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Influence of periodontal disease, Porphyromonas gingivalis and cigarette smoking on systemic anti-citrullinated peptide antibody titres

Background Anti‐citrullinated protein antibody (ACPA) responses may precede clinical onset of rheumatoid arthritis. Porphyromonas gingivalis peptidylarginine deiminase can citrullinate proteins possibly inducing autoimmunity in susceptible individuals. Aim To determine whether periodontitis, carriag...

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Published in:Journal of clinical periodontology 2013-10, Vol.40 (10), p.907-915
Main Authors: Lappin, David F., Apatzidou, Danae, Quirke, Anne-Marie, Oliver-Bell, Jessica, Butcher, John P., Kinane, Denis F., Riggio, Marcello P., Venables, Patrick, McInnes, Iain B., Culshaw, Shauna
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Language:English
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Summary:Background Anti‐citrullinated protein antibody (ACPA) responses may precede clinical onset of rheumatoid arthritis. Porphyromonas gingivalis peptidylarginine deiminase can citrullinate proteins possibly inducing autoimmunity in susceptible individuals. Aim To determine whether periodontitis, carriage of P. gingivalis, smoking and periodontal therapy influence ACPA titres. Methods Serum and plaque samples were collected from 39 periodontitis patients before and after non‐surgical periodontal treatment, and from 36 healthy subjects. Carriage of P. gingivalis was determined by PCR of plaque DNA. ACPA was determined by anti‐cyclic citrullinated peptide (CCP) enzyme‐linked immunosorbent assay (ELISA). Anti‐P. gingivalis titres were determined by ELISA. Results Untreated periodontitis patients had higher anti‐CCP antibody titres than healthy controls [three patients (8%) greater than manufacturer suggested assay diagnostic threshold (5 Assay Units/AU) versus none (0%); mean ± SEM: 1.37 ± 0.23 versus 0.40 ± 0.10 AU, p 
ISSN:0303-6979
1600-051X
DOI:10.1111/jcpe.12138