In spite of intensive research, many of the events involved in the initiation of calcification of hard tissues have yet to be clarified [1-11]. At the present, the mechanisms underlying the initiation of calcification may be accounted by two alternative hypotheses. The first, considers that the [Ca]x[Pi] ion product reaches the threshold of precipitation as a consequence of accumulation of inorganic phosphate, by alkaline phosphatase activity [12]. The second hypothesis sustains that [Ca]x(Pi] ion product may remain at physiological levels, but a number of concerted physico-chemical and biochemical factors elicit the deposition of a mineral solid phase into a specific organic matrix [13]. While hypophosphatasia, a rare inheritable form of rickets, supports the role of alkaline phosphatase in the mineralization process in humans [6], the occurrence of an active form of this enzyme in many soft tissues which do not calcify, argues against Robison`s hypothesis. Moreover, the phosphoester concentrations required to provide sufficient inorganic phosphate to initiate calcium phosphate precipitation, should be far greater than the physiological levels. It should be stressed that the actual phosphoester concentration at the calcification front is unknown and that an increase in phosphate concentration alone is not sufficient to trigger mineralization in vitro [14]. Glucose-phosphate esters produced by glycolytic activity have also been suggested to be an important source of phosphoesters [15, 16]. However, other workers failed to confirm these observations [17].