Zhao Hong-Mou, Diao Jia-Yu, Liang Xiao-Jun, Zhang Feng, Hao Ding-Jun
Foot and Ankle Surgery Department, Honghui Hospital of Xi'an Jiaotong University College of Medicine, No. 76 Nanguo Road, Xi'an, 710054, People's Republic of China.
Cardiovascular Medicine Department, The Second Affiliated Hospital of Xi'an Jiaotong University College of Medicine, No. 157 West Fifth Road, Xi'an, 710004, People's Republic of China.
J Orthop Surg Res. 2017 Oct 2;12(1):142. doi: 10.1186/s13018-017-0634-8.
Diabetic neuropathic osteoarthropathy (DNOAP) is an uncommon, but with considerable morbidity and mortality rates, complication of diabetes. The real pathogenesis is still unclear. The two popular theories are the neuro-vascular theory and neuro-traumatic theory. Most theories and pathways focused on the uncontrolled inflammations that resulted in the final common pathway, receptor activator of nuclear factor κβ ligand (RANKL)/osteoprotegerin (OPG) axis, for the decreased bone density in DNOAP with an osteoclast and osteoblast imbalance. However, the RANKL/OPG pathway does not explain all the changes, other pathways and factors also play roles. A lot of DNOAP potential relative risk factors were evaluated and reported in the literature, including age, gender, weight, duration and type of diabetes, bone mineral density, peripheral neuropathy and arterial disease, trauma history, and some others. However, most of them are still in debates. Future studies focus on the pathogenesis of DNOAP are still needed, especially for the genetic factors. And, the relationship between DNOAP and those potential relative risk factors are still need to further clarify.
糖尿病性神经病变性骨关节炎（DNOAP）是糖尿病一种不常见但发病率和死亡率颇高的并发症。其真正的发病机制仍不清楚。两种流行的理论是神经血管理论和神经创伤理论。大多数理论和途径聚焦于失控的炎症，这些炎症导致了最终的共同途径，即核因子κβ配体受体激活剂（RANKL）/骨保护素（OPG）轴，从而造成DNOAP中破骨细胞与成骨细胞失衡，骨密度降低。然而，RANKL/OPG途径并不能解释所有变化，其他途径和因素也发挥作用。文献中评估并报道了许多DNOAP潜在的相关危险因素，包括年龄、性别、体重、糖尿病病程和类型、骨矿物质密度、周围神经病变和动脉疾病、创伤史等。然而，其中大多数仍存在争议。仍需要对DNOAP的发病机制进行进一步研究，尤其是针对遗传因素。而且，DNOAP与那些潜在相关危险因素之间的关系仍需进一步阐明。
