Clarissa Araújo Silva Gurgel

Distribution of mast cells in benign odontogenic tumors.

The aim of this study was to investigate the presence of mast cells in a series of odontogenic tumors. Forty-five cases of odontogenic tumors were investigated using immunohistochemistry for mast cell triptase, and differences between groups were statistically evaluated. Mast cells were present in 96% of odontogenic tumors. Mast cells present in solid ameloblastoma were observed in the tumor stroma surrounding more solid and follicular epithelial islands, with or without squamous metaplasia. The odontogenic mixoma showed few mast cells. In odontogenic tumors with a cystic structure, the mast cells were distributed throughout all areas of the lesions, mainly in keratocystic odontogenic tumor. In addition, the total density of mast cells between all odontogenic tumors showed no significant difference (pu2009>u20090.05). A greater mast cells distribution was found in keratocystic odontogenic tumor in relation to adenomatoid odontogenic tumor (pu2009<u20090.01), and when the unicystic ameloblastoma and keratocistic odontogenic tumor were compared to the odontogenic myxoma (pu2009<u20090.05). Syndrome keratocystic odontogenic tumor showed a higher mean of mast cells when compared with the other tumors of the sample. Mast cells values presented by syndrome keratocystic odontogenic tumor were significantly greater than those of the sporadic keratocystic odontogenic tumor that were not associated with the syndrome (pu2009=u20090.03). Mast cells are probably one of the major components of the stromal scaffold in odontogenic tumors. We found significant differences of mast cells between syndrome nonsyndrome keratocystic odontogenic tumors, although their distribution did not seem to have any influence on the biologic behavior of benign odontogenic tumors.

Sclerosing Polycystic Adenosis of the minor salivary gland: case report

Gurgel, Clarissa Araujo Silva; Ramos, Eduardo Antonio Goncalves “Documento produzido em parceria ou por autor vinculado a Fiocruz, mas nao consta a informacao no documento”.

Transcriptional profiles of SHH pathway genes in keratocystic odontogenic tumor and ameloblastoma

BACKGROUNDnSonic hedgehog (SHH) pathway activation has been identified as a key factor in the development of many types of tumors, including odontogenic tumors. Our study examined the expression of genes in the SHH pathway to characterize their roles in the pathogenesis of keratocystic odontogenic tumors (KOT) and ameloblastomas (AB).nnnMETHODSnWe quantified the expression of SHH, SMO, PTCH1, SUFU, GLI1, CCND1, and BCL2 genes by qPCR in a total of 23 KOT, 11 AB, and three non-neoplastic oral mucosa (NNM). We also measured the expression of proteins related to this pathway (CCND1 and BCL2) by immunohistochemistry.nnnRESULTSnWe observed overexpression of SMO, PTCH1, GLI1, and CCND1 genes in both KOT (23/23) and AB (11/11). However, we did not detect expression of the SHH gene in 21/23 KOT and 10/11 AB tumors. Low levels of the SUFU gene were expressed in KOT (P = 0.0199) and AB (P = 0.0127) relative to the NNM. Recurrent KOT exhibited high levels of SMO (P = 0.035), PTCH1 (P = 0.048), CCND1 (P = 0.048), and BCL2 (P = 0.045) transcripts. Using immunolabeling of CCND1, we observed no statistical difference between primary and recurrent KOT (P = 0.8815), sporadic and NBCCS-KOT (P = 0.7688), and unicystic and solid AB (P = 0.7521).nnnCONCLUSIONSnOverexpression of upstream (PTCH1 and SMO) and downstream (GLI1, CCND1 and BCL2) genes in the SHH pathway leads to the constitutive activation of this pathway in KOT and AB and may suggest a mechanism for the development of these types of tumors.

Histopathological study of radicular cysts diagnosed in a Brazilian population

The aim of this study was to investigate the histopathological features of radicular cysts (RCs) diagnosed in a Brazilian population. Seventy-three cases of RCs, from a total of 1480 biopsies diagnosed between 2001 and 2008 at the Laboratory of Oral Surgical Pathology of the Dental School of the Federal University of Bahia were investigated regarding their histopathological features. Morphological results showed that exocytosis (n = 50), spongiosis (n = 40), acanthosis (n = 28), atrophic epithelium (n = 27) and apoptotic bodies (n = 21) were the most common findings. Other morphological findings included: foamy macrophages (n = 10), Russells bodies (n = 7), cholesterol crystals (n = 7) and glandular-like odontogenic epithelial rests (n = 1). Evidence of exogenous material was seen in 16 samples. It was concluded that the clinical and histopathological findings observed in Brazilian patients were comparable with those described for other populations.

Density of mast cells and microvessels in minor salivary gland tumors

The aim of this study was to investigate the density of mast cells and microvessels in minor salivary gland tumors. Forty-one cases of minor salivary gland tumors (pleomorphic adenoma, nu2009=u200910; adenoid cystic carcinoma, nu2009=u200911; mucoepidermoid carcinoma, nu2009=u200910; and polymorphous low-grade adenocarcinoma) were investigated using immunohistochemistry for mast cell tryptase and von-Willebrand factor. Density of mast cells was higher in mucoepidermoid carcinoma; however, no differences in the number of these cells were observed between the different types of tumors (pu2009>u20090.05). The number of mast cells was higher in periparenchymal areas in all tumors, but the difference was not significant (pu2009>u20090.05). Mucoepidermoid carcinoma showed the largest number of periparenchymal mast cells, whereas pleomorphic adenomas showed the smallest number of intraparenchymal mast cells (pu2009>u20090.05). The highest microvessel density was observed in mucoepidermoid carcinomas, being this difference statistically significant when mucoepidermoid carcinoma was compared to pleomorphic adenoma (pu2009=u20090.0034) and polymorphous low-grade adenocarcinoma (pu2009=u20090.004). Microvessel density was significantly higher in adenoid cystic carcinoma when compared to pleomorphic adenoma (pu2009=u20090.0406) and polymorphous low-grade adenocarcinoma (pu2009=u20090.0123). Comparison of mast cells and microvessel densities showed no significant difference between tumors. A quantitative difference in mast cells and microvessels was observed, particularly in mucoepidermoid carcinoma, a finding supporting the aggressive behavior of malignant salivary gland tumors without myoepithelial differentiation. Further studies are needed to determine the role of mast cells in angiogenesis, as well as in the development and biological behavior of these tumors.

CD1a-positive Langerhans cells and their relationship with E-cadherin in ameloblastomas and keratocystic odontogenic tumors

BACKGROUNDnAmeloblastomas and keratocystic odontogenic tumors (KOTs) are lesions that are characterized by locally invasive growth and cause extensive bone destruction. In addition, it is known that E-cadherin influences the adhesion of Langerhans cells (LCs) to keratinocytes.nnnOBJECTIVE AND METHODSnThe aim of this study was to investigate, using immunohistochemistry, the distribution of CD1a-positive cells in ameloblastomas and KOTs and their relationship with E-cadherin, in comparison to calcifying cystic odontogenic tumor (CCOT).nnnRESULTSnThe CD1a-positive LCs were observed in 11 ameloblastomas and KOTs. All of the cases of CCOT showed CD1a-positive LCs and a significant difference was found when this tumor was compared with ameloblastomas (P < 0.05, Mann-Whitney test). A statistically significant difference was also noted when comparing CD1a-positive LCs between CCOTs and KOTs (P < 0.05, Mann-Whitney test). Lower expression of E-cadherin in ameloblastomas (AMs) in relation to KOTs and CCOTs (P < 0.05, Fisher test) was observed. There was no correlation between E-cadherin and CD1a-positive LCs between all odontogenic tumors that were studied (P > 0.05, Spearman test).nnnCONCLUSIONnA quantitative difference of CD1a-positive cells between AMs and KOTs in comparison to CCOTs was observed. This permits to speculate that a depletion of CD1a-positive LCs might influence the local invasiveness of ameloblastomas and KOTs. Furthermore, it is suggested that E-cadherin mediates cell adhesion in these tumors.

Effects of imiquimod and low-intensity laser (λ660nm) in chemically induced oral carcinomas in hamster buccal pouch mucosa

Squamous cell carcinoma (SCC) is the most common neoplasm of the oral cavity. It is aggressive, highly proliferative, and metastatic. This study aimed to evaluate the effect of LLLT and imiquimod on DMBA chemically induced lesions on the oral mucosa of hamsters. SCCs were induced on 25 hamsters. Animals of G1 (control 1) were killed and the presence of tumors confirmed; G2 (control 2) suffered no interventions for additional 4xa0weeks; animals of G3 (laser treatment) were irradiated (λ660nm, 50xa0mW, CW, Øu2009=u20093xa0mm, 0.07xa0cm2, 714.2xa0mW/cm2, 133xa0s, 95xa0J/cm2, 6.65xa0J) at every other day for 4xa0weeks; animals of G4 (imiquimod treatment) received 5xa0% imiquimod three times a week for 4xa0weeks; and animals of G5 (imiquimod and laser treatment) received both treatments for the same period. Samples were taken and underwent histological analysis by light microscopy and were investigated using immunohistochemistry for S-100+ dendritic cells. In G1, G2, and G3, the evaluations showed malignant tumors and the absence of S-100+ dendritic cells in the tumor stroma. In G4, 60xa0% of the animals had no malignant tumors, and S-100+ dendritic cells were present in the stroma of the tumors as well as dysplasia. In G5, 40xa0% of the animals presented SCC, with scarce or no S-100+ dendritic cells. The imiquimod treatment played a direct effect on SCC, demonstrated by the increased number of S-100+ dendritic cells, which could suggest an important role of immune surveillance against neoplastic proliferation. Furthermore, its association with laser needs to be further investigated.

Elastin Accumulation in Actinic Cheilitis with Different Degrees of Epithelial Dysplasia

La matriz extracelular (MEC) juega un papel importante en la regulacion de los eventos biologicos, tales como, el desarrollo de la migracion celular, proliferacion y diferenciacion. La exposicion solar cronica provoca cambios presentes en la MRC de la queilitis actinica (QA), una lesion premaligna del labio inferior que contribuye a entender la carcinogenesis del labio. Este estudio tuvo como objetivo investigar la elastina, el componente principal de la elastosis solar en corriente alterna en un intento de establecer la relacion entre esta proteina y la MEC en displasia epitelial. Se incluyeron en parafina cortes de tejido de las lesiones de 35 casos de QC fueron analizadas mediante tecnicas de inmunohistoquimica para elastina, y se hizo la asociacion con los grados de displasia epitelial y la edad. La mas alta puntuacion de la elastina (+3) fue predominante en el 45,7% de los casos de QA, especialmente en los casos de displasia severa (n = 3). Al comparar las puntuaciones de elastina entre los diferentes grados de displasia epitelial, no mostro diferencia significativa (P> 0,05, Kruskall-Wallis). Este estudio no fue capaz de demostrar la influencia de la elastina sobre gravedad de la displasia epitelial en QA. Estudios adicionales sobre otras proteinas de la MEC deben llevarse a cabo en un intento por comprender mejor el mecanismo de progresion maligna de la QC.

E-cadherin regulators are differentially expressed in the epithelium and stroma of keratocystic odontogenic tumors

BACKGROUNDnThe epithelial-mesenchymal transition (EMT) is the process where cells lose their epithelial features and acquire properties of typical mesenchymal cells. The dissociation of tumor cells due to changes in cell-cell adhesion is one of the key principles of tumor invasion and EMT. Thus, the knowledge of the molecular features of EMT in keratocyst odontogenic tumor (KOT) can provide useful markers to aid in the diagnosis and prognosis and perhaps contribute to an alternative therapeutic approach as it shows an aggressive clinical behavior and high recurrence rates. This study aimed to evaluate the EMT in KOT by the immunoexpression of E-cadherin, N-cadherin, Snail, and Slug and comparing to radicular cysts and dental follicles.nnnMETHODSnThirty-two KOTs, 15 radicular cysts, and 08 dental follicles were used for immunohistochemistry, evaluating the extent, intensity, labeling pattern, cellular compartment in the epithelium and stroma, and the presence of inflammation.nnnRESULTSnE-cadherin was preserved in most cases of keratocystic odontogenic tumor. N-cadherin was increased in the tumor epithelium, a result that was positively correlated with the heterogeneous and nuclear immunoexpression of Slug in the epithelium; Slug also correlated with high Snail immunoexpression. N-cadherin was positively correlated with Slug in the stroma of keratocystic odontogenic tumors.nnnCONCLUSIONSnThe high immunoexpression of Snail and nuclear Slug in keratocystic odontogenic tumors suggests these proteins as transcription factors without necessarily participating in cadherin switching. However, the knowledge of their induction of the epithelial-mesenchymal transition in odontogenic tumors is still limited.

Insulin-like Growth Factor II Messenger RNA-binding Protein 3 in Salivary Gland Tumors

Insulin-like growth factor II mRNA-binding protein 3 (IMP3) is strongly expressed in malignant tumors and has been associated with their aggressive behavior. The aim of this study was to evaluate the presence of IMP3 in a series of salivary gland tumors. The sample consisted of 9 pleomorphic adenomas (PA), 14 adenoid cystic carcinomas (ACC), and 13 mucoepidermoid carcinomas (MEC) that were investigated by immunohistochemical technique. All cases of PA and MEC were positive for IMP3 particularly in the cytoplasm. PA showed 4 cases as high expression and 6 as low expression. MEC showed 10 cases as low expression and 3 as high expression. For ACC, 4 cases were high expression, whereas 6 cases were low expression. No significant difference was observed between tumors (P>0.05, Fisher’s test) when both scores of IMP3 were compared. This study showed that MEC seems to be more sensitive to IMP3 than ACC and provided an insight into this protein in salivary gland tumors. Furthermore, although IMP3 is not a specific diagnostic marker to distinguish the tumors studied, it seems to mediate cell adhesion and migration in these tumors. Further studies should be performed to better understand the IMP3 biology in salivary gland tumors.