Arancha R Gortázar1,2, Juan A Ardura3,4. 1. Bone Physiopathology laboratory, Applied Molecular Medicine Institute (IMMA), Universidad San Pablo-CEU, CEU Universities, Campus Monteprincipe, 28925, Alcorcón, Madrid, Spain. argortazar@ceu.es. 2. Departamento de Ciencias Médicas Básicas, Facultad de Medicina, Universidad San Pablo-CEU,CEU Universities, Campus Monteprincipe, 28925, Alcorcón, Madrid, Spain. argortazar@ceu.es. 3. Bone Physiopathology laboratory, Applied Molecular Medicine Institute (IMMA), Universidad San Pablo-CEU, CEU Universities, Campus Monteprincipe, 28925, Alcorcón, Madrid, Spain. 4. Departamento de Ciencias Médicas Básicas, Facultad de Medicina, Universidad San Pablo-CEU,CEU Universities, Campus Monteprincipe, 28925, Alcorcón, Madrid, Spain.
Abstract
PURPOSE OF REVIEW: Diabetes mellitus is a prevalent chronic disease affecting millions of people in the world. Bone fragility is a complication found in diabetic patients. Although osteoblasts and osteoclasts are directly affected by diabetes, herein we focus on how the diabetic state-based on hyperglycemia and accumulation of advanced glycation end products among other features-impairs osteocyte functions exerting deleterious effects on bone. RECENT FINDINGS: In the last years, several studies described that diabetic conditions cause morphological modifications on lacunar-canalicular system, alterations on osteocyte mechanoreceptors and intracellular pathways and on osteocyte communication with other cells through the secretion of proteins such as sclerostin or RANKL. This article gives an overview of events occurring in diabetic osteocytes. In particular, mechanical responses seem to be seriously affected in these conditions, suggesting that mechanical sensibility could be a target for future research in the field.
PURPOSE OF REVIEW: Diabetes mellitus is a prevalent chronic disease affecting millions of people in the world. Bone fragility is a complication found in diabetic patients. Although osteoblasts and osteoclasts are directly affected by diabetes, herein we focus on how the diabetic state-based on hyperglycemia and accumulation of advanced glycation end products among other features-impairs osteocyte functions exerting deleterious effects on bone. RECENT FINDINGS: In the last years, several studies described that diabetic conditions cause morphological modifications on lacunar-canalicular system, alterations on osteocyte mechanoreceptors and intracellular pathways and on osteocyte communication with other cells through the secretion of proteins such as sclerostin or RANKL. This article gives an overview of events occurring in diabetic osteocytes. In particular, mechanical responses seem to be seriously affected in these conditions, suggesting that mechanical sensibility could be a target for future research in the field.
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