Immunological mechanisms behind inflammaging in the pathogenesis of chronic generalized periodontitis

Abstract

Aim of study. To examine the specific features pertaining to periodontal status and immunological reactivity in elderly individuals with chronic generalized periodontitis (CGP). Materials and methods. Clinical, radiographic, and immunological examinations were performed in patients (n=67) aged 21–74 with moderate chronic generalized periodontitis (main group). The main group was divided into two subgroups: individuals in their first period of mature age (Subgroup 1; n=31) and elderly individuals (Subgroup 2; n=36). The control group were 29 persons aged 21-35 featuring intact periodontium. The clinical assessment implied oral hygiene evaluation using the Green-Vermillion Index (Green J.C., Vermillion J.R., 1964) and periodontal tissue condition assessment relying on the following indices: PBI (Mühlemann-Sukser, 1977); PMA (modified by Parma, 1960), and PI (Russel, 1956); probing pocket depth (PPD), and gingival recession height. The radiological studies were conducted using the Orthopantomograph™ OP 3D Pro device in Low Dose Technology™ mode. The levels of immune regulatory mediators (IL-1β, TNF-α, IL-6, IL-10, MCP-1, IL-8, VEGF) in unstimulated saliva were identified through enzyme-linked immunosorbent assay (ELISA) using Vector-Best reagents following the manufacturer’s instructions. Results. The evaluation of the periodontal status revealed that, compared with the respective parameters (Me) of Subgroup 1, patients in Subgroup 2 demonstrated an increase in factors like OHI-S (by 1.22×; p ≥ 0.05), PMA (by 1.05×; p ≥ 0.05), PI (by 1.05×; p ≥ 0.05), and gingival recession height (by 1.54×; p ≤ 0.05) against a reduced probing depth (PBI – by 1.28×; p ≥ 0.05). The analysis of local immunity parameters in saliva showed that, compared to the control group, the patients in Subgroup 2 exhibited more pronounced changes in immune mediator levels (Me): an increase in IL-1β (by 2.33×, p ≤ 0.05), TNF-α (by 5.70×, p ≤ 0.05), IL-6 (by 3.43×, p ≤ 0.05), MCP-1 (by 1.24×, p ≥ 0.05), IL-8 (by 3.01×, p ≤ 0.05), with a decrease in IL-10 (by 2.88×, p ≤ 0.05) and VEGF (by 5.29×, p exceeding similar changes in Subgroup 1: TNF-α (by 2.87×, p ≤ 0.05), IL-6 (2.12×, p ≤ 0.05), IL-8 (1.64×, p ≤ 0.05); with a decrease in IL-10 (3.40×, p ≤ 0.05), and VEGF (2.03×, p ≤ 0.05). Spearman’s correlation analysis revealed strong positive correlations between IL-1β, IL-8 and the PMA index (ρ > 0.71 and ρ > 0.74, respectively, p < 0.001), TNF-α and PI (ρ > 0.73, p < 0.001), as well as a moderate positive correlation between VEGF and probing depth (ρ > 0.68, p < 0.001). 129 Conclusion. The interpretation of clinical and immunological findings in elderly and mature patients with CGP offered proof to the previously detected age-related patterns of immune alterations. In older individuals with CGP, the chronic pro-inflammatory profile can be characterized by elevated levels of pro-inflammatory cytokines combined with age-dependent immune dysregulation. The cytokine imbalance, marked by a significant shift toward pro-inflammatory activity, exacerbates respective pathological processes at the molecular level, whereas cellular senescence contributes significantly to inflammaging, thereby potentiating premature systemic aging.