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World J Orthop. Nov 18, 2010; 1(1): 3-9
Published online Nov 18, 2010. doi: 10.5312/wjo.v1.i1.3
Bone fragility in type 2 diabetes mellitus
Toru Yamaguchi
Toru Yamaguchi, Internal Medicine 1, Shimane University Faculty of Medicine, Shimane 693-8501, Japan
Author contributions: Yamaguchi T contributed solely to this paper.
Correspondence to: Toru Yamaguchi, MD, PhD, Associate Professor, Internal Medicine 1, Shimane University Faculty of Medicine, 89-1, Enya-cho, Izumo, Shimane 693-8501, Japan. yamaguch@med.shimane-u.ac.jp
Telephone: +81-853-202183 Fax: +81-853-238650
Received: June 24, 2010
Revised: July 27, 2010
Accepted: August 4, 2010
Published online: November 18, 2010

The number of patients with osteoporosis or type 2 diabetes mellitus (T2DM) is increasing in aging and westernized societies. Both disorders predispose elderly people to disabling conditions by causing fractures and vascular complications, respectively. It is well documented that bone metabolism and glucose/fat metabolism are etiologically related to each other through osteocalcin action and Wnt signaling. Bone fragility in T2DM, which is not reflected by bone mineral density (BMD), depends on bone quality deterioration rather than bone mass reduction. Thus, surrogate markers are needed to replace the insensitivity of BMD in assessing fracture risks of T2DM patients. Pentosidine, the endogenous secretory receptor for advanced glycation endproducts, and insulin-like growth factor-I seem to be such candidates, although further studies are required to clarify whether or not these markers could predict the occurrence of new fractures of T2DM patients in a prospective fashion.

Keywords: Osteoporosis, Type 2 diabetes mellitus, Fracture risk, Osteocalcin, Wnt signaling