Potential role of Hedgehog signaling pathway and myofibroblastic differentiation in central giant cell granuloma-A preliminary study.

OBJECTIVE: This study investigated components of the Hedgehog (HH) signaling pathway (SHH, GLI1), cyclin D1, and smooth muscle actin (SMA) in central giant cell granulomas (CGCG). The relationship between these proteins and myofibroblasts was also studied. MATERIAL AND METHODS: Twelve cases of non-aggressive CGCG and 11 cases of aggressive CGCG were studied using immunohistochemistry for SHH, GLI1, Cyclin D1, and SMA. RESULTS: Associations between all proteins in non-aggressive and aggressive CGCG were not significant (P > .05). All cases of CGCG showed significantly higher expression of SMA compared with the other proteins (P < .01). A positive correlation (P = .04) was only observed between SHH and GLI1 for all cases of CGCG. Furthermore, a positive correlation between SHH and GLI1 in non-aggressive CGCG (P = .04) and between GLI1 and cyclin D1 in aggressive CGCG (P = .03) were observed. There was also a negative correlation between the expression of SHH and SMA in non-aggressive CGCG (P = .031). CONCLUSIONS: This study provided insights into the activation of the HH signaling pathway in CGCG. In addition, the activation of this pathway (SHH and GLI1) might play some role in the differentiation of stromal myofibroblasts, although these markers including Cyclin D1 and SMA do not indicate aggressiveness of the CGCG. Furthermore, this myofibroblastic differentiation process would occur at the expense of maturation of these lesions.

Glypican-3 distinguishes aggressive from non-aggressive odontogenic tumors: a preliminary study.

BACKGROUND: Glypican-3 is a cell surface proteoglycan that is found in embrionary tissues, and there are no studies investigating this protein in odontogenic tumor. Thus, the aim of this study was to investigate glypican-3 in a series of aggressive and non-aggressive odontogenic tumors. METHODS: Fifty-nine cases of tumors were divided into aggressive odontogenic tumors (20 solid ameloblastomas, four unicystic ameloblastoma, 28 KOTs including five associated with Gorlin-Goltz syndrome) and non-aggressive odontogenic tumors (five adenomatoid odontogenic tumors and two calcifying cystic odontogenic tumors) and analyzed for glypican-3 using immunohistochemistry. RESULTS: Glypican-3 was observed in seven solid ameloblastoma and eighteen keratocystic odontogenic tumors including three of the five syndromic cases, but there was no significant difference between syndromic and sporadic cases (P > 0.05; Fisher's exact Test). All cases of unicystic ameloblastoma (n = 4), adenomatoid odontogenic tumor (n = 5), and calcifying cystic odontogenic tumor (n = 2) were negative. CONCLUSIONS: This provided insights into the presence of glypican-3 in odontogenic tumors. This protein distinguished aggressive from non-aggressive odontogenic tumors.

Histochemical and immunohistochemical differences between solitary oral fibroma and fibrous papule of the face.

BACKGROUND:: The morphological similarities between fibrous papules of the face and multiple sporadic oral fibromas were mentioned long ago and a relationship between them has been reported in the literature. OBJECTIVE:: The aim of this study was to evaluate the participation of mast cells, elastin and collagen in a series of oral fibromas and fibrous papules of the face in order to better understand the possible role of these factors in fibrosis and the formation of these lesions. METHODS:: Thirty cases of oral fibroma involving the buccal mucosa and 30 cases of fibrous papules of the face were selected. Tissue samples were submitted to picrosirius red staining and immunohistochemistry using anti-elastin and anti-tryptase antibodies. RESULTS:: The percentage of tryptase-positive mast cells and expression of elastin were higher in cases of fibrous papules of the face (p < 0.05). In contrast, a higher intensity of collagen deposition was observed in oral fibromas. The results showed mast cell accumulation and higher elastin synthesis in fibrous papules of the face, and mast cell accumulation with higher collagen fiber synthesis in oral fibromas. CONCLUSION:: These findings support the hypothesis that mast cells influence the development and growth of these lesions through different mechanisms.

Histochemical and immunohistochemical differences between solitary oral fibroma and fibrous papule of the face

Abstract: Background: The morphological similarities between fibrous papules of the face and multiple sporadic oral fibromas were mentioned long ago and a relationship between them has been reported in the literature. Objective: The aim of this study was to evaluate the participation of mast cells, elastin and collagen in a series of oral fibromas and fibrous papules of the face in order to better understand the possible role of these factors in fibrosis and the formation of these lesions. Methods: Thirty cases of oral fibroma involving the buccal mucosa and 30 cases of fibrous papules of the face were selected. Tissue samples were submitted to picrosirius red staining and immunohistochemistry using anti-elastin and anti-tryptase antibodies. Results: The percentage of tryptase-positive mast cells and expression of elastin were higher in cases of fibrous papules of the face (p < 0.05). In contrast, a higher intensity of collagen deposition was observed in oral fibromas. The results showed mast cell accumulation and higher elastin synthesis in fibrous papules of the face, and mast cell accumulation with higher collagen fiber synthesis in oral fibromas. Conclusion: These findings support the hypothesis that mast cells influence the development and growth of these lesions through different mechanisms.

Involvement of mast cells and microvessels density in reactive lesions of oral cavity: A comparative immunohistochemical study.

In view of the similarity of clinicopathological features between reactive lesions of the oral cavity, the objective of the present study was to investigate the density of MCs (mast cells) and microvessels in a series of these lesions. Thirty-seven cases of reactive lesions including fibrous hyperplasia (FH, n=10), inflammatory fibrous hyperplasia (IFH, n=10), peripheral giant cell lesion (PGCL, n=10) and lobular capillary hemangioma (LCH, n=7) were investigated using immunohistochemistry for mast cell tryptase and CD34. For comparative purposes, central giant cell lesions (CGCL, n=5) were included. A higher MC density was observed in LCH (37.01), while CGCL exhibited the lowest density (n=8.14). There was a significant difference in MC density when all reactive lesions were compared to CGCL (p=0.001). The largest mean density of microvessels was observed in LCH (n=21.69). The smallest number was observed in CGCL (n=6.24). There was a significant difference in microvessel density when the reactive lesions were compared to CGCL (p=0.003). There was a significant and direct correlation between the density of MCs and microvessels only for IFH (p=0.048) and CGCL (p=0.005). A significant and direct correlation between the mean density of MCs and microvessels was observed when the reactive lesions were analyzed as a whole (p=0.005). Our results suggest that mast cells contribute to the connective tissue framework and angiogenic function, as well as the development, of reactive lesions of the oral cavity, including FH, IFH, LCH and PGCL.

Interaction of stromal and microvascular components in keratocystic odontogenic tumors.

OBJECTIVE: Little is known about the interaction of stromal components in odontogenic tumors. Thus, the aim of this study was to investigate mast cells (MCs), myofibroblasts, macrophages, and their possible association with angiogenesis and lymphangiogenesis in keratocystic odontogenic tumors (KCOTs). MATERIAL AND METHODS: Thirty cases of KCOTs were included and analyzed by immunohistochemistry for mast cell tryptase, α-SMA, CD34, CD163, and D240. For comparative purpose, 15 radicular cysts (CRs) and 7 pericoronal follicles (PFs) were included. RESULTS: There was an increase in MCs for RCs and this difference was significant when they were compared to KCOTS and PFs. A significant increase in the density of MFs was observed for KCOTs when compared to RCs and PFs (P = 0.00). No significant difference in CD163-positive macrophages (P = 0.084) and CD34-positive vessels (P = 0.244) densities was observed between KCOTs, RCs, and PFs, although KCOTs showed a higher density of all proteins. Significant difference in lymphatic vessel density was observed for KCOTs when compared to RCs and PFs (P = 0.00). Positive correlation was observed between mast cell tryptase and CD34 in KCOTs (P = 0.025). CONCLUSIONS: A significant interaction between the MC population and CD34-positive vessels in KCOTs supported the hypothesis that MCs and blood vessels contribute to the stromal scaffold of KCOT.

The sonic hedgehog signaling pathway contributes to the development of salivary gland neoplasms regardless of perineural infiltration.

The pleomorphic adenoma (PA), mucoepidermoid carcinoma (MEC), and adenoid cystic carcinoma (ACC) are common tumors arising from salivary glands whose histopathology is heterogeneous. The sonic hedgehog signaling pathway (Hh) and signal transducer and activator of transcription 3 (STAT3) play important roles in cell proliferation, favoring tumor growth. The aim of this investigation was to study components of the Hh pathway, as well as STAT3 in salivary gland neoplasms in an attempt to add information about the biological characteristics of these neoplasms. We used 9 cases of PA, 17 cases of ACC, and 20 cases of MEC. Using immunohistochemistry, SHH, GLI1, SUFU, HHIP, and STAT3 were investigated. For comparative purposes, MCM3 (cellular proliferation marker) was also included. In PA, there was high expression of cytoplasmic SHH and SUFU and low expression of STAT3 and MCM3. In the ACC, there was high expression of GLI1, HHIP, and STAT3 and low expression of SHH, SUFU, and MCM3. In the MEC, we observed high expression of SHH, GLI1, SUFU, and HHIP and low expression of STAT3 and MCM3. There was a statistically significant difference between SHH (p = 0.0064), STAT3 (p = 0.0003), and MCM3 (p = 0.0257) when all tumors were compared and a higher expression in parenchyma for all tumors when stroma and parenchyma were compared (p < 0.05). These findings suggests a possible role of Hh pathway in the development and maintenance of the cytoarchitectural pattern of PA, ACC, and MEC, as well as the participation of STAT3 in the development of ACC, irrespective perineural infiltration.

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

BACKGROUND: The 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. METHODS: Thirty-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. RESULTS: E-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. CONCLUSIONS: The 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.

Epithelioid hemangioma in the oral mucosa ­ A case report.

Introduction: Epithelioid hemangioma is an uncommon benign vasoproliferative neoplasm that usually manifests as multiple red nodules in middle-aged adults Case Outline: 52-year-old male patient presented with a one-year history of a nodular lesion in the left buccal mucosa measuring 3 cm. The clinical hypothesis was lipoma. An excisional biopsy revealed a circumscribed lesion composed of lobules of vessels with perceptible or poor lumina, associated with a prominent inflammatory infiltrate consisting of eosinophils, histiocytes and chronic inflammatory cells. The endothelial cells composing the lesion had an epithelioid morphology and contained abundant eosinophilic cytoplasm. Immunohistochemistry for CD34, factor VIII, collagen IV, alpha-smooth muscle actin, and mast cells, as well as histochemical staining with Weigert's orcein were performed. Conclusion: Vascular proliferations of soft tissues are a diverse and morphologically complex group of lesions that are difficult to diagnose. This report presents a case of oral epithelioid hemangioma, highlighting relevant morphological and immunohistochemical features that could help distinguish this condition from other neoplasms.

Oral lichen sclerosus expressing extracellular matrix proteins and IgG4-positive plasma cells.

Lichen sclerosus (LS) is a mucocutaneous disease with uncommon oral involvement. The etiology is not yet well understood, but LS has been associated with autoimmune, genetic, and immunological factors. We report a 47-year-old man with LS that exhibited an asymptomatic white plaque with red patches on the maxillary alveolar mucosa extending to the labial mucosa. He had no other skin disease. Positive immunostaining for tenascin and scarcity of fibronectin suggested extracellular matrix reorganization. Elastin immunostaining indicated a reduction of elastic fibers. Immunoexpression of collagen IV in blood vessels and its absence in the epithelial basement membrane, together with diffuse MMP-9 immunoexpression, suggested altered proteolytic activity. Mast cell staining bordering areas of sclerosis indicated a possible role in the synthesis of collagen. IgG4 positivity in plasma cells suggested a role in the fibrogenesis. This is an unusual presentation of oral LS and we discuss immunohistochemical findings regarding cellular and extracellular matrix components.

Infrared LED light therapy influences the expression of fibronectin and tenascin in skin wounds of malnourished rats--a preliminary study.

The aim of this investigation was to evaluate the effect of infrared (λ 846±20nm) LED irradiation on the expression profile of the extracellular matrix protein components, tenascin and fibronectin on skin wounds induced in well nourished and malnourished rats. Eighteen albino rats (21 days old) were randomly divided into a well-nourished group (standard diet) and a malnourished group (regional basic diet). After receiving the diet for 70 days, skin wounds were created and the animals were subdivided into three groups: well-nourished control (n=6), malnourished control (n=6), and malnourished+LED irradiated (λ 846±20nm, 100mW, 4J/cm(2)) (n=6). The animals were sacrificed 3 and 7 days after injury and histological sections were immunostained for both proteins. They were examined for the presence, intensity, distribution and pattern of immunolabeling. At 3 days, the distribution of tenascin was shown to be greater in the wound bed of malnourished animals compared to the well-nourished group. The intensity and distribution of tenascin was shown to be lower in the malnourished LED irradiated group compared to the malnourished control. There was a significant difference regarding the presence of fibronectin in the malnourished and well-nourished groups after 7 days (p=0.03). The intensity of fibronectin was slight (100%) in the irradiated group and moderate to intense in the malnourished control group. The results of the present study indicate that infrared LED irradiation modulates positively the expression of tenascin and particularly fibronectin.

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

BACKGROUND: Sonic 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). METHODS: We 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. RESULTS: We 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). CONCLUSIONS: Overexpression 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.

Immunohistochemistry assessment of Langerhans cells and microvascular density in oral squamous cell carcinomas / Avaliação imuno-histoquímica de células de Langerhans e densidade microvascular em carcinoma oral de células escamosas

The aim of this study was to assess and correlate microvascular density (MVD) and the quantity of Langerhans cells (LC) present in oral squamous cell carcinoma (OSCC), well as the correlation between this microvascular density and number of Langerhans cells (LCs) with the intensity of the infiltrate, the histologic grading and staging, according to the TNM system. Twenty-three paraffin-embedded blocks of SCC lesions were analyzed using the immunohistochemical technique in which the two anti-CD1a and anti-CD207 markers were used to quantify the Langerhans cells and the CD34 marker to assess MVD. Immunostaining for CD1a, CD207 and CD34 was observed in 100% of the cases analyzed, showing a statistically significant association (p = 0.0001, Fisher’s test). No statistical correlation between MVD and LC or between immunostainings and histological grading of malignancy were found. However, immunostaining for CD1a and CD207 showed a statistically significant correlation (p value = 0.001, Spearman test) and a positive correlation was found between MVD and lymph node involvement. The LCs and MVD seem to involved in immunopathogenesis of oral carcinoma, although no statistically significant correlation was found between these two findings

O objetivo deste estudo foi avaliar e correlacionar a densidade microvascular (MVD) e a quantidade de células de Langerhans (LC) presente no carcinoma epidermoide de boca (CEB), bem como a correlação entre esta densidade microvascular e número das células de Langerhans (CL), com a intensidade do infiltrado, a classificação histológica e de teste, de acordo com o sistema TNM. Vinte e três blocos de parafina-encaixados de lesães SCC foram analisados utilizando a técnica de imuno-histoquímica em que os dois marcadores anti-CD1a e anti-CD207 foram usados para quantificar as células de Langerhans e o marcador CD34 para avaliar MVD. A imunocoloração para CD1a, CD207 e CD34 foi observada em 100% dos casos analisados, demonstrando uma associação estatisticamente significativa (p = 0,0001, teste de Fisher). Não houve correlação estatística entre MVD e LC ou entre imunomarcações e gradação histológica de malignidade foram encontrados. No entanto, a imunocoloração para CD1a e CD207 mostraram uma correlação estatisticamente significativa (p = 0,001, teste de Spearman) e foi encontrada uma correlação positiva entre MVD e comprometimento de linfonodos. O LCs e MVD parecem envolvidos em imunopatogênese de carcinoma oral, embora não foi encontrada correlação estatisticamente significativa entre estes dois resultados.

Oral mucoceles: a clinical, histopathological and immunohistochemical study.

The aim of study was to evaluate the clinicopathological features of oral mucoceles and the immunohistochemical expression of cellular and extracellular matrix components in these lesions. One hundred cases of oral mucoceles were examined for clinicopathological features. The expression of mast cell tryptase, CD68, MMP-1 (matrix metalloproteinase-1), MMP-9 (matrix metalloproteinase-9) and CD34 was investigated immunohistochemically in 32 cases. The lesions arose as nodules or blisters of variable color. The mean age was 23.2 years and a higher male frequency was observed. The most common locations were the lower lip (92%), followed by the floor of the mouth (7%), and palate (1%). The lesion size ranged from 0.4 to 3.0cm. Unusual histopathological findings as superficial mucoceles (n=16, 16%), pseudopapillary projections (n=3, 3%), epithelioid histiocytes (n=4, 4%), multinucleated giant cells (n=1, 1%) and myxoglobulosis (n=9, 9%) were also seen. Mast cells and CD68-positive macrophages, MMP-1, MMP-9 and CD34-positive blood vessels were seen in all cases. A significant association was seen between mast cells and MMP-1 (p=0.03) and between macrophages and MMP-1 (p=0.01). This study provided important insight into the demographic and histopathological occurrence of oral mucoceles. The tissue remodeling seen in these lesions mainly involved the migration and interaction of mast cells, macrophages and MMP-1.

Tumor-infiltrating macrophage and microvessel density in oral squamous cell carcinoma.

Tumor-associated macrophages (TAM) are the main cellular component in stroma of many tumors and participate in tumor angiogenesis. The aim of present study was to compare the microvascular density (MVD) and infiltrating macrophage density (IMD) in oral squamous cell carcinomas (OSCCs) with different histological grades. A histomorphometric analysis was performed after immunohistochemistry using antibodies such as von-Willebrand factor and CD68. A significant difference in MVD was found between well and moderately differentiated OSCCs (p<0.05). TAM were largely present in all studied tumors and the IMD was not different among OSCCs with different histological grades (p=0.381). Significant correlation between MVD and IMD was not observed (p=0.870). In conclusion, these results suggest that TAM and angiogenesis have an influence at different histological grades of OSCC. However, the lack of correlation between MVD and IMD could suggest that angiogenesis does not depend on the number of macrophages present in OSCC, but their predominant phenotype. Further studies involving distinct phenotypes of macrophages should be done to better understand the influence of TAM on the tumor angiogenesis.

Tumor-Infiltrating Macrophage and Microvessel Density in Oral Squamous Cell Carcinoma

Tumor-associated macrophages (TAM) are the main cellular component in stroma of many tumors and participate in tumor angiogenesis. The aim of present study was to compare the microvascular density (MVD) and infiltrating macrophage density (IMD) in oral squamous cell carcinomas (OSCCs) with different histological grades. A histomorphometric analysis was performed after immunohistochemistry using antibodies such as von-Willebrand factor and CD68. A significant difference in MVD was found between well and moderately differentiated OSCCs (p<0.05). TAM were largely present in all studied tumors and the IMD was not different among OSCCs with different histological grades (p=0.381). Significant correlation between MVD and IMD was not observed (p=0.870). In conclusion, these results suggest that TAM and angiogenesis have an influence at different histological grades of OSCC. However, the lack of correlation between MVD and IMD could suggest that angiogenesis does not depend on the number of macrophages present in OSCC, but their predominant phenotype. Further studies involving distinct phenotypes of macrophages should be done to better understand the influence of TAM on the tumor angiogenesis.

Macrófagos associados a tumores (MAT) representam o componente principal do estroma de muitos tumores, além de participar da angiogênese tumoral. Este estudo comparou a microdensidade vascular (MDV) e densidade de macrófagos infiltrando o tumor (DMIT) em carcinoma escamocelular da boca (CEC) com diferentes graus histológicos de malignidade. Análise histomorfométrica foi empregada após técnica imuno-histoquímica para os anticorpos fator von-Willebrand e CD68. Uma diferença significante entre MDV e carcinomas bem e moderadamente diferenciados foi observada (p<0,05). MAT estavam fortemente presentes em todos os tumores estudados e a DMIT não foi diferente entre os diferentes graus histológicos de malignidade do CEC (p=0,381). Correlação significante entre MDV e DMIT não foi observada (p=0,870). Em conclusão, os resultados desse estudo sugerem a influência de MAT e angiogênese nos diferentes graus histológicos de malignidade do CEC. Entretanto, a ausência de correlação entre MDV e DMIT sugere que a angiogênese não depende do número de macrófagos presentes neste tipo de câncer, mas do fenótipo predominante. Outros estudos devem ser realizados a fim de contribuir para melhor compreensão da participação de MAT na angiogênese tumoral.

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

BACKGROUND: Ameloblastomas 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. OBJECTIVE AND METHODS: The 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). RESULTS: The 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). CONCLUSION: A 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 (λ660 nm) 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 4 weeks; animals of G3 (laser treatment) were irradiated (λ660 nm, 50 mW, CW, Ø=3 mm, 0.07 cm(2), 714.2 mW/cm(2), 133 s, 95 J/cm(2), 6.65 J) at every other day for 4 weeks; animals of G4 (imiquimod treatment) received 5 % imiquimod three times a week for 4 weeks; 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, 60 % 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, 40 % 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.