In most arthritis studies, TRPA1 was reported to be increased and acted as a promoter of joint destruction, mediating inflammatory and catabolic effects (Nummenmaa et al., 2016), oxidative stress (Phull et al., 2018), apoptosis (Yin et al., 2018), edema, and pain (Garrison and Stucky, 2014). This evidence concerns the gene TRPA1 and arthritic joint disease.