This review explores the emerging relationship between obstructive sleep apnea (OSA) and periodontal disease (PD), emphasizing shared inflammatory pathways, overlapping risk factors, and potential systemic health implications. Both conditions are characterized by chronic inflammation and oxidative stress, which independently contribute to cardiovascular disease, diabetes, and other systemic disorders. Evidence suggests a bidirectional relationship, with OSA-related hypoxia exacerbating periodontal tissue breakdown and PD-induced inflammation potentially influencing OSA severity. However, the causative nature of the relationship between OSA and PD remains uncertain, largely due to inconsistencies in diagnostic criteria, methodological variability, and study heterogeneity. This review highlights the essential role of systematic reviews (SRs) in synthesizing current evidence, identifying research gaps, and guiding future studies. To maximize their impact, SRs should adhere to rigorous methodological quality standards, improve transparency in data reporting, and address the heterogeneity of included studies. Future research should focus on longitudinal and interventional designs, standardize diagnostic protocols, and investigate biomarkers, oral microbiome profiles, and inflammatory mediators to elucidate the mechanisms linking OSA and PD. Multidisciplinary collaboration between dental and sleep specialists is crucial to advancing evidence-based strategies that improve patient outcomes and address the broader health implications of these often coexisting conditions.

Periodontitis is a chronic, progressive inflammatory disease characterized by the gradual destruction of the supporting structures of the teeth, including the periodontal ligament and alveolar bone. This condition primarily originates from microbial dysbiosis in the oral cavity, further influenced by the host’s immune responses and a variety of environmental and behavioral factors. As the leading cause of tooth loss and edentulism among adults, periodontitis also has far-reaching systemic consequences. An expanding body of scientific evidence has established strong associations between periodontitis and numerous systemic conditions, including cardiovascular disease, diabetes mellitus, respiratory disorders, thyroid dysfunction, and obstructive sleep apnea (OSA). This review examines the potential biological and clinical connections between periodontitis and these systemic diseases by first providing an overview of the normal physiological functions and pathological changes of each condition. It then explores the shared immunological and pathophysiological pathways, with particular focus on inflammatory mediators, immune system dysregulation, and microbial translocation. By integrating perspectives from disciplines such as microbiology, immunology, and clinical research, this review underscores the integral role of oral health in systemic well-being. It also highlights the necessity of early detection, interdisciplinary cooperation, and preventive strategies—including lifestyle modifications—to manage common risk factors and improve comprehensive patient outcomes.

Periodontitis (PD) and rheumatoid arthritis (RA) are chronic inflammatory disorders that impose substantial individual and societal burdens worldwide. PD is characterized by progressive destruction of the periodontal ligament and alveolar bone, leading to tooth loss, impaired oral function, and sustained systemic inflammatory burden. RA, affecting approximately 0.5–1% of the population, is a chronic autoimmune disease marked by persistent synovial inflammation, progressive joint destruction, disability, and reduced quality of life. Increasing evidence indicates that these conditions are biologically and clinically interconnected. Both diseases share key pathogenic pathways, including microbial dysbiosis, immune dysregulation, chronic inflammation, genetic susceptibility, and aberrant autoantibody responses. Particular attention has focused on keystone periodontal pathogens such as Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans, which may promote protein citrullination and the formation of anti-citrullinated protein antibodies (ACPA), thereby providing a plausible mechanistic bridge between periodontal infection and systemic autoimmunity. Shared genetic risk factors, including HLA-DRB1 susceptibility alleles, further support a common host predisposition. Clinical, epidemiological, and translational studies increasingly support a bidirectional association. Individuals with PD appear to have a higher risk of RA development, whereas patients with RA demonstrate greater prevalence, severity, and progression of periodontal disease. Interventional studies suggest that nonsurgical periodontal therapy may reduce local periodontal inflammation, circulating inflammatory biomarkers, and RA disease activity indices, while effective pharmacological control of RA may also improve periodontal outcomes. This narrative review critically evaluates the PD–RA relationship across four interconnected domains: (i) epidemiological and clinical associations between PD and RA, (ii) key mechanisms underlying RA pathogenesis, (iii) shared biological pathways linking both diseases, and (iv) the extent to which treatment of one condition influences the other. Particular emphasis is placed on major sources of heterogeneity and confounding—including smoking, metabolic comorbidities, disease stage, therapeutic exposure, and variable diagnostic definitions—that may explain inconsistencies across the literature. By integrating current mechanistic and clinical evidence, this review provides a structured synthesis that extends beyond a descriptive overview of association studies. A clearer understanding of the periodontal–rheumatologic axis may facilitate risk stratification, identify novel therapeutic targets, and support integrated multidisciplinary care. Targeting both oral and systemic inflammation may improve outcomes in patients with coexisting PD and RA and may potentially reduce the risk or severity of one condition in individuals already affected by the other.