Jan Lessem

Short-Term Effects of an Anti-Inflammatory Treatment on Clinical Parameters and Serum Levels of C-Reactive Protein and Proinflammatory Cytokines in Subjects With Periodontitis

BACKGROUND Periodontal disease is the most common multifactorial disease, afflicting a very large proportion of the adult population. Periodontal disease secondarily causes increases in the serum levels of C-reactive protein (CRP) and other markers of inflammation. An increased level of CRP reflects an increased risk for cardiovascular disease. The aim of the current randomized clinical trial was to evaluate the short-term effect of a combination of dipyridamole and prednisolone (CRx-102) on the levels of high-sensitivity (hs)-CRP, proinflammatory markers in blood, and clinical signs of periodontal disease. METHODS Fifty-seven patients with >/=10 pockets with probing depths >/=5 mm were randomized into two groups in this masked single-center placebo-controlled study: CRx-102 (n = 28) and placebo (n = 29). hs-CRP levels, inflammatory markers (interleukin [IL]-6, -1beta, -8, and -12, tumor necrosis factor-alpha, and interferon-gamma [IFN-gamma]), bleeding on probing (BOP), and changes in probing depths were evaluated. The subjects received mechanical non-surgical therapy after 42 days, and the study was completed after 49 days. RESULTS At day 42, the differences in the hs-CRP, IFN-gamma, and IL-6 levels between the two groups were statistically significant (P <0.05), whereas no difference was found for the other inflammatory markers. There was no change in probing depth or BOP between the two groups. CONCLUSION The administration of CRx-102 resulted in significant decreases in hs-CRP, IFN-gamma, and IL-6, but it did not significantly change BOP or probing depths.

Effects of an anti-inflammatory treatment on clinicalparameters and serum levels of CRP and pro-inflammatorycytokines in subjects with periodontitis

Background: Infection and inflammation in tissues adjacent to dental implants are common. There are few controlled studies assessing interventions. We assessed if mechanical debridement with titanium curettes, is equally effective as an ultrasonic device in reducing clinical signs of inflammation and the total bacterial load. Materials and methods: Thrity two subjects (mean age 62.5 S.D ± 11.7) with one implant each demonstrating peri-implantitis were randomized in two intervention groups. Clinical and microbiological data were obtained before and during 6 months. Group one received debridement using titanium hand-instruments and group two received ultrasonic treatment using a coated working end. Results: At the different time-points, data analysis by independent t–test, or Mann–Whitney U tests failed to demonstrate group differences. Comparing baseline data with results at 6 months (merged groups) demonstrated that overall PI scores and at implants decreased (mean diff: 20.2%, S.E ± 6.3, 95%CI: 7.0 to 32.7, P < 0.002) and (mean diff: 27.2% S.E ± 7.9, 95%CI: 11.3 to 43.1, P < 0.001). Bleeding scores at implants improved (P < 0.01). PPD scores at implants did not improve (P = 0.30). Conclusions: No differences in treatment outcomes between the two treatment methods studied were found. While PI and BOP scores improved no effects in PPD were identified.Aims: To assess whether recurrence of acute coronary syndrome (ACS) can be linked to periodontitis in subjects followed over a 3 year period. Methods and results: Consecutive 163 hospital admitted subjects with ACS, and 158 medically healthy matched control subjects were followed through medical records review over 3 years. At baseline, subjects received medical and dental examinations. Periodontitis was defined as alveolar bone loss (ABL) > 2 S.D. above normal mean values. Subgingival bacterial samples were collected and processed by checkerboard DNA–DNA hybridization. ACS recurrence was found in 66/163 (40.5%) subjects, and a first ACS event in 7/158 (4.4%) control subjects. ABL was a risk marker of future ACS with OR: 3.6 (95%CI: 2.0-6.5, P < 0.001). Subject age was also an explanatory factor for a new ACS event (P < 0.001). Significantly higher subgingival bacterial counts for 20/37 species (i.e., Streptococcus anginosus, Streptococcus mitis, Tannerella forsythia) in ACS cases than in healthy controls. None of traditional serum markers (CRP, high and low density lipoprotein, cholesterol, triglycerides) were explanatory. Conclusions: Age, and periodontitis (ABL) are robust markers of risk for future ACS. Subgingival bacterial counts are elevated in subjects with ACS.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.