Department of Biomedical Sciences, Tufts University - Cummings School of Veterinary Medicine, 200 Westboro Rd, North Grafton, MA, 48109, USA.
Department of Surgery, Faculty of Veterinary Medicine, Universidade de São Paulo, São Paulo, Brazil.
Musculoskelet Surg. 2020 Dec;104(3):303-311. doi: 10.1007/s12306-019-00621-2. Epub 2019 Aug 12.
The nonunion fracture is a relatively frequent complication in both human and veterinary medicine. Specifically, atrophic fracture nonunions are difficult to treat, with revision surgery usually providing the best prognosis. Anabolic steroids, such as nandrolone decanoate (ND), have been reported to have beneficial clinical effects on bone mass gain during osteoporosis; however, their utility in promoting regeneration in atrophic nonunions has not been documented. Our objective was to examine morphological changes induced by the ND in experimental fracture nonunion with vascular deficit in the rat model.
Fourteen adult Wistar rats had an atrophic fracture nonunion induced in the diaphysis of their left femur. Rats were allocated into two groups: control group and nandrolone decanoate group. Rats in the latter group were given nandrolone decanoate (1.5 mg/kg IM, once a week, during 4 weeks after confirmation of fracture nonunion radiographically). Radiographic and anatomopathological examination, micro-tomography and histological analysis were assessed to characterize the morphological changes promoted by the nandrolone decanoate use.
Based on radiology, anatomopathological evaluation, computed micro-tomography and conventional microscopy, nandrolone decanoate promoted bone regeneration at the fracture nonunion site by increasing the cellularity at the fracture site. Percentage of collagen was not significantly different between groups, consistent with high-quality regenerated bone.
The anabolic steroid nandrolone decanoate improved bone mass and regeneration without affecting collagen production and therefore has potential for improving outcomes for atrophic fracture nonunion.
骨折不愈合是人类和兽医医学中相对常见的并发症。具体来说，萎缩性骨折不愈合较难治疗，通常需要进行翻修手术才能获得最佳预后。同化类固醇，如癸酸诺龙（ND），已被报道对骨质疏松症患者的骨量增加具有有益的临床效果；然而，它们在促进萎缩性骨折不愈合的再生方面的效用尚未得到证实。我们的目的是在大鼠模型中研究具有血管缺陷的实验性骨折不愈合中 ND 引起的形态变化。
14 只成年 Wistar 大鼠的左股骨骨干发生萎缩性骨折不愈合。大鼠被分为两组：对照组和癸酸诺龙组。后者组大鼠给予癸酸诺龙（1.5mg/kg 肌内注射，每周一次，在骨折不愈合影像学确认后 4 周内）。进行影像学和解剖病理学检查、微断层扫描和组织学分析，以评估癸酸诺龙使用所引起的形态变化。
基于放射学、解剖病理学评估、计算微断层扫描和常规显微镜检查，癸酸诺龙通过增加骨折部位的细胞数量促进了骨折不愈合部位的骨再生。两组之间的胶原百分比没有显著差异，表明再生骨质量较高。
同化类固醇癸酸诺龙改善了骨量和再生，而不影响胶原的产生，因此有望改善萎缩性骨折不愈合的预后。
