Cristiano Macabú Badauy

Ehlers-Danlos Syndrome (EDS) type IV. Review of the literature

Ehlers-Danlos syndrome (EDS) is a heterogeneous group of connective tissue heritable disorders. EDS type IV is a rare form that presents typical clinical signs, such as easy bruising and haematomas at sites of trauma, skin manifestations (translucent skin with visible veins), and joint hyperlaxity. To illustrate the dermatological features and describe an aggressive periodontitis, a symptom not yet reported in this EDS type, we present a case of a 23-year-old young man. This patient has been suffering from bruised skin, haematomas, and varicose veins in his legs. These lesions, typical of EDS type IV, were associated with trauma followed by slow and difficult cicatrization. Teeth loss and clinical attachment loss in all the remaining teeth, a symptom compatible with a severe destruction of the periodontal support, was reported after orthodontic treatment. The treatment is limited to control the disease and teeth loss. Considering this new clinical symptom associated with EDS type IV, we suggest that the use of orthodontic apparatus should be carefully considered in such patients.

Exploring the mechanisms of alcohol-related damage in oral mucosa – is oxidative stress associated with the increase in cell proliferation in rat tongue epithelium?

Context: Alcohol consumption has been related to a cell proliferation increase in oral epithelium but its mechanism remains unclear. Objective: The aim of this study was to investigate whether oxidative stress parameters are implicated in the induction of cell proliferation in rat tongue epithelium after different times of chronic alcohol consumption. Materials and methods: Cell proliferation was assessed in tongue epithelium using AgNOR (argyrophilic proteins related to active nucleolar organizer regions) quantification. Oxidative stress parameters [lipid peroxidation, protein carbonyls, superoxide dismutase activity and catalase (CAT) activity and immunocontent] and Nrf2 immunocontent were quantified in tongue homogenates. Results and discussion: Mean AgNOR numbers (mAgNOR) per nucleus was 2.22 ± 0.30 in ventral tongue epithelium after 120 days of alcohol consumption (vs. 1.87 ± 0.18 for control animals and 1.91 ± 0.23 for animals treated with alcohol for 60 days) indicating cell proliferation increase (p < 0.05, ANOVA followed by Tukey post hoc). Interestingly, 60 days of alcohol consumption induced changes in oxidative stress parameters, but no alteration in cell proliferation. Vitamin E co-treatment was conduced in order to evaluate its possible protective effects. The 120 day Tween + vitamin E + alcohol treatment induced an increase in mAgNORs when compared to the Tween + vitamin E treated group (respectively 2.10 ± 0.30 vs. 1.77 ± 0.11, p < 0.05, ANOVA followed by Tukey post hoc), showing that vitamin E co-treatment had no protective effects. In addition, an inverse association was observed between CAT activity and AgNORs quantity (R = −0.32; p < 0.05, Person’s correlation) as well as the possible involvement of Nrf2 in alcohol-related damage. Conclusions: Our findings suggest that the increase in cell proliferation associated with alcohol-related damage has no direct relation with an imbalance in oxidative parameters. In contrast, our results indicate that hydrogen peroxide may be implicated in cellular signaling during proliferation in the oral mucosa.