###### Abstract  
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. s +
Footnote †: journal: Applied sciences  
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the Apnea-Hypopnea Index (AHI), which in adults categorizes the condition as mild (5-15 events/hour), moderate (15-30 events/hour), or severe (>30 events/hour), depending on the frequency of apneas and hypopneas per hour of sleep [1]. Recognized by the World Health Organization as a chronic condition, OSA requires continuous management due to its progressive nature and multiple associated comorbidities [4]. The systemic impact of OSA extends beyond respiratory disturbances, influencing cardiovascular health (with an increased risk for conditions like hypertension and coronary artery disease) and neurological function, often manifesting as mood disturbances and cognitive decline [5; 6; 7; 8; 9]. A distinctive feature of OSA is intermittent hypoxia, which repeatedly triggers the production of reactive oxygen species (ROS), activating inflammatory responses and elevating levels of pro-inflammatory cytokines, such as interleukin-6 (IL-6) and C-reactive protein (CRP), and interleukin-18 (IL-18) [10; 11]. This inflammatory state is associated with various chronic inflammatory diseases, including cardiovascular disorders, type II diabetes, and insulin resistance [12; 13; 14]. The chronic inflammation and oxidative stress characteristic of OSA closely resemble the mechanisms observed in periodontal disease (PD), a highly prevalent condition in which immune responses and inflammation also play a central role [15; 16]. Gingivitis is confined to inflammation of the gingival tissues, whereas periodontitis involves alveolar bone loss and is clinically characterized by periodontal pockets and bleeding on probing. In severe cases, features such as deep lesions, truncation involvement, tooth mobility, flaring, and tooth loss can significantly impair masticatory function, aesthetics, and oral-health-related quality of life [17; 18; 19]. An emerging body of research suggests a potential association between OSA and PD, highlighting the role of shared inflammatory and oxidative stress pathways [20]. Common risk factors, such as obesity, diabetes, alcohol consumption, and smoking, support the hypothesis of a bidirectional relationship between OSA and PD, with significant implications for systemic health [20].