Differential lectin-bindings in normal and precancerous epithelium and squamous cell carcinoma of the oral mucosa

In order to establish a useful and objective marker of malignancy of oral mucosa, the binding sites for Ulex europaeus agglutinin I (UEA-I). Bandeiraea simplicifolia agglutinin I (BSA-I) and peanut agglutinin (PNA) were comparatively examined in the surgical materials from the normal, dysplastic and cancerous epithelium of the oral mucosa by a novel lectin-antilectin immunoperoxidase method. Based on the staining patterns of the normal keratinized epithelium, UEA-I was regarded as the marker for the prickle cells, BSA-I for the cells in the upper prickle to the horny layers, and PNA for those in the basal layer. As the degree of dysplasia advanced, all layers of epithelium came to react with UEA-I and PNA, whereas the BSA-I binding was negative. Positive reactions for UEA-I and PNA were seen in most carcinoma cells other than the keratinizing foci stained by BSA-I. The results indicate that a UEA-I-positive reaction in the basal cells, a PNA-positive in the prickle cells and loss of receptor for BSA-I occur in the course of malignant transformation of oral mucosa, and that these lectins may be regarded as useful markers of oral epithelial cytoplasmic differentiation.     

Lectin histochemistry of ameloblastomas and odontogenic keratocysts

The cell membrane carbohydrate components of 10 simple (follicular and/or plexiform pattern) and 5 acanthomatous ameloblastomas, one plexiform unicystic ameloblastoma, one soft tissue ameloblastoma and 11 odontogenic keratocysts were studied in paraffin-embedded tissues using horseradish peroxidase-conjugated lectins. The presence of glucose and mannose was demonstrated by intense labelling with Concanavalin ensiforme (Con A) in 73% of the ameloblastomas examined, while periodate oxidation of the specimens prior to Con A (PA/Con A) stained 53% of the cases. Ameloblastomas did not express receptors for Triticum vulgaris (WGA), Erythrina chrystagalli (ECA), Arachis hypogea (PNA), and Ulex europaeus (UEA-1). The plexiform unicystic ameloblastoma and the soft tissue ameloblastoma examined showed the same cell membrane glycoproteins as the simple and acanthomatous ameloblastomas. Forty-five per cent of the keratocysts demonstrated Con A reactivity from the basal to the keratinized layer, while 72% of these specimens showed positive PA/Con A reactivity from the parabasal to the keratinized layer. Staining with WGA, ECA, PNA, and UEA lectins also revealed the presence of N-Acetyl-glucosamine and fucose oligosaccharides in the plasma membrane of basal, spinous and keratinized cell layers of the odontogenic keratocysts. The distinct cell surface carbohydrate composition of the ameloblastoma and odontogenic keratocyst may be responsible for the differences in biological behavior in these conditions.     

A comparative study of epithelial cell proliferation between the odontogenic keratocyst, orthokeratinized odontogenic cyst, dentigerous cyst, and ameloblastoma

OBJECTIVES: The aim of the present study was to compare the proliferation index of the epithelial cells between odontogenic keratocysts (OKC), orthokeratinized odontogenic cysts (OOC), dentigerous cysts (DC), and ameloblastomas. MATERIALS AND METHODS: The proliferation index, employing a novel cell proliferation marker IPO-38, was studied by the immunohistochemical technique in 10 OKC, seven OOC, eight DC and 10 ameloblastomas. RESULTS: The ameloblastoma had no higher labeling index (LI) of IPO-38 than the OKC (P = 0.910) but had higher LI than the OOC (P = 0.001) and DC (P = 0.000); the OKC had higher LI than the OOC (P = 0.002) and DC (P = 0.000); and the OOC had higher LI than the DC (P = 0.011). IPO-38-positive cells in the OKC and OOC were located principally in the suprabasal cell layers while the ameloblastoma were found in the peripheral portion in particularly, the follicular and plexiform types. CONCLUSION: These findings support previous studies that the proliferation indices are useful in predicting the different biological behavior of the odontogenic lesions and the OKC should be regarded as a benign tumor rather than simply an odontogenic cyst.     

Ameloblastoma, calcifying epithelial odontogenic tumor, and glandular odontogenic cyst show a distinctive immunophenotype with some myoepithelial antigen expression

Background:  Odontogenic neoplasms have some morphologic overlap with salivary gland neoplasms, many of which show myoepithelial differentiation. In the 1980s, an ultrastructural study identified a population of myoepithelial-like cells in calcifying epithelial odontogenic tumor. Myoepithelial derived tumors have since been shown to have distinct immunohistochemical profiles.
Methods:  We examined a series of odontogenic neoplasms, including 11 ameloblastomas, four calcifying epithelial odontogenic tumors, five glandular odontogenic cysts (GOCs), and five keratocystic odontogenic tumors with a panel of myoepithelial-associated immunohistochemical stains. We also assessed representative control examples of oral mucosa, odontogenic rests, and dentigerous cysts.
Results:  All of the neoplastic and non-neoplastic oral epithelium-derived entities share a p63-positive, high molecular weight cytokeratin (CK5/6)-positive immunophenotype. Calponin reactivity was at least focally present in two of four calcifying epithelial odontogenic tumors, three of five GOCs, and 10 of 11 ameloblastomas; the sole completely non-reactive ameloblastoma represents a lung metastasis. One case of calcifying epithelial odontogenic tumor was focally positive for glial fibrillary acidic protein. However, other more definitive markers of myoepithelial differentiation, including S-100 and smooth muscle actin, were negative. Two of three calcifying epithelial odontogenic tumors and five of five GOCs were also positive for a low molecular weight cytokeratin (CK7).
Conclusions:  Ameloblastomas, GOCs, and calcifying epithelial odontogenic tumors show a distinctive immunophenotype which overlaps with that of myoepithelial-derived salivary gland neoplasms but does not provide definitive support for myoepithelial differentiation.     

单囊型成釉细胞瘤临床病理及凝集素免疫组织化学研究

目的 研究单囊型成釉细胞瘤的临床病理及凝集素免疫组织化学特点，探索有助于诊断和临别诊断的组织学标记物。方法 对４０例单囊型成釉细胞瘤行ＨＥ染色及组织学观察；并对其中的２５例行荆豆凝集素（ＵＥＡ－１）、兀鹰血凝集素（ＢＳＡ－１）免疫组织化学染色。结果 ４０例 单囊型成釉细胞瘤，组织学上可分为３个亚型：第一型５例（１２．５％），第二型２０例（５０．０％），第三型１５例（３７．５％）；ＵＥＡ－１、ＢＳＡ     

Synchronous ameloblastoma and orthokeratinized odontogenic cyst of the mandible

The simultaneous occurrence of ameloblastomas with odontogenic cysts or other non-odontogenic lesions have already been described as combined lesions. However, we are unaware of any report in the English literature of simultaneous occurrence of ameloblastoma and orthokeratinized odontogenic cyst (OOC) occurring as completely distinct lesions. This report shows a case of synchronous ameloblastoma and OOC, located on posterior regions of the mandible, but in distinct sides.     

牙源性角化囊肿细胞增殖抗原和表皮生长因子受体表达

目的　探讨牙源性角化囊肿衬里上皮细胞的增殖特点。方法　采用免疫组化染色方法 ,对牙源性角化囊肿、成釉细胞瘤、含牙囊肿、正常口腔粘膜上皮中细胞增殖抗原 Ki- 6 7和表皮生长因子受体 (EGFR)的表达进行分析比较。结果　牙源性角化囊肿中 Ki- 6 7表达较含牙囊肿高 ,与正常口腔上皮相似 ;复发的与未复发的牙源性角化囊肿 Ki- 6 7指数无显著性差异。牙源性角化囊肿中 EGFR表达呈阳性。结论　牙源性角化囊肿上皮增殖活跃 ,上皮增殖生长可能与表皮生长因子家族有关。     

Age-standardized incidence rates of ameloblastoma and dentigerous cyst on the Witwatersrand, South Africa

Although a great deal is known about the incidence of cancer, including oral cancer, no such study has been done on odontogenic tumors and jaw cysts. There are therefore no standardized data which would allow for comparative incidences in different countries and between different groups. In the present study, cases of ameloblastomas and dentigerous cysts derived from the records of all the hospital pathology departments and private pathology practices on the Witwatersrand, were recorded for the 10-year period 1965--1974. The population at risk (1970 census) was 974,390 Whites and 1,567,280 Blacks. The annual incidence rates, standardized against the standard world population, for ameloblastomas per million population are 1.96, 1.20, 0.18 and 0.44 for Black males, females and White males, females, respectively. The equivalent four figures for dentigerous cysts are 1.18, 1.22, 9.92 and 7.26. These figures show that ameloblastoma is very much more common in Blacks than Whites in the population at risk. Conversely, dentigerous cysts are much more common in Whites. This makes it unlikely that dentigerous cysts predispose to ameloblastoma formation. These epidemiologic observations give rise to speculation as to whether some component of the South African Black diet or other environmental substance might possibly be an etiologic factor in ameloblastoma.     

Syndecan‐1 (CD 138) surface expression marks cell type and differentiation in ameloblastoma,keratocystic odontogenic tumor,and dentigerous cyst

J Oral Pathol Med (2013) 42 : 186–193 Background: The altered expression of syndecan‐1 (SD‐1), a transmembrane heparan sulfate proteoglycan, in ameloblastomas and cysts of odontogenic origin suggests that this molecule could have prognostic value in assessing the clinical outcome of those lesions. The purpose of this study was to analyze SD‐1 expression profile immunohistochemically in archival, paraffin‐embedded tissue sections of ameloblastomas and in common odontogenic cysts arising from the same locale. Methods: SD‐1 expression was investigated in 32 ameloblastomas, 26 keratocystic odontogenic tumors (KCOT), and 21 dentigerous cysts from the archives of the histopathology laboratory which were routinely processed. The cases were reviewed and assessed according to the established criteria. Sections were immunostained with monoclonal antibody against SD‐1 (CD138). Sections of normal oral mucosa, site matched, were stained in parallel as positive controls. The plasma cells in sections served as internal positive controls. Results: SD‐1 expression was observed in the epithelial and stromal elements of the sections, and the expression was significantly associated with the lesion’s extension and involvement of adjacent structures (P = 0.025). Stellate‐reticulum cells showed higher expression than the ameloblasts, which was at a significant level (P < 0.0001). Highly significant difference was reported among the three groups of lesion for the epithelial staining (P < 0.0001). The mean rank scores (Kruskal–Wallis test) of ameloblastomas were significantly lower than those of KCOT and dentigerous cysts. Non‐significant comparison was made between KCOT and dentigerous cyst groups. Conclusions: The present study revealed SD‐1 immunoreactivity in the stromal cells of ameloblastoma, KCOT, and dentigerous cysts rather uniformly. This reported SD‐1 expression by the tumor stroma is considered to be associated with poor prognosis of the lesions.     

Calretinin Expression in Unicystic Ameloblastoma: An Aid in Differential Diagnosis

Calretinin is a 29 kDa calcium-binding protein, which is widely expressed in the central and peripheral neural tissue. It has also been demonstrated in odontogenic epithelium during odontogenesis and in neoplastic odontogenic tissues. The lining epithelium of eight cases of unicystic ameloblastoma, six cases of dentigerous cyst, six cases of odontogenic keratocyst, reclassified as keratocystic odontogenic tumor (KCOT), and four cases of solid/multicystic ameloblastoma was examined for the expression of calretinin. No positive staining was observed in any of the dentigerous cysts and keratocystic odontogenic tumor linings. In comparison, coarse dark brown staining was seen in the stellate reticulum of solid multicystic ameloblastoma and more superficial epithelial layers of unicystic ameloblastoma. In conclusion, we have highlighted calretinin to be a specific immunohistochemical marker for neoplastic ameloblastic tissue that can be used as an important diagnostic aid in the differential diagnosis of unicystic ameloblastoma and cystic odontogenic lesions.     

Granular cell — Peripheral ameloblastoma: a rare variant

Ameloblastoma is an epithelial odontogenic tumour of the jaw and exhibits diverse microscopic patterns which occurs either singly or in combination with other patterns. Peripheral ameloblastoma is a rare odontogenic soft tissue tumor, derived from epithelial and/or mesenchymal elements being part of the tooth-forming apparatus. The lesions responsible for approximately 1% to 5% of all cases of ameloblastoma affecting alveolar mucosa and gingiva occurring mainly, in the middle age. This article describes a case of peripheral ameloblastoma affecting a 35-year-old female. The lesion was located in the right buccal space. The occurrence and pathogenesis of peripheral ameloblastomas in general, are reviewed. The tumour was excised and no recurrence has been observed after twenty four months of surgery.     

Infrequent clinicopathological findings in 108 ameloblastomas

One hundred and eight ameloblastomas diagnosed in a rural black Africa population were analysed for clinicopathologic findings other than those classically described. One patient had a polycystic ameloblastoma adjacent to an ameloblastic fibroma. Two other polycystic ameloblastomas showed aneurysmal bone cyst formation and one mandibular tumour was diagnosed as a keratoameloblastoma. Microscopic changes resembling an adenomatoid odontogenic tumour were present in association with two unicystic ameloblastomas and a HPV18-positive verrucous lesion occurred in the lining of a cystic space of a polycystic ameloblastoma. Two ameloblastomas contained eosinophilic granules in all tumor cells and melanocytes were diffusely present in another. One case exhibited a focus of mucous cell metaplasia. Two polycystic ameloblastomas showed diffuse interstitial ossification. One mandibular tumor was diagnosed as a desmoplastic ameloblastoma and another as an odontoameloblastoma. This study demonstrated that although ameloblastomas are regarded as a fairly homogeneous group of neoplasms, detailed investigations prove clinicopathologic diversity in a significant number of lesions.     

Discrimination of parakeratinised odontogenic keratocysts from other odontogenic and non-odontogenic cyst types by expression of a 38kd cell-surface glycoprotein

We have identified strong expression of a 38-kD cell surface glycoprotein (gp38), a marker of basal cell carcinomas (BCCs), in basal and suprabasal epithelial cell membranes of parakeratinised odontogenic keratocysts. In contrast, orthokeratinised cysts and most other odontogenic cyst types, ameloblastomas, normal stratified oral epithelium, cell rests of Malassez and glands of Serres, all proved negative. To our knowledge this is the first histochemical marker to distinguish between these major cyst types. It has obvious uses in the diagnosis of inflamed keratocysts and the separation of ameloblastomas from BCCs and may find a role in studies of the developmental biology of other odontogenic structures.     

How to name it: a rare case of odontogenic cyst

Odontogenic cysts and tumors are well-recognized entities to the specialist oral pathologist and they seldom pose problems in differential diagnosis. This paper deals with an aggressive cystic lesion in the maxilla of a 65-year-old male that was characterized by a large radiographically multilocular lesion and a multicystic pattern microscopically. The categorization of this lesion was complicated by the presence of features suggestive of both glandular odontogenic cyst and cystic ameloblastoma with aggressive histologic phenotypes.     

Histopathologic study of epithelial components in the connective tissue wall of unilocular type of calcifying odontogenic cyst

Histopathologic study of satellite cysts and odontogenic epithelial islands in connective tissue wall of unilocular type of calcifying odontogenic cyst (COC) was made. The material was 13 cases consisting of 3 simple unicystic COCs, 9 odontome producing COCs and 1 ameloblastomatous proliferating COC. Satellite cysts were found in 6 cases, and were histologically classified into following types: simple cystic, odontome producing and ameloblastomatous. Histologic types of satellite cysts did not coincide with those of main cystic lesions in some cases. Odontogenic epithelial islands with or without proliferating feature were found in 9 cases, and were found in all cases with satellite cysts. Melanin and melanocytes were seen in an ameloblastomatous satellite cysts of 1 of 3 pigmented COCs.     

Detection of apoptosis-related factors and apoptotic cells in ameloblastomas: analysis by immunohistochemistry and an in situ DNA nick end-labelling method

To clarify the possible role of apoptosis in odontogenic epithelium, apoptosis-related factors and apoptotic cells were examined by immunohistochemistry and an in situ DNA nick end-labelling method. Expression of bcl-2 protein was detected in both normal and neoplastic odontogenic epithelium, whereas expression of p53 protein was detected only in neoplastic but not in normal odontogenic epithelium. The prevalence of cases positive for Lewis^y antigen in ameloblastomas was significantly lower than in enamel organs. Correlation between these factors and apoptotic cells presented by an in situ DNA nick end-labelling method was not clear. The number of apoptotic cells in ameloblastomas was significantly greater than in normal odontogenic epithelium, and apoptotic reactions in the granular cell type ameloblastoma tended to be more frequently detected than in other types of ameloblastomas. These results suggested that apoptotic cell death might play an important role in oncogenesis and-or tissue differentiation in odontogenic epithelium.     

Frequency of odontogenic cysts and tumors: a systematic review

A systematic review of the literature from 1993 to 2011 was undertaken examining frequency data of the most common odontogenic cysts and tumors. Seven inclusion criteria were met for the paper to be incorporated. In the preliminary search 5231 papers were identified, of these 26 papers met the inclusion criteria. There were 18 297 odontogenic cysts reported. Of these there were 9982 (54.6%) radicular cysts, 3772 (20.6%) dentigerous cysts and 2145 (11.7%) keratocystic odontogenic tumors. With the reclassification of keratocystic odontogenic tumor in 2005 as an odontogenic tumor, there were 8129 odontogenic tumors reported with 3001 (36.9%) ameloblastomas, 1163 (14.3%) keratocystic odontogenic tumors, 533 (6.5%) odontogenic myxomas, 337 (4.1%) adenomatoid odontogenic tumors and 127 (1.6%) ameloblastic fibromas. This systematic review found that odontogenic cysts are 2.25 times more frequent than odontogenic tumors. The most frequent odontogenic cyst and tumor were the radicular cyst and ameloblastoma respectively.     

Calcifying odontogenic cyst. A review of ninety-two cases with reevaluation of their nature as cysts or neoplasms, the nature of ghost cells, and subclassification.

Ninety-two cases of calcifying odontogenic cyst (COC) were reviewed with special consideration of their nature as cysts or neoplasms, the nature of ghost cells, and classification on the basis of clinicopathologic features. The cases were divided into 79 (85.9%) cysts and 13 (14.1%) neoplasms. The cysts occurred as four variants: (1) nonproliferative COC (35 cases), characterized by a simple unicystic structure; (2) proliferative COC (17 cases), characterized by a cystic structure with multiple daughter cysts, extensive ghost cell formations, and marked tendency for calcification; (3) ameloblastomatous COC (11 cases), characterized by ameloblastoma-like, cyst-lining epithelium with ghost cells and calcifications; and (4) COC associated with odontoma (16 cases), which combined features of COC and odontoma. The neoplasms occurred as three variants: (1) ameloblastoma ex COC (two cases), which showed unifocal and multifocal intraluminal and intramural ameloblastoma proliferating from the COC-lining epithelium; (2) peripheral epithelial odontogenic ghost cell tumor (eight cases), which occurred in the gingiva and resembled peripheral ameloblastoma except for clustered ghost cells in the central portion of epithelial islands and the presence of juxtaepithelial dentinoid; and (3) central epithelial odontogenic ghost cell tumor (three cases). The latter showed ameloblastomatous or adenomatoid odontogenic tumor-like epithelial clusters with ghost cell formation and juxtaepithelial dentinoid. The clinical features of cystic and neoplastic variants were tabulated and described. On the basis of histopathologic features and their immunohistochemical reaction to polyclonal antikeratin antibody, it is suggested that ghost cells might be the result of coagulative necrosis.     

Clinicopathological evaluation of 164 dental follicles and dentigerous cysts with emphasis on the presence of odontogenic epithelium in the connective tissue. The hypothesis of “focal ameloblastoma”

Objectives: Some ameloblastomas presumably originate from odontogenic epithelium within the connective tissue of dental follicles and dentigerous cysts. Therefore, it would seem reasonable to discuss as whether odontogenic epithelium proliferations, frankly displaying ameloblastomatous features (“focal ameloblastoma”), should be considered as an “early” ameloblastoma. Study Design: Histopathological reports from 164 dental follicles and dentigerous cysts from the Department of Oral and Maxillofacial Surgery/Oral Pathology of the VU Free University medical center in Amsterdam, The Ne-therlands, were reviewed. Histopathological slides from 39 cases reporting the presence of odontogenic epithelium within the connective tissue were re-evaluated in order to assess the possible presence of focal ameloblastomas. Results: Focal ameloblastomas were detected in one dental follicle and in two dentigerous cysts. During a follow-up period of 6, 8 and 22 years, respectively, no clinical signs of (recurrent) ameloblastoma have occurred in these patients. Conclusions: Focal ameloblastoma possibly represents the early stage of ameloblastoma development. Key words:Ameloblastoma, odontogenic epithelium, dentigerous cyst, dental follicle.