Candida albicans is a dimorphic yeast strongly gram positive able to live as normal commensal organism in the oral cavity of healthy people. It is the yeast more frequently isolated in the oral cavity. Under local and systemic factors related to the host conditions, it becomes virulent and responsible of oral diseases known as oral candidiasis. It has been shown that the presence of denture is a predisposing factor to the onset of pathologies related to C. albicans. Clinical studies have shown that C. albicans is not only able to adhere to the mucous surfaces, but also to stick to the acrylic resins of the dental prostheses. Both the plaque accumulated on the denture and the poor oral hygiene contribute to the virulence of Candida, offering the clinical picture of Candida-associated denture stomatitis. The therapeutic strategies currently adopted in the clinical practice to overcome these fungal infections provide for the use of topical and/or systemic antifungal and topical antiseptics and disinfectants, the irradiation with microwaves and the accurate mechanical removal of the bacterial plaque from the denture surfaces and from the underlying mucosa. A correct oral hygiene is important for the control of the bacterial biofilm present on the denture and on the oral mucosa and it is the fundamental base for the prophylaxis and the therapy of the Candidaassociated denture stomatitis.

. Cell death and the subsequent post-mortem changes, called necrosis, are integral parts of normal development and maturation cycle. Despite the importance of this process, the mechanisms underlying cell death are still poorly understood. In the recent literature, cell death is said to occur by two alternative, opposite modes: apoptosis, a programmed, managed form of cell death, and necrosis, an unordered and accidental form of cellular dying. The incorrect consequence is the overlapping of: a) the process whereby cells die, cell death; and b) the changes that the cells and tissues undergo after the cells die. Only the latter process can be referred to as necrosis and represents a 'no return' process in cell life. In this review, we discuss the excellent basic research developed in this field during last decades and problems that remain to be resolved in defining both experimentally and mechanicistically the events that lead to and characterize cell death. IntroductionCell death is part of normal development and maturation cycle, and is the component of many response patterns of living tissues to xenobiotic agents (i.e. micro organisms and chemicals) and to endogenous modulations, such as inflammation and disturbed blood supply (1,2). Cell death is an important variable in cancer development, cancer prevention and cancer therapy (3-5). In the treatment of cancer, the major approach is the removal, by surgery, of the neoplasm and/or the induction of cell death in neoplastic cells by radiation, toxic chemicals, antibodies and/or cells of the immune system (6-9). On the other hand, this pathobiological process remains poorly understood and the physiological and biochemical factors that lead to cell death are still not clear. One main factor is the existing confusion between 'apoptosis' process, as compared and contrasted with 'necrosis', leading to the overlapping of the ante mortem changes, i.e. the process of cell death, and the post-mortem changes, i.e. the necrosis process. The pathobiology of cell deathThe elegant scientific exploration of sub-cellular molecular anatomy of the last decades have reinforced the cell concept as 'the smallest integrating unit in biology: a pseudo-intelligent computer that receives, screens, changes, reacts to and adapts to a host of environmental signals, all of this activity apparently

Systemic capsaicin is therapeutically effective for the short-term treatment of BMS but major gastrointestinal side-effects may threaten its large-scale, long-term use. This preliminary study suggests that more, adequately powered, randomized controlled trials are necessary and worthy to come to a definitive assessment of this matter.

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Cyclooxygenase (COX), the key enzyme in prostaglandin cascade, is expressed in two isoforms: the constitutive COX-! and the inducible COX-2. Hyper-expression of COX-2 has been implicated in the pathogenesis of colon-rectal cancer in humans but it appears to play a significant role as a tumour progression factor also in other forms of human cancer, including oral cancer. The aim of this study was to analyze the expression of COX-2, at the protein level, in 45 cases of oral squamous cell carcinoma. Standard immunohistochemical streptavidin-biotin peroxidase analysis was carried out with a highly specific antibody against human COX-2 and cell specific markers, in 45 oral squamous cell carcinomas. Our study revealed a moderate to high COX-2 expression in 35 out of the 45 oral squamous cell carcinoma specimens (77.8 %). COX-2 expression appeared particularly abundant in the superficial ulcerated layers of relatively well differentiated carcinomas. However, we were unable to assess any statistically significant association between COX-2 hyper-expression and tumor site, tumor grading, tumor size, presence oflymph node metastases, tumor stage and age at onset, respectively. Interestingly, COX-2 expression was detected not only in areas of epithelial dysplasia adjacent to the primary layers (86 % of the cases) but also in normalappearing epithelium at the boundaries of squamous cell carcinomas (77% ), indicating a possible involvement in tumour progression by the apparently normal tissue surrounding the lesion. Moreover, intense COX-2 staining was observed in endothelial cells of intra-tumour vessels and extra-tumour vessels adjacent to the tumour nests, in a high proportion of cases (82 %). COX-2 positivity was associated with CD34 and VEGF positivity, indicating that these vessels were probably neo-formed. From this study, as well as from other works, it appears that COX-2 is over-expressed in this important human malignancy. However, further studies are necessary to understand the exact magnitude of this overexpression and, mostly, the possible role of COX-2 in the pathogenesis and progression of oral cancer.Several lines of evidence suggest that prostanoids may be involved in the pathobiology of human oral carcinogenesis (1-3). The enzyme cyclooxygenase (COX) catalyzes the first two steps of a cascade of biochemical reactions, leading to prostaglandin formation from arachidonic acid. COX is the rate-limiting enzyme in prostaglandin biosynthesis and is expressed in a constitutive (COX-I) and in an inducible (COX-2) isoform (4). Enhanced biosynthesis of prostaglandins, as a

Low E-Cadherin expression is a negative prognostic factor of OSCC and is likely due to the hypermethylation of CDH1 promoter. The delocalization of E-cadherin from membrane to cytoplasm could be also due to the increased expression of EGFR in OSCC and the consequent increase of E-cadherin co-internalization with EGFR.