[Calcitonin in treating bone and joint lesions--clinical and experimental findings and personal experience]

Several experimental studies in the animal models and the use of calcitonin in patients with osteoarthritis, rheumatoid arthritis, and osteoporosis have shown multiple actions of this hormone, justifying its use in the wide range of osteoarthritic pathologies. We used well known animal models of tests to study chondro-tropic drugs such as: post-corticoid arthropathy, partial meniscectomy, immobilization of the lower extremity of rabbits, follow-up of the natural knee degeneration in the black mouse C57, and radiolabelled sulphates uptake by the cartilage, and have shown: (a) anticatabolic effect of salmon calcitonin as measured as GAG levels, width of articular space, and histochemical and morphologic examination of the cartilage in some model arthropathies, (b) anti-osteoporotic properties counteracting an effect of corticosteroids, (c) increased uptake of sulphates by the articular cartilage of the rat following calcitonin administration in vivo. The studies explaining mechanisms of calcitonin actions included IGF-1 assays and beta-endorphins. The former increased transiently after calcitonin administration whereas the latter increased after non-steroid anti-inflammatory agents use. Calcitonin decreased gastrin secretion with negligible effect on calcium ions and prostaglandin E2 levels in blood plasma while it potently acid secretion and increasing gastric mucus content in the stomach. The use of calcitonin in patients with arthrosis, rheumatoid arthritis, and osteoporosis with accompanying peptic and/or duodenal ulcers produced healing of peptic and/or duodenal ulcers in 75% of patients within 4 weeks with simultaneous shortening of the morning stiffness, increase in hand grip strength (in rheumatoid arthritis), and significant decrease in pain as well as an improvement in the quality of life in the majority of the treated patients.(ABSTRACT TRUNCATED AT 250 WORDS)