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

David F. Lappin, Danae Apatzidou, Anne-Marie Quirke, Jessica Oliver-Bell, John P. Butcher, Denis F. Kinane, Marcello P. Riggio, Patrick Venables, Iain B. McInnes, Shauna Culshaw

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Abstract

BackgroundAnti-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. 
AimTo determine whether periodontitis, carriage of P. gingivalis, smoking and periodontal therapy influence ACPA titres. 
MethodsSerum 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. 
ResultsUntreated 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 +/- 0.10AU, p<0.0001]. Periodontitis patients who smoked demonstrated lower anti-P. gingivalis (15956 +/- 4385 versus 2512 +/- 1290Units/ml, p<0.05), but similar anti-CCP than non-smoking periodontitis patients (smokers: 1.31 +/- 0.35; non-smokers: 1.41 +/- 0.32AU). Healthy smokers demonstrated elevated anti-CCP titres (0.75 +/- 0.19AU), at levels between healthy non-smokers (0.15 +/- 0.05AU) and non-smoker periodontitis patients. Six months after periodontal treatment, there were significant reductions in anti-CCP (non-smokers p<0.05) and anti-P. gingivalis (all participants p<0.01).

ConclusionIn subjects with periodontitis, P. gingivalis infection may be responsible for inducing autoimmune responses that characterize rheumatoid arthritis.
Original languageEnglish
Pages (from-to)907-915
Number of pages9
JournalJournal of Clinical Periodontology
Volume40
Issue number10
DOIs
Publication statusPublished - 1 Aug 2013
Externally publishedYes

Cite this

Lappin, D. F., Apatzidou, D., Quirke, A-M., Oliver-Bell, J., Butcher, J. P., Kinane, D. F., ... Culshaw, S. (2013). Influence of periodontal disease, Porphyromonas gingivalis and cigarette smoking on systemic anti-citrullinated peptide antibody titres. Journal of Clinical Periodontology, 40(10), 907-915. https://doi.org/10.1111/jcpe.12138
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. / Influence of periodontal disease, Porphyromonas gingivalis and cigarette smoking on systemic anti-citrullinated peptide antibody titres. In: Journal of Clinical Periodontology. 2013 ; Vol. 40, No. 10. pp. 907-915.
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title = "Influence of periodontal disease, Porphyromonas gingivalis and cigarette smoking on systemic anti-citrullinated peptide antibody titres",
abstract = "BackgroundAnti-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. AimTo determine whether periodontitis, carriage of P. gingivalis, smoking and periodontal therapy influence ACPA titres. MethodsSerum 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. ResultsUntreated 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 +/- 0.10AU, p<0.0001]. Periodontitis patients who smoked demonstrated lower anti-P. gingivalis (15956 +/- 4385 versus 2512 +/- 1290Units/ml, p<0.05), but similar anti-CCP than non-smoking periodontitis patients (smokers: 1.31 +/- 0.35; non-smokers: 1.41 +/- 0.32AU). Healthy smokers demonstrated elevated anti-CCP titres (0.75 +/- 0.19AU), at levels between healthy non-smokers (0.15 +/- 0.05AU) and non-smoker periodontitis patients. Six months after periodontal treatment, there were significant reductions in anti-CCP (non-smokers p<0.05) and anti-P. gingivalis (all participants p<0.01).ConclusionIn subjects with periodontitis, P. gingivalis infection may be responsible for inducing autoimmune responses that characterize rheumatoid arthritis.",
author = "Lappin, {David F.} and Danae Apatzidou and Anne-Marie Quirke and Jessica Oliver-Bell and Butcher, {John P.} and Kinane, {Denis F.} and Riggio, {Marcello P.} and Patrick Venables and McInnes, {Iain B.} and Shauna Culshaw",
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Lappin, DF, Apatzidou, D, Quirke, A-M, Oliver-Bell, J, Butcher, JP, Kinane, DF, Riggio, MP, Venables, P, McInnes, IB & Culshaw, S 2013, 'Influence of periodontal disease, Porphyromonas gingivalis and cigarette smoking on systemic anti-citrullinated peptide antibody titres', Journal of Clinical Periodontology, vol. 40, no. 10, pp. 907-915. https://doi.org/10.1111/jcpe.12138

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

In: Journal of Clinical Periodontology, Vol. 40, No. 10, 01.08.2013, p. 907-915.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Influence of periodontal disease, Porphyromonas gingivalis and cigarette smoking on systemic anti-citrullinated peptide antibody titres

AU - Lappin, David F.

AU - Apatzidou, Danae

AU - Quirke, Anne-Marie

AU - Oliver-Bell, Jessica

AU - Butcher, John P.

AU - Kinane, Denis F.

AU - Riggio, Marcello P.

AU - Venables, Patrick

AU - McInnes, Iain B.

AU - Culshaw, Shauna

PY - 2013/8/1

Y1 - 2013/8/1

N2 - BackgroundAnti-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. AimTo determine whether periodontitis, carriage of P. gingivalis, smoking and periodontal therapy influence ACPA titres. MethodsSerum 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. ResultsUntreated 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 +/- 0.10AU, p<0.0001]. Periodontitis patients who smoked demonstrated lower anti-P. gingivalis (15956 +/- 4385 versus 2512 +/- 1290Units/ml, p<0.05), but similar anti-CCP than non-smoking periodontitis patients (smokers: 1.31 +/- 0.35; non-smokers: 1.41 +/- 0.32AU). Healthy smokers demonstrated elevated anti-CCP titres (0.75 +/- 0.19AU), at levels between healthy non-smokers (0.15 +/- 0.05AU) and non-smoker periodontitis patients. Six months after periodontal treatment, there were significant reductions in anti-CCP (non-smokers p<0.05) and anti-P. gingivalis (all participants p<0.01).ConclusionIn subjects with periodontitis, P. gingivalis infection may be responsible for inducing autoimmune responses that characterize rheumatoid arthritis.

AB - BackgroundAnti-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. AimTo determine whether periodontitis, carriage of P. gingivalis, smoking and periodontal therapy influence ACPA titres. MethodsSerum 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. ResultsUntreated 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 +/- 0.10AU, p<0.0001]. Periodontitis patients who smoked demonstrated lower anti-P. gingivalis (15956 +/- 4385 versus 2512 +/- 1290Units/ml, p<0.05), but similar anti-CCP than non-smoking periodontitis patients (smokers: 1.31 +/- 0.35; non-smokers: 1.41 +/- 0.32AU). Healthy smokers demonstrated elevated anti-CCP titres (0.75 +/- 0.19AU), at levels between healthy non-smokers (0.15 +/- 0.05AU) and non-smoker periodontitis patients. Six months after periodontal treatment, there were significant reductions in anti-CCP (non-smokers p<0.05) and anti-P. gingivalis (all participants p<0.01).ConclusionIn subjects with periodontitis, P. gingivalis infection may be responsible for inducing autoimmune responses that characterize rheumatoid arthritis.

U2 - 10.1111/jcpe.12138

DO - 10.1111/jcpe.12138

M3 - Article

VL - 40

SP - 907

EP - 915

JO - Journal of Clinical Periodontology

JF - Journal of Clinical Periodontology

SN - 0303-6979

IS - 10

ER -