Vashishth Deepak
Center of Biotechnology and Interdisciplinary Studies, Rensselaer Polytechnic Institute, Troy, NY 12180, USA.
Curr Osteoporos Rep. 2007 Jun;5(2):62-6. doi: 10.1007/s11914-007-0004-2.
The collagen network in bone provides resistance against fracture and may be susceptible to changes with aging and disease. This review identifies the changes in quality of collagen matrix as contributors to bone fragility. With aging and in diabetes, cross-links accumulate in bone collagen as a result of nonenzymatic glycation and consequently impair matrix properties, increasing bone fragility. Cell-culture and animal studies suggest that the accumulation of cross-links induced by nonenzymatic glycation may be related to a reduction in bone turnover resulting from the altered responses of osteoblasts and osteoclasts to advanced glycation end products.
骨骼中的胶原蛋白网络可抵抗骨折,并且可能会随着衰老和疾病而发生变化。本综述确定胶原蛋白基质质量的变化是导致骨脆性增加的因素。随着年龄增长以及在糖尿病状态下,由于非酶糖基化作用,交联物在骨胶原蛋白中积累,从而损害基质特性,增加骨脆性。细胞培养和动物研究表明,非酶糖基化诱导的交联物积累可能与成骨细胞和破骨细胞对晚期糖基化终产物反应改变导致的骨转换减少有关。