Percutaneous balloon humeroplasty for Hill-Sachs lesions: a novel technique.

INTRODUCTION: Hills-Sachs lesions are commonly associated with anterior shoulder dislocations and can be a source of recurrent instability. Studies have shown that, even after soft tissue repair of a Bankart lesion, there is still a risk for redislocation in a patient with significant bony defects. The purpose of this study is to ascertain whether balloon humeroplasty is an effective technique of reducing acute Hill-Sachs defect in a cadaveric model. METHODS: Eighteen cadaveric humerii dissected free of soft tissue were used for this study. Hill-Sachs lesions were created in a reproducible manner in the anatomical posterolateral aspect of the head with a mallet edge. An inflatable balloon tamp (balloon, IBT) was used to reduce the lesion via a small transcortical window. Cement was used to fill the void created by the balloon. We utilized computed tomography (CT) to collect volume data of each humeral head pre- and post-procedure. From this data, we calculated the volume of the Hill-Sachs defect and the percent corrected. A paired t test was performed to analyze the data statistically. RESULTS: The average prereduction Hill-Sachs defect volume was 1515.5 mm(3). The average post-reduction lesion residual volume was 31 mm(3) with 99.3% reduction to the original humeral head volume. The Hill-Sachs lesion reduction was statistically significant with P value of .0004. CONCLUSION: Balloon humeroplasty proved to be an effective technique for reducing Hill-Sachs lesions in a cadaveric model. This technique may be used as an adjunct to arthroscopic versus open Bankart procedure for engaging acute Hill-Sachs lesions.

Oxidative stress inhibits caveolin-1 palmitoylation and trafficking in endothelial cells.

During normal and pathological conditions, endothelial cells (ECs) are subjected to locally generated reactive oxygen species, produced by themselves or by other vessel wall cells. In excess these molecules cause oxidative injury to the cell but at moderate levels they might modulate intracellular signalling pathways. We have investigated the effect of oxidative stress on the palmitoylation and trafficking of caveolin-1 in bovine aortic ECs. Exogenous H2O2 did not alter the intracellular localization of caveolin-1 in ECs. However, metabolic labelling experiments showed that H2O2 inhibited the trafficking of newly synthesized caveolin-1 to membrane raft domains. Several mechanisms potentially responsible for this inhibition were examined. Impairment of caveolin-1 synthesis by H2O2 was not responsible for diminished trafficking. Similarly, the inhibition was independent of H2O2-induced caveolin-1 phosphorylation as shown by the markedly different concentration dependences. We tested the effect of H2O2 on palmitoylation of caveolin-1 by the incorporation of [3H]palmitic acid. Exposure of ECs to H2O2 markedly inhibited the palmitoylation of caveolin-1. Comparable inhibition was observed after treatment of cells with H2O2 delivered either as a bolus or by continuous delivery with glucose and glucose oxidase. Kinetic studies showed that H2O2 did not alter the rate of caveolin-1 depalmitoylation but instead decreased the 'on-rate' of palmitoylation. Together these results show for the first time the modulation of protein palmitoylation by oxidative stress, and suggest a cellular mechanism by which stress might influence caveolin-1-dependent cell activities such as the concentration of signalling proteins and cholesterol trafficking.