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DOI: 10.1055/s-0030-1262825
© Georg Thieme Verlag KG Stuttgart · New York
Diabetes and Bone
Publikationsverlauf
received 03.02.2010
accepted 07.07.2010
Publikationsdatum:
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.
Key words
diabetes mellitus - advanced glycosylation endproducts - osteocalcin - thiazolidinediones - runx2 - PPARγ
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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
Telefon: +43/140/400 5126
Fax: +43/140/400 5130
eMail: peter.pietschmann@meduniwien.ac.at