Long-duration type 1 diabetes is associated with deficient cortical bone mechanical behavior and altered matrix composition in human femoral bone
Authors' conclusion
Thus, the impairment of cortical bone to absorb energy following long-duration T1D is well explained by AGE accumulation and modifications to the bone matrix.
Study context
- Population
- Cadaveric femora from older adults with long-duration T1D (≥50 yr) and age- and sex-matched nondiabetic controls
- Participants
- 20 vs 14
- Exposure
- Long-duration T1D vs nondiabetic controls
- T1Dn = 20
- Nondiabetic controlsn = 14reference
- Outcome
- Cortical bone material behavior: mechanical testing, AGE quantification and matrix composition via Raman spectroscopy
Methodological detailscadaveric femora, age- and sex-matched controls
- Cadaveric femora
- Age- and sex-matched controls
Main finding
As reported in the abstract
Cortical bone properties, T1D vs nondiabetics
- Postyield toughness to fracture, T1D vs nondiabetics
- −30%, p = .036
- AGEs (pentosidine), T1D vs nondiabetics
- +17%, p = .039
- Mineral crystallinity, T1D vs nondiabetics
- −1.4%, p = .010
- Proline hydroxylation, T1D vs nondiabetics
- +1.9%, p = .009
- Glycosaminoglycan (GAG) content, T1D vs nondiabetics
- −1.3%, p < .03
Observational data: associations, not effects.
Further findings
Multiple regression models predicting cortical bone toughness
- Cortical tissue mineral density, carboxymethyl lysine (CML), and Raman measures of enzymatic collagen crosslinks and GAG content remained highly significant predictors; diabetic status no longer significant
- adjusted R2 > 0.60, p < .001
Original publication
Long-duration type 1 diabetes is associated with deficient cortical bone mechanical behavior and altered matrix composition in human femoral bone. J Bone Miner Res. Published 19 November 2024. doi:10.
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