Purpose: Periodontitis is an infectious disease caused predominantly by gram-negative anerobes. The host inflammatory response to these bacteria causes alveolar bone loss that is characterized as periodontitis. Omega-3 fatty acids (ω-3 FAs) have anti-inflammatory properties, thus have been used to treat some chronic inflammatory diseases such as cardiovascular disease and rheumatoid arthritis. We aimed to evaluate the effect of dietary supplementation with ω-3 FAs as a host modulating agent in patients with chronic periodontitis. Methods: Sixty otherwise healthy subjects with moderate and severe chronic periodontitis were enrolled in our randomised, double-blind, placebo-controlled trial. The control group (CG, n = 30) was treated with scaling and root planing (SRP) and given a placebo; the treatment group (TG, n = 30) was treated with SRP and dietary supplementation of ω-3 FAs (one 300 mg tablet daily for 12 weeks). Periodontal clinical parameters and serum C-reactive protein (CRP) levels were evaluated in all patients at baseline, a 6-week and 12-week period after treatment. Results: A significant reduction in the gingival index, sulcus bleeding index, pocket depth, and clinical attachment level was found in the TG compared to the CG at a 12-week period. However, no statistically significant changes in serum CRP levels were found. Conclusions: Our findings suggest that ω-3 FAs can successfully reduce gingival inflammation, pocket depth, and attachment level gain. Dietary supplementation with ω-3 FAs may have potential benefits as a host modulatory agent in the prevention and/or adjunctive management of chronic periodontitis.

European Journal of Breast Health (Eur J Breast Health) is an international, scientific, open access periodical published by independent, unbiased, and double-blinded peer-review principles. It is the official publication of the Turkish Federation of Breast Diseases Societies, and Senologic International Society is the official supporter of the journal.

Expression of Bcl-2 family proteins in tumours can modulate apoptosis, influencing tumour behaviour and treatment. To investigate their role in oral tumourigenesis, nine Bcl-2 family transcripts were examined in three oral cell lines and 25 oral tumours, using ribonuclease protection assay. Since Mcl-1 mRNA was elevated in these samples, Mcl-1 splice variants were assessed by RT-PCR and Mcl-1 protein was studied in normal, premalignant and malignant oral tissues and cell lines, by immunohistochemistry and/or immunoblotting. The cell lines exhibited significantly higher levels of 7/9 Bcl-2 family transcripts as compared to those in normal tongue, and significantly higher (p=0.030, p=0.004) anti-apoptotic versus pro-apoptotic transcripts. Elevated Mcl-1 mRNA was observed in 11/25 (44%) tumours as compared to normal tissues with a five- to ten-fold higher expression of full-length anti-apoptotic Mcl-1 transcript versus the pro-apoptotic short isoform. Strong cytoplasmic Mcl-1 immunoreactivity was detected predominantly in differentiated epithelia in 27/33 (82%) oral tumours, 18/20 (90%) leukoplakia, 25/30 (83%) submucous fibrosis and 3/3 oral cell lines, with weak staining in 8/15 (53%) normal mucosa samples. Mcl-1 positivity in malignant and premalignant tissues was comparable but significantly higher (p<0.01) than that in normal mucosa. The expression of bcl-2 family genes, including Mcl-1 in tumours, did not correlate significantly with clinicopathological parameters. This is the first report delineating the in vivo expression patterns of Mcl-1 protein and Mcl-1 transcripts in oral cancers and premalignant lesions. The observed imbalance between expression of anti-apoptotic and pro-apoptotic Bcl-2 family genes may promote survival in the oral cell lines. Since the majority of oral tumours associated with tobacco-chewing evolve from premalignant lesions, the sustained expression of full-length anti-apoptotic Mcl-1 protein in these tissues suggests an important role for Mcl-1, early in oral cancer pathogenesis in protecting cells from apoptosis via neutralization of pro-apoptotic members and could be a potential therapeutic target for oral cancers.

The results suggest that the p53 protein expression does not necessarily imply an association with malignant disease and/or p53 gene mutation, but a tendency to be expressed in an increasing quantitative and qualitative manner, as the biologic behavior of odontogenic cyst or tumors becomes more aggressive. p53 over-expression may promote cell proliferation in odontogenic lesions. Thus, it can be stipulated that Ki-67 and p53 protein expression can be used as a prognostic marker in odontogenic lesions.

The results revealed no significant difference with respect to the lipid profile levels between the four groups. Interpreting the results of the study, periodontal disease did not cause an increase in total CHL, LDL or triglyceride levels or a decrease in the HDL levels in an otherwise systemically healthy individual or in a CHD patient. Periodontitis in a CHD patient did not seem to exacerbate the destruction of periodontal tissue. Higher triglyceride levels did not have any correlation with the severity of attachment loss in a periodontitis subject.