人体骨骼具有显著的再生能力。然而,5-10%的骨折未能愈合并发展为不愈合,这是一种具有挑战性的骨科并发症,需要复杂且昂贵的治疗。这篇综述论文将讨论四种不同的计算模型,每个捕获不愈合的特定临床病例:由骨髓管扩孔和骨膜剥离引起的不愈合,由于较大的碎片间隙而导致不愈合,由于遗传性疾病[即NF1相关的先天性胫骨假关节炎(CPT)]导致的不愈合和由于机械超负荷导致的不愈合。一起,这四种计算模型能够捕获各种骨折不愈合类型的病因,并设计其新颖的治疗策略。需要进一步的研究来证实动物和人类环境中的计算模型,并将它们从工作台转换到床边。
The human skeleton has a remarkable regeneration capacity. Nevertheless, 5-10 % of the bone fractures fails to heal and develops into a non-union which is a challenging orthopedic complication requiring complex and expensive treatment. This review paper will discuss four different computational models, each capturing a particular clinical
case of non-union: non-union induced by reaming of the marrow canal and periosteal stripping, non-union due to a large interfragmentary gap, non-union due to a genetic disorder [i.e. NF1 related congenital pseudoarthrosis of the tibia (CPT)] and non-union due to mechanical overload. Together, the four computational models are able to capture the etiology of a wide range of fracture non-union types and design novel treatment strategies thereof. Further research is required to corroborate the computational models in both animal and human settings and translate them from bench to bed side.