Alterations in static and dynamic topological properties of brain functional network after chronic high altitude exposure: a panel study.

Periodontitis (PD) is a chronic inflammatory disease characterized by the progressive destruction of the periodontal supporting tissues (encompassing the gums, alveolar bone, and periodontal ligaments), and represents a major contributor to compromised oral health worldwide. PD is the predominant cause of tooth loss in adults (accounting for 45% to 50% of cases) and is bidirectionally associated with systemic diseases such as diabetes and cardiovascular diseases. Recent NHANES-based evidence further indicates that edentulism is independently associated with higher all-cause mortality, underscoring that compromised oral health carries prognostic implications well beyond the oral cavity. The Global Burden of Disease Study (GBD) reports that PD ranks as the sixth most prevalent disease worldwide. PD imposes significant physical and psychological burden on patients and leads to substantial productivity losses, and has therefore become a major global public health challenge. A recent bibliometric review has further confirmed its broad associations with nutritional, metabolic, cardiovascular, and musculoskeletal disorders, highlighting growing interest in the connection between oral and systemic health. The pathogenesis of PD is fundamentally a dynamic imbalance caused by the interaction between the immune system of the host and the dysbiotic microbial community in the dental plaque biofilm. Specific pathogenic bacteria in the biofilm (such as and ) activate the TLR signaling pathway of the host, leading to the excessive release of pro-inflammatory cytokines (e.g., IL-6 and TNF-α), which ultimately result in bone resorption and loss of periodontal attachment. Beyond local tissue damage, these inflammatory mediators can enter the bloodstream and induce systemic low-grade inflammation, thereby affecting overall health. A network of inflammatory and oxidative stress (OS) mediators is thought to link the oral environment with the systemic circulation. Serum cytokines have been recognized as key signals connecting periodontal disease activity to systemic inflammatory burden, and their circulating profiles can serve as informative readouts of both periodontal and overall health status. In parallel, the field is gradually moving beyond purely clinical phenotyping, including probing depth and attachment loss, toward host response biomarkers derived from saliva, blood, and gingival crevicular fluid, which provide more biologically grounded indicators of oral disease processes. At the molecular level, the balance between reactive oxygen species, reactive nitrogen species, and antioxidant defences critically shapes oral health. Under homeostatic conditions, nitric oxide generated from oral microbial nitrate reduction supports microbial eubiosis and immune regulation, whereas chronic inflammation shifts this balance toward nitric oxide scavenging, NOS uncoupling, and oxidative tissue damage. Together, these observations suggest that circulating inflammatory and OS markers may not only mirror periodontal status but also reflect a broader continuum of oral health that closely interacts with systemic metabolism. Among the systemic conditions that may interact with oral health through inflammatory and oxidative pathways, sarcopenic obesity (SO) has received increasing attention. SO is a comorbid condition characterized by a decrease in skeletal muscle mass index (MMI) and an abnormal increase in body fat percentage. The prevalence of SO increases with age. It is estimated that approximately 11% of older adults globally suffer from SO, with a sharp rise after the age of 70 years. SO is associated with an increased the risk of metabolic syndrome, functional impairment, and mortality. The pathophysiology of SO is driven by the interplay of four main factors: chronic inflammation, insulin resistance, hormonal disturbances, and oxidative stress (OS), among which OS plays a central role. OS damages muscle homeostasis through three primary mechanisms: mitochondrial dysfunction, endoplasmic reticulum stress, and disrupted regulation of muscle mass.