ArticleJBMR plus2026
Advanced glycation end-product adducts alter the bone collagen network and human cortical bone fracture resistance.
Article in JBMR plus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
5 citing papers in PubMed.
- Is direct oxidative damage of bone collagen associated with poor human cortical bone tissue fracture resistance?JBMR plus · 2026Article
- Sites of non-enzymatic crosslinks pentosidine and glucosepane in collagen I of human cortical bone.Bone · 2026Article
- Comprehensive profiling of the competitive interplay among carbamylation, glycation, and enzymatic cross-links in human bone.JBMR plus · 2026Article
- Regenerative Therapies for Cosmetic Dermatology for Patients with Diabetes Mellitus: Skin Aging, Aesthetic Concerns, and Evidence-Based Best Practices.International journal of molecular sciences · 2026Review
- Differences and similarities in cortical bone of the femur between donors with and without type 2 diabetes.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2026Article
Corrections and comments
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Authors and funding
7 authors.
Funding
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. Specifically, the relationships between AGEs, bone collagen network properties, and cortical bone fracture toughness are poorly understood. Three AGE adducts (carboxy-methyl-lysine, carboxy-ethyl-lysine, 5-hydro-5-methyl-4-imidazolon-2-yl-ornithine 1), pentosidine, collagen network measures, and the fracture toughness of cortical bone specimens from a large heterogenous group of 80 human donors with and without a history of T2D and/or CKD were measured ex vivo. The AGE adducts contents were 57%-63% higher in the T2D/CKD group compared to the controls and were 70-830 times more abundant than pentosidine. The AGE adducts also correlated negatively and strongly with hydroxylysinonorleucine (HLNL), an immature lysyl oxidase-mediated crosslink (
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Registered trials
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