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Oral lichen planus (OLP), is considered premalignant condition. This study tried to investigate the possibility of malignant transformation in OLP patients, by measuring the level of tumor suppressor protein p16INK4A, which is a product of the cyclin-dependent kinase inhibitor 2 (CDK2). CDK inhibitors may be responsible for maintenance of cell cycle. An imbalance in the cell cycle regulatory pathway involving p16/pRb may lead to unrestricted proliferation and tumorigenesis.40 patients with OLP underwent biopsy. Two control groups were included in this research, 13 healthy persons and 12 patients with oral squamous cell carcinoma (OSCC). All tissue samples were treated immunohistochemically using avidin-biotin peroxidase complex method.The number of patients with p16 positive cells was significantly higher in OLP (72.5%) in comparison to OSCC (33.33%). Although the prevalence of patients with p16 positive cells in OSCC was low, they expressed the highest percentage of p16 positive keratinocytes. Staining intensity of cytoplasm was also higher in p16 positive keratinocytes of OSCC in comparison to OLP.These results suggest that inactivation of p16 is an early detectable event in oral tumorigenesis. P16 expression could also be connected with tumor grading and may be useful marker in oral tumor progression.

Paper description: The toxicity of dental alloys in terms of continuous and prolonged exposure of cells in the oral cavity to certain materials is extensively documented. Our results showed that the cytotoxic effect of the Ag-Pd alloy against L929 cells was mediated by metal ion release in culture medium and provoked by recasting. Induction of senescence and cell death are basic mechanisms of alloy toxicity and are in correlation with casting number and endogenous ROS/RNS production. The data presented here underline the risk of Ag-Pd alloy reuse which compromises its biocompatibility, provoking complications observed in dental practice. Abstract: The biological quality and chemical composition of alloys used in dental practice changes during heat treatment. Often the residues of the previous cast are not disposed of but are reused and recycled until consumed. Thus, manufactured dental restorations have modified biological quality and chemical composition, and compromised biocompatibility. The aim of this study was to investigate the influence of repeated casting on the cytotoxicity of the silver-palladium (Ag-Pd) alloy. Our results showed that repeated casting of the Ag-Pd dental alloy affected its biocompatibility by promoting toxicity against transformed fibroblasts in a contact-independent manner. A strong decrease in cell proliferation, induction of senescence and massive cell death were observed in cultures exposed only to a medium previously incubated with dental alloy samples. The obtained data indicated that toxicity mediated by the accumulation of the Ag, Pd, Cu and Zn cations released from the Ag-Pd material was enhanced by recasting. The induction of cell senescence and subsequent apoptotic and necrotic death was accompanied by amplified intracellular production of reactive oxygen and nitrogen species, suggesting their involvement in the cell destruction process. Therefore, compromised biocompatibility after recasting with the Ag-Pd alloy can be the cause of serious local cell destruction, as observed in clinical practice. https://doi.org/10.2298/ABS190305017C Received: March 5, 2019; Revised: March 15, 2019; Accepted: March 21, 2019; Published online: March 25, 2019 How to cite this article: Cairovic AD, Stanimirovic DM, Krajnovic TT, Dojcinovic BP, Maksimovic VM, Cvijovic-Alagic ILj. Recasting as a booster of Ag-Pd alloy cytotoxicity: Induction of cell senescence prior to mass cell death. Arch Biol Sci. 2019;71(2):347-56.

Oral lichen planus (OLP) is an autoimmune skin and mucosal disorder. The range of malignant transformation in OLP varies between 0.1-3%. p53 is a tumor suppressor protein. Defective p53 could allow abnormal cells to proliferate, resulting in cancer. p53 plays an important role in cell cycle control and apoptosis and loss of p53 function has been demonstrated in about half of all human cancers. The purpose of the study was to investigate the malignant potential of OLP on the basis of p53 expression and to correlate p53 expression with clinical and histopathological features of OLP.40 patients with OLP underwent biopsy. All tissue samples were treated immunohistochemicaly using avidin-biotin peroxidase complex method.In 80% of OLP specimens the nuclei of basal and parabasal keratinocytes were p53-positive, but in low numbers. Low percentage of p53-positive cells in older and medium percentage of p53-positive cells in younger group of OLP patients were noted. Higher intensity of p53 stained keratinocytes, no matter their low number, could represent mutant and more stable form of p53 protein, and at the same time signal for monitoring of disease due to potential malignant transformation. Low percentage and weak intensity of p53-positive cells was detected mostly in OLP specimens with highly expressed civatte bodies (CB). Upregulation of apoptosis didn't correspond with the expression of CB.We believe that low percentage of p53-positive and well-marked keratinocytes in OLP represent the influence of mutant p53 protein, and that increasing expression of this protein could serve as a valuable diagnostic sign of early carcinogenesis. According to our results intensity of p53 coloration of keratinocytes could help assessing the malignant potential of OLP.