PEMFs, as a non-invasive method, could positively affect bone and cartilage metabolism. However, the bio-effect and underlying mechanisms remain poorly understood. The present study is designed to investigate the effect of PEMFs on osteoporotic bone and degenerative cartilage together with its potential molecular mechanisms in mice with different gene background.

Twenty 12-week male and female wild-type (WT), TNFα knockout (TNFα^−/−) or IL6 knockout (IL6^−/−) mice, respectively, were sham-operated (SHAM) or subjected to destabilization of the medial meniscus (DMM) and ovariectomy (OVX) surgeries. After surgeries, WT mice were equally assigned to the non-treatment and PEMFs groups. After surgeries, WT mice were equally assigned to the non-treatment and PEMFs groups. Mice in PEMFs group were subjected to daily 1-hour PEMFs exposure with 8Hz, 3.8mT (peak value). Then all mice were euthanized after 4 weeks.

The surgical models of osteoporosis and osteoarthritis were proved successful evidenced by the analysis of micro-CT data and histological analysis. The bone loss and damaged cartilage were largely repaired by TNF-α and IL-6 gene knockout and partially inhibited by PEMFs exposure. Interestingly, no difference in Micro-CT data analysis was found between PEMFs group and gene knockouts, although a slight increase could be observed in TNFα^−/− mice when compared to the PEMFs group. Negative effects on bone and cartilage were proved by testing key cytokines in anabolism and catabolism. PEMFs treatment and gene knockouts corrected the negative effects by targeting mediators in molecular pathways like Wnt and RANK in a similar way.

PEMFs alleviated surgeries induced bone loss and cartilage degeneration by promoting anabolism and inhibiting catabolism possibly in a similar mechanism to TNF-α and IL-6 gene knockouts, which imply that TNF-α and IL-6 may become new potential targets for PEMFs in treating degenerative bone diseases.