Capsaicin inhibits Porphyromonas gingivalis growth, biofilm formation, gingivomucosal inflammatory cytokine secretion, and in vitro osteoclastogenesis.

The prevention and treatment of periodontitis requires not only the control of causative pathogens, especially Porphyromonas gingivalis, but also the regulation of inflammatory immune response. Investigating auxiliary drugs for periodontitis during conventional treatments is, thus, quite important. Capsaicin, an agonist for the vanilloid receptor subtype 1 (TRPV1), due to its bacteriostatic activity against Gram-negative bacteria and anti-inflammatory effects, appears to be a promising drug. In this work, the antimicrobial activity of capsaicin against P. gingivalis and biofilm formation, inflammatory cytokine levels in experimental periodontitis, osteoclast precursor proliferation, and osteoclastogenesis in vitro were fully investigated. The results showed that capsaicin inhibited P. gingivalis growth with a minimum inhibitory concentration (MIC) and a minimum bactericidal concentration (MBC) of 16 and 64 mg/l, respectively. Capsaicin also inhibited P. gingivalis biofilm formation, with minimum biofilm inhibition concentrations MBIC50 and MBIC90 of 16 and 32 mg/l, respectively, and reduced pre-formed biofilms' viability with a minimum biofilm reduction concentration MBRC50 of 64 mg/l, as demonstrated by confocal laser scanning microscopy. In experimental periodontitis, except for IL-10, TNF-α, IL-1β, IL-6, IL-12, and iNOS were depressed after capsaicin treatment. Moreover, capsaicin also suppressed osteoclast precursor proliferation and osteoclastogenesis, as demonstrated by NF-ĸB p65. However, this favorable effect was attenuated by the TRPV1 antagonist, camphor. It, thus, suggests that capsaicin is a potential drug for the auxiliary treatment of periodontitis. TRPV1 activation may involve in beneficial roles of capsaicin on periodontitis.