U.O. Medicina Nucleare, Centro per la Diagnosi e la Terapia delle Osteoporosi, Fondazione IRCCS Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena, Via F. Sforza 35, 20122, Milan, Italy.
J Orthop Traumatol. 2009 Jun;10(2):55-8. doi: 10.1007/s10195-009-0047-5. Epub 2009 Mar 19.
Bone repair alteration is hypothesized for nonunion fracture pathogenesis. Since it is involved in osteoclast regulation, the RANK/RANKL/OPG system (receptor activator of nuclear factor kB/its ligand/osteoprotegerin) may play a role.
Serum OPG, free RANKL, bone alkaline phosphatase (BAP), osteocalcin (OC), and urinary deoxypyridinoline (DPD) were determined in 16 male patients (20-39 years) with long bone atrophic nonunion fractures. Serum markers were also measured in 18 age-matched male controls who healed from the same type of fractures within six months, and in 14 age-matched male controls who were healing from the same fractures one month after injury. One-way ANOVA and Bonferroni's test were used for statistical analysis.
Only OPG was significantly higher (0.56 sd 0.11 ng/ml) in the patients compared to healed (0.26 sd 0.04 ng/ml; P < 0.001) and healing (0.29 sd 0.09 ng/ml; P < 0.001) controls. The patients' DPD levels were normal. No correlations were found between bone markers and the characteristics of the subjects in all groups.
A normal steady state of bone metabolism seems to be present in patients with atrophic nonunion fractures, despite the high serum OPG. The reason for the inability of the patients' OPG to inhibit osteoclastic activity is unknown. Osteoblast activity also appears normal, so another cellular source of OPG can be hypothesized.
骨修复改变被认为是骨折不愈合发病机制。由于它涉及破骨细胞的调节，RANK/RANKL/OPG 系统（核因子 κB 受体激活剂/其配体/骨保护素）可能发挥作用。
在 16 名男性（20-39 岁）长骨萎缩性骨折不愈合患者中测定血清 OPG、游离 RANKL、骨碱性磷酸酶（BAP）、骨钙素（OC）和尿脱氧吡啶啉（DPD）。还测定了 18 名年龄匹配的男性对照者（在 6 个月内从同一类型骨折愈合）和 14 名年龄匹配的男性对照者（在受伤后一个月从同一骨折愈合）的血清标志物。采用单因素方差分析和 Bonferroni 检验进行统计学分析。
与愈合组（0.26 sd 0.04 ng/ml；P < 0.001）和愈合组（0.29 sd 0.09 ng/ml；P < 0.001）相比，患者的 OPG 明显升高（0.56 sd 0.11 ng/ml）。患者的 DPD 水平正常。在所有组中，骨标志物与受试者的特征之间均无相关性。
尽管血清 OPG 升高，但萎缩性骨折不愈合患者似乎存在正常的骨代谢稳态。患者 OPG 无法抑制破骨细胞活性的原因尚不清楚。成骨细胞活性也似乎正常，因此可以假设 OPG 的另一种细胞来源。
