Horm Metab Res 2010; 42(11): 763-768
DOI: 10.1055/s-0030-1262825
Review

© Georg Thieme Verlag KG Stuttgart · New York

Diabetes and Bone

P. Pietschmann1 , J. M. Patsch1 , G. Schernthaner2
  • 1Department of Pathophysiology and Allergy Research, Center of Pathophysiology, Infectiology and Immunology, Medical University of Vienna, Vienna, Austria
  • 2Department of Medicine I, Rudolfstiftung Hospital, Vienna, Austria
Further Information

Publication History

received 03.02.2010

accepted 07.07.2010

Publication Date:
13 August 2010 (online)

Abstract

Traditionally, patients with type 1 diabetes were regarded to be at an increased risk of fractures whereas type 2 diabetics were assumed to be protected from fractures since many of them have high bone mineral density. Nevertheless, several clinical studies consistently demonstrated that type 2 diabetes is a paradigm of a disease with an increased risk of fractures in the presence of high bone mass. The pathophysiology of decreased bone strength in diabetes mellitus is multifactorial: insulin deficiency, insulin resistance, osteoblast insufficiency, vitamin D deficiency, formation of advanced glycation endproducts in bone, and microvascular complications appear to contribute. Drugs used for the treatment of type 2 diabetes also may influence bone fragility: thiazolidinedione use has been associated with an increased risk of fractures.

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Correspondence

P. PietschmannMD 

Associate Professor

Department of Pathophysiology

and Allergy Research

Center of Pathophysiology,

Infectiology and Immunology

Medical University of Vienna

Währinger Gürtel 18–20

1090 Vienna

Austria

Phone: +43/140/400 5126

Fax: +43/140/400 5130

Email: peter.pietschmann@meduniwien.ac.at

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