Abstract

We examined cultured osteoblasts derived from paired samples from the greater tuberosity and acromion from eight patients with large chronic tears of the rotator cuff. We found that osteoblasts from the tuberosity had no apparent response to mechanical stimulation, whereas those derived from the acromion showed an increase in alkaline phosphatase activity and nitric oxide release which is normally a response of bone cells to mechanical strain. By contrast, we found that cells from both regions were able to respond to dexamethasone, a well-established promoter of osteoblastic differentiation, with the expected increase in alkaline phosphatase activity. Our findings indicate that the failure of repair of the rotator cuff may be due, at least in part, to a compromised capacity for mechanoadaptation within the greater tuberosity. It remains to be seen whether this apparent decrease in the sensitivity of bone cells to mechanical stimulation is the specific consequence of the reduced load-bearing history of the greater tuberosity in these patients.

Highlights

  • We found that osteoblasts from the tuberosity had no apparent response to mechanical stimulation, whereas those derived from the acromion showed an increase in alkaline phosphatase activity and nitric oxide release which is normally a response of bone cells to mechanical strain

  • Previous studies have shown that both increases in mechanical loading in vivo and the application of direct mechanical strain to cells derived from normal bone in vitro induce the differentiation of osteoblasts.[22,23]

  • We found that acromial osteoblasts had statistically significant increases in alkaline phosphatase activity/cell when exposed to mechanical strain, but not in response to medium perturbation alone (Fig. 2)

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Summary

Introduction

We found that osteoblasts from the tuberosity had no apparent response to mechanical stimulation, whereas those derived from the acromion showed an increase in alkaline phosphatase activity and nitric oxide release which is normally a response of bone cells to mechanical strain. Re-implantation of the ruptured tendon of supraspinatus into the greater tuberosity of the humerus fails in up to 50% of cases.[2] A tear of the rotator cuff is often accompanied by thinning of the trabecular and cortical bone in the greater tuberosity as well as loss of the normal cortical contour This would appear to be the result of disuse osteoporosis which, in turn, seems to be a factor contributing to the poor outcome of repairs of the rotator cuff.[3] It is not known if the bone of the greater tuberosity in these patients has an impaired mechanoadaptive response to re-implantation of the tendon of supraspinatus, and, if so, whether this contributes to the high rate of failure. These findings suggest that the healing of tendon to bone is likely to be impaired in larger chronic tears

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