Abstract
Background: Greater tuberosity disuse osteoporosis is a consequence of rotator cuff tear. This is a significant problem as the tendon is implanted into a trough within the greater tuberosity during repair. Failure of the repair is a common complication (up to 50%). We hypothesise that failure in re-implantation is due to deficient bone cell response to mechanical stimulation in the tuberosity.
Methods: In order to establish whether these cells are capable of responding appropriately to mechanical stimuli, the response of bone cells derived from the tuberosity was compared with that of cells derived from the acromion. This was measured in terms of strain related increases in alkaline phosphatase (ALP) activity and nitric oxide (NO) production (which are recognised markers of osteoblast differentiation and their response to mechanical strain). Primary osteoblasts were cultured from samples of acromion and greater tuberosity taken during routine rotator cuff repair (n=10 pairs). The derived cells were:
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Placed under cyclic strain at a physiological magnitude for 10 minutes at 1Hz using well established controls. Samples of media were analyzed for changes in NO and the cells were reacted for ALP activity, or:
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Stimulated with dexamethasone, (an established mediator of osteoblast differentiation) then reacted for ALP activity.
Results: The results suggest that cells derived from the acromion exhibit significant strain related increases in cellular NO release and in ALP activity, whereas cells derived from the humeral greater tuberosity fail to exhibit any such increases. In marked contrast, cells derived from both sites exhibit increases in ALP activity in response to dexamethasone treatment.
Conclusions: Our results suggest that whilst cells derived from the tuberosity, after rotator cuff tear, respond appropriately to chemical and hormonal stimuli, they are compromised in their ability to respond to mechanical stimulation. Therefore, it is tempting to speculate that such relationships are also evident in vivo and that they underpin re-implantation failures.
The abstracts were prepared by David Stanley. Correspondence should be addressed to him c/o British Orthopaedic Association, Royal College of Surgeons, 35–43 Lincoln’s Inn Fields, London WC2A 3PN.
