Serum anti-CCP antibodies in periodontitis associated with rheumatoid arthritis - relative value for the severity of periodontitis

Keywords

Periodontitis, rheumatoid arthritis, ACPA, anti-CCP test

How to Cite

[1]
Stefanov, L., Bolyarova-Konova, T., Kolarov, Z., Pavlova, P. and Ivanova, M. 2020. Serum anti-CCP antibodies in periodontitis associated with rheumatoid arthritis - relative value for the severity of periodontitis. Revmatologiia (Bulgaria). 28, ONLINE (Dec. 2020).

Abstract

Antibodies against cyclic citrullinated peptides (ACPA) have significant prognostic value for the onset or progression of rheumatoid arthritis (RA). Extraarticular citrullination and the production of ACPA as an immune response have been well documented in a number of tissues, including inflamed gingiva associated with periodontal disease. The aim of this study was to analyze the relative value of serum ACPA, determined by anti-CCP test, in the periodontitis (P) associated with RA severity`s assessment. The study included 60 patients with a mean age of 58 ± 10 (34 to 74 years), of whom 44 were women and 16 were men with concomitant P and RA. All patients underwent clinical and laboratory tests for the diagnosis of RA and clinical periodontal examination for the diagnosis of P, after signed informed consent. In the studied cohort we found that the average number of lost teeth was 8 ± 5 (0-18), and the average depth of periodontal pockets in mm was 4.4 ± 1.1. In 50% of patients there was a loss of attachment> 5 mm, and in 43% we found furcation lesions. Fifty-eight patients (96.7%) had a 100% prevalence of probing bleeding (BoP), and 47 patients (78.3%) had PISA ≥ 934.71mm². The mean value of PISA in the studied patients was 1727.04 ± 873.64 (214.37 - 4324.00). We did not find a statistically significant difference in serum ACPA levels depending on the severity of periodontal parameters PD (p = 0.357), CAL (p = 0.589) and PISA (p = 0.788). We found that the ROC-based cutoff values ​​for ACPA were high (123.85 IU / ml) and had low sensitivity and specificity in distinguishing between severe and moderate / mild forms of periodontal disease.

References

  1. Papapanou PN, Sanz M, Buduneli N, et al. Periodontitis: Consensus report of workgroup 2 of the 2017 World Workshop on the Classification of periodontal and Peri-Implant Diseases and Conditions. J Periodontol 2018;89(1):173-182.
  2. Consensus Report: Chronic Periodontitis. 1999 International Workshop for a classification of Periodontal Diseases and Conditions. Ann Periodontol 1999;4:38.
  3. Коларов Зл. Съвременни аспекти в патогенезата на ревматоидния артрит. Дисертация. Университетско издателство "Св. Климент Охридски", 1997.
  4. Rodrıguez-Rodrıguez L, Lamas JR, et al. Combined influence of genetic and environmental factors in age of rheumatoid arthritis onset. Rheumatol Int 2012;32:3097-3102.
  5. Aletaha D, Neogi T, Silman AJ, et al. 2010 Rheumatoid arthritis classification criteria: An American College of Rheumatology/European League Against Rheumatism collaborative initiative. Arthritis Rheum 2010;62:2569-2581.
  6. Bright R, Proudman SM, Rosenstein ED et al. Is there a link between carbamylation and citrullination in periodontal disease and rheumatoid arthritis? Med Hypotheses 2015;84(6):570-576.
  7. Pruijn GJ, Wiik A, van Venrooij WJ. The use of citrullinated peptides and proteins for the diagnosis of rheumatoid arthritis. Arthritis Res Ther 2010;12:203.
  8. Bartold PM, Marshal RI, Haynes DR. Periodontitis and rheumatoid arthritis: a review. J Periodontol 2005;76(11S):2066-2074.
  9. Ebersole JL, Machen RL, Steffen M J et al. Systemic acute phase reactants, C-reactive protein and haptoglobin in adult periodontitis. Clin Exp Immunol 1997;107:347-352.
  10. The J, Ebersole JL. Rheumatoid factor (RF) distribution in periodontal disease. J Clin Immunol 1991;11:132-142.
  11. Snyderman R, McCarty GA. Analogous mechanisms of tissue destruction in rheumatoid arthritis and periodontal disease. Host-Parasite interaction in periodontal diseases. American Society of Microbiology, Washington, DC, 1982, 354-362.
  12. Gleissner, C, Willershausen B, Käßer U et al. The role of risk factors for periodontal disease in patients with rheumatoid arthritis. Eur J Med Res 1998 ;3 :387-392.
  13. Kaßer, U, Gleissner C, Dehne F, et al. Risk for periodontal disease in patients with longstanding rheumatoid arthritis. Arthritis Rheum 1997;40:2248-2251.
  14. Mercado FB, Marshall RI, Klestov AC et al. Relationship between rheumatoid arthritis and periodontal disease. J Periodontol 2001;72:779-787.
  15. Ramamurthy NS, Greenwald RA, Celiker MY et al. Experimental arthritis in rats induces biomarkers of periodontitis which are ameliorated by gene therapy with tissue inhibitor of matrix metalloproteinases. J Periodontol 2005;76:229-233.
  16. Papapanou PN, Sanz M, Buduneli N, et al. Periodontitis: Consensus report of workgroup 2 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Clin Periodontol 2018;45(20):S162-S170.
  17. Prevoo MLL, Van‘t Hof MA, Kuper HH et al. PLCM: Modified disease activity scores that include twenty-eight-joint counts. Development and validation in a prospective longitudinal study of patients with rheumatoid arthritis. Arthritis Rheum 1995;38:44-48.
  18. Nesse W, Abbas F, van der Ploeg I, et al. Periodontal inflamed surface area: quantifying inflammatory burden. J Clin Periodontol 2008;35(8):668-673.
  19. Leira Y, Martin-Lancharo P, Blanco J. Periodontal inflamed surface area and periodontal case definition classification. Acta Odontologica Scandinavica 2017;76(3) :195-198.
  20. Białowąs K, Radwan-Oczko M, Duś-Ilnicka I et al. Periodontal disease and influence of periodontal treatment on disease activity in patients with rheumatoid arthritis and spondyloarthritis. Rheumatol Int 2020;40:455-463.
  21. Holtfreter B, Albandar JM, Dietrich T, et al. Standards for reporting chronic periodontitis prevalence and severity in epidemiological studies – proposed standards from the Joint EU/USA Periodontal Epidemiology Working Group. J Clin Periodontol 2015;42:407-412.
  22. Yamashita M, Kobayashi T, Ito S, et al. The periodontal inflamed surface area is associated with the clinical response to biological disease-modifying antirheumatic drugs in rheumatoid arthritis: a retrospective study, Modern Rheumatology 2020;30:6,990-996.
  23. de Smit M, Westra J, Vissink A, et al. Periodontitis in established rheumatoid arthritis patients: a cross-sectional clinical, microbiological and serological study. Research and therapy 2012; 14:R222
  24. Loutan L, Alpizar-Rodriguez D, Courvoisier DS, et al. Periodontal status correlates with anti‐citrullinated protein antibodies in first‐degree relatives of individuals with rheumatoid arthritis. J Clin Periodontol 2019;46:690-698.
  25. Harvey GP, Fitzsimmons TR, Dhamarpatni AA, et al. Expression of peptidylarginine deiminase-2 and -4, citrullinated proteins and anti-citrullinated protein antibodies in human gingiva. J Рeriodontal Res 2013;48:252-261.
  26. Nesse W, Westra J, van der Wal JE, et al. The periodontium of periodontitis patients contains citrullinated proteins which may play a role in ACPA (anti-citrullinated protein antibody) formation. J Clin Periodontol 2012, 39, 599-607.
  27. Bolyarova-Konova TN, Stefanov LD, Kolarov ZG, et al. ACPA in Saliva and their Association with Periodontitis and Rheumatoid Arthritis. Revmatologiia (Bulgaria). 2020; XXVIII(1), 20-30.
Creative Commons License

This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License.