Porphyromonas gingivalis Accumulates in Human CAVS Valves and Drives IL-1β-Dependent Calcification in Mice

Researchers quantified bacterial DNA in explanted human aortic valves, comparing CAVS cases to non-calcified valves from other diseases. P. gingivalis was not the most abundant species but exhibited one of the largest case-control differences, prompting targeted mouse studies. Repeated oral or intravenous exposure to live bacteria produced valve colonization, calcium deposition, and echocardiographic stenosis; heat-killed organisms and antibiotic pretreatment attenuated these effects.

Prior observational cohorts have linked periodontitis to coronary plaque and stroke, yet valve-specific mechanisms remained unclear. The present data isolate a direct IL-1β pathway: genetic IL-1β deletion blocked calcification despite bacterial challenge, distinguishing this from generic systemic inflammation. This finding aligns with earlier reports of P. gingivalis invasion of endothelial cells and with IL-1 receptor antagonist trials showing reduced cardiovascular events.

No approved pharmacotherapy slows CAVS progression; valve replacement remains the only option once symptoms appear. The results suggest periodontal therapy or targeted IL-1β blockade could be testable adjuncts, but require prospective cohorts linking oral bacterial load to serial valve imaging and randomized trials of periodontal intervention with CAVS endpoints.

Next steps include longitudinal human studies measuring P. gingivalis antibody titers against progression rates on echocardiography and safety trials of IL-1 inhibitors in patients with both periodontitis and mild CAVS.