ArticleScientific reports2019
In vivo Labeling of Bone Microdamage in an Animal Model of Type 1 Diabetes Mellitus.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Integrated apoptotic extracellular vesicle-recruitment peptide coating reprograms the diabetic bone microenvironment and orchestrates enhanced implant osseointegration.Bioactive materials · 2026Article
- Microdamage in biological hard tissues and its repair mechanisms.Biomedical engineering online · 2025Review
- Phytochemicals in Bone Therapy: Exploring Natural Alternatives for Bone Health.International journal of nanomedicine · 2025Review
- Gender-Specific Risk Factors for Asymmetric Bone Density in Adult Degenerative Lumbar Scoliosis: A Retrospective Cohort Analysis.Medical science monitor : international medical journal of experimental and clinical research · 2024Article
- Review
- Effect of non-enzymatic glycation on collagen nanoscale mechanisms in diabetic and age-related bone fragility.Biocell : official journal of the Sociedades Latinoamericanas de Microscopia Electronica ... et. al · 2023Article
- Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type 1 diabetes mellitus (DM1) is linked to a decrease in bone strength. Bone strength entails both bone mineral density and bone quality. Limited data are available regarding diabetes-induced microdamage, which can severely influence bone quality. This study has investigated bone microdamage as a measure of bone quality in an animal model of DM1. Microdamage in the neck of the femur was labelled in vivo using multiple fluorochromes at 4, 12 and 24 weeks after the onset of DM1. Microcracks were quantified and their morphology analyzed using microscopy techniques. The mean length of microcracks at 24 weeks, and crack numerical and surface densities were significantly higher (p < 0.05) 4 weeks after the onset of DM1 when compared with control. Diffuse damage density was highest at 12 weeks after the onset of DM1. The arrangement of the collagen fibrils became progressively more irregular from 4 to 24 weeks of DM. This is the first study to analyze microdamage in vivo at different time points of DM1. DM1is associated with microcracks from the early stage, however bone microstructure shows toughening mechanisms that arrest their growth but disease progression further deteriorates bone quality resulting in longer microcracks which may increase fracture risk.
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