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Published on: July 8, 2021
Pentosidine effects on human osteoblasts in vitro.
Roberta Sanguineti1, Daniela Storace, Fiammetta Monacelli
1Division of Geriatrics, Deptartment of Internal Medicine and Medical Specialities, University of Genoa, Genoa, Italy.
Annals of the New York Academy of Sciences
|May 2, 2008
Summary
Advanced glycation end products (AGEs), like pentosidine, negatively impact bone health by reducing osteoblast function and mineralization. This study shows AGEs impair key bone-building processes, contributing to age-related bone loss and osteoporosis.
Area of Science:
- Biochemistry
- Cell Biology
- Bone Metabolism
Background:
- Osteoporosis is a metabolic bone disease marked by low bone mass and micro-architectural deterioration, increasing fracture risk.
- Age-related bone loss may be linked to the glycoxidative process, involving the formation of advanced glycation end products (AGEs).
Purpose of the Study:
- To investigate the in vitro effects of pentosidine, a specific AGE, on human osteoblasts (HOb).
- To evaluate the impact of pentosidine on osteoblast mineralization, specific bone markers, and receptor for advanced glycation end products (RAGE) gene expression.
Main Methods:
- Human osteoblasts (HOb) were incubated with pentosidine.
- Assessed mineralization rate, alkaline phosphatase (ALP), collagen Ialpha1 (COL Ialpha1), osteocalcin (BGP) gene expression, and RAGE gene expression.
- Evaluated the formation of bone nodules.
Main Results:
- Pentosidine significantly decreased ALP, Col Ialpha1, and RAGE mRNA levels in HOb.
- RAGE gene expression reduction was not dose-dependent.
- Pentosidine incubation inhibited bone nodule formation.
- No effect on BGP gene expression was observed.
Conclusions:
- Advanced glycation end products (AGEs) have a detrimental effect on bone by causing functional alterations in osteoblasts.
- Protein glycoxidation plays a critical role in bone mineralization.
- AGEs accumulation in bone may be an early pathogenetic step in bone remodeling during aging and age-related diseases, contributing to bone mass loss.
