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In vitro Induction of Human Dental Pulp Stem Cells Toward Pancreatic Lineages

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Circulating osteogenic precursor cells in type 2 diabetes mellitus.

J S Manavalan¹, S Cremers, D W Dempster

¹Department of Medicine, College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA.

The Journal of Clinical Endocrinology and Metabolism

|June 29, 2012

Summary

Type 2 diabetes (T2D) is linked to lower bone formation due to fewer circulating osteogenic precursor cells. Mature osteogenic cells increase, indicating impaired bone building in T2D patients.

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Area of Science:

Endocrinology
Bone Biology
Metabolic Diseases

Background:

Type 2 diabetes (T2D) is associated with increased fracture risk and reduced bone formation.
The underlying mechanisms for impaired bone formation in T2D remain unclear.
Circulating osteogenic precursor (COP) cells are critical for bone formation and have been identified in peripheral blood.

Purpose of the Study:

To characterize the number and maturity of circulating osteogenic precursor (COP) cells in postmenopausal women with T2D.
To investigate potential mechanisms linking T2D to reduced bone formation.

Main Methods:

Cross-sectional study involving 18 postmenopausal women with T2D and 27 controls.
Flow cytometry used to quantify COP cells expressing osteocalcin (OCN) and CD146.
Histomorphometric and molecular analyses of bone turnover and oxidative stress markers were performed.

Main Results:

T2D patients had a lower percentage of circulating OCN(+) cells (0.8% vs. 1.6%) but a higher percentage of OCN(+)/CD146(+) cells (33.3% vs. 12.0%).
Reduced bone formation indices were observed in T2D, including lower mineralizing surface, bone formation rate, and osteoblast surface.
T2D subjects exhibited decreased Runx2 gene expression and increased oxidative stress markers (p66Shc, SOD2).

Conclusions:

T2D is characterized by decreased circulating osteogenic precursor cells (OCN+) and increased immature/mature OCN+/CD146+ cells.
Impaired osteoblast activity and increased oxidative stress contribute to reduced bone formation in T2D.
Therapeutic strategies targeting bone formation stimulation may benefit skeletal health in T2D.