Primary human osteoblast proliferation and prostaglandin E2 release in response to mechanical strain in vitro.
The application of mechanical loads to bone cells in vitro has been found to generate variable responses, which may in part be due to the source of the cell used and the characteristics of the strain applied. The aim of this study was to establish a system for applying well-defined physiological levels of mechanical strain to a well-defined population of human osteoblast-like cells. Human bone-derived cells obtained from the greater trochanter of the femur during total hip arthroplasty for osteoarthritis were cultured in the presence of 10 nmol/L dexamethasone and 100 mumol/L L-ascorbate-2-phosphate. Replicates of cells from each patient were loaded on separate occasions using controlled cyclical strains of 4000 microstrain (mu epsilon) or less. Strain gauges recorded reliable, reproducible strains between 1000 and 6000 mu epsilon. To establish reproducibility, sequential explant cultures derived from two patients were studied. A consistent increase (p < 0.05) in proliferation between replicates and explants derived from one patient subjected to 1600 mu epsilon on separate occasions was observed. Cells derived from sequential explants of the second patient showed no consistent increase in proliferation between replicates and explants. Three of six patients showed a significant increase (p < 0.05) in PGE2 production after 5 h in response to stretch (4000 mu epsilon) in all replicates on separate occasions, whereas, in the other three populations of cells, no increase in PGE2 was measured in any of the replicates. These results show that the application of highly controlled strains causes a significant effect on human bone cells, but only in a proportion of subjects. The response is consistent between sequential explants derived from the same patient. The implications of this study are that human osteoblast-like cells do respond to physiological strain in vitro, although some cells are more strain sensitive than others.
Fermor
B
B
Nuffield Department of Orthopaedic Surgery, Nuffield Orthopaedic Centre, Oxford, UK. Beverley.Fermor@ndos.ox.ac.uk
Gundle
R
R
Evans
M
M
Emerton
M
M
Pocock
A
A
Murray
D
D
D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D019644:Arthroplasty, Replacement, Hip; D001205:Ascorbic Acid / Q000031:analogs & derivatives* / Q000494:pharmacology; D002455:Cell Division; D002478:Cells, Cultured; D003907:Dexamethasone / Q000494:pharmacology*; D015232:Dinoprostone / Q000378:metabolism*; D005269:Femur / Q000502:physiology*; D006801:Humans; D010003:Osteoarthritis / Q000601:surgery; D010006:Osteoblasts / Q000378:metabolism / Q000502:physiology*; D015203:Reproducibility of Results; D013314:Stress, Mechanical
D000893:Anti-Inflammatory Agents; C011669:ascorbate-2-phosphate; D003907:Dexamethasone; D015232:Dinoprostone; D001205:Ascorbic Acid