Abstract
Calcitonin has been used in the treatment of Paget's Disease of bone because of its ability to inhibit osteoclastic bone resorption. This results in a return of bone turnover towards normal, as reflected by urinary hydroxyproline and serum alkaline phosphatase. A plateau is reached with these parameters, at about 50% of the pre-treatment level. The cause of this plateau is unknown, but does not indicate resistance to treatment, since it occurs with all forms of calcitonin. Most treated patients experience pain relief, and there is radiological and histological evidence of arrested progression of Paget's Disease in patients treated with calcitonin. Both primary and secondary resistance to calcitonin occur with all calcitonins, including homologous hormone. Antibodies develop commonly in patients treated with pig or salmon calcitonin, but antibody-based clinical resistance has been demonstrated only in a few patients. Methods of selection of patients for treatment and of assessment of response are discussed, and treatment schedules summarized.