We further advanced the understanding of TiO2-induced arthritis’s physiopathology and HMC’s activity by demonstrating that HMC reduces the activation of TRPV1+ and TRPA1+ nociceptive neurons, which are already activated in basal conditions in TiO2-induced arthritis and present a boosted response to their standard agonists, and that HMC reduces such neuronal activation. This evidence concerns the gene TRPA1 and arthritic joint disease.