Aim: Discussing a protocol involving xylene-ethanol deparaffinization on slides followed by a kit-based extraction that allows for the extraction of high quality DNA from FFPE tissues.

The aim of the present study was to assess the prevalence of Herpes Simplex virus, Epstein Barr virus and Human Papilloma virus -16 in oral lichen planus cases and to evaluate whether any clinical variant, histopathological or demographic feature correlates with these viruses. The study was conducted on 65 cases. Viruses were detected immunohistochemically. We evaluated the histopathological and demographic features and statistically analysed correlation of these features with Herpes Simplex virus, Epstein Barr virus and Human Papilloma virus-16 positivity. Herpes Simplex virus was positive in six (9%) cases and this was not statistically significant. The number of Epstein Barr virus positive cases was 23 (35%) and it was statistically significant. Human Papilloma virus positivity in 14 cases (21%) was statistically significant. Except basal cell degeneration in Herpes Simplex virus positive cases, we did not observe any significant correlation between virus positivity and demographic or histopathological features. However an increased risk of Epstein Barr virus and Human Papilloma virus infection was noted in oral lichen planus cases. Taking into account the oncogenic potential of both viruses, oral lichen planus cases should be detected for the presence of these viruses.

It is frequently assumed that pre-invasive lesions are simpler precursors of cancer and will contain a limited subset of the genomic changes seen in their associated invasive disease. Driver mutations are thought to occur early, but it is not known how many of these are present in pre-invasive lesions. These assumptions need to be tested with the increasing focus on both personalised cancer treatments and early detection methodologies. We examined genomic copy number changes in 256 pre-invasive and invasive samples from 69 oral cancer patients. Forty-eight samples from 16 patients were further examined using exome sequencing. Evidence of a shared ancestor of both dysplasia and carcinoma was seen in all but one patient. One-third of dysplasias showed independent copy number events. The remainder had a copy number pattern that was similar to or simpler than that of the carcinoma. All dysplasias examined contained somatic mutations absent in the related carcinoma. Previously observed copy number changes and TP53 mutations were very frequently observed, and almost always shared between dysplasia and carcinoma. Other gene changes were more sporadic. Pathway analysis confirmed that each patient’s disease developed in a different way. Examining the numbers of shared mutations and the rate of accumulation of mutations showed evidence that all samples contain a population of sub-clones, with little evidence of selective advantage of a subset of these. These findings suggest that most of the genomic changes driving oral cancer occur in the pre-cancerous state by way of gradual random accumulation rather than a dramatic single event.

In jawbones, ameloblastomas and odontogenic keratocysts share many clinical features in common such as aggressiveness, high recurrence rates and radical management options. Understanding the pathogenesis and biological aspects of these tumors would improve the success of diagnose and treatment procedures. The aim of this study was to exhibit the reasons of high recurrence rates and growth potentials of ameloblastomas and keratocystic odontogenic tumours by investigating the expression of IL-1α and IL-6 and IL-1α -889 gene polymorphism. IL-1α and IL-6 are shown as very effective tissue degrading factors in bone remodelling. This study included 25 cases of ameloblastomas, 41 cases of keratocystic odontogenic tumors (parakeratinized odontogenic keratocysts) and 8 cases of orthokeratinized odontogenic keratocysts. All histological slides were stained immunohistochemically to show the expression of IL-1α and IL-6. Restriction fragment length analysis was used to investigate the cytokine gene polymorphism. The higher expression rates of IL-1α and IL-6 were associated with tumor size in ameloblastomas and with cyst wall thickness in keratocystic odontogenic tumors. This finding suggested us that the cytokines IL-1α and IL-6 play a role on aggressive behaviour of ameloblastomas and keratocystic odontogenic tumors by making easy bone resorption. In addition, IL-1α (-889) T polymorphism was found consistent with increased IL-1α expression but not seem as a risk factor on the development of these tumors.

Background: Bisphosphonates (BPs) and low‐dose doxycycline (LDD) have been shown to inhibit bone resorption and to improve the levels of proinflammatory mediators and destructive enzymes in gingival tissues, respectively. The purpose of this study is to evaluate the effect of mono and combined BP clodronate and LDD therapies in reducing gingival levels of matrix metalloproteinase‐9 (MMP‐9), interleukin‐1β (IL‐1β), and alveolar bone loss in rats with diabetes.Methods: Fifty adult Wistar rats were divided into five study groups as follows: 1) group 1 = diabetes control; 2) group 2 = diabetes + periodontitis; 3) group 3 = diabetes + periodontitis + LDD; 4) group 4 = diabetes + periodontitis + clodronate; and 5) group 5 = diabetes + periodontitis + LDD + clodronate. LDD and clodronate were given as a single agent or as combination therapy during the 7 days of the post‐experimental periodontitis period. On day 7, the rats were sacrificed, the mobility of the tooth was recorded, and block biopsies were removed. The gingival tissues were analyzed histologically and immunohistochemically for expression of MMP‐9 and IL‐1β. Alveolar bone loss was evaluated morphometrically under a light microscope. Data analysis was performed statistically by Kruskal‐Wallis and post hoc Tukey and Spearman correlation tests.Results: Alveolar bone loss was significantly greater in groups 2 through 5 than group 1 (P 0.05). Animals with periodontitis (group 2) expressed significantly higher levels of MMP‐9 and IL‐1β compared with those without periodontitis (group 1) (P <0.05). MMP‐9 expression was significantly lower in group 3 than groups 1, 2, and 5 (P <0.05). IL‐1β expression was significantly lower in the groups 1, 3, 4, and 5 than 2 (P <0.01) but was not significantly different among groups 1, 3, 4, and 5. Positive correlations were found between alveolar bone loss and density of inflammation (ρ = 0.319, P = 0.021) and between MMP‐9 and IL‐1β (ρ = 0.418, P = 0.002), respectively.Conclusion: Our findings suggest that ligature‐induced periodontitis in animals with diabetes results in significantly higher levels of MMP‐9 and IL‐1β expression in gingiva. The use of mono and combined clodronate and LDD administrations may significantly reduce levels of MMP‐9 and IL‐1β expression. However, drug administration did not affect alveolar bone levels during the study period.