Osteomyelitis is one of the most challenging diseases in the field of orthopedics for its complex pathogenesis and unsatisfactory treatment. The mechanism underlying its occurrence and development is still unclear. In our previous study, we found that long non-coding RNA (lncRNA) NONHSAT009968 inhibited the ability of osteogenic differentiation in staphylococcal protein A (SPA)-treated human bone marrow mesenchymal stem cells (hBMMSCs), but the underlying mechanism remains unclear. The current study was aimed at elucidating the possible mechanism of NONHSAT009968 in regulating osteogenic differentiation and bone defect repairability of hBMMSCs under infection. It was revealed that Wnt3a played a key role in promoting osteogenic differentiation of hBMMSCs treated with SPA in vitro. In addition, NONHSAT009968 inhibited osteogenic differentiation of hBMMSCs treated with SPA via Wnt3a, both in vivo and in vitro. In sum, the results suggested that lncNONHSAT009968 inhibited osteogenic differentiation of hBMMSCs in SA-induced inflammation through Wnt3a, which may have affected the occurrence and development of osteomyelitis. This study might provide novel insights regarding osteomyelitis and infectious bone defects.

骨髓炎发病机制复杂，治疗效果不佳，是骨科领域最具挑战性的疾病之一。其发生和发展的机制尚不清楚。在我们之前的研究中，我们发现长链非编码 RNA (lncRNA) NONHSAT009968 抑制葡萄球菌蛋白 A (SPA) 处理的人骨髓间充质干细胞 (hBMMSCs) 的成骨分化能力，但潜在机制尚不清楚。本研究旨在阐明NONHSAT009968在调节感染下hBMMSCs的成骨分化和骨缺损修复能力方面的可能机制。结果表明，Wnt3a在体外促进 SPA 处理的 hBMMSCs 的成骨分化中起关键作用。此外，NONHSAT009968在体内和体外均通过 Wnt3a 抑制用 SPA 处理的 hBMMSCs 的成骨分化。总之，结果提示lncNONHSAT009968通过W​​nt3a抑制SA诱导炎症中hBMMSCs的成骨分化，这可能影响了骨髓炎的发生发展。这项研究可能会提供有关骨髓炎和感染性骨缺损的新见解。