In 20 intact and 20 parathyroidectomized female Sprague-Dawley rats, holes with a diameter of 1.8 mm were bored into the proximal third of the tibia. Half the animals served as controls and received the vehicle, the remainder received daily subcutaneous injections of 100 MRCmU calcitonin in 5 % gelatin. Tetracycline labelling was performed weekly. 5 animals from each group were sacrificed after 3 weeks, the other 5 after 6 weeks. Nondecalcified ground sections through the center of the holes were evaluated with an integration ocular; the surface of the newly formed bone was compared with the original size of the defect. The course of the regeneration for the control animals was in agreement with previous data in the literature. Calcitonin treatment produced a distinct acceleration of the healing process. Presumably, the hormone does not only act via inhibition of bone resorption, but also by stimulating the activity of osteoblasts and by increasing the mineralization of the osteoid seams.