Abstract
The association between rheumatoid arthritis (RA) and periodontal disease (PD) has been the focus of numerous investigations driven by their common pathological features. RA is an autoimmune disease characterized by chronic inflammation, the production of anti-citrullinated proteins antibodies (ACPA) leading to synovial joint inflammation and destruction. PD is a chronic inflammatory condition associated with a dysbiotic microbial biofilm affecting the supporting tissues around the teeth leading to the destruction of mineralized and non-mineralized connective tissues. Chronic inflammation associated with both RA and PD is similar in the predominant adaptive immune phenotype, in the imbalance between pro- and anti-inflammatory cytokines and in the role of smoking and genetic background as risk factors. Structural damage that occurs in consequence of chronic inflammation is the ultimate cause of loss of function and disability observed with the progression of RA and PD. Interestingly, the periodontal pathogen Porphyromonas gingivalis has been implicated in the generation of ACPA in RA patients, suggesting a direct biological intersection between PD and RA. However, more studies are warranted to confirm this link, elucidate potential mechanisms involved, and ascertain temporal associations between RA and PD. This review is mainly focused on recent clinical and translational research intends to discuss and provide an overview of the relationship between RA and PD, exploring the similarities in the immune-pathological aspects and the possible mechanisms linking the development and progression of both diseases. In addition, the current available treatments targeting both RA and PD were revised.
Highlights
The possible association between rheumatoid arthritis (RA) and periodontal disease (PD) has been investigated because of the numerous similarities in pathological and immunological characteristics, including: (1) Increased infiltration of inflammatory and immune cells including neutrophils, monocytes, and T and B lymphocytes; (2) increased release of pro-inflammatory mediators such as the tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), and matrix-degrading enzymes (MMPs, Cathepsin); (3) increased activation of the receptor activator of the factor nuclear kappa B (NF-κB) ligand (RANK-L) pathway induced by soluble mediators released by immune cells [1], with subsequent osteoclast differentiation and maturation
The lack of influence of PD on arthritis progression in this study [141] compared to the work made by Bartold et al [150] might be attributed to differences in the bacterial species (P. gingivalis versus A. actinomycetemcomitans), the specific strain of bacteria used, route of bacterial infection, experimental animal species and arthritis experimental model
The findings suggest that Non-Surgical Periodontal Treatment (NSPT) decreases Disease Activity Score including 28-joint count (DAS28)-C-Reactive Protein (CRP) and the serum levels of Immunoglobulin G (IgG) to P. gingivalis and citrulline in the RA patients and may reflect a role of P. gingivalis in the protein citrullination
Summary
The possible association between rheumatoid arthritis (RA) and periodontal disease (PD) has been investigated because of the numerous similarities in pathological and immunological characteristics, including: (1) Increased infiltration of inflammatory and immune cells including neutrophils, monocytes, and T and B lymphocytes; (2) increased release of pro-inflammatory mediators such as the tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), and matrix-degrading enzymes (MMPs, Cathepsin); (3) increased activation of the receptor activator of the factor nuclear kappa B (NF-κB) ligand (RANK-L) pathway induced by soluble mediators released by immune cells [1], with subsequent osteoclast differentiation and maturation. It is important to bear in mind that several studies in the literature mention statistical or selection adjustment/control for smoking, and most of them (if not all) consider smoking as a categorical variable (current, former or never-smoker) and do not account for the frequency, type or duration of smoking. This is true for the socioeconomic status of patients suffering from PD and/or RA. This review discusses the information on mechanisms underlying the possible reciprocal influences between RA and PD, those related to the similarities in the immune-pathological aspects, and the current available therapeutic strategies targeting RA and PD
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