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Advanced glycation end products and bone loss during aging
Patrizio Odetti1, Simona Rossi, Fiammetta Monacelli
1Division of Geriatrics, Department of Internal Medicine and Medical Specialties (D.I.M.I.), Viale Benedetto XV, 6, 16132 Genova, Italy. odetti@unige.it
Annals of the New York Academy of Sciences
|July 23, 2005
Summary
Advanced glycation end product pentosidine increases with age in cortical bone, correlating with bone density loss. Plasma pentosidine also rises with age and may reflect bone turnover rates.
Area of Science:
- Biochemistry
- Gerontology
- Orthopedics
Background:
- Bone mass density naturally declines with aging.
- Nonenzymatic glycation is a potential contributor to age-related bone loss.
- Advanced glycation end products (AGEs) accumulate in tissues over time.
Purpose of the Study:
- To investigate the concentration of pentosidine, an AGE, in human cortical bone, trabecular bone, and plasma.
- To assess the relationship between pentosidine levels and age.
- To correlate pentosidine concentrations with a clinical index of osteoporosis (Singh index).
Main Methods:
- Quantified pentosidine levels in cortical bone, trabecular bone, and plasma from 104 non-diabetic subjects (mean age 72).
- Determined pentosidine using High-Performance Liquid Chromatography (HPLC) after bone decalcification and hydrolysis.
- Assessed osteoporosis severity using the radiologic Singh index, evaluated by orthopedic surgeons.
Main Results:
- Cortical bone pentosidine showed a significant exponential increase with age (r=0.610, P<0.001).
- Trabecular bone pentosidine levels were highly variable and did not show a clear age-related trend.
- Cortical pentosidine correlated negatively with the Singh index (r(s)=-0.274, P<0.01), indicating a link to osteoporosis.
- Plasma pentosidine exhibited a significant exponential correlation with age (r=+0.339, P<0.001) and a linear correlation with cortical pentosidine (r=+0.248, P<0.05).
Conclusions:
- Pentosidine accumulation in cortical bone increases exponentially with aging, serving as a biomarker for bone density loss.
- Trabecular bone pentosidine variability may be due to turnover rates and local factors.
- Plasma pentosidine levels correlate with age and cortical bone pentosidine, potentially indicating bone turnover status.