Tibiae from rachitic weanling rats were studied during healing to examine the mechanism of bone mineralization. Rickets was induced by feeding the animals a low phosphate, low vitamin D diet for five weeks. Calcification was reinstituted in three ways; group I animals received 1.0 ml of NaH2PO4 i.p. and the rachitogenic diet in a darkened room; group II animals were placed in a lighted room and given standard laboratory chow; group III animals were placed in lighted room, given standard laboratory chow and received 1.0 ml of 0.1M NaH2PO4 i.p. Group I healed slowly while II and III were found to heal rapidly and at nearly identical rates. Groups II and III revealed a significantly elevated serum alkaline phosphatase activity and became hyperphosphatemic as the rickets healed suggesting a more vigorous recovery. Ultrastructurally, numerous matrix vesicles were noted in unhealed rachitic bone matrix and these structures acquired mineral upon initiation of healing. Vesicle-associated mineral aggregates increased in size penetrating through and beyond the vesicle membrane and were incorporated into the advancing mineralization front. By 48 hrs. post-healing initiation, the osteoid borders were almost completely mineralized in groups II and III. These observations suggest that in addition to pre-existing mineral, matrix vesicles can also serve as nucleating sites in the osteoid of post-fetal bone.