Clinical and experimental studies indicate that calcification of bioprosthetic valves depends on host, implant, and biomechanical factors. The earliest mineral deposits in both clinical and experimental bioprosthetic tissue are localized to transplanted connective tissue cells; collagen involvement occurs later. Passive calcium entry occurs unimpeded in cells modified by aldehyde cross-linking, but the mechanisms for calcium removal are dysfunctional; calcium influx contributes to apatite formation by reacting with compartmentalized, bound phosphorus. Specific strategies for prevention of biopros- thetic tissue mineralization involve modification of either valve preparation details or the local implant environment. Efficacy, mechanisms and safety must be demonstrated for any antimineralization strategy. (Eur J Cardio-thorac Surg (1992) 6 (Suppl 11: S91-S94)