Gingival crevicular fluid IL-6, tPA, PAI-2, albumin levels following initial periodontal treatment in chronic periodontitis patients with or without type 2 diabetes

To evaluate initial periodontal treatment effects on gingival crevicular fluid (GCF) interleukin-6 (IL-6), tissue-type plasminogen activator (tPA), plasminogen activator inhibitor-2 (PAI-2), albumin levels in type 2 diabetic patients. GCF samples were collected from 20 type 2 diabetic, 22 non-diabetic non-smokers all with chronic periodontitis at baseline, 1-, 3-months following initial periodontal treatment. Biochemical analysis was performed by ELISA. Data were tested by Mann-Whitney U, Wilcoxon tests. The total amounts of albumin, IL-6, tPA, PAI-2 decreased significantly in diabetics after treatment (1- and 3-months) whereas, only PAI-2 decreased in non-diabetic group at 3-months (p < 0.05). There were statistically significant differences between the diabetics and non-diabetics at all time points for albumin, PAI-2 and at 1-, 3-months for GCF volume (p < 0.050) but only at baseline for IL-6 (p < 0.050). Present data suggest clinical improvements are less apparent in diabetic chronic periodontitis patients as reflected by disease markers in GCF and by an increase in concentrations of inflammatory proteins IL-6, tPA, and PAI-2 in GCF of this patient group following initial periodontal treatment

Gingival Crevicular Fluid MMP-8 and-13 and TIMP-1 Levels in Patients With Rheumatoid Arthritis and Inflammatory Periodontal Disease

WOS: 000269024700015PubMed ID: 19656031Background: The purpose of this study was to compare gingival crevicular fluid (GCF) levels of matrix metalloproteinase (MMP)-8 and -13 and tissue inhibitor of MMP (TIMP)-1 in patients with rheumatoid arthritis (RA) and systemically healthy counterparts with inflammatory periodontal disease. Methods: Subjects (N = 74) were divided into five groups: 12 patients with RA and gingivitis; 13 patients with RA and periodontitis; 12 systemically healthy patients with gingivitis; 13 systemically healthy patients with periodontitis; and 24 periodontally and systemically healthy volunteers. Full-mouth clinical periodontal measurements were performed at six sites/tooth. GCF samples obtained from two sites in single-rooted teeth were analyzed by immunofluorometric assay and enzyme-linked immunosorbent assay. Data were assessed statistically by parametric tests. Results: The total amounts of MMP-8 were lower in the healthy control group than in RA-gingivitis, RA-periodontitis, and healthy-periodontitis groups (P0.05). Patients with RA and gingivitis or periodontitis exhibited levels of MMP-8 and -13 and TIMP-1 that were similar to systemically healthy counterparts (P>0.05). Conclusions: The coexistence of RA and periodontitis did not significantly affect the investigated parameters. GCF MMP-8 levels increased with periodontal inflammation. Despite the long-term usage of corticosteroids and non-steroidal anti-inflammatory drugs, similar GCF MMP-8 and -13 levels in patients with RA and systemically healthy counterparts suggest that RA may create a tendency to overproduce these enzymes. J Periodontol 2009;80:1307-1314

Dietary supplementation of omega-3 fatty acid and circulating levels of interleukin-1 beta, osteocalcin, and C-reactive protein in rats

WOS: 000245450900008PubMed ID: 29539164Background: In this study, we evaluated the effects of two different regimes of dietary supplementation of omega-3 fatty acid on serum levels of interleukin-1 beta (IL-1 beta), osteocalcin (OC), and C-reactive protein (CRP) in experimental periodontitis. Methods: Experimental periodontitis was induced by repeated injections of Escherichia coli lipopolysaccharide (LPS). Thirty-nine adult male Sprague-Dawley rats were divided into four study groups as follows: an LPS positive control group; a saline (negative) control group; and two different groups with omega-3 fatty acid dietary supplementation, one in which we gave the supplement subsequent to disease induction (TO3) and the other in which the agent was started prior to and continued subsequent to LPS injections (P + TO3). In the TO3 group, omega-3 fatty acid administration was performed for 14 days following induction of experimental periodontitis. In the P + TO3 group, omega-3 fatty acid was given for 14 days prior to the start of LPS injections and was continued for another 14 days subsequent to the induction of experimental periodontitis. On day 15 of the first LPS injection, serum samples were obtained and rats were sacrificed. Serum samples were analyzed for IL-1 beta, OC, and CRP concentrations by enzymelinked immunosorbent assay. Defleshed jaws were analyzed morphometrically for alveolar bone loss. Data were evaluated statistically by non-parametric tests. Results: LPS injection resulted in statistically significantly more bone loss compared to the saline control group (P < 0.05). None of the omega-3 fatty acid administration groups showed evidence that this fatty acid was effective in preventing LPS-induced alveolar bone loss. TO3 and P + TO3 groups revealed significantly higher IL-1 beta and OC levels than the LPS group (P < 0.05). The study groups exhibited no significant differences in the serum CRP levels. Conclusions: Omega-3 fatty acid administration does not seem to influence circulating levels of CRP. The significantly increased serum OC level observed in both omega-3 fatty acid regimes is curious and could have an effect on bone turnover, as could the further significant increase in serum IL-1 beta, which could counteract any osteoblastic induction by OC through promotion of osteoclast activity. The lack of a therapeutic benefit of omega-3 fatty acid in this study, despite the effects on OC and IL-1 beta, is difficult to explain, and further studies are required to more fully assess the potential role of this fatty acid in periodontal treatment