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Author Spotlight: An Economic and Efficient Method for Quantitative Evaluation of Bone Microarchitecture in a Murine Osteoporosis Model
Published on: September 8, 2023
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[Bone quality].
Nihon Rinsho. Japanese Journal of Clinical Medicine
|November 5, 2015
Summary
Bone collagen crosslinking is vital for bone strength. Deterioration of these crosslinks, indicated by pentosidine and homocysteine levels, may signal increased fracture risk in conditions like diabetes and kidney disease.
Area of Science:
- Biomedical Engineering
- Orthopedics
- Metabolic Diseases
Background:
- Bone quality is determined by structural and material properties.
- Collagen crosslinking is crucial for bone strength.
- Lysyl oxidase control and non-enzymatic crosslinks (AGEs, pentosidine) are key collagen components.
Purpose of the Study:
- To investigate the role of collagen crosslinking in bone quality.
- To explore the association between collagen crosslink deterioration and osteoporotic fractures in patients with diabetes and chronic kidney disease.
- To evaluate pentosidine and homocysteine as potential biomarkers for bone collagen deterioration.
Main Methods:
- Analysis of quantitative and qualitative changes in collagen crosslinks.
- Assessment of lysyl oxidase control and non-enzymatic crosslinks (AGEs, pentosidine).
- Measurement of urinary or plasma pentosidine and homocysteine levels.
Main Results:
- Deterioration of collagen crosslinking, including advanced glycation end products (AGEs) and pentosidine, is observed in patients with osteoporotic femoral neck fracture, diabetes, and chronic kidney disease.
- Increased oxidative stress and glycation may contribute to this deterioration.
- Higher urinary or plasma pentosidine and homocysteine levels are independently associated with osteoporotic fracture risk.
Conclusions:
- Measurements of serum homocysteine and serum or urine pentosidine may serve as markers for bone collagen deterioration.
- These findings, if confirmed in prospective trials, could aid in assessing fracture risk.
- Targeting oxidative stress and glycation pathways may be beneficial for bone health in at-risk populations.
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