant of ameloblastoma of the jaws observed during the years 1967-1991. There were 12 females and 5 males, and these consisted of 7 Chinese, 6 Malays, 2 Indians, 1 Sikh and 1 Kadazan. Their ages at diagnosis ranged from 21-60 years with a mean of 36.6 years. There were 10 mandibular and 7 maxillary tumours. Of these, 14 cases involved the anterior segment with extension to the premolar region in 5 cases. 60% of cases were radiologically suggestive of fibro-osseous lesions. The main mode of treatment was resection and 1 case presented with recurrence. The findings of this study were compared with those of previous reports.

Matched MeSH terms: Ameloblastoma/pathology*

Peripheral ameloblastoma with clear cell differentiation

Ng KH, Siar CH

Oral Surg. Oral Med. Oral Pathol., 1990 Aug;70(2):210-3.

PMID: 2290651

This report details a case of mandibular peripheral ameloblastoma having a clear cell component. The latter consisted of ovoid cells with vacuolated or clear cytoplasm and vesicular or pyknotic nuclei that may be disposed as discrete clusters or show direct transition from typical acanthomatous areas. Comparison of this lesion with other odontogenic and nonodontogenic tumors that contain clear cells is discussed in the context of the differential diagnosis.

Matched MeSH terms: Ameloblastoma/pathology*

Granular ameloblastoma: report of two cases with atypical cytological aspects

Arora S, Urs AB, Kumar P, Augustine J, Saran RK

Rom J Morphol Embryol, 2017;58(3):997-1001.

PMID: 29250680

Ameloblastoma is an aggressive odontogenic tumor, which arises from odontogenic epithelium. Ameloblastomas can present in several clinical and histomorphological patterns. The granular cell variant accounts for only 3.5% to 5% of ameloblastomas. We have presented two cases of granular cell ameloblastoma (GCA) occurring in a 44-year-old and 50-year-old man, respectively. Case No. 1 on incisional biopsy was diagnosed as unicystic ameloblastoma (UA), which later after excisional biopsy was finally diagnosed as GCA owing to the features observed in excisional biopsied tissue. Case No. 2 on incisional biopsy showed darker and lighter stained cells arranged in small follicular pattern, and anastomosing cords. Meticulous immunohistochemistry, histochemical examination and careful literature search helped us to diagnose it as GCA. We have made an attempt to elucidate the diagnosis of GCA especially in cases of GCA with unusual granular component.

Matched MeSH terms: Ameloblastoma/pathology

Fulltext Ameloblastomas--a clinicopathologic study of 133 cases in peninsular Malaysia

Ramanathan K, Chelvanayagam PI, Ng KH, Ramanathan J

Med J Malaysia, 1982 Mar;37(1):18-24.

PMID: 7121342

Ameloblastomas formed 1.1 percent of all oral pathology cases reported. The race, sex and age group distribution of 133 cases are shown. The peak age incidence (70.6 percent) was between 11-40 years. The mandible was involved 9 times more commonly than the maxilla. The anatomical sites of distribution, clinical and radiological features, histological variants and their correlation are discussed. Twenty two patients (15 percent) had ameloblastomas associated with a dentigerous cyst and/or unerupted teeth. Ameloblastomas with the above clinical features represented a much less aggressive form of neoplasm. The authors could not correlate histological variants of ameloblastoma with recurrence rates. The various treatment methods and the respective recurrence rates are outlined. Radiotherapy and marsupialization as treatment of ameloblastoma are not recommended. The indications for enucleation curettage, resection en bloc, segmental resection and hemimandibulectomy
are emphasized. Ameloblastomas involving the maxilla should be treated by complete removal en bloc with a margin of normal tissue. Since ameloblastoma has the capacity to recur after several years of apparent cure patients who have been treated for ameloblastoma must be followed up periodically during their life time. So far no case of ameloblastoma in this study has shown evidence
ofmetastasis.

Matched MeSH terms: Ameloblastoma/pathology*

RANK, RANKL, and OPG in recurrent solid/multicystic ameloblastoma: their distribution patterns and biologic significance

Siar CH, Tsujigiwa H, Ishak I, Hussin NM, Nagatsuka H, Ng KH

Oral Surg Oral Med Oral Pathol Oral Radiol, 2015 Jan;119(1):83-91.

PMID: 25446507 DOI: 10.1016/j.oooo.2014.09.017

To determine the distribution patterns of bone resorption regulators, receptor activator of nuclear factor κ-B (RANK), RANK ligand (RANKL), and osteoprotegerin (OPG) in recurrent ameloblastoma (RAs) and to clarify their impact on the biologic behavior of these neoplasms.

Matched MeSH terms: Ameloblastoma/pathology*

Podoplanin, E-cadherin, β-catenin, and CD44v6 in recurrent ameloblastoma: their distribution patterns and relevance

Siar CH, Ishak I, Ng KH

J Oral Pathol Med, 2015 Jan;44(1):51-8.

PMID: 25059841 DOI: 10.1111/jop.12203

Ameloblastoma is a benign but locally infiltrative odontogenic epithelial neoplasm with a high risk for recurrence. Podoplanin, a lymphatic endothelium marker, putatively promotes collective cell migration and invasiveness in this neoplasm. However, its role in the recurrent ameloblastoma (RA) remains unclear. As morphological, signaling, and genetic differences may exist between primary and recurrent tumors, clarification of their distribution patterns is of relevance.

Matched MeSH terms: Ameloblastoma/pathology

Differential expression of transcription factors Snail, Slug, SIP1, and Twist in ameloblastoma

Siar CH, Ng KH

J Oral Pathol Med, 2014 Jan;43(1):45-52.

PMID: 23560539 DOI: 10.1111/jop.12065

Epithelial-to-mesenchymal transition (EMT) via the mechanism of transcription repression is a crucial process for the induction of invasiveness in many human tumors. Ameloblastoma is a benign odontogenic epithelial neoplasm with a locally infiltrative behavior. Twist, an EMT promoter, has been implicated in its invasiveness. The roles of the other transcription factors remain unclarified.

Matched MeSH terms: Ameloblastoma/pathology

Ameloblastoma of the jaws: a retrospective analysis of 340 cases in a Malaysian population

Siar CH, Lau SH, Ng KH

J Oral Maxillofac Surg, 2012 Mar;70(3):608-15.

PMID: 21723654 DOI: 10.1016/j.joms.2011.02.039

Ameloblastoma of the human jaw is an uncommon but clinically significant odontogenic epithelial neoplasm. The aim was to analyze the clinicopathologic characteristics of ameloblastoma in a Malaysian population.

Matched MeSH terms: Ameloblastoma/pathology

Invadopodia proteins, cortactin, N-WASP and WIP differentially promote local invasiveness in ameloblastoma

Siar CH, Rahman ZA, Tsujigiwa H, Mohamed Om Alblazi K, Nagatsuka H, Ng KH

J Oral Pathol Med, 2016 Sep;45(8):591-8.

PMID: 26752341 DOI: 10.1111/jop.12417

BACKGROUND: Cell migration and invasion through interstitial tissues are dependent upon several specialized characteristics of the migratory cell notably generation of proteolytic membranous protrusions or invadopodia. Ameloblastoma is a benign odontogenic epithelial neoplasm with a locally infiltrative behaviour. Cortactin and MMT1-MMP are two invadopodia proteins implicated in its local invasiveness. Other invadopodia regulators, namely N-WASP, WIP and Src kinase remain unclarified. This study addresses their roles in ameloblastoma.

MATERIALS AND METHOD: Eighty-seven paraffin-embedded ameloblastoma cases (20 unicystic, 47 solid/multicystic, 3 desmoplastic and 17 recurrent) were subjected to immunohistochemistry for expression of cortactin, N-WASP, WIP, Src kinase and F-actin, and findings correlated with clinicopathological parameters.

RESULTS: Invadopodia proteins (except Src kinase) and F-actin were widely detected in ameloblastoma (cortactin: n = 73/87, 83.9%; N-WASP: n = 59/87; 67.8%; WIP: n = 77/87; 88.5%; and F-actin: n = 87/87, 100%). Protein localization was mainly cytoplasmic and/or membranous, and occasionally nuclear for F-actin. Cortactin, which functions as an actin-scaffolding protein, demonstrated significantly higher expression levels within ameloblastoma tumoral epithelium than in stroma (P < 0.05). N-WASP, which coordinates actin polymerization and invadopodia-mediated extracellular matrix degradation, was overexpressed in the solid/multicystic subtype (P < 0.05). WIP, an upstream regulator of N-WASP, and F-actin were significantly upregulated along the tumour invasive front compared to tumour centres (P < 0.05). Except for males with cortactin overexpression, other clinical parameters (age, ethnicity and anatomical site) showed no significant correlations.

CONCLUSIONS: Present results suggest that local invasiveness of ameloblastoma is dependent upon the migratory potential of its tumour cells as defined by their distribution of cortactin, N-WASP and WIP in correlation with F-actin cytoskeletal dynamics.

Matched MeSH terms: Ameloblastoma/pathology

'Combined ameloblastoma and odontogenic keratocyst' or 'keratinising ameloblastoma'

Siar CH, Ng KH

Br J Oral Maxillofac Surg, 1993 Jun;31(3):183-6.

PMID: 7685634

Four cases of either combined occurrence of ameloblastoma and odontogenic keratocyst or a rare keratinising variant of ameloblastoma are presented. The cardinal histomorphologic characteristics are simultaneous occurrence of ameloblastomatous epithelial islands with central keratinisation and multiple keratinising cysts. Immunohistochemically the tumour elements were keratin positive and occasionally S-100 protein and desmin positive. Major differential diagnosis of these neoplasms are discussed.

Matched MeSH terms: Ameloblastoma/pathology*

Unusual granular cell odontogenic tumor. Report of two undescribed cases with features of granular cell ameloblastoma and plexiform granular cell odontogenic tumor

Siar CH, Ng KH

J Nihon Univ Sch Dent, 1993 Jun;35(2):134-8.

PMID: 7692017

Granular cell ameloblastoma (GCA) is a well recognized variant of follicular ameloblastoma with extensive granular cell change. In contrast, plexiform granular cell odontogenic tumor (PGCOT) is a rare and recently described lesion characterized histologically by a monophasic plexiform pattern of granular cells. In this paper, two cases of an unusual granular cell odontogenic tumor exhibiting combined features of these two entities are described along with their immunohistochemical characteristics. The granular cells of both the GCA and PGCOT areas showed similar patterns of expression for keratin and S-100, which differed from those of typical ameloblastoma. No reactivity for desmin or vimentin was noted. The histomorphologic and immunohistochemical features of these hybrid tumors suggest that the granular cells present have a common origin, most probably the odontogenic epithelium.

Matched MeSH terms: Ameloblastoma/pathology*

Patterns of expression of intermediate filaments and S-100 protein in desmoplastic ameloblastoma

Siar CH, Ng KH

J Nihon Univ Sch Dent, 1993 Jun;35(2):104-8.

PMID: 7692015

Seventeen cases of desmoplastic ameloblastoma were examined immunohistochemically. Immunoperoxidase techniques were applied for detection of keratin, desmin, vimentin and S-100 protein expression in these tumors. The tumor epithelium of desmoplastic ameloblastoma exhibited weak, focal, inconstant keratin staining, weak, variable expression of S-100 protein, desmin immunoreactivity of mild to moderate intensity and vimentin non-reactivity. The pertinent literature on the immunohistochemistry of ameloblastomas is briefly reviewed.

Matched MeSH terms: Ameloblastoma/pathology

Aggressive (malignant?) epithelial odontogenic ghost cell tumour of the maxilla

Siar CH, Ng KH

J Laryngol Otol, 1994 Mar;108(3):269-71.

PMID: 8169519

A case is described of ameloblastoma of the mandible presenting with multiple recurrences and subsequent extension to the maxilla with resultant transformation into an aggressive (malignant?) epithelial odontogenic ghost cell tumour. The latter is a rare, biologically virulent entity that affects mainly males, exhibits a preference for the maxilla and is histologically characterized by atypical malignant odontogenic epithelium associated with areas of ghost cell formation and varying amounts of dentinoid.

Matched MeSH terms: Ameloblastoma/pathology*

Calcifying and keratinizing ameloblastoma of the maxilla

Siar CH, Ng KH

J Laryngol Otol, 1991 Nov;105(11):971-2.

PMID: 1722237

A case is described of ameloblastoma of maxilla presenting with numerous calcified keratin pearls. The significance of cellular variation in relation to the behavioural potential of the ameloblastoma in general is briefly discussed.

Matched MeSH terms: Ameloblastoma/pathology*

Epithelial-to-mesenchymal transition in ameloblastoma: focus on morphologically evident mesenchymal phenotypic transition

Siar CH, Ng KH

Pathology, 2019 Aug;51(5):494-501.

PMID: 31262562 DOI: 10.1016/j.pathol.2019.04.004

The ameloblastoma is the most common and clinically significant odontogenic epithelial neoplasm known for its locally-invasive behaviour and high recurrence risk. Epithelial-to-mesenchymal transition (EMT) is a fundamental process whereby epithelial cells lose their epithelial characteristics and gain mesenchymal properties. EMT induction via transcription repression has been investigated in ameloblastoma. However, morphologically evident mesenchymal phenotypic transition remains ill-defined. To determine this, 24 unicystic (UA), 34 solid/multicystic (SA) and 18 recurrent ameloblastoma (RA) were immunohistochemically examined for three EMT-related mesenchymal markers, alpha smooth muscle actin (α-SMA), osteonectin and neuronal cadherin (N-cadherin). All three factors were heterogeneously detected in ameloblastoma samples (α-SMA, n=71/76, 93.4%; osteonectin, n=72/76, 94.7%; N-cadherin, n=24/76, 31.6%). In the tumoural parenchyma, immunoreactive cells were not morphologically distinct from their non-reactive cellular counterparts. Rather, α-SMA and osteonectin predominantly labelled the cytoplasm of central polyhedral > peripheral columnar/cuboidal tumour cells. N-cadherin demonstrated weak-to-moderate circumferential membranous staining in both neoplastic cell types and cytoplasmic expression in spindle-celled epithelium of desmoplastic amelobastoma. For all tumour subsets, α-SMA and osteonectin scored significantly higher in the stroma > parenchyma whilst α-SMA was overexpressed along the tumour invasive front > centre (p<0.05). Stromal N-cadherin scored higher in SA > UA and RA > UA (p<0.05). Other clinicopathological parameters showed no significant associations. Taken together, acquisition of mesenchymal traits without morphologically evident mesenchymal alteration suggests partial EMT in ameloblastoma. Stromal upregulation of these proteins in SA and RA implicates a role in local invasiveness.

Matched MeSH terms: Ameloblastoma/pathology*

Parenchyma-stromal interactions induce fibrosis by secreting CCN2 and promote osteoclastogenesis by stimulating RANKL and CD68 through activated TGF-β/BMP4 in ameloblastoma

Takebe Y, Tsujigiwa H, Katase N, Siar CH, Takabatake K, Fujii M, et al.

J Oral Pathol Med, 2017 Jan;46(1):67-75.

PMID: 27327904 DOI: 10.1111/jop.12467

BACKGROUND: Tumor parenchyma-stromal interactions affect the properties of tumors and their dynamics. Our group previously showed that secreted frizzled related protein (sFRP)-2 impairs bone formation and promotes bone invasion in ameloblastoma. However, the effects of the secreted growth factors CCN2, TGF-β, and BMP4 on stromal tissues in ameloblastoma remain unclear.

MATERIALS AND RESULTS: Thirty-five paraffin-embedded ameloblastoma cases, ameloblastoma-derived cell lines (AM-1), and primary cultures of ameloblastoma stromal fibroblasts (ASF) were used. Immunohistochemistry, MTT assay, Western blotting, and RT-PCR were performed on these samples. Parenchyma-stromal CCN2 overexpression correlated significantly with fibrous-type stroma, but not with myxoid-type stroma, suggesting a role of CCN2 in fibrosis (P < 0.05). Recombinant CCN2 induction of enhanced ASF proliferation in AM-1 medium supports this view. Conversely, BMP4 and TGF-β were expressed in myxoid-type fibroblasts, but little expression was found in parenchyma. RANKL-positive and CD68-positive stromal cell populations were significantly greater in myxoid-type tumor areas than in fibrous-type tumor areas, while a higher Ki-67 labeling index was recorded in ameloblastoma with fibrous-type stroma. These data suggest that stromal properties influence bone resorption-related activities and growth rates, respectively.

CONCLUSIONS: These results suggest that the effects of secreted growth factors are governed by ameloblastoma parenchyma-stromal interactions. CCN2 promotes fibrogenesis independent of TGF-β signaling. Absence of CCN2 expression is associated with a phenotypic switch to a myxoid-type microenvironment that is conducive for TGF-β/BMP4 signaling to promote osteoclastogenesis.

Matched MeSH terms: Ameloblastoma/pathology

Fulltext Traumatic neuroma in wall of recurrent unicystic ameloblastoma: a case report

Zain R, Ling KC

Med J Malaysia, 1985 Mar;40(1):49-51.

PMID: 3831736

This is a case report of a recurrent lesion diagnosed histologically as a unicystic ameloblastoma. The concomitant presence of a traumatic neuroma was observed within the wall of the recurrent lesion. The mode of development of the traumatic neuroma, and the reason for the recurrence were presented.

Matched MeSH terms: Ameloblastoma/pathology*

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