Associations Between Immune-inflammatory Markers, Age, and Periodontal Status: a Cross-sectional Study

Since periodontal disease is associated with many systemic diseases, it is important to evaluate its effects on host responses in elderly individuals. To this end, this study investigated salivary interleukin (IL)-17, IL-18, toll-like receptor (TLR) 2, TLR4, and tumor necrosis factor-alpha (TNF-α) levels in patient groups with different periodontal health statuses and immunologically evaluated the relationship between age and periodontal health status. A total of 60 individuals aged 18-40 years (young individuals) and 60 individuals aged 65 years or older (elderly individuals) were included in this study. According to periodontal disease status, the patients were divided into periodontally healthy, gingivitis, and periodontitis subgroups. Clinical periodontal parameters, including probing depth (PD), clinical attachment level (CAL), plaque index (PI), and gingival index (GI), were recorded. Saliva samples were collected and analyzed using ELISA to determine the levels of IL-17, IL-18, TLR2, TLR4, and TNF-α. Higher clinical periodontal parameter (PD, CAL, PI, and GI) and inflammatory marker (IL-17, IL-18, TNF-α, TLR2, and TLR4) levels were found in patients with periodontitis than those in periodontally healthy individuals and patients with gingivitis (P < 0.05). Salivary inflammatory marker levels were significantly higher in elderly individuals than those in young individuals in all subgroups (P < 0.05). A positive correlation was found between inflammatory marker levels and clinical periodontal parameters, but there was no correlation between TLR2 and PI or GI. This study suggests a significant increase in host response to periodontal disease as the disease progresses, with the levels of cytokines and TLR expression exhibiting an increasing trend with age. Increased IL-17, IL-18, TLR2, TLR4, and TNF-α levels in elderly individuals in all periodontal health subgroups might suggest the role of these cytokines and TLR pathway in the pathogenesis of periodontal diseases.