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World J Rheumatol. Nov 12, 2014; 4(3): 80-87
Published online Nov 12, 2014. doi: 10.5499/wjr.v4.i3.80
Does a biological link exist between periodontitis and rheumatoid arthritis?
Rosamma Joseph, MG Jose Raj, Shobha Sundareswaran, Priyanka Chand Kaushik, Amol Vijay Nagrale, Susan Jose, Sreeraj Rajappan
Rosamma Joseph, Priyanka Chand Kaushik, Amol Vijay Nagrale, Sreeraj Rajappan, Department of Periodontics, Government Dental College, Kottayam 686008, Kerala, India
MG Jose Raj, Department of Biochemistry, Government Medical College, Calicut 673008, Kerala, India
Shobha Sundareswaran, Department of Orthodontics, Government Dental College, Calicut 673008, Kerala, India
Susan Jose, Medical College Campus, Calicut 673008, Kerala, India
Author contributions: All authors have contributed to literature search, intellectual content, drafting and editing of the manuscript and language revision; all authors approved the final version to be published.
Correspondence to: Dr. Rosamma Joseph, Professor and Head, Department of Periodontics, Government Dental College, Medical College PO, Calicut 673008, Kerala, India. drrosammajoseph@gmail.com
Telephone: +91-944-6070599 Fax: +91-495-2356781
Received: June 28, 2014
Revised: September 25, 2014
Accepted: October 14, 2014
Published online: November 12, 2014
Abstract

Periodontitis or Periodontal disease (PD) and Rheumatoid arthritis (RA) are two the most common chronic inflammatory diseases. Periodontitis is a biofilm associated destructive inflammatory disease of the periodontium caused by specific microorganisms. Rheumatoid arthritis is an autoimmune condition and is identified by elevated serum autoantibody titre directed against citrullinated peptides or rheumatoid factor. Periodontitis may involve some elements of autoimmunity. Recent studies have established that PD and RA show a common pathway and could be closely associated through a common dysregulation and dysfunction in inflammatory mechanism. The enzyme peptidyl arginine deiminase (PAD), expressed by Porphyromonas gingivalis (P. gingivalis) is responsible for the enzymatic deimination of arginine residuals to citrulline resulting in protein citrullination and its increased accumulation in RA. Citrullination by PAD may act as a putative biologic link between PD and RA. Association of Human leukocytic antigen-DR4 antigen has been established both with RA and PD. Several interleukins and inflammatory mediators (ILs) and Nuclear factor kappa beta ligand are linked to these common chronic inflammatory diseases. Antibodies directed against heat shock protein (hsp 70 ab) of P. gingivalis, P. melanogenicus and P. intermedia are raised in PD as well as RA. Both the conditions share many pathological and immunological similarities. Bacterial infection, genetic susceptibility, altered immune reaction and inflammatory mediators considered responsible for RA are also associated with PD. So it is plausible that a biological link may exist between PD and RA. Therapies aimed at modifying the expression and effect of inflammatory mediators and effector molecules such as matrix metalloproteinases, proinflammatory cytokines and autoantibodies of structural proteins may probably reduce the severity of both RA and PD.

Keywords: Periodontal disease, Rheumatoid arthritis, Citrullinated peptidase, Porphyromonas gingivalis, Inflammatory marker, Inflammation and autoantibody

Core tip: Periodontal disease (PD) and Rheumatoid arthritis (RA) share many pathological and immunological similarities. Recent studies have established significant association between the two. Bacterial infection, genetic susceptibility, altered immune reaction and inflammatory mediators considered responsible for RA are also associated with PD. So it is plausible that a biological link may exist between PD and RA. Therapies aimed at reduction of inflammatory mediators and effector molecules can probably reduce the severity of both RA and PD.