Advanced glycation end-product adducts alter the bone collagen network and human cortical bone fracture resistance.

ABSTRACT: Elevated levels of AGEs have been implicated in the increased fracture risk of type 2 diabetes (T2D) and CKD patients. AGEs are widely thought to "over-crosslink" bone collagen, making it stiff and less ductile, leading to reduced cortical bone fracture resistance. This idea is primarily based on in vitro studies where predominately pentosidine, an AGE crosslink, has been used as a biomarker for AGEs. However, more recent studies have found that non-crosslinking AGE adducts to be roughly 40-200 times more abundant than pentosidine in human specimens. In addition, ex vivo studies have shown a denatured and less connected collagen network is associated with reduced fracture resistance. This highlights a disconnect in understanding regarding how AGEs impact cortical bone fragility. Specifical

SUBMITTER: Dapaah DY 

PROVIDER: S-EPMC12771375 | biostudies-literature | 2026 Jan

REPOSITORIES: biostudies-literature