Background: Understanding the mechanism of calcium deposition in soft tissues is of great importance in a variety of pathological conditions such as chronic kidney disease. The present study examined the role of phytate and osteopontin during the development of soft tissue calcification in an animal model.
Methods: Male Wistar rats (16 rats per treatment) were fed with a diet (AIN-76A) in which phytate is undetectable (non-phytate-treated group), or with a phytin-enriched AIN-76A diet (phytate-treated group). After 21 days on the respective diets, all rats were subjected to calcinosis induction by subcutaneous injection with KMnO4 at 2 sites on either side of the interscapular region. At 2, 5, 8 and 10 days after the calcinosis induction, 4 rats of each group were sacrificed, and the injured tissues were removed for histological analysis and for calcium determination.
Results: Calcification was notably and significantly reduced in phytate-treated rats compared with non-phytate-treated rats. Calcified deposits appeared as soon as 2 days after calcinosis induction, but inflammation with the presence of macrophages, lymphocytes and eosinophils was not typically observed until 5 days postinduction. Osteopontin was only detected 8 days postinduction, and was clearly associated with calcified areas.
Conclusions: The results suggest an important role for crystallization inhibitors such as phytate in reducing hydroxyapatite crystal formation in the first steps of soft tissue calcification. Histological analysis indicated that osteopontin was not involved during initiation of soft tissue calcification. Osteopontin appears be involved in the control of calcification rather than its genesis.