Trpv4 Activation Aggravates Temporomandibular Joint Osteoarthritis Via P38 Mapk Pathway

This study aimed to explore the underlying mechanisms after transient receptor potential vanilloid 4 (TRPV4) activation in disc during the progress of temporomandibular joint osteoarthritis (TMJOA). The study utilized a rat model of traumatic occlusion to induce TMJOA in vivo (seven-week-old, female). The disc cell-related chemokine release was screened by transcriptome sequencing analysis. The regulatory effects of TRPV4/p38 mitogen-activated protein kinase (MAPK) pathway on disc-derived chemokine release was confirmed both in vivo and in vitro. The therapeutic effects of blocking p38 MAPK pathway was demonstrated in a rat model of traumatic occlusion-induced TMJOA in vivo. The study utilized a rat model of traumatic occlusion to induce TMJOA in vivo (seven-week-old, female). The disc cell-related chemokine release was screened by transcriptome sequencing analysis. The regulatory effects of TRPV4/p38 mitogen-activated protein kinase (MAPK) pathway on disc-derived chemokine release was confirmed both in vivo and in vitro. The therapeutic effects of blocking p38 MAPK pathway was demonstrated in a rat model of traumatic occlusion-induced TMJOA in vivo. This study clarifies the key role of TRPV4/p38 MAPK axis in regulating the synthesis and release of CXCLs in TMJ disc cells during the pathogenesis of TMJOA, thus blocking p38 MAPK pathway provides a promising approach for clinical treatment of TMJOA.