Dental Biomaterials Research Unit (d-BRU), Faculty of Medicine, University of Liege, Liège, Belgium.
Clinic of Oral Surgery, School of Dental Medicine, University of Belgrade, Belgrade, Serbia.
Calcif Tissue Int. 2017 Dec;101(6):553-563. doi: 10.1007/s00223-017-0327-7. Epub 2017 Oct 24.
Diabetes mellitus (DM) has been associated with increased bone fracture rates, impaired bone regeneration, delayed bone healing, and depressed osteogenesis. However, the plausible pathogenic mechanisms remain incompletely understood. The aim of the present systematic review was to investigate whether oxidative stress (OS) plays a role in altered characteristics of diabetic bone under in vivo conditions. An electronic search of the MEDLINE (via PubMed) and Embase databases was performed. In vivo animal studies involving DM and providing information regarding assessment of OS markers combined with analyses of bone histology/histomorphometry parameters were selected. A descriptive analysis of selected articles was performed. Ten studies were included in the present review. Both bone formation and bone resorption parameters were significantly decreased in the diabetic groups of animals compared to the healthy groups. This finding was consistent regardless of different animal/bone models employed or different evaluation periods. A statistically significant increase in systemic and/or local OS status was also emphasised in the diabetic groups in comparison to the healthy ones. Markers of OS were associated with histological and/or histomorphometric parameters, including decreased trabecular bone and osteoid volumes, suppressed bone formation, defective bone mineralisation, and reduced osteoclastic activity, in diabetic animals. Additionally, insulin and antioxidative treatment proved to be efficient in reversing the deleterious effects of high glucose and associated OS. The present findings support the hypotheses that OS in the diabetic condition contributes at least partially to defective bone features, and that antioxidative supplementation can be a valuable adjunctive strategy in treating diabetic bone disease, accelerating bone healing, and improving osteointegration.
糖尿病(DM)与骨折发生率增加、骨再生受损、骨愈合延迟和成骨作用下降有关。然而,其潜在的发病机制尚不完全清楚。本系统评价的目的是研究氧化应激(OS)是否在糖尿病骨骼的特征改变中发挥作用。对 MEDLINE(通过 PubMed)和 Embase 数据库进行了电子检索。选择了涉及 DM 并提供有关 OS 标志物评估信息以及骨组织学/组织形态计量学参数分析的体内动物研究。对选定的文章进行了描述性分析。本综述纳入了 10 项研究。与健康组相比,糖尿病动物组的骨形成和骨吸收参数均显著降低。无论使用不同的动物/骨骼模型还是不同的评估期,这一发现都是一致的。与健康组相比,糖尿病组的全身和/或局部 OS 状态也明显升高。OS 标志物与组织学和/或组织形态计量学参数相关,包括骨小梁和类骨质体积减少、骨形成受抑制、骨矿化缺陷和破骨细胞活性降低,在糖尿病动物中。此外,胰岛素和抗氧化治疗已被证明能有效逆转高血糖和相关 OS 的有害影响。目前的研究结果支持以下假说:糖尿病状态下的 OS 至少部分导致了骨骼特征的缺陷,抗氧化补充剂可以作为治疗糖尿病性骨病、加速骨愈合和改善骨整合的一种有价值的辅助策略。