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The effects of calcium regulating hormones on bone resorption by isolated human osteoclastoma cells
Author(s) -
Chambers T. J.,
Fuller K.,
McSheehy P. M. J.,
Pringle J. A. S.
Publication year - 1985
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/path.1711450403
Subject(s) - bone resorption , resorption , calcitonin , endocrinology , medicine , chemistry , parathyroid hormone , prostaglandin e2 , calcium , stimulation , multinucleate , bone cell , osteoclast , cytoplasm , hormone , biology , microbiology and biotechnology , in vitro , biochemistry
Abstract Cells were disaggregated from osteoclastomas, and the response of the giant cells to calcium‐regulating hormones, prostaglandin (PG)E 1 and dibutyryl cyclic AMP (dbcAMP) was observed by phase‐contrast time‐lapse video microscopy. The pattern and nature of their response was very similar to that previously found to be characteristic of osteoclasts: calcitonin (CT), PGE 1 , and dbcAMP induced cytoplasmic quiescence, while parathyroid hormone (PTH) showed no influence on cytoplasmic motility or behaviour. The cells were also cultured on slices of devitalized cortical bone for 5 or 18 h. After this time the giant cells were associated with the appearance in the scanning electron microscope of characteristic resorption pits, the volume of which was calculated by computer‐assisted morphometric and stereophotogrammetric techniques after removal of cells. Calcitonin caused a dramatic reduction in the volume of bone resorbed by these isolated cells compared with control cultures, while PTH was without significant effect. This result supports the view that PTH does not increase bone resorption in intact bone through a direct effect on osteoclasts. PGE 1 which stimulates bone resorption when added to intact bone, paradoxically reduced resorption in our cultures. It thus appears possible that PGE 1 acts as a direct inhibitor of osteoclastic bone resorption but has an additional effect on other cells in bone, which are induced by PGE 1 to cause osteoclastic stimulation.