作者: Jeffry S. Nyman
DOI: 10.1007/S12018-012-9124-Z
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摘要: Diabetes increases the likelihood of suffering a fracture, and in case type 2 diabetes mellitus (T2D), low bone mass does not explain this loss fracture resistance. Insulin contributes to accrual mass. As such, elevated risk among those with 1 (T1D) could be due deficit structure, especially if is poorly controlled. Clinical studies involving computed tomography scans do suggest that moment inertia cross-sectional area cortical accompany T1D. However, typically T2D, resistance arises from all hierarchical levels comprising organization bone’s constituents. One consequence diabetes, hyperglycemia, causes an increase non-enzymatic collagen crosslinks, also known as advanced glycation end products (AGEs). Increases AGEs within matrix are strongly correlated age-related decrease ability dissipate energy during failure (toughness toughness). While associated higher incidence mechanism by which crosslinking lowers fully delineated. The general concept cause phase become brittle, reducing capacity tissue resist formation propagation microdamage. certainly more research into diabetic effects on necessary before clear therapeutic options identified, should considered problem brittleness, just one strength.