SAT0691 Influence of smoking in the expression of chronic periodontitis and anti-citrullinated proteins antibodies in rheumatoid arthritis
Authors: J González Febles, JL Rodríguez Garnier, F Sánchez Alonso, S Dadlani, Y Barrios, S Bustabad, F González Díaz, M Sanz Alonso, B Rodríguez Lozano
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> Environmental, genetic and epigenetic factors can induce citrullination of structural peptides by the enzyme PAD,which induce anti-citrullinated protein antibodies (ACPA) preceding RA. Among the environmental factors are cigarette smoke, infections, such as <i>P. gingivalis</i> in periodontitis (PD) and <i>Prevotella copri</i> of intestinal microflora, and silica dust. Given the implication of these two exogenous factors, tobacco and PD,in citrullination, and tobacco enhancer factor in PD, we studied: <h3>Objectives</h3> 1. The risk of smoking for developing advanced PD in patients with RA. 2. Possible influence of smoking on the expression of severe PD and ACPA in RA patients. <h3>Methods</h3> Observational, descriptive, cross-sectional study in RA patients older tan 18y.o.(ACR/EULAR 2010), with ≥4 teeth, without tooth cleaning nor antibiotic intake 6 months previously. Socio-demographic and anthropometric variables included smoking status, social indicators such as Graffar scale, stress level, annual dental prophylaxis, and co-morbidities such as diabetes mellitus, dyslipidemia, ischemic cardiovascular disease. Serum ACPA detection: semiquantification Ab IgG against citrullinated peptides (ELISA) with Immunoscan CCPlus®test kit. Eurodiagnostica: positive &gt;25; ACPA title stratification: Low (25–75), moderate (76–300) and high (&gt;300). Periodontal parameters: plaque index (PI), Bleeding on probing (Bop), probing pocket depth, recession, clinical attachment level (CAL). CAL loss was categorized according to European Workshop 2005 (Tonetti)<sup>1</sup>: T level 0 (abscence), TL1 (mild), TL2 (severe). Statistical analysis: t-student, Kruskal Wallis, Chi-cuadrado by Stata program 13.1. <h3>Results</h3> We studied 187 patients, F/M 78.6%/21.4%, mean age 54.4 y.o. Follow-up time 8.8 y.o. RF+ 74.2%, ACPA positive in 114/168 patients (67.86%). Smoking habit:Current smoker (19.25%), former smoker (24.6%); low socioeconomical status (36.4%)/ relative poverty (33.7%).PD was observed in 97.3%: TL1 52.4%, TL2 44.9%. A "risk gradient" was observed for PD related to smoking habit: former smoker OR 1.62 (95% CI 0.81–3.27),p=0.174; smokers, OR 2.27 (95% CI 1.05–4.91), p=0.037. When analyzing the influence of smoking on PD development according to ACPA profile, a gradient effect of developing severe PD was observed from former smokers OR 2.37 (IC95% 0.52–7.64) to current smokers OR 6.99 (IC95% 1.53–32.07) (p=0.029) in ACPA(-) patients. This relationship was not observed in ACPA (+) patients (p=0.383). <h3>Conclusions</h3> 1.There is a "risk gradient" to develop PD in RA in relation to past or current exposure to tobacco, so that, although not significant, former smokers are at greater risk than non-smokers, and current smokers have a significant risk 2.3 times higher. 2. This risk gradient is shown in ACPA (-) patients, but not in ACPA (+) patients, which suggests an independent relationship between PD and ACPA (+) RA. <h3>References</h3> Tonetti MS, et al. J Clin Periodontol 2005. <h3>Disclosure of Interest</h3> None declared