TY - JOUR
T1 - Update on the pathogenesis and treatment of skeletal fragility in type 2 diabetes mellitus
AU - Khosla, Sundeep
AU - Samakkarnthai, Parinya
AU - Monroe, David G.
AU - Farr, Joshua N.
N1 - Publisher Copyright:
© 2021, Springer Nature Limited.
PY - 2021/11
Y1 - 2021/11
N2 - Fracture risk is increased in patients with type 2 diabetes mellitus (T2DM). In addition, these patients sustain fractures despite having higher levels of areal bone mineral density, as measured by dual-energy X-ray absorptiometry, than individuals without T2DM. Thus, additional factors such as alterations in bone quality could have important roles in mediating skeletal fragility in patients with T2DM. Although the pathogenesis of increased fracture risk in T2DM is multifactorial, impairments in bone material properties and increases in cortical porosity have emerged as two key skeletal abnormalities that contribute to skeletal fragility in patients with T2DM. In addition, indices of bone formation are uniformly reduced in patients with T2DM, with evidence from mouse studies published over the past few years linking this abnormality to accelerated skeletal ageing, specifically cellular senescence. In this Review, we highlight the latest advances in our understanding of the mechanisms of skeletal fragility in patients with T2DM and suggest potential novel therapeutic approaches to address this problem.
AB - Fracture risk is increased in patients with type 2 diabetes mellitus (T2DM). In addition, these patients sustain fractures despite having higher levels of areal bone mineral density, as measured by dual-energy X-ray absorptiometry, than individuals without T2DM. Thus, additional factors such as alterations in bone quality could have important roles in mediating skeletal fragility in patients with T2DM. Although the pathogenesis of increased fracture risk in T2DM is multifactorial, impairments in bone material properties and increases in cortical porosity have emerged as two key skeletal abnormalities that contribute to skeletal fragility in patients with T2DM. In addition, indices of bone formation are uniformly reduced in patients with T2DM, with evidence from mouse studies published over the past few years linking this abnormality to accelerated skeletal ageing, specifically cellular senescence. In this Review, we highlight the latest advances in our understanding of the mechanisms of skeletal fragility in patients with T2DM and suggest potential novel therapeutic approaches to address this problem.
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U2 - 10.1038/s41574-021-00555-5
DO - 10.1038/s41574-021-00555-5
M3 - Review article
C2 - 34518671
AN - SCOPUS:85114810311
SN - 1759-5029
VL - 17
SP - 685
EP - 697
JO - Nature Reviews Endocrinology
JF - Nature Reviews Endocrinology
IS - 11
ER -