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 (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.

Periodontitis is a multifactorial disease that leads to the progressive destruction of the tooth’s supporting apparatus in the presence of bacterial plaque, the primary etiological agent; as responsible for systemic inflammation, it can activate the host’s immune response. Alzheimer’s disease (AD) is a persistent neurodegenerative disorder characterized by a progressive cognitive decline in which inflammation plays a significant pathogenic role. This narrative review examines the most recent scientific evidence on the already established association between periodontal disease and Alzheimer’s disease. Articles published between 1984 and June 2024 were selected through searches conducted in the PubMed and Google Scholar databases, using the keywords “Periodontitis and Alzheimer’s disease”, “Periodontitis”, and “Alzheimer’s disease”. No language restrictions were applied, and only full-text articles were considered. Eligible studies included those involving humans, animals, and in vitro models, as well as systematic reviews and meta-analyses. Duplicates and studies not directly relevant to the topic were excluded. After applying these initial criteria, 179 articles were identified. Following a more detailed assessment, 72 articles were selected for inclusion in this review. The excluded studies were omitted due to limited relevance, redundancy with more comprehensive or recent publications, methodological limitations, or insufficient data for meaningful analysis. The final 72 articles were evaluated based on their methodology, key findings, and clinical implications. Periodontitis and AD often coexist. Periodontal patients are more likely to suffer from AD. Bacterial colonization of the periodontium, responsible either for a chronic and acute local inflammatory process, can extend to the brain via the bloodstream or the trigeminal nerve, as showed by post-mortem studies. Etiopathogenesis of periodontitis and AD is different; however, these pathologies share common risk factors that can influence their development, severity, and progression. Among those mechanisms, the most relevant is systemic inflammation, and a connection between periodontitis and AD was found in most papers; however, longitudinal and large-scale studies are needed to fully understand the deep mechanisms of this relationship.