Abstract Growth plate fractures present a significant challenge to the healing process due to the formation of bone bridges. However, the microenvironment and the regulatory mechanisms underlying growth plate fracture healing remain poorly understood. In this study, we analyzed growth plate and cortical bone tissues from mice at various stages, before and after bone callus formation, using RNA sequencing to compare gene expression profiles. A distinct chemokine activity signature was observed in growth plate injuries, with CCL9 emerging as a dynamically regulated chemokine. Recombinant CCL9 was found to inhibit osteogenesis, promote osteoclast formation under non-inflammatory conditions, and induce macrophage activation ex vivo. Notably, treatment with CCL9 in growth plate injuries preserved chondrocyte activity and significantly reduced the accumulation of bony matrix. These findings collectively suggest a potential protective role for CCL9 in growth plate injuries, likely through the suppression of bone turnover and the enhancement of cartilage anabolism. Elevating CCL9 levels during the appropriate remodeling phase may offer novel opportunities for promoting cartilage regeneration.
Zhu et al. (Mon,) studied this question.