Abstract
Background:
The global incidence of frozen shoulder (FS) and osteoporosis (OP) is high. Although FS patients may experience localized OP in the shoulder, there is still insufficient strong evidence to confirm the relationship between FS and OP. The main objective of this current research is to investigate the pathogenesis mechanism of FS and explore the connection between FS and OP.
Methods:
We obtained FS and OP datasets from GEO and identified crosstalk genes. We screened the p38 MAPK signaling pathway and its specific inhibitor, TAK715. We conducted flow cytometry, western blot, and PCR analyses to assess the treatment effect of TAK715 on FS synovium fibroblasts at concentrations of 1μM, 5μM, and 10μM. Additionally, we employed SD rats to validate the treatment effects of TAK715 in vivo.
Results:
TAK715 was found to also intervene in the activation of osteoclasts. We successfully established a FS and OP rat model, with the FS with OP rat displaying more severe symptoms. Results demonstrated that TAK715 effectively corrected both fibrosis and osteoporosis simultaneously in vivo.
Conclusions:
The frozen shoulder with osteoporosis may exhibit more severe symptoms, and TAK715 is effective in protecting fibrosis and osteoporosis both in vitro and vivo. The therapy to correct FS and OP simultaneously by TAK715 provides novel approach in FS treatment and study.