Date: Monday, November 6, 2017
Session Type: ACR Poster Session B
Session Time: 9:00AM-11:00AM
Background/Purpose: 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 P. gingivalis and A. actinomycetemcomitans in periodontitis (PD) and Prevotella copri 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: 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.
Methods: Observational, cross-sectional study in RA patients older tan 18yo (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, 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. Euro Diagnostica: positive >25 U/mL; ACPA title stratification: Low (25–75), moderate (76–300) and high (>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)1: T level 0 (abscence), TL1 (mild), TL2 (severe). Statistical analysis: t-student, Kruskal Wallis, Chi-cuadrado by Stata program 13.1.
Results: We studied 187 patients, F/M 78.6%/21.4%, mean age 54.4 yo Follow-up time 8.8 yo Rheumatoid Factor positive 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).
Conclusion: 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.
To cite this abstract in AMA style:González Febles J, Garnier Rodríguez JL, Sánchez-Alonso F, Bustabad S, Díaz-González F, Sanz Alonso M, Rodriguez Lozano B. IMPACT of Smoking in the Expression of Periodontitis and Anticitrullinated Protein Antibodies in Rheumatoid Arthritis [abstract]. Arthritis Rheumatol. 2017; 69 (suppl 10). https://acrabstracts.org/abstract/impact-of-smoking-in-the-expression-of-periodontitis-and-anticitrullinated-protein-antibodies-in-rheumatoid-arthritis/. Accessed August 3, 2021.
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