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The aim of this review is to address controversies in the management of dislocations of the acromioclavicular joint. Current evidence suggests that operative rather than non-operative treatment of Rockwood grade III dislocations results in better cosmetic and radiological results, similar functional outcomes and longer time off work. Early surgery results in better functional and radiological outcomes with a reduced risk of infection and loss of reduction compared with delayed surgery.Surgical options include acromioclavicular fixation, coracoclavicular fixation and coracoclavicular ligament reconstruction. Although non-controlled studies report promising results for arthroscopic coracoclavicular fixation, there are no comparative studies with open techniques to draw conclusions about the best surgical approach. Non-rigid coracoclavicular fixation with tendon graft or synthetic materials, or rigid acromioclavicular fixation with a hook plate, is preferable to fixation with coracoclavicular screws owing to significant risks of loosening and breakage.The evidence, although limited, also suggests that anatomical ligament reconstruction with autograft or certain synthetic grafts may have better outcomes than non-anatomical transfer of the coracoacromial ligament. It has been suggested that this is due to better restoration horizontal and vertical stability of the joint.Despite the large number of recently published studies, there remains a lack of high-quality evidence, making it difficult to draw firm conclusions regarding these controversial issues.Cite this article: Bone Joint J2013;95-B:1595–1602.

Between 1976 and 2004, 38 revision arthroplasties (35 patients) were performed for aseptic loosening of the humeral component. The mean interval from primary arthroplasty to revision was 7.1 years (0.4 to 16.6). A total of 35 shoulders (32 patients) were available for review at a mean follow-up of seven years (2 to 19.3).Pre-operatively, 34 patients (97%) had moderate or severe pain; at final follow-up, 29 (83%) had no or only mild pain (p < 0.0001). The mean active abduction improved from 88° to 107° (p < 0.01); and the mean external rotation from 37° to 46° (p = 0.27). Excellent or satisfactory results were achieved in 25 patients (71%) according to the modified Neer rating system. Humeral components were cemented in 29, with ingrowth implants used in nine cases. There were 19 of standard length and 17 were longer (two were custom replacements and are not included). Bone grafting was required for defects in 11 humeri. Only two glenoid components were left unrevised. Intra-operative complications included cement extrusion in eight cases, fracture of the shaft of the humerus is two and of the tuberosity in four. There were four re-operations, one for recurrent humeral loosening, with 89% survival free of re-operations at ten years.Revision surgery for aseptic loosening of the humeral component provides reliable pain relief and modest improvement of movement, although there is a substantial risk of intra-operative complications. Revision to a total shoulder replacement gives better results than to a hemiarthroplasty.

The p53 tumor-suppressor protein binds DNA and activates the expression of a 21-kDa protein that inhibits both the activity of cyclin-dependent kinases and the function of proliferating cell nuclear antigen. Since p21 expression has been reported to increase 10- to 20-fold as human diploid fibroblasts lose the ability to replicate, we examined the expression and activity of p53 during replicative aging. Similar levels of total p53 mRNA and protein were expressed in low-passage (young) and high-passage (old) cells but both DNA binding activity in vitro and transcriptional activity of p53 in vivo were increased severalfold in high-passage cells. While the basis of increased p53 activity is presently unclear, it is not correlated with differential phosphorylation or changes in p53-mouse double minute 2 gene product interactions. These results provide evidence for the activation of a protein involved in the control of cell cycle checkpoints during cellular aging, in the absence of increased expression.