Diabetes, Collagen, and Bone Quality

被引：110
作者：
Saito, Mitsuru [1 ]
Kida, Yoshikuni [1 ]
Kato, Soki [1 ]
Marumo, Keishi [1 ]
机构：
[1] Jikei Univ, Sch Med, Dept Orthopaed Surg, Minato Ku, Tokyo 1058461, Japan
来源：
CURRENT OSTEOPOROSIS REPORTS | 2014年 / 12卷 / 02期
关键词：
Diabetes; Bone quality; Collagen; Cross-links; Advanced glycation end products; Pentosidine; Homocysteine; Fracture risk; GLYCATION END-PRODUCTS; AGE-RELATED-CHANGES; PROTEIN CROSS-LINK; LYSYL OXIDASE; I COLLAGEN; BIOMECHANICAL PROPERTIES; NONENZYMATIC GLYCATION; FRACTURE RISK; GROWTH-FACTOR; OSTEOBLASTIC DIFFERENTIATION;
D O I：
10.1007/s11914-014-0202-7
中图分类号：
R5 [内科学];
学科分类号：
1002 ; 100201 ;
摘要：
Diabetes increases risk of fracture, although type 2 diabetes is characterized by normal or high bone mineral density (BMD) compared with the patients without diabetes. The fracture risk of type 1 diabetes as well as type 2 diabetes increases beyond an explained by a decrease of BMD. Thus, diabetes may reduce bone strength without change in BMD. Whole bone strength is determined by bone density, structure, and quality, which encompass the micro-structural and tissue material properties. Recent literature showed that diabetes reduces bone material properties rather than BMD. Collagen intermolecular cross-linking plays an important role in the expression of bone strength. Collagen cross-links can be divided into beneficial enzymatic immature divalent and mature trivalent cross-links and disadvantageous nonenzymatic cross-links (Advanced glycation end products: AGEs) induced by glycation and oxidation. The formation pathway and biological function are quite different. Not only hyperglycemia, but also oxidative stress induces the reduction in enzymatic cross-links and the formation of AGEs. In this review, we describe the mechanism of low bone quality in diabetes and the usefulness of the measurement of plasma or urinary level of AGEs for estimation of fracture risk.
引用
收藏
页码：181 / 188
页数：8
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