Bone union was not always achieved after arthroscopic bony Bankart repair, and union was often delayed. Recurrence of instability was significantly more frequent when bone union failed. The size of the glenoid defect decreased significantly in shoulders with bone union.

Osteoarthritis (OA) is a potentially disabling disease whose progression is dependent on several risk factors. OA management usually involves the use of non-steroidal anti-inflammatory drugs (NSAIDs) that are the primary pharmacological treatments of choice. However, NSAIDs have often been associated with unwanted side effects. Cyclooxygenase (COX)-2 specific inhibitors, such as celecoxib, have been successfully used as an alternative in the past for OA treatment and have demonstrated fewer side effects. While abundant data are available for the clinical efficacy of drugs used for OA treatment, little is known about the disease-modifying effects of these agents. A previous review published by Zweers et al. (2010) assessed the available literature between 1990 and 2010 on the disease-modifying effects of celecoxib. In the present review, we aimed to update the existing evidence and identify evolving concepts relating to the disease-modifying effects of not just celecoxib, but also other NSAIDs. We conducted a review of the literature published from 2010 to 2016 dealing with the effects, especially disease-modifying effects, of NSAIDs on cartilage, synovium, and bone in OA patients. Our results show that celecoxib was the most commonly used drug in papers that presented data on disease-modifying effects of NSAIDs. Further, these effects appeared to be mediated through the regulation of prostaglandins, cytokines, and direct changes to tissues. Additional studies should be carried out to assess the disease-modifying properties of NSAIDs in greater detail.

The prevalence of bipolar lesions was approximately 60%. As glenoid defects became larger, Hill-Sachs lesions also enlarged, but there was no strong correlation. Bipolar lesions were frequent in patients with recurrent instability, patients with repetitive dislocation/subluxation, and those playing collision/contact sports. Instability showed a high recurrence rate in shoulders with bipolar lesions.

Background:Large glenoid rim defects in patients with traumatic anterior shoulder instability are often regarded as a contraindication for arthroscopic Bankart repair, with a defect of 20% to 27% considered as the critical size. While recurrence of dislocations, male sex, and collision sports were reported to be the significant factors influencing large glenoid defects, the influences of subluxations and more detailed types of sports were not investigated.Purpose:To investigate the influence of the number of dislocations and subluxations and type of sport on the occurrence and size of glenoid defects in detail.Study Design:Case-control study; Level of evidence, 3.Methods:A total of 223 shoulders (60 with primary instability, 163 with recurrent instability) were prospectively examined by computed tomography. Glenoid rim morphology was compared between primary and recurrent instability. In patients with recurrent instability, the relationship between the glenoid defect and the number of dislocations and subluxations was investigated. In addition, glenoid defects were compared among 49 male American football players, 41 male rugby players, 27 male baseball players, and 25 female athletes.Results:The mean extent of the glenoid defect was 3.5% in shoulders with primary instability and 11.3% in those with recurrent instability. A glenoid defect was detected in 108 shoulders (66.2%) with recurrent instability versus 12 shoulders (20%) with primary instability. Regarding the influence of the total number of dislocations/subluxations, the average extent of the glenoid defect was 6.3% in 85 shoulders with 2 to 5 events, 12.9% in 34 shoulders with 6 to 10 events, and 19.6% in 44 shoulders with 11 or more events. The glenoid defect became significantly larger along with an increasing number of recurrences. Although recurrent subluxation without dislocation also influenced the glenoid defect size, the number of dislocations did not. The average extent of the glenoid defect was 12.0% in rugby players, 8.9% in American football players, 4.7% in female athletes, and 4.5% in baseball players. Glenoid defects were significantly smaller in male baseball players and female athletes than in male collision athletes.Conclusion:The glenoid defect is significantly enlarged by damage due to recurrent dislocation and subluxation; therefore, glenoid rim morphology differs markedly between primary and recurrent instability. Glenoid defect size is also influenced by sex and by the type of sport.

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