Periodontitis-induced Systemic Multi-organ Aging Mediated by the NF-κB Signalling Pathway

Area of Science:

• Gerontology
• Oral Medicine
• Molecular Biology

Background:

• Periodontitis, a chronic inflammatory disease, is linked to systemic health issues.
• Cellular senescence and the senescence-associated secretory phenotype (SASP) are key drivers of aging.
• The NF-κB signaling pathway is implicated in inflammation and cellular senescence.

Purpose of the Study:

• To investigate the causal role of periodontitis in promoting aging in distal organs.
• To elucidate the mechanism linking periodontitis to multi-organ aging, focusing on NF-κB signaling.
• To assess the role of NF-κB in mediating periodontitis-induced cellular senescence.

Main Methods:

• Established a ligature-induced periodontitis mouse model.
• Examined senescence markers (SASP genes, telomere length, p16INK4a, p21CIP1/WAF1, β-galactosidase) in various tissues.
• Utilized the NF-κB inhibitor BAY 11-7082 to study pathway mediation.

Main Results:

• Periodontitis mice showed elevated SASP-related gene expression in peripheral blood.
• Distal organs exhibited molecular aging hallmarks: increased SASP genes, shortened telomeres, and higher p16 expression.
• NF-κB inhibition significantly reduced these aging markers, confirming its mediating role.

Conclusions:

• Periodontitis actively promotes systemic multi-organ aging through NF-κB pathway activation.
• This study provides evidence for NF-κB as a critical mediator of periodontitis-induced aging.
• Findings establish a theoretical basis for therapeutic interventions targeting periodontitis-related aging.