Analyses of VEGFC/VEGF-D expressions, density and endothelial lymphatic proliferation in salivary gland neoplasms.

OBJECTIVE: The aim of this study was to assess vascular endothelial growth factor C (VEGF-C) and VEGF-D expressions, tumor lymphatic density (D2-40) and endothelial lymphatic proliferation (D2-40/Ki-67 double labeling) in a series of salivary gland neoplasm cases. MATERIALS AND METHODS: Twenty pleomorphic adenomas (PA), 20 adenoid cystic carcinomas (ACC) and 20 mucoepidermoid carcinomas (MEC) were assessed, as well as 10 normal minor salivary gland (SG) tissues for comparison. RESULTS: All cases presented positive VEGF-C expression in the peritumoral and intratumoral regions, and no differences in immunoexpression were detected between groups. However, the ACC group presented a significant difference in VEGF-C immunoexpression according to the predominant histological pattern. Most cases presented poor VEGF-D labeling in the peritumoral and intratumoral regions. Concerning peritumoral, intratumoral and total lymphatic endothelial density, the assessed groups revealed an increasing gradient, with lower values for PA, followed by MEC and ACC. CONCLUSION: No correlation was detected between VEGF-C and VEGF-D immunoexpression in relation to lymphatic tumor density and endothelial lymphatic proliferation. Western blotting (WB) revealed no difference between VEGF-C and VEGF-D expression among the lesions, corroborating the immunohistochemistry findings.

Relationship between mast cells and E-cadherin in odontogenic keratocysts and radicular cysts.

OBJECTIVE: This study aimed to evaluate tryptase and E-cadherin protein expression in odontogenic keratocysts (OKCs) and radicular cysts (RCs) and their relationship with lesion size. MATERIALS AND METHODS: Thirty OKC and 30 RC cases were analyzed by immunohistochemistry. Tryptase expression was quantitatively assessed using the quantification of mast cells, and expression of E-cadherin was semi-quantitatively analyzed estimating the proportion of positive cells: 1 = less than 25% of immunopositive cells; 2 = 26 to 50% of immunopositive cells; 3 = 51 to 75% of immunopositive cells; 4 = more than 75% of immunopositive cells. Data on cystic lesion sizes were obtained from patients' clinical files, based on previous radiographic exams, and the lesions were categorized into three groups: group 1 (< 2 to 2 cm); group 2 (> 2 to 4 cm), and group 3 (> 4 cm). RESULTS: Higher mast cell means were found for RCs, with the predominance of degranulated mast cells in both OKCs and RCs (p = 0.082). Concerning the epithelial component, a higher concentration of degranulated mast cells was detected in RCs (p = 0.000). Regarding connective tissue, degranulated mast cells were more evident in OKCs (p = 0.762). A negative correlation was observed between E-cadherin expression and total number of mast cells (p = 0.011), degranulated mast cells (p = 0.040), and degranulated mast cells in both superficial (p = 0.035) and deep connective tissues (p = 0.009). Concerning lesion size, a negative correlation with total number of mast cells (p = 0.016) and number of degranulated mast cells (p = 0.049) was observed, both in the epithelial components. Herein, the larger the lesion size, the lower the number of degranulated mast cells in the epithelium (r = - 0.271; p = 0.49), suggesting that these cells play a role in the initial cystic expansion phase. CONCLUSION: The higher expression of tryptase in degranulated mast cells was linked to a lower expression of E-cadherin, which may be related to a change in the epithelial permeability in these lesions, contributing to increased cystic content and lesion growth. CLINICAL RELEVANCE: Evidence of the relationship between mast cells and E-cadherin in the growth of odontogenic cysts was studied.

Immunohistochemical analysis of MMP-13 and EMMPRIN in epithelial odontogenic lesions.

PURPOSE: To investigate the contribution of MMP-13 in tumor aggressiveness, by acting on the reorganization of the extracellular matrix, regulating the biological activity of cytokines in odontogenic epithelial lesions, as well as to evaluate the role of EMMPRIN as an inducer of MMP-13. METHODS: Twenty solid ameloblastomas (SAs), 10 unicystic ameloblastomas (UAs), 20 odontogenic keratocysts (OKCs), and 20 adenomatoid odontogenic tumors (OATs) were selected. The expression of MMP-13 and EMMPRIN was evaluated in epithelial/connective tissue by determining the score of immunoreactive cells. RESULTS: Higher concentration of MMP-13 was observed in epithelium of SAs and OKCs (p = 0.316), while in connective, MMP-13 was more expressed in OKCs and UAs (p = 0.213). OKCs exhibited the highest immunoreactivity score for EMMPRIN in the epithelium (p = 0.091). In connective tissue, a larger number of immunoreactive cells were observed in OKCs and UACs (p = 0.357). There was a moderate correlation (r = 0.343/p = 0.004) between MMP-13/EMMPRIN in epithelium and strong correlation (r = 0.474/p < 0.001) in connective tissue. CONCLUSION: We suggest that the OKCs, SAs and UAs presented greater immunoexpression for MMP-13 and EMMPRIN, since they were lesions of more aggressive behavior, with smaller expressions in the AOTs that are admittedly indolent. However, we did not find a statistically significant difference between the expression of MMP-13 and EMMPRIN in lesions studied. The positive correlation found between MMP-13 and EMMPRIN in the epithelial and connective tissue of odontogenic lesions analyzed, seems to be related to the role of EMMPRIN as an inducer of MMP-13 expression.

Oral lymphoid lesions: a 47-year clinicopathological study in a Brazilian population.

We performed an epidemiological, clinical and histopathological analysis of oral lymphoid lesions (OLLs) during a 47-year period. Data regarding patient age, sex, duration, location, symptomatology, type of growth, implantation, staining, presence of ulceration and bleeding of all cases were compiled from the clinical data. For the histopathological analyses, all slides stained by H/E were reassessed. During the analyzed period, 14,565 patients with oral and maxillofacial lesions were diagnosed, with 45 cases diagnosed as OLLs. The most prevalent location was the tongue. Females were more affected, and the mean age was 40.8 years. OLLs presented a heterogeneous frequency, with the prevalence of reactive lesions (42.3%) followed by developmental lesions (35.6%). Among the reactive lesions, foreign body granulomas were the most common. Regarding diagnosed neoplasms, malignant represented 13.2% of the cases. The average time of evolution of OLLs in general was of 22.2 months. Regarding the histopathological characteristics, the presence of primary lymphoid follicles was observed in 37.8% of the cases, while inflammatory infiltrates were diffuse in 66.7% and epimyoepithelial islands were observed in 13.3%. Our study concludes that OLLs involves a broad spectrum of lesions that share the presence of the lymphoid component, which can range from indolent to more aggressive behavior.

Expression of matrix metalloproteinases (MMPs-2, -7, -9, and -26) and tissue inhibitors of metalloproteinases (TIMPs-1 and -2) in pleomorphic adenomas and adenoid cystic carcinomas.

PURPOSE: To compare the immunohistochemical expression of matrix metalloproteinases-2, -7, -9 and -26 and tissue inhibitors of metalloproteinases-1 and -2 in pleomorphic adenomas and adenoid cystic carcinomas of the minor salivary glands. METHODS: Twenty cases of pleomorphic adenomas and 20 cases of adenoid cystic carcinomas were evaluated for the immunohistochemical expression of matrix metalloproteinases-2, -7, -9, and -26 and tissue inhibitors-1 and -2 in tumor parenchyma. RESULTS: Most pleomorphic adenomas and adenoid cystic carcinomas showed high expression of matrix metalloproteinases and tissue inhibitors, predominantly located in the tumor cells. There was no statistically significant difference in the expression of the metalloproteinases-2 (p = 0.359), -7 (p = 0.081), and -26 (p = 0 553), as well as the tissue inhibitors-1 (p = 0.657), and -2 (p = 0.248) between the parenchyma of the studied tumors. Only matrix metalloproteinase-9 showed a significant difference in expression between the two tumors, with adenoid cystic carcinoma showing a more intense staining for this gelatinase (p = 0.041). CONCLUSIONS: The expression of the studied metalloproteinases suggests the involvement of these enzymes in the tissue remodeling process in pleomorphic adenomas and adenoid cystic carcinomas, but only MMP-9, significantly expressed in the adenoid cystic carcinomas, appears to be involved in the process of invasiveness and more aggressive behavior of these tumors. Additionally, results point that TIMPs-1 and -2 may have more complex functions besides metalloproteinase inhibition, which may be related to the pathogenesis and biological behavior of salivary gland tumors.

Clinicopathological evaluation and survival of patients with squamous cell carcinoma of the tongue

BACKGROUND: Early detection of oral cancer is the most effective means of reducing morbidity, complexity, and extent of treatment. This study evaluated the clinicopathological profile of epidermoid carcinoma of the tongue, including treatment and survival. MATERIAL AND METHODS: This observational, retrospective cross-sectional study evaluated patients with squamous cell carcinoma of the tongue treated at the Dr. Luiz Antônio Hospital, Natal, Brazil, from January 2001 to December 2011. Survival variables were calculated using the Kaplan-Meier method and compared by log rank tests. RESULTS: Of the 412 patients diagnosed in this period, 298 (72.3%) were men; their mean age was 60.5 years, and 69.2% were diagnosed with stage III/IV tumours. Improved survival was associated with early stage diagnosis, absence of affected lymph nodes at diagnosis, and treatment with surgery alone. CONCLUSIONS: Late stage diagnosis of oral cancer negatively affects patient survival. In addition, the general public should be made aware of the prognostic factors for oral SCC of the tongue and of the importance of periodic examinations of the oral cavity

Immunohistochemical expression of myofibroblasts, TGF-ß1 and IFN-γ in oral fibrous lesions.

OBJECTIVE: Analyze the presence of myofibroblasts (MFBs) in oral fibrous lesions and investigate TGF-ß1 and IFN-γ expression by immunohistochemistry during their differentiation. DESIGN: Twenty giant cell fibromas (GCFs), 20 fibromas (FIBs), and 20 fibrous hyperplasias (FHs) were selected. To evaluate the presence of MFBs, anti-α-SMA-immunoreactive cells were quantified in connective tissue. TGF-ß1 and IFN-γ expressions were evaluated in epithelial and connective tissue by determining the percentage of immunoreactive cells. RESULTS: Higher MFBs concentrations were observed in GCFs (median of 20.00), followed by FHs (15.00) and FIBs (14.00) (P = 0.072). No significant correlation between TGF-ß1 or IFN-γ immunoexpression and the number of MFBs in oral fibrous lesions was observed (P > 0.05). CONCLUSIONS: The higher density of MFBs found in GCFs, followed by FHs and FIBs, reaffirms the fibrogenic role of these cells, while the higher concentrations detected in GCFs, including evidence of giant MFBs, also suggest a role in the neoplastic behavior of these lesions. No correlation was observed between TGF-ß1 and IFN-γ in the myofibroblastic transdifferentiation process of the analyzed lesions.

Assessment of CTNNB1 gene mutations and ß-catenin immunoexpression in salivary gland pleomorphic adenomas and adenoid cystic carcinomas.

ß-Catenin exerts multiple functions in several neoplasms, playing a major role in cell signaling and tumor progression. This study analyzed possible CTNNB1 mutations in salivary gland pleomorphic adenomas (PAs) and adenoid cystic carcinomas (ACCs), and determined possible differences in ß-catenin immunoexpression in relation to these mutations, as well as histopathological aspects of these tumors. Twenty-four PAs (15 cell-rich and 9 cell-poor tumors) and 24 ACCs (10 tubular, 8 cribriform, and 6 solid tumors) were selected for the analysis of ß-catenin distribution and cellular localization. Furthermore, ß-catenin expression was evaluated using the H-score scoring system. Mutations in CTNNB1 exon 3 were investigated by the single-strand conformational polymorphism test. Diffuse ß-catenin expression was more frequently observed in ACCs compared to PAs (P = 0.008). No significant difference in ß-catenin cellular localization was observed between these tumors (P = 0.098). Comparisons between PA and ACC cases revealed a higher median H-score in the latter (P = 0.036). Cell-rich PAs exhibited a trend for higher H-score than cell-poor tumors (P = 0.060), whereas lower H-scores were observed in cribriform ACCs when compared to tubular and solid ACCs (P = 0.042). Mutations in CTNNB1 were observed in 6 PAs and 7 ACCs, with no significant difference in H-scores for ß-catenin according to mutation status (P = 0.135). ß-Catenin is important in the pathogenesis of salivary gland PAs and ACCs. In addition, CTNNB1 exon 3 mutations do not seem to significantly influence ß-catenin cytoplasmic/membranous expression or nuclear translocation in these tumors.

Analysis of GLUT-1, GLUT-3, and angiogenic index in syndromic and non-syndromic keratocystic odontogenic tumors.

The aim of this study was to evaluate the immunoexpression of glucose transporters 1 (GLUT-1) and 3 (GLUT-3) in keratocystic odontogenic tumors associated with Gorlin syndrome (SKOTs) and non-syndromic keratocystic odontogenic tumors (NSKOTs), and to establish correlations with the angiogenic index. Seventeen primary NSKOTs, seven recurrent NSKOTs, and 17 SKOTs were selected for the study. The percentage of immunopositive cells for GLUT-1 and GLUT-3 in the epithelial component of the tumors was assessed. The angiogenic index was determined by microvessel count. The results were analyzed statistically using the nonparametric Kruskal-Wallis test and Spearman's correlation test. High epithelial immunoexpression of GLUT-1 was observed in most tumors (p = 0.360). There was a higher frequency of negative cases for GLUT-3 in all groups. The few GLUT-3-positive tumors exhibited low expression of this protein in epithelial cells. No significant difference in the angiogenic index was observed between groups (p = 0.778). GLUT-1 expression did not correlate significantly with the angiogenic index (p > 0.05). The results suggest that the more aggressive biological behavior of SKOTs when compared to NSKOTs may not be related to GLUT-1 or GLUT-3 expression. GLUT-1 may play an important role in glucose uptake by epithelial cells of KOTs and this process is unlikely related to the angiogenic index. GLUT-1 could be a potential target for future development of therapeutic strategies for KOTs.

Immunohistochemical analysis of myofibroblasts, TGF-ß1, and IFN-γ in epithelial odontogenic lesions.

AIM: To investigate the presence of myofibroblasts (MFBs) in epithelial odontogenic lesions by immunohistochemistry and to correlate the findings with tumor aggressiveness, as well as to analyze the expression of TGF-ß1 and IFN-γ during the differentiation of these cells. METHODS AND RESULTS: Twenty solid ameloblastomas (SAs), 10 unicystic ameloblastomas (UAs), 20 keratocystic odontogenic tumors (KCOTs), and 20 adenomatoid odontogenic tumors (AOTs) were selected. For evaluation of the presence of MFBs, anti-α-SMA-immunoreactive cells were quantified in connective tissue near the epithelium. The expression of TGF-ß1 and IFN-γ was evaluated in epithelial and connective tissue by determining the percentage of immunoreactive cells. A higher concentration of MFBs was observed in SAs (mean of 30.55), followed by KCOTs (22.50), UAs (20.80), and AOTs (19.15) (P = 0.001). There was no significant correlation between the immunoexpression of TGF-ß1 or IFN-γ and the number of MFBs (P > 0.05). CONCLUSIONS: The larger number of MFBs suggests that these cells are one of the factors responsible for the more aggressive biological behavior of these lesions. The lack of correlation between the number of MFBs and immunoexpression of TGF-ß1 and IFN-γ indicates that these proteins are not involved in the differentiation of this type of contractile cell in the lesions studied and that only the use of immunohistochemistry to establish such a correlation is a limiting factor.

Immunoexpression of BMP-2 and BMP-4 and their receptors, BMPR-IA and BMPR-II, in ameloblastomas and adenomatoid odontogenic tumors.

OBJECTIVES: The present study evaluated the immunohistochemical expression of BMP-2 and BMP-4 and of their receptors (BMPR-IA and BMPR-II) in solid ameloblastoma (SA), unicystic ameloblastoma (UA) and adenomatoid odontogenic tumor (AOT) in order to obtain a better understanding of their role in the development and biological behavior of these tumors. DESIGN: This study analyzed these proteins in 30 cases of SA, 10 cases of UA, and 30 cases of AOT. Immunoexpression was evaluated in the parenchyma and stroma by attributing the following scores: 0, no stained cells; 1, ≤10%; 2, >10% and ≤25%; 3, >25% and ≤50%; 4, >50% and ≤75%.; 5, >75% stained cells. RESULTS: In SAs, positive correlations were observed between the stromal and parenchymal expression of BMP-2 (p<0.001) and between the stromal expression of BMP-2 and BMP-4 (p=0.020), as well as between the stromal expression of BMPR-II and BMP-4 (p=0.001) and the stromal and parenchymal expression of BMPR-II (p<0.001). In UAs, correlations were detected between the stromal and parenchymal expression of BMP-4 (p=0.035) and between the stromal expression of BMP-4 and BMPR-IA (p=0.022). In AOTs, analysis of immunoexpression in the parenchyma revealed positive correlations between all proteins. CONCLUSION: BMPs and their receptors play an important role in the differentiation and development of ameloblastomas and AOTs, but may not explain the different biological behaviors of these lesions. The positive correlation observed in AOTs might be related to the formation of mineralized material in this tumor.

Analysis of GLUT-1, GLUT-3, and angiogenic index in syndromic and non-syndromic keratocystic odontogenic tumors

Abstract The aim of this study was to evaluate the immunoexpression of glucose transporters 1 (GLUT-1) and 3 (GLUT-3) in keratocystic odontogenic tumors associated with Gorlin syndrome (SKOTs) and non-syndromic keratocystic odontogenic tumors (NSKOTs), and to establish correlations with the angiogenic index. Seventeen primary NSKOTs, seven recurrent NSKOTs, and 17 SKOTs were selected for the study. The percentage of immunopositive cells for GLUT-1 and GLUT-3 in the epithelial component of the tumors was assessed. The angiogenic index was determined by microvessel count. The results were analyzed statistically using the nonparametric Kruskal-Wallis test and Spearman’s correlation test. High epithelial immunoexpression of GLUT-1 was observed in most tumors (p = 0.360). There was a higher frequency of negative cases for GLUT-3 in all groups. The few GLUT-3-positive tumors exhibited low expression of this protein in epithelial cells. No significant difference in the angiogenic index was observed between groups (p = 0.778). GLUT-1 expression did not correlate significantly with the angiogenic index (p > 0.05). The results suggest that the more aggressive biological behavior of SKOTs when compared to NSKOTs may not be related to GLUT-1 or GLUT-3 expression. GLUT-1 may play an important role in glucose uptake by epithelial cells of KOTs and this process is unlikely related to the angiogenic index. GLUT-1 could be a potential target for future development of therapeutic strategies for KOTs.

Immunoexpression of α2ß1, α3ß1, and α5ß1 integrins in pleomorphic adenoma and adenoid cystic carcinoma.

The aim of the present study was to compare the expression of α2ß1, α3ß1, and α5ß1 integrins between 28 pleomorphic adenomas (PAs) and 10 adenoid cystic carcinomas (ACCs), and investigate differences in the expression of these integrins according to histologic subtypes of ACCs. It was taken into consideration the presence or absence, distribution, and localization of integrin immunoexpression. There was immunoreactivity in the intercellular contacts of the strands, nests, and solid sheets of PAs, as well as in the luminal and nonluminal cells of the duct-like structures, with a predominant immunoexpression in the luminal cells. The immunoexpression in ACCs varied with histologic subtype of the tumor. It was verified for a tendency of absence and/or reduced expression of all integrins in the solid subtype of ACCs. In general, PAs revealed a more diffuse and remarkable immunoexpression of all studied integrins than ACCs. The reduced integrins expression in ACC may be related to a lesser degree of cell differentiation in this neoplasm. Moreover, the absence and/or reduced expression of the studied integrins in solid ACC suggest a possible role in pathogenesis and more aggressive biological behavior of this histologic subtype.

Mast cells and matrix metalloproteinase 9 expression in actinic cheilitis and lip squamous cell carcinoma.

OBJECTIVES: The aim of this study was to evaluate mast cell (MC) density and migration and their association with matrix metalloproteinase (MMP) 9 expression in squamous cell carcinoma (SCC) and actinic cheilitis (AC). STUDY DESIGN: Tryptase, c-Kit, and MMP-9 expression was evaluated in 20 cases of SCC, 20 cases of AC, and 7 cases of normal lip (control samples) by immunohistochemistry techniques. RESULTS: Tryptase(+) and c-Kit(+) MC densities were significantly higher in SCCs than in ACs and control samples (P < .001). However, no significant difference was found when comparing tryptase(+) and c-Kit(+) MC densities between ACs and control samples (P values .185 and .516, respectively). MMP-9 was strongly expressed in SCCs and moderately expressed in ACs and control samples. A highly significant association was found between tryptase(+) MC density and the expression of MMP-9 (P < .001). CONCLUSIONS: The increase in MC density associated with the strong expression of MMP-9 may favor SCC progression.

Immunohistochemical expression of matrix metalloproteinases 1, 2, and 9 in odontogenic myxoma and dental germ papilla.

The aim of this study was to compare the immunohistochemical expression of matrix metalloproteinases (MMPs) 1, 2, and 9 in odontogenic myxomas and dental germ papillae. Twelve cases of odontogenic myxoma and eight tooth germ specimens were selected for analysis of the immunohistochemical expression and the pattern of distribution of MMPs 1, 2, and 9 in extracellular matrix (ECM), as well as of the number of MMP-positive cells. MMP-2 was expressed only in the ECM of myxomas (p<0.05). No significant difference was observed between ECM immunoreactivity for MMP-9 in myxomas and dental papillae (p>0.05). MMP-1 immunoreactivity was detected in most myxoma cases at a proportion similar to that observed in dental papillae (p>0.05). A significant difference was observed in the number of immunoreactive cells in myxomas (p<0.05), MMP-1 being present at higher proportions than MMPs 2 and 9. There was a gradient in the expression of MMPs in the ECM and in neoplastic cells of odontogenic myxomas, with higher immunoreactivity to MMP-1 and lower immunoreactivity to MMP-9. Taken together, our results suggest the existence of a coordinated mechanism between MMPs 1, 2, and 9 that aimed at the efficient degradation of extracellular matrix in odontogenic myxomas.

Immunoexpression of integrins in ameloblastoma, adenomatoid odontogenic tumor, and human tooth germs.

The expression of integrins alpha2beta1, alpha3beta1, and alpha5beta1 in 30 ameloblastomas (20 solid and 10 unicystic tumors), 12 adenomatoid odontogenic tumors (AOTs), and 5 human tooth germs in different stages of odontogenesis was analyzed. The distribution, location, pattern, and intensity of immunohistochemical expression were evaluated. Intensity was analyzed using scores (0 = absence, 1 = weak staining, and 2 = strong staining). No difference in the immunoexpression of the integrins was observed between solid and unicystic ameloblastomas. When these two ameloblastoma types were pooled into a single group, the following significant differences were found: immunoexpression of integrin alpha2beta1 was stronger in ameloblastomas than in AOTs and tooth germs, and the expression of integrin alpha5beta1 was stronger in ameloblastomas than in AOTs. The lack of detection of integrin alpha3beta1 in tooth germs and its detection in the odontogenic tumors studied suggest that this integrin might be used as a marker of neoplastic transformation in odontogenic tissues.

Prevention of oral lesions in children with acute lymphoblastic leukemia.

UNLABELLED: Acute lymphoblastic leukemia (ALL) is the most common form of cancer in children and is responsible for severe stomatologic complications. Treatment consists of four phases of chemotherapy, the main side effect of methotrexate, the drug most used during the intensification phase, is oral mucositis. OBJECTIVE: To evaluate the clinical aspects of the oral mucosa of children with ALL and to determine the effect of 0.12% chlorhexidine gluconate on the prevention of stomatologic complications in these patients. PATIENTS AND METHODS: Thirty-three children treated for ALL ranging in age from 2 to 15 years, without distinction of gender or race, were submitted to visual examination, digital palpation of the oral mucosa and cytologic examination of the buccal mucosa, and divided into two groups: group I consisted of 23 children using an oral solution of 0.12% chlorhexidine gluconate twice a day, and group II consisted of 10 children who did not receive this solution. All children received daily oral hygiene care guided by the dentist throughout treatment. RESULTS: Mucositis was observed in six children of group I and eight of group II, and was characterized by erythema, edema and ulcers. Uniform cytologic findings were obtained for the two groups, with a clear predominance of cells of the intermediate layer in all smears, in addition to a perinuclear halo in 18% of the smears. CONCLUSION: The present results suggest that systematic preventive treatment with 0.12% chlorhexidine gluconate and oral hygiene care reduce the occurrence of oral complications in children with ALL undergoing antineoplastic chemotherapy.

Estudo clínico e histopatológico de lesões centrais de células gigantes e tumores de células gigantes / Clinic and histopathological study of central giant cells lesions and giant cells tumors

Objetivo: Avaliar os aspectos clínicos e histopatológicos de um grupo de Lesões de Células Gigantes Centrais e Tumoresde Células Gigantes dos Ossos Longos, objetivando o diagnóstico diferencial entre essas lesões, bem como, correlacionaros resultados com o comportamento biológico de cada lesão. Material e Método: A amostra consistiu de oito casos de Lesão de Células Gigantes Centrais e sete casos de Tumores de Células Gigantes dos Ossos Longos, obtidos nos arquivos do Serviço de Anatomia Patológica da Disciplina de Patologia Oral de uma Universidade e do Laboratório de Patologia e Citologia Ltda. de um município, respectivamente. Os espécimes seccionados foram corados pela técnica da Hematoxilina/ Eosina (H/E) e analisados em microscopia de luz. Resultados: Similaridades marcantes foram observadas em alguns aspectos clínicos e histopatológicos, entre as lesões analisadas. Conclusão: Os resultados desta pesquisasuportam a hipótese da existência de um único processo patológico.

Proliferating cell nuclear antigen (PCNA) and p53 protein expression in ameloblastoma and adenomatoid odontogenic tumor.

In this study, proliferating cell nuclear antigen (PCNA) and p53 protein expressions were analyzed in 16 cases of ameloblastoma and 8 cases of adenomatoid odontogenic tumor (AOT). The cases of ameloblastoma consisted of solid type tumors and histologic arrangements of different subtypes were observed. In some specimens, more than one histologic subtype was identified in the same lesion, and each tumor was categorized according to the predominant cell pattern. The odontogenic tumors were grouped as follows: follicular ameloblastoma (n=7), plexiform ameloblastoma (n=4), acanthomatous + follicular ameloblastoma (n=3), basal cell ameloblastoma (n=2), adenomatoid odontogenic tumor (n=8). PCNA immunohistochemical expression revealed stronger quantitative labeling index for the follicular ameloblastoma, while for p53 protein the strongest quantitative labeling index was detected in the plexiform type. Nevertheless, statistical analysis using ANOVA and Tukey's test did not detect significant differences (p>0.05) among the histologic subtypes of ameloblastoma. The findings of this study suggest that the different histologic patterns of ameloblastoma did not show a direct correlation with their clinical behavior and consequently with the prognosis of the cases. The results also indicated that the ameloblastoma has greater proliferative potential than the AOT, which can contribute to explain its more aggressive and invasive characteristics.