Is obesity a possible modifier of periodontal disease as a chronic inflammatory process? A case-control study.

BACKGROUND AND OBJECTIVE: This cross-sectional case-control study was conducted to provide a comparative evaluation of clinical periodontal measurements, together with serum levels of certain bioactive peptides and inflammatory cytokines, in relation to obesity. For this purpose, clinical periodontal measurements and the levels of serum leptin, adiponectin, interleukin-6 (IL-6), C-reactive protein and soluble intercellular adhesion molecule-1 of obese female individuals and their nonobese counterparts were compared. MATERIAL AND METHODS: Sixty obese (body mass index (BMI) > 30) and 31 nonobese (BMI < 30) female subjects were recruited for the present study. Before any periodontal intervention, serum samples were obtained and full-mouth clinical periodontal measurements were recorded at six sites per tooth. ELISA was used for the biochemical analysis. Data were tested statistically. RESULTS: Clinical attachment level was significantly higher in the obese group compared with the nonobese control group (p < 0.05). Serum levels of leptin and IL-6 were significantly higher in the obese group (p < 0.05). BMI correlated with the serum levels of inflammatory molecules (p < 0.05), but not with clinical periodontal parameters, in the obese group. CONCLUSION: In conclusion, obesity does not seem to have a prominent effect on clinical periodontal parameters but it does have many correlations with circulating inflammatory molecules. As suggested in the literature, increased levels of leptin and IL-6 in the obese group might be one explanation for a possible relationship between obesity and periodontal disease. A prospective study is warranted to clarify, in greater detail, the effects of obesity on periodontal health.

Fatty acid profiles in smokers with chronic periodontitis.

We hypothesized that tobacco smoke induces alterations to the 3-OH fatty acids present in lipid A in a manner consistent with a microflora of reduced inflammatory potential. Whole saliva samples and full-mouth clinical periodontal recordings were obtained from persons with (22 smokers; 15 non-smokers) and without (14 smokers; 15 non-smokers) chronic periodontitis. Clear differences in the contributions of multiple saturated 3-OH fatty acid species were noted in the group with disease compared with healthy individuals. Increases in the long-chain fatty acids associated with anaerobic bacterial periodontopathogens, particularly 3-OH-C(i17.0) (146.7%, relative to controls), were apparent. Significant reductions in the 3-OH fatty acids associated with the consensus (high potency) enteric LPS structure (3-OH-C(12.0) and 3-OH-C(14.0); 33.3% and 15.8% reduction, respectively) were noted in smokers compared with non-smokers with chronic periodontitis. Thus, smoking is associated with specific structural alterations to the lipid-A-derived 3-OH fatty acid profile in saliva that are consistent with an oral microflora of reduced inflammatory potential. These findings provide much-needed mechanistic insight into the established clinical conundrum of increased infection with periodontal pathogens but reduced clinical inflammation in smokers.

Crevicular fluid matrix metalloproteinase-8, -13, and TIMP-1 levels in type 2 diabetics.

OBJECTIVES: To evaluate whether type 2 diabetes mellitus (DM) enlarged and if so the quantum of such increase in the gingival crevicular fluid (GCF) levels of matrix metalloproteinase-8 (MMP-8), MMP-13 and tissue inhibitor of metalloproteinases-1 (TIMP-1). METHODS: Subjects (n = 73) were divided into five groups as follows: 12 DM patients with gingivitis (DM-G), 12 DM patients with periodontitis (DM-P), 12 systemically healthy patients with gingivitis (H-G), 13 systemically healthy patients with periodontitis (H-P) and 24 periodontally, systemically healthy volunteer subjects (H-C). Full-mouth clinical periodontal measurements were performed at six sites per tooth. Gingival crevicular fluid samples were obtained from two sites representing the clinical periodontal diagnosis in single-rooted teeth. Gingival crevicular fluid levels of MMP-8, MMP-13 and TIMP-1 were analysed by immunofluorometric MMP assay (IFMA), enzyme-linked immunosorbent assay (ELISA). Data were tested statistically by parametric tests. RESULTS: All clinical periodontal measurements were similar in both diabetic and systemically healthy patients with periodontal disease (all P > 0.05). Total amounts of MMP-8 in GCF samples were significantly lower in H-C group than DM-G, DM-P, H-P groups (all P < 0.05). Matrix metalloproteinase-13, TIMP-1 total amounts were similar in study groups (P > 0.05). Diabetes mellitus patients exhibited similar levels of MMP-8, MMP-13, TIMP-1 with systemically healthy gingivitis/periodontitis patients (P > 0.05). CONCLUSIONS: Within the limits of this study, DM does not seem to significantly affect GCF levels of MMP-8, MMP-13, TIMP-1 or clinical periodontal status.