Hormonal receptor site alterations in the etiopathogenesis of otosclerosis.

The authors have studied calcium 45 uptake and cAMP intracellular levels in normal and otosclerotic bone cell cultures after stimulation with calcitonin in the presence or absence of propranolol. The results seem to demonstrate that poststimulatory 45Ca incorporation is slightly different in normal and otosclerotic cell cultures, being slower but longer lasting in the latter. Propranolol administration markedly inhibits 45Ca uptake in normal cells, while in otosclerotic cells a massive intracellular penetration becomes evident after an initial inhibitory phase. Also cAMP intracellular levels behave differently; a marked increase, followed by a rapid decrease, can be detected in normal cells after stimulation with calcitonin, while in otosclerotic cells, the increase is slower and followed by a long lasting reduction. Adding propranolol reduces cAMP levels in normal cells, while it increases levels in otosclerotic cells. The different behavior of calcium metabolism and cAMP levels after stimulation with calcitonin, depending upon the presence or absence of propranolol, seems to indicate an alteration of the transducing mechanism between stimulus, receptor, and cellular effector in otosclerotic cells.