PTH induces modification of transductive events in otosclerotic bone cell cultures.

We studied the effect of PTH (10-100 nM) on transductive mechanisms (adenylate cyclase activity, Ca2+ metabolism, IP3 levels) in cell cultures derived from normal and otosclerotic human bone fragments. The cultured cells were osteoblast-like but with calcitonin-receptors still present and with PTH receptors coupled with the adenylate cyclase system. The results showed that PTH activated adenylate cyclase and increased the intracellular Ca2+ levels with qualitative and quantitative differences between the two cellular populations. In particular, otosclerotic cells responded less to hormone stimulation, which is in accord with the current hypothesis of a desensitization of the receptor/enzyme complex associated with the pathological status.