title: Periodontal treatment decreases levels of antibodies to Porphyromonas gingivalis and citrulline in patients with rheumatoid arthritis and periodontitis.
abstract: BACKGROUND
  Porphyromonas gingivalis has been implicated as an etiologic agent of rheumatoid arthritis (RA) because of the expression of peptidylarginine deiminase. The present study evaluates whether periodontal treatment may affect serum antibodies to P. gingivalis and citrulline levels in relation to disease activity of RA.
  
  
  METHODS
  Fifty-five patients with RA were randomly assigned to receive oral hygiene instruction and supragingival scaling (treatment group, n = 26) or no periodontal treatment (control group, n = 29). Periodontal and rheumatologic parameters and serum levels of cytokine and inflammatory markers citrulline and immunoglobulin (Ig)G to P. gingivalis were examined at baseline and 8 weeks later.
  
  
  RESULTS
  Both groups did not differ statistically in any parameters except percentage of sites with probing depth and clinical attachment level ≥ 4 mm at baseline. The treatment group exhibited a significantly greater decrease in disease activity score including 28 joints using C-reactive protein (DAS28-CRP) (P = 0.02), serum levels of IgG to P. gingivalis hemin binding protein (HBP)35 (P = 0.04), and citrulline (P = 0.02) than the control group. Serum levels of IgG to P. gingivalis HBP35 were significantly correlated positively with those of anti-cyclic citrullinated peptide antibodies (P = 0.0002). The same correlation was obtained between serum levels of IgG to P. gingivalis-sonicated extracts and those of rheumatoid factor (P = 0.02).
  
  
  CONCLUSIONS
  These results suggest that supragingival scaling decreases DAS28-CRP and serum levels of IgG to P. gingivalis HBP35 and citrulline in patients with RA. These observations may reflect a role of P. gingivalis in the protein citrullination, which is related to the pathogenesis of RA.
authors.affiliation: Division of Periodontology, Department of Oral Biological Science, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
authors.forename: Moe
authors.initials: M
authors.lastname: Okada
authors.forename: Tetsuo
authors.initials: T
authors.lastname: Kobayashi
authors.forename: Satoshi
authors.initials: S
authors.lastname: Ito
authors.forename: Tomoko
authors.initials: T
authors.lastname: Yokoyama
authors.forename: Asami
authors.initials: A
authors.lastname: Abe
authors.forename: Akira
authors.initials: A
authors.lastname: Murasawa
authors.forename: Hiromasa
authors.initials: H
authors.lastname: Yoshie
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000907:Antibodies, Bacterial / Q000097:blood*; D000942:Antigens, Bacterial / Q000097:blood; D001172:Arthritis, Rheumatoid / Q000276:immunology* / Q000382:microbiology; D002097:C-Reactive Protein / Q000032:analysis; D002352:Carrier Proteins / Q000097:blood; D002956:Citrulline / Q000097:blood / Q000276:immunology*; D012534:Dental Scaling / Q000379:methods; D005260:Female; D005500:Follow-Up Studies; D000081062:Heme-Binding Proteins; D006420:Hemeproteins; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D019278:Matrix Metalloproteinase 3 / Q000097:blood; D008875:Middle Aged; D009910:Oral Hygiene / Q000193:education; D017622:Periodontal Attachment Loss / Q000628:therapy; D010514:Periodontal Pocket / Q000628:therapy; D010518:Periodontitis / Q000382:microbiology / Q000628:therapy*; D016966:Porphyromonas gingivalis / Q000276:immunology*; D012217:Rheumatoid Factor / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D000907:Antibodies, Bacterial; D000942:Antigens, Bacterial; D002352:Carrier Proteins; D000081062:Heme-Binding Proteins; D006420:Hemeproteins; D007074:Immunoglobulin G; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D002956:Citrulline; D002097:C-Reactive Protein; D012217:Rheumatoid Factor; C511768:MMP3 protein, human; D019278:Matrix Metalloproteinase 3