Nonenzymatic glycation, bone quality, and microdamage in patients with type 2 diabetes

Individuals with type 2 diabetes paradoxically have increased fracture risk despite normal or greater bone density relative to non-diabetics, suggesting that impaired glucose metabolism degrades bone material properties. Formation of advanced glycation endproducts (AGEs) through nonenzymatic glycation of collagen associated with hyperglycemia has been proposed as a mechanism of impaired bone quality in diabetic bone, but the effect of AGEs on bone mechanical properties has not yet been investigated in bone tissue of patients with type 2 diabetes. The objective of this study is to relate alterations in collagen crosslinking, microdamage morphology, and structural properties that occur in the bone tissue of patients with type 2 diabetes relative to control patients. We expect to identify changes in collagen properties and microdamage patterns in patients with type 2 diabetes and to yield important new insights into the pathogenesis of diabetic fractures.

Collaborators:
Deepak Vashishth, PhD: Biomedical Engineering, Rensselaer Polytechnic Institute
Joseph Lane, MD: Orthopedics, Hospital for Special Surgery

Funding:
NIH/NIAMS K01AR064314