Introduction: Periodontitis is associated with many chronic health conditions including diabetes, cardiovascular disease, and rheumatoid arthritis (RA). RA and periodontitis have similarities in inflammatory mechanism, morphology, and histopathology. Osteoarthritis (OA) is a chronic, multifactorial degenerative disease characterized by the deterioration of cartilage in joints. Objective: The aim of this study was to evaluate the prevalence and severity of periodontal disease in patients with established RA and OA. Materials and Methods: A total of 200 patients reporting to the Department of Orthopaedics, KIMSDU, Karad were included in the study. Patients were divided into two groups: Group 1 that included 100 patients with established RA diagnosed according to American College of Rheumatology (ACR) classification 1987 criteria and Group 2 that comprised 100 patients diagnosed with OA. Demographic profile, medical and dental history, oral hygiene practices, and smoking status of study participants were recorded. Periodontal status of the patients were evaluated using the simplified oral hygiene index (OHI-S), Loe and Silness gingival index (GI), probing pocket depth (PPD), and clinical attachment level (CAL). On the basis of the CAL score periodontitis severity was defined as slight, moderate, and severe. Rheumatoid Factor (RF) and C-reactive protein (CRP) were considered as a serological marker in RA. Serological tests were performed to measure RF and CRP. Periodontal parameters and serological tests were correlated. Results: This study reported 45% severe periodontitis prevalence in RA compared to OA group, which was 33%. Severity of periodontitis is significantly greater in RF positive RA group with mean CAL 5.38 mm compared to RF negative RA group with mean CAL 2.81 mm ( P = 0.001). There was moderate positive correlation found between RF titer and severity of periodontitis (r = 0.311). Conclusion: The severity of periodontitis was significantly higher among the patients with established RA as compared to patients with OA. RF positive patients had higher periodontal disease compared to RF negative patients. There was an increase in the mean clinical attachment loss with increase in RF titer.

Aim: This review aims to highlight the emerging role of toll-like receptors (TLRs) in pathogenesis of periodontitis and negative regulation of TLR signaling. Background: Periodontal disease is the common chronic bacterial infection of the supporting structures of the teeth characterized by the tissue destruction. Bacterial plaque stimulates the host inflammatory response. It is now known that the immune response utilizes a family of pattern-recognition receptors (PRRs) called TLR as a tool to trigger an inflammatory response to microbial invasion. The TLRs expressed by epithelial cells of gingiva are constantly stimulated which release cytokines and defensins required for maintenance of oral health. The chronic stimulation of TLRs may leas to the disruption of epithelial barrier and allows microorganisms to enter the underlying connective tissue. This further activates TLRs present on additional cells of the periodontium, i.e., resident and non-resident cells. These TLRs activation may cause host tissue destruction due to an overproduction of proinflammatory cytokines as well other biological mediators. Review results: The electronic databases PubMed, MEDLINE, Cochrane, Scopus and Google Scholar were searched for available data in the present review. A database search yielded a total of 94 articles out of 56 included based on the core data. The results and subsequent conclusions were extracted and reviewed. Conclusion:It may be concluded that TLR signaling is crucial for maintenance of periodontal health as well as initiation and progression of periodontal disease. In spite of this, there are still lacks of information regarding the functional polymorphisms of genes that are involved in the stimulation and regulation of lipopolysaccharide mediated inflammatory processes. Clinical significance: Overactive TLRs might pivot into chronic inflammation, and so targeting TLRs might therefore lead to remission from this chronic inflammation. Therefore, further investigations are necessary to expand our knowledge to understand and develop therapies for major pathologic conditions.