Microscopic aspects of angiogenesis and lymphangiogenesis in oral squamous cell carcinoma.

Despite various great scientific and financial efforts, head and neck carcinomas represent a public health problem, being the eighth cause of cancer death worldwidely. The rate of tumor growth, its local expansion, as well as the metastasis of cancerous cells depend on the tumor vascularization, on the ability of blood vessels to provide a constant supply of nourishing substances and oxygen and to eliminate the residual products resulted from tumor growth. That is why angiogenesis and lymphogenesis are considered to be essential processes within the neoplastic process. The assessment of tumoral neoformed blood vessels in oral squamous carcinomas, using the CD34 antibody, showed a significant growth of the microvascular density, the average number being 504.66±177.65 vessels/mm². The diameter of angiogenesis vessels varied between 3.42 and 121.27 µm. The density of lymphogenesis vessels was 508.78±235.93 vessels/mm², while the diameter varied from 2.82 to 165.28 µm. Both angiogenesis and lymphogenesis vessels were more numerous in the areas where the inflammatory infiltrate was more abundant, which suggests that chronic inflammation plays the part of a promoter factor of neoplastic lesions.

Squamous cell carcinoma of the oral cavity: clinical and pathological aspects.

Oral cavity cancer is a public health problem as the sixth leading cause of cancer worldwide. Most tumor lesions are detected in stage III and IV, leading to a poor prognosis, five-year survival rate ranging between 10% and 40%. Oral cancer etiology is multifactorial, known still incomplete. The main etiopathogenic factors are exposure to cigarette smoke and alcohol consumption. We conducted a retrospective study of oral cavity tumors hospitalized in 2008-2012 in Oral and Maxillofacial Surgery Clinic of the Emergency County Hospital of Craiova, Romania. Of 143 tumors of the oral cavity, 125 were malignant, and of these, 115 (92%) were represented by squamous cell carcinoma. Tumor lesions were more common in males (69%), patients from rural areas (64%) and those over 50-year-old (87.71%).

Inflammatory reaction in chronic periodontopathies in patients with diabetes mellitus. Histological and immunohistochemical study.

Chronic periodontopathies and diabetes mellitus are two clinical entities, which reciprocally condition one another. The periodontal disease is considered a major complication, which induces an unfavorable evolution of diabetes mellitus. Diabetes mellitus is an endocrine disease which favors the occurrence of periodontopathy through gum's microvascular disorders, the selection and development of an aggressive bacterial plaque and through an exaggerate inflammatory response to the microflora within the oral cavity. Both diabetes mellitus and periodontal disease have an increasing incidence in the whole world. Development of periodontopathy is related to the aggression of bacterial flora in dental plaque, flora that is influenced on its turn by the evolution of diabetes mellitus. In our study, we have evaluated the inflammatory reaction in periodontium in patients with slowly and progressive periodontitis in patients with diabetes mellitus who had diabetes longer than five years. It has been found that all patients presented a chronic inflammatory infiltrate, abundant, with round mononuclear cells of lymphocyte, plasma cells and macrophage type, with non-homogenous arrangement, more intensely where the covering epithelium presented erosions or necrotic areas. Out of the immunity system cells, the most numerous where of T-lymphocytes type.

VEGFR1 and VEGFR2 immunohistochemical expression in oral squamous cell carcinoma: a morphometric study.

Vascular endothelial growth factor (VEGF) is considered one of the main molecules involved in tumor angiogenesis and is largely expressed in oral squamous cell carcinoma (OSCC). His signal is transmitted intracellulary by binding with class III tyrosine kinase receptors, known as VEGF receptor family (VEGFRs). Therefore, we designed this study for quantification of VEGFR1 and VEGFR2 immunohistochemical expression in the tumor cells of OSCC, and compare this expression with clinicopathologic parameters. For this purpose, 46 formalin-fixed, paraffin-embedded tissue blocks of OSCC were processed by immunohistochemistry. The immunohistochemical signal was assessed by estimating the area of the objects and the medium pixel intensity per object, as the integrated optical density (IOD). In our study, VEGFR1 staining intensity was significantly higher for tongue localization, while VEGFR2 was higher for the lip. Both markers were higher expressed in the center of the tumor compared to the tumor front. Moderate differentiated tumors exert higher expression levels for VEGFR1 but lower for VEGFR2. pT1 tumors had higher VEGFR1 levels, and when lymph node involvement was present, this was accompanied by elevated expression levels for VEGFR2 and lower levels for VEGFR1. These results point to an inverse profile of these receptors in OSCC, suggesting their involvement in a sequential manner in VEGF signaling regulation. In conclusion, our study revealed that VEGFR1 and VEGFR2 correlate with tumor localization, tumoral area (front vs. center of the tumor), histological differentiation degree, and lymph node involvement, while only VEGFR1 correlated with pT stage.