The bone formation of periarticular connective tissue after head injury and total hip arthroplasty is included in the category of heterotopic ossification. Induction of a new bone formation in the soft tissue is related to various materials such as bone morphogenic protein. The alkaline phosphatase and acid phosphatase act as important factors in the formation and absorption of the bone. The acid phospatase has the important function of acting as the control with specific activity of phosphatase in vivo. Cholecalciferol induces absorption of the calcium in the alimentary tract and bone resorption and increment of bone calcification, whereas disodium etidronate inhibits the deposition and dissolution of calcium salt and formation of heterotopic bone. This paper reports on the relationship of alkaline phosphatase and various phosphoaminoacid phosphatase which affect the cellular differentiation and remodelling in the heterotopic ossification, with the effect of cholecalciferol and disodium etidronate on the heterotopic bone induction in rats. The following results were obtained: 1. The contents of the calcium in the implanted bone matrix increased markedly from two to five weeks. There was no changes in the calcium content by cholecalciferol or in the administration of small doses of disodium etidronate (5mg/kg). However, in the administration of large dose of disodium etidronate (25mg/kg), calcium mobilization was totally suppressed for the whole period of the experiment. 2. The protein content in the implanted bone matrix did not much change for the whole period of the experiment and the administratinn of cholecalciferol or disodium etidronate also had no effect on the protein content. 3. The activities of alkaline phosphatase in the implanted bone matrix peaked at two weeks in control or cholecalciferol group, whereas disodium etidronate admninstration caused the highest activity in the third week. 4. The activity of acid phosphatase in the implanted bone matrix increased in first and third weeks by cholecalciferol treatment. Disoidum etidronate inhibited the activity of the acid phosphatase in the first, fourth & sixth weeks of implantation. 5. The activity of phosphoserine phosphatase increased due to cholecalciferol treatment, but was significantly inhibited by disodium etidronate (25mg/kg) treatment. 6. The activity of phosphothreonine phosphatase in the implanted bone matrix slightly increased due to cholecalciferol treatment, whereas the activity decreased significantly for the whole period of the experiment by disodium etidronate (25mg/kg) treatment. 7. The activity of phosphotyrosine phosphatase in the implanted bone matrix was not change much for the whole period of the experiment and the administration of cholecalciferol or disodium etidronate had no effect on the activity of phosphotyrosine phosphatase. In conclusion, the disodium etidronate (25mg/kg) almost completely inhibited the molilization of calcium and the activities of acid phosphatase, phosphoserine and phosphothreonine phosphatases. Therefore, it can be suggested that the above phosphatases are closely related to the action mechanism of disodium etidronate.