Adalberto Mosqueda-Taylor

Odontogenic tumors in Mexico: a collaborative retrospective study of 349 cases.

Reports about the frequency of odontogenic tumors are scarce, and diagnostic criteria used in the reports are not uniform. This article presents the results of a retrospective study of odontogenic tumors recorded in four services of diagnostic pathology in Mexico City (two dental schools, one cancer hospital, and one private oral pathology service). The final diagnosis in each case was based on the 1992 histologic criteria of the World Health Organization. The frequency of odontogenic tumors, expressed as a percent of all oral and maxillofacial specimens, ranged from 0.8% in the cancer hospital (0.02% of all biopsies) to 3.7% in the private oral pathology service. The frequency was identical for the two dental schools (2.5%). We found a total of 349 odontogenic tumors; of these, 345 were benign (98.8%), and 4 (1.1%) were malignant (3 were primary intraosseous carcinomas and 1 was a malignant ameloblastoma). The most frequently occurring tumors were odontoma (34.6%), ameloblastoma (23.7%), myxoma (17.7%), adenomatoid odontogenic tumor (7.1%), and calcifying odontogenic cyst (6.8%). Although relatively rare, odontogenic tumors are still an important cause of extensive surgical procedures in Mexico.

International collaborative study on ghost cell odontogenic tumours: calcifying cystic odontogenic tumour, dentinogenic ghost cell tumour and ghost cell odontogenic carcinoma.

BACKGROUND Calcifying odontogenic cyst was described first by Gorlin et al. in 1962; since then several hundreds of cases had been reported. In 1981, Praetorius et al. proposed a widely used classification. Afterwards, several authors proposed different classifications and discussed its neoplastic potential. The 2005 WHO Classification of Odontogenic Tumours re-named this entity as calcifying cystic odontogenic tumour (CCOT) and defined the clinico-pathological features of the ghost cell odontogenic tumours, the CCOT, the dentinogenic ghost cell tumour (DGCT) and the ghost cell odontogenic carcinoma (GCOC). METHODS The aim of this paper was to review the clinical-pathological features of 122 CCOT, DGCT and GCOC cases retrieved from the files of the oral pathology laboratories from 14 institutions in Mexico, South Africa, Denmark, the USA, Brazil, Guatemala and Peru. It attempts to clarify and to group the clinico-pathological features of the analysed cases and to propose an objective, comprehensive and useful classification under the 2005 WHO classification guidelines. RESULTS CCOT cases were divided into four sub-types: (i) simple cystic; (ii) odontoma associated; (iii) ameloblastomatous proliferating; and (iv) CCOT associated with benign odontogenic tumours other than odontomas. DGCT was separated into a central aggressive DGCT and a peripheral non-aggressive counterpart. For GCOC, three variants were identified. The first reported cases of a recurrent peripheral CCOT and a multiple synchronous, CCOT are included. CONCLUSIONS Our results suggest that ghost cell odontogenic tumours comprise a heterogeneous group of neoplasms which need further studies to define more precisely their biological behaviour.

Comparison of the value of PCNA and Ki-67 as markers of cell proliferation in ameloblastic tumors

Objectives: The aim of this study was to compare among PCNAand Ki-67 as the most reliable immunohistochemical marker for evaluating cell proliferation in ameloblastic tumors. Study Design: Observational, retrospective, and descriptive study of a large series of ameloblastic tumors, composed of 161 ameloblastomas and four ameloblastic carcinomas, to determine and compare PCNA and Ki-67 expression using immunohistochemistry techniques. Results: When analyzing Ki-67 positivity, the desmoplastic ameloblastoma demonstrated a significantly lower proliferation rate (1.9%) compared with the solid/multicystic and unicystic ameloblastomas and ameloblastic carcinomas (p<0.05), whereas the ameloblastic carcinomas displayed a significantly higher rate compared with all of the other ameloblastomas (48.7%) (p<0.05). When analyzing cell proliferation with PCNA, we found significant differences only between the ameloblastic carcinomas (93.3%) and the desmoplastic ameloblastomas (p<0.05). When differences between the immunopositivity for PCNA and Ki-67 were compared, the percentages were higher for PCNA in all types of ameloblastomas and ameloblastic carcinomas. In all cases, the percentages were greater than 80%, whereas the immunopositivity for Ki-67 was significantly lower; for example, the ameloblastic carcinoma expressed the highest positivity and only reached 48.7%, compared to 93.3% when we used PCNA. Conclusions: In the present study, when we used the proliferation cell marker Ki-67, the percentages of positivity were more specific and varied among the different types of ameloblastomas, suggesting that Ki-67 is a more specific marker for the proliferation of ameloblastic tumor cells. Key words:Ameloblastomas, ameloblastic carcinoma, PCNA, Ki-67, cell proliferation markers.

Syndecan-1 (CD138) and Ki-67 expression in different subtypes of ameloblastomas

Ameloblastoma is the most frequent odontogenic tumor and is considered a benign, but locally invasive, neoplasm with variable clinico-pathological expression. Syndecan-1 is a cell surface proteoglycan that binds cells to the extracellular matrix and its expression is down-regulated in many cellular transformation models. The aims of this study were to examine the pattern of syndecan-1 expression, to evaluate the proliferating activity in a large series of solid/multicystic (SA) and unicystic ameloblastomas (UA), and to study its possible correlation to their biological behavior. Immunohistochemical studies were performed for syndecan-1 (clone MI15) and Ki-67 (clone MIB-1) in 120 ameloblastomas (75 SA and 45 UA). The salient finding was that expression of syndecan-1 was related to the histological subtype of tumors, as there was a lower expression in SA (40.2%) as compared to UA (49.7%) (p<0.05). These findings did not correlate with Ki-67 expression, as this was similar in both types of ameloblastomas. Our results suggest that the reduced expression of syndecan-1 supports the view that SA has a more aggressive biological behavior than the UA. The lack of correlation between reduction of the syndecan-1 and Ki-67 index may be due to the different histomorphologies of both types of ameloblastoma, and more studies are necessary to better understand the role of this protein in the biological behavior of these tumors.

Comparative expression of syndecan-1 and Ki-67 in peripheral and desmoplastic ameloblastomas and ameloblastic carcinoma

The aims of the present study were to examine whether the pattern of syndecan‐1 expression correlates with cellular proliferation index in desmoplastic ameloblastomas (DA), peripheral ameloblastomas (PA) and ameloblastic carcinomas (AC), and to compare with that previously reported for solid (SA) and unicystic (UA) variants of ameloblastoma. Immunohistochemistry was performed for syndecan‐1 and Ki‐67 in seven ameloblastomas (four DA and three PA) and three AC. Expression of syndecan‐1 was related to the histological subtype of tumors and, in the case of malignancy, to lower expression levels observed in AC (22.5%) than in PA (47.5%) or DA (77.5%) (P < 0.05). Syndecan‐1 expression correlated inversely with Ki‐67 proliferative index: the expression was lower in both types of ameloblastomas (1.5% in DA and 6.4% in PA) than in AC (41.2%; P < 0.05). The present results suggest that the decrease in syndecan‐1 expression and increase in the Ki‐67 index observed in AC is in accordance with its higher aggressiveness as compared to the rare DA and PA. Interestingly, DA had a lower proliferation index as well as the highest levels of syndecan‐1 expression. These data suggest that DA differ from the other types of intraosseous ameloblastomas but more studies are necessary to better understand the role of this protein as a marker in the biological behavior of the epithelial odontogenic neoplasms.

Odontoameloblastoma. Clinico-pathologic study of three cases and critical review of the literature

The odontoameloblastoma (OA), is an infrequent neoplasm. To date, there are less than 50 cases reported as OA or ameloblastic odontoma in the English dental literature, but only 14 (including three of our own material), fulfill the histological criteria of the current WHO histological classification of odontogenic tumours. Nine occurred in men and five in women (male to female ratio 1.8:1). Age ranged from 2 to 50 years (mean 20.2 years), and nine cases (64.2%) were diagnosed during the first two decades. Maxilla and mandible were equally involved, and most cases occurred posterior to the canines (71.4%). Follow-up ranged from 6 months to 8 years (mean: 25.5 months). Of the 12 cases with informed follow-up, two recurred once (at 24 and 18 months, respectively), and one case had two documented recurrences, at 6 and 49 months. Although OA tends to occur at an earlier age than conventional ameloblastoma, it has practically the same potential to produce bone expansion, root resorption and recurrence. For these reasons OA should be treated in a similar fashion, with wide surgical excision and close follow-up for at least 5 years.

Central odontogenic fibroma: new findings and report of a multicentric collaborative study

OBJECTIVE The aim of this study was to describe the clinicopathologic and immunohistochemical characteristics of 14 cases of central odontogenic fibroma (COF), and the ultrastructural features of 2 of them. STUDY DESIGN Collaborative retrospective study based on the records of 4 oral pathology diagnostic services in Latin America based on the current World Health Organization classification. RESULTS There were 7 male and 7 female patients (mean age 31.8 years). Eight tumors occurred in the maxilla and 6 in the mandible. Thirteen cases were epithelium-rich and 1 epithelium-poor COF. Three were classified as hybrid COF with giant cell lesion. Mean size of the hybrid lesions were larger than pure COF (3.8 vs. 2.4 cm). Odontogenic epithelial islands were immunoreactive for cytokeratin (CK) AE1/AE3, CK5, CK14, CK19, and 34BE12 and negative for CK1 and CK18. Langerhans cells positive for S-100 and CD1a were found within the epithelial islands in 6/6 tested cases. CD68 was expressed in the giant cells of the hybrid lesions and in a few mononuclear cells of 2 cases of COF. Ki-67 index was <1% in all cases. In 6 tumors (42.8%), there were small globular eosinophilic droplets within the epithelial islands, which were positive for collagen type IV, and 9/13 cases (69.2%) were focally positive for smooth muscle actin. In addition to fibroblasts, myofibroblastic differentiation was found in the 2 cases studied ultrastructurally. CONCLUSIONS Immunohistochemistry was useful to confirm the presence of epithelium and to exclude other central fibrous tumors. COF also contains a variable number of mast cells, Langerhans cells, and myofibroblasts, and further studies are needed to better understand the participation of these cells in COF histogenesis.

Cell proliferation associated with actions of the substance P/NK-1 receptor complex in keratocystic odontogenic tumours

The expression of substance P (SP) and its NK-1 receptor (NK-1R) in keratocystic odontogenic tumours (KOTs) was studied to determine whether the intrinsic growth potential of these lesions is related to a cell proliferation stimulus mediated by the SP/NK-1R complex. A total of 65 tissue samples of solitary non-recurrent KOTs, solitary recurrent KOTs, KOTs associated with nevoid basal cell carcinoma syndrome (NBCCS) and KOTs with chondroid wall were studied by immunohistochemistry, using anti-SP, anti-NK-1R and anti-Ki-67 monoclonal antibodies. Expression of these markers was analysed in infiltrating lymphocytes, in fibrous capsule, and in membrane, cytoplasm and nucleus of epithelial cells. SP expression in infiltrating lymphocytes was significantly associated with SP in fibrous capsule and epithelial cells. KOTs associated with NBCCS showed a significantly higher SP expression in all tissues and cell compartments compared with other KOT types. Finally, SP expression in epithelial cells was associated with positive Ki-67 expression in dysplastic epithelium. This first published report on SP and NK-1R expressions in KOTs demonstrates that actions of the SP/NK-1R complex may constitute a mechanism to stimulate epithelial cell proliferation in KOT. This pathway may be of special relevance in the multiple KOTs associated with NBCCS.

Odontogenic tumors: A retrospective study of four Brazilian diagnostic pathology centers

Objective: This article presents the results of a retrospective study of the frequency and classification of odontogenic tumors recorded at four centers of diagnostic pathology in Rio de Janeiro, Brazil. Study Design: All medical records and microscopic slides of odontogenic tumor specimens for the years 1997 to 2007 were retrieved from the files of four services of diagnostic pathology in Rio de Janeiro City. Diagnoses were re-evaluated and the tumors classified according to the latest (2005) World Health Organization Classification of Tumors. Results: A total of 201 odontogenic tumors were found among 15,758 oral biopsies (1.3%). The frequencies of these tumors at the four centers ranged from 0.5% at the National Cancer Institute to 3.3% in a private laboratory. Chi-square analysis revealed statistically significant differences (p<0.05) between the proportions of odontogenic tumors in the studied centers. Of these, 94.5% were benign and 5.5% were malignant. Keratocystic odontogenic tumor (32.3%) was the most frequent lesion, followed by ameloblastoma (29.8%) and odontoma (18.4%). Conclusions: Odontogenic tumors are uncommon in Brazil. Different pathology laboratories reported divergent frequencies of odontogenic tumors, which may reflect institutional specializations and the patient populations served. Key words:Odontogenic tumors, jaw neoplasms, epidemiology, WHO classification.

Adenoid cystic carcinoma of the tongue – clinicopathological study and survival analysis

BackgroundTo review the demographic data of a series of adenoid cystic carcinoma (ACC) of the tongue, as well as to analyze c-kit expression, histopathologic patterns, prognostic factors, evolution, recurrences and/or persistence and survival.MethodsRetrospective study from 1986 to 2006, which reviews a database of 68 patients with diagnosis of head and neck ACC.ResultsWe found eight cases of ACC of the tongue (11.7% of all head and neck ACCs). There were 7 female (87.5%) and 1 male (12.5%) patients, with an average age of 51 years (range 33 to 67 years). Seven patients were surgically treated, three of which required adjuvant treatment. Only one female patient did not accept treatment. Average follow-up time was 5.3 years. Metastases developed in 37% of cases during the follow-up period. Histopathologically, the cribriform pattern predominated (6/8 cases). All cases presented perineural invasion, and one patient also presented vascular invasion. c-kit positivity was observed in all cases. Global survival in the seven treated cases was 51% and 34% at 5 and 10 years, respectively, while the disease-free period was of 64% at 3 years and 42% at 10 years.ConclusionACC of the tongue is a rare neoplasm, in which early diagnosis is important because these are slowly-growing tumors that produce diffuse invasion. As the role of c-kit could not be assesed in this series, surgery continues to be the cornerstone of treatment and radiotherapy is indicated when surgical margins are compromised. Metastatic disease is still hard to handle because of the lack of adequate therapies for these tumors. Hence, survival has not changed in the last years.