There are remarkable similarities in the pathogenesis of periodontal diseases and rheumatoid arthritis. The mechanisms that drive antigen induced sequelae of oxidative stress are discussed in this review. A poorly modulated inflammatory response drives both diseases resulting in oxidative stress induced tissue injury. Immune complex formation in response to the periodontal pathogen Porphyromonas gingivalis triggering the production of ROS in both gingivae and synovium of RA patients has been reported. Elevated antibody levels to several periodontal pathogens in RA patients has implications on both RA and periodontal diseases. Periodontal patients are challenged individuals representing a multifactorial aetiopathogenesis with potential for therapeutic intervention in the context of free radical damage. Subjects with moderate to severe periodontal bone loss are significantly more likely than healthy individuals to have several co-existing systemic conditions resulting in ROS mediated damage. There is potential for dual induction of periodontal disease by existing inflammatory mechanisms of systemic diseases rather than exacerbation of low grade inflammation only; emphasizing the relevance of reducing inflammatory burden for disease control. Therapeutic strategies based on disease mechanisms include combined low dose non-steroidal anti-inflammatory drugs and doxycycline for synergistic reduction of matrix metalloproteinase activity in periodontal tissues and RA; sub-optimal dosing with CMT-8 and a biphosphonate clodronate to reduce pathologically elevated levels of MMPs, elastase and to restore alveolar bone in experimental periodontits demonstrating dual applications. Therapeutic interventions relevant to both diseases discussed in this review, have scope for a double hit in periodontal patients with co-existing RA and vice versa.
Keywords: Periodontal diseases, Rheumatoid arthritis, MMPs, Oxidative stress, ROS, Anti-inflammatory agents
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