Characterization of deposits in patients with calcific tendinopathy of the supraspinatus. Role of phytate and osteopontin.

Calcific tendinopathy of the tendons of the rotator cuff is common in adults. These calcifications tend to be reabsorbed after a period of acute pain. This study evaluated the morphologic characteristics of calcific deposits and the participation of phytate and osteopontin (OPN) in their development. Calcific deposits were removed from 21 patients with calcific tendinopathy by ultrasound-guided needle puncture under local anesthesia. The removed deposits were evaluated by scanning electron microscopy, X-ray diffraction and Fourier transform infrared spectroscopy. The amounts of calcium and phosphorus in the deposits were semi-quantitatively determined by energy dispersive X-ray analysis. Phytate was determined in 2 h urine samples, and OPN was extracted from a pool of deposits. The calcific deposits consisted of amorphous and poorly crystalline carbonated hydroxyapatite containing molecular water and organic matter. OPN was associated with the hydroxyapatite deposits. Phytate concentrations were significantly lower in the urine of patients with calcific tendinopathy than in healthy controls. The deficit in crystallization inhibitors such as phytate, and the presence of regulators such as OPN, may play important roles in the development of calcific tendinopathy.

Phytate (Myo-inositol hexakisphosphate) inhibits cardiovascular calcifications in rats.

Calcification is an undesirable disorder, which frequently occurs in the heart vessels. In general, the formation of calcific vascular lesions involves complex physicochemical and molecular events. Calcification (hydroxyapatite) is initiated by injury and is progressed by promoter factors and/or the deficit of inhibitory signals. Myo-inositol hexakisphosphate (phytate, InsP6) is found in organs, tissues and fluids of all mammals and exhibits an important capacity as a crystallization inhibitor of calcium salts in urine and soft tissues. The levels found clearly depend on the dietary intake but it can also be absorbed topically. In this paper, the capacity of InsP6 as a potential inhibitor of cardiovascular calcifications was assessed in Wistar rats. Three groups were included, a control group, an InsP6 treated group (subjected to calcinosis induction by Vitamin D and nicotine and treated with standard cream with a 2% of InsP6 as potassium salt) and an InsP6 non-treated group (only subjected to calcinosis induction). All rats were fed AIN 76-A diet (a purified diet in which InsP6 is undetectable). Animals were monitorized every 12 hours. After 60 hours of calcinosis treatment, all rats of the InsP6 non-treated group died and the rest were sacrificed. Aortas and hearts were removed. A highly significant increase in the calcium content of aorta and heart tissue was observed in the InsP6 non-treated rats (21 +/- 1 mg calcium/g dry aorta tissue, 10 +/- 1 mg calcium/g dry heart tissue) when compared with controls (1.3 +/- 0.1 mg calcium/g dry aorta tissue, 0.023 +/- 0.004 mg calcium/g heart dry tissue) and InsP6 treated (0.9 +/- 0.2 mg calcium/g dry aorta tissue, 0.30 +/- 0.03 mg calcium/g dry heart tissue) animals. Only InsP6 non-treated rats displayed important mineral deposits in aorta and heart. These findings are consistent with the action of InsP6, as an inhibitor of calcification of cardiovascular system.