Hydroxyapatite (Calcium phosphate) (HAP)

Calcium-based mineral deposits, primarily in the form of hydroxyapatite [Ca10(PO4)6(OH)2], are the hallmark of vascular calcification, a pathological process where mineral is deposited in the intimal or medial layers of blood vessels (Schiantarelli et al., 2020, Frontiers in Cardiovascular Medicine). This process is highly prevalent in patients with chronic kidney disease (CKD), diabetes, and advanced age, leading to increased arterial stiffness, hypertension, and high cardiovascular mortality (Durham et al., 2018, Circulation Research). While traditionally viewed as a passive process of calcium-phosphate precipitation, it is now recognized as an active, cell-mediated biological event resembling osteogenesis (Leopold, 2015, Circulation). Therapeutic strategies target these deposits by inhibiting the nucleation and growth of hydroxyapatite crystals or by enhancing endogenous inhibitors like pyrophosphate (Perelló et al., 2018, British Journal of Clinical Pharmacology). Drugs such as SNF472 (myo-inositol hexaphosphate) and sodium thiosulfate are used to interact directly with the mineral phase to prevent further deposition or facilitate dissolution (Nigwekar et al., 2013, CJASN). Managing these deposits is critical for reducing cardiovascular risk, though care must be taken to avoid interfering with systemic bone mineralization (O'Neill et al., 2011, Kidney International). The presence of these deposits is often quantified using the Coronary Artery Calcium (CAC) score, which serves as a powerful predictor of future cardiovascular events (Budoff et al., 2018, JACC).

Other names

Vascular calcificationCalcium phosphate depositsMedial arterial calcificationIntimal calcificationAortic calcificationEctopic mineralization

Inhibition of hydroxyapatite crystal nucleation and growth through surface binding or calcium chelation (Perelló et al., 2018; Nigwekar et al., 2013).