Ligature-induced periodontitis in mice potentially accelerates CD4+ T-cell senescence and exacerbates rheumatoid arthritis

IntroductionAging impairs immunity, sustains chronic inflammation, and enhances autoimmunity–a process termed “immunosenescence” that contributes to the pathogenesis of type 2 diabetes and rheumatoid arthritis (RA). Post-pubertal thymic involution depletes naïve T-cell pool, promoting the emergence of senescent CD4+ T cells.

To maintain T-cell homeostasis, these cells undergo extensive homeostatic proliferation, eventually reaching their replicative limit. Characterized by PD-1 and CD153 expression, these senescent cells exhibit diminished proliferative capacity and an enhanced senescence-associated secretory phenotype (SASP).

While chronic periodontitis, which typically affects middle-aged individuals, is known to influence systemic conditions like RA (periodontal medicine), the underlying mechanisms remain elusive. This study investigates whether periodontitis accelerates CD4+ T-cell senescence and its subsequent impact on systemic disease.MethodsBALB/c mice (5–42 weeks old) underwent silk ligation of the maxillary second molars to induce experimental periodontitis (LIP).