创伤性异位骨化形成的细胞及分子机制研究进展

Advances in cell and molecular mechanisms of traumatic heterotopic ossification

创伤性异位骨化为创伤后骨外成骨。不同的损伤因素常诱导多种前体细胞参与这一过程。多种细胞因子如骨形态发生蛋白、缺氧诱导因子1-α、炎症、纤维蛋白沉积等会影响这一过程。异位骨化的形成常导致患肢功能受限及疼痛,而预防与治疗异位骨化又常带来骨不愈合并伴随高复发率。何种治疗方法能够在抑制异位骨化形成的同时,又不影响骨折愈合成为目前临床医师所关注的问题。这就需要探究异位骨化的形成机制并从中寻找有效且安全的治疗方法。笔者对参与创伤性异位骨化形成的细胞及分子机制进行综述,旨在对影响异位骨化形成的因素有更多了解,为新的治疗方式提供参考。

Objective Traumatic heterotopic ossification is the formation of extra-skeletal bone within soft tissues or joints after trauma.Injury factors induce many types of precursor cells to participate in this process.Many cytokines such as bone morphogenetic proteins,hypoxia inducible factor 1-α,inflammation factors and fibrin,can influence this process.Formation of heterotopic ossification often leads to the limitation of limb function and pain.However,prevention and treatment of heterotopic ossification often lead to bone nonunion and high recurrence rate.To find a treatment that can inhibit the formation of heterotopic ossification without affecting fracture healing has become a concern of clinicians.It is necessary to explore the formation mechanism of heterotopic ossification and find effective and safe methods.The authors document the cellular and molecular mechanisms involved in formation of traumatic heterotopic ossification for better understanding the factors affecting the formation of heterotopic ossification so as to provide references for new treatment methods.