title: Mechanisms of diabetes mellitus-induced bone fragility.
abstract: The risk of fragility fractures is increased in patients with either type 1 diabetes mellitus (T1DM) or type 2 diabetes mellitus (T2DM). Although BMD is decreased in T1DM, BMD in T2DM is often normal or even slightly elevated compared with an age-matched control population. However, in both T1DM and T2DM, bone turnover is decreased and the bone material properties and microstructure of bone are altered; the latter particularly so when microvascular complications are present. The pathophysiological mechanisms underlying bone fragility in diabetes mellitus are complex, and include hyperglycaemia, oxidative stress and the accumulation of advanced glycation endproducts that compromise collagen properties, increase marrow adiposity, release inflammatory factors and adipokines from visceral fat, and potentially alter the function of osteocytes. Additional factors including treatment-induced hypoglycaemia, certain antidiabetic medications with a direct effect on bone and mineral metabolism (such as thiazolidinediones), as well as an increased propensity for falls, all contribute to the increased fracture risk in patients with diabetes mellitus.
authors.affiliation: Unit of Endocrinology and Diabetes, Department of Medicine, Università Campus Bio-Medico di Roma, Via Alvaro di Portillo 21, 00128 Roma, Italy.|Division of Bone and Mineral Diseases, Washington University in St Louis, St Louis, Missouri, USA.|Diabetes and Bone Network.
authors.forename: Nicola
authors.initials: N
authors.lastname: Napoli
authors.affiliation: Osteoporosis and Bone Metabolism Unit, Department of Endocrinology, Singapore General Hospital, Outram Road, 169608 Singapore.
authors.forename: Manju
authors.initials: M
authors.lastname: Chandran
authors.affiliation: International Osteoporosis Foundation (IOF), Rue Juste-Olivier 9, 1260 Nyon, Switzerland.
authors.forename: Dominique D
authors.initials: DD
authors.lastname: Pierroz
authors.affiliation: University of Southern Denmark, Department of Medicine, Faculty of Health, Holbaek Hospital, Holbaek, Denmark.
authors.forename: Bo
authors.initials: B
authors.lastname: Abrahamsen
authors.affiliation: Department of Epidemiology and Biostatistics, University of California, 550 16th Street, San Francisco, California 94158, USA.
authors.forename: Ann V
authors.initials: AV
authors.lastname: Schwartz
authors.affiliation: Service of Bone Diseases, Geneva University Hospital and Faculty of Medicine, Rue Gabrielle-Perret-Gentil 4, 1205 Geneva, Switzerland.
authors.forename: Serge L
authors.initials: SL
authors.lastname: Ferrari
mesh_terms: D000058:Accidental Falls / Q000517:prevention & control; D000818:Animals; D015519:Bone Density / Q000187:drug effects / Q000502:physiology; D016723:Bone Remodeling / Q000187:drug effects / Q000502:physiology*; D003922:Diabetes Mellitus, Type 1 / Q000150:complications / Q000188:drug therapy / Q000378:metabolism*; D003924:Diabetes Mellitus, Type 2 / Q000150:complications / Q000188:drug therapy / Q000378:metabolism*; D050723:Fractures, Bone / Q000209:etiology / Q000378:metabolism*; D006801:Humans; D006943:Hyperglycemia / Q000150:complications / Q000188:drug therapy / Q000378:metabolism; D007004:Hypoglycemic Agents / Q000009:adverse effects / Q000627:therapeutic use
chemical_list: D007004:Hypoglycemic Agents