Osteoporosis and vascular calcifications.

Area of Science:

• Bone biology and vascular health
• Metabolic and endocrine regulation

Background:

• Post-menopausal women, elderly individuals, and patients with diabetes or chronic kidney disease experience decreased bone mineral density (BMD) and arterial calcifications (ACs).
• Low BMD and fragility fractures are associated with increased cardiovascular events and mortality.
• Abdominal aorta calcifications correlate with reduced BMD in adjacent bones, indicating a link between vascular pathology and bone fragility.

Purpose of the Study:

• To explore the reciprocal relationship between bone metabolism and vascular calcification.
• To identify shared regulatory pathways and molecular mechanisms involved in bone loss and arterial calcification.

Main Methods:

• Review of animal and in vitro models investigating bone-vascular interactions.
• Analysis of potential molecular regulators including vitamin K, vitamin D, advanced glycation end-products, osteoprotegerin/RANKL/RANK system, Fetuin A, estrogen, and microbiota.

Main Results:

• Ectopic biomineralization in ACs involves osteogenic transdifferentiation of vascular smooth muscle cells.
• Shared regulatory molecules, often acting in reverse for bone and vascular health, have been identified.
• Potential mechanisms include vitamin sufficiency, RAGE interaction, hormonal status, and microbiota.

Conclusions:

• The interplay between bone and vascular health is complex, involving shared molecular pathways.
• Further clinical validation of identified mechanisms is needed.
• Elucidating these mechanisms could pave the way for interventions promoting simultaneous bone and vascular health.