Background: Periodontal disease affect a large proportion of the adult population and cause an increasein serum levels of C- reactive protein (CRP), and other markers of inflammation. An increased level of CRP reflects an increased risk of cardiovascular disease. The aim of the current randomized clinical trial was to evaluate the short term effect of CRx-102 alone on the levels of hs-CRP, pro-inflammatory markers in blood and clinical signs of periodontal disease. Methods: Fifty seven patients with at least 10 pockets, with a probing depth of 5 mm or more, were randomized into two groups either CRx-102 (n = 28) or placebo (n = 29) in this blinded single-centre placebo controlled study. High sensitivity CRP (Hs-CRP) levels, inflammatory markers (IL-6, Il-1b, TNFa, IL12, IL-8, IFN c), bleeding on probing (BOP) and change in probing depths were evaluated. After 42 days the subjects received mechanical non-surgical therapy and the study was completed after 49 days. Results: At day 42 the difference in hs-CRP and IFN c levels between the two groups was statistically significant (P = 0.02 and P = 0.03, respectively) whereas no difference was found for the other inflammatory markers. There was no change in periodontal probing depth or BOP between the two groups. Conclusion: The current study demonstrated that the administration of CRx-102, resulted in significant decreases in hs- CRP and IFN c, but did not significantly change BOP or probing depths. 10:15–10:30 Ref no: EUABS065318 Anti TNF-a therapy and periodontal parameters in rheumatoid arthritis patients Y. MAYER*, A. GURMAN-BALBIR AND E. E. MACHTEI Unit of Periodontology, Rambam HCC, Haifa, Israel Aim: To evaluate the influence of anti TNF-a therapy on the clinical and immunological parameters of the periodontium. Materials and methods: Ten patients with RA who received infusion of 200 mg infliximab routinely (RA+), 10 patients with RA without anti TNF-a therapy (RA-) and 10 healthy patients (C) were included. Clinical parameters PI, GI, PD, CAL and BOP were assessed and total GCF TNF-a level was determined using ELISA. ANOVA with Fisher’s modification and Pearson correlation test were used for statistical analysis. Results: Patients’ age ranged between 22 and 76 years (mean 50.73 ± 9.1). Mean PI was similar between the groups. However, mean inflammatory parameters in the 3 groups varied significantly; GI was greater in the RA- compared with RA+ and C (P = 0.0042). RA+ exhibit less BOP than RA- and C (21.1% ± 3.0%, 45.9% ± 6.2% and 39.1% ± 7.2%; respectively, P = 0.0146) The mean PD in RA+ was shallower than RA- and C (3.22 ± 0.13, 3.85 ± 0.22, 3.77 ± 0.20; P = 0.055). CAL in RA+ was lower than RA- and C (3.68 ± 0.11, 4.52 ± 0.26, 4.35 ± 0.24; P = 0.0273). TNF-a levels in the GCF of RA+ were the lowest (0.663 pg/ml, 1.23 pg/ml and 0.949 pg/ml; P = 0.0401). A significant positive correlation was found between TNF-a levels in the GCF and CAL (r = 0.448, P = 0.0283). Conclusion: Rheumatoid arthritis patients receiving anti TNF-a medications have lower periodontal indices and GCF TNF-a levels. Thus, suppression of pro-inflammatory cytokines might prove beneficial in suppressing periodontal diseases.