Concomitant rotator cuff repair and instability surgery provide good patient-reported functional outcomes in patients aged 40 years or older with shoulder dislocation

Background: Recurrent anterior shoulder dislocation in patients aged \u3e /= 40 years is not as rare as once thought. The mechanism of instability in this patient population is different-more likely to be attributed to rotator cuff pathology-compared with that in younger individuals. With an increasingly aging active population, surgical management has a rising role in preventing morbidity associated with recurrent instability. Our purpose was to evaluate outcomes of anterior shoulder instability repair (ie, Bankart or bony Bankart repair) with and without rotator cuff repair (RCR) in patients aged \u3e /= 40 years. Methods: We conducted a retrospective chart review of all patients aged \u3e /= 40 years who underwent surgical repair for anterior shoulder instability from 2008-2016. Patients were categorized into 4 cohorts: Bankart repair only, bony Bankart repair only, Bankart repair with concomitant RCR, and bony Bankart repair with concomitant RCR. Demographic and history-of-instability data were collected. Clinical and functional outcomes assessed included the Single Assessment Numeric Evaluation score, American Shoulder and Elbow Surgeons score, Penn Shoulder Score, visual analog scale score for pain, Western Ontario Shoulder Instability Index score, and patient satisfaction score. Results: A total of 146 patients were included in this study, with 103 patients (71%) having \u3e /=2-year outcome scores. Outcome scores were not significantly different among groups. For patients who underwent Bankart repair only, bony Bankart repair only, Bankart repair with RCR, and bony Bankart repair with RCR, the Single Assessment Numeric Evaluation scores were 80.8 +/- 19.7, 90.0 +/- 10.7, 79.3 +/- 29.4, and 87.2 +/- 10.6, respectively (P = .284); American Shoulder and Elbow Surgeons scores, 83.8 +/- 19.7, 92.4 +/- 17.4, 82.5 +/- 25.6, and 85.6 +/- 12.7, respectively (P = .114); Penn Shoulder Scores for function, 84.5 +/- 17.9, 90.9 +/- 15.3, 83.6 +/- 25.1, and 95.7 +/- 13.0, respectively (P = .286); and Western Ontario Shoulder Instability Index scores, 481.0 +/- 519.5, 292.1 +/- 414.3, 548.9 +/- 690.5, and 320.6 +/- 258.7, respectively (P = .713). Age at the time of surgery significantly differed between cohorts (P \u3c .001). No patients had recurrence of instability during the study period. Conclusion: Similar functional outcomes can be achieved in the surgical management of anterior instability in patients aged \u3e /= 40 years. Rotator cuff tears should be suspected and repaired in patients with anterior instability, especially those aged \u3e /= 50 years

Thymosin Β4 And Its Degradation Product, Ac-Sdkp, Are Novel Reparative Factors In Renal Fibrosis

Previously we found thymosin β4 (Tβ4) is up-regulated in glomerulosclerosis and required for angiotensin II-induced expression of plasminogen activator inhibitor-1 (PAI-1) in glomerular endothelial cells. Tβ4 has beneficial effects in dermal and corneal wound healing and heart disease yet its effects in kidney disease are unknown. Here we studied renal fibrosis in wild type and PAI-1 knockout mice following unilateral ureteral obstruction to explore the impact of Tβ4 and its prolyl oligopeptidase tetrapeptide degradation product, Ac-SDKP, in renal fibrosis. Additionally, we explored interactions of Tβ4 with PAI-1. Treatment with Ac-SDKP significantly decreased fibrosis in both wild type and PAI-1 knockout mice, as observed by decreased collagen and fibronectin deposition, fewer myofibroblasts and macrophages, and suppressed pro-fibrotic factors. In contrast, Tβ4 plus a prolyl oligopeptidase inhibitor significantly increased fibrosis in wild type mice. Tβ4 alone also promoted repair and reduced late fibrosis in wild type mice. Importantly, both pro-fibrotic effects of Tβ4 plus the prolyl oligopeptidase inhibitor, and late reparative effects of Tβ4 alone, were absent in PAI-1 knockout mice. Thus, Tβ4 combined with prolyl oligopeptidase inhibition, is consistently pro-fibrotic, but by itself, has anti-fibrotic effects in late stage fibrosis, while Ac-SDKP has consistent anti-fibrotic effects in both early and late stages of kidney injury. These effects of Tβ4 are dependent on PAI-1.PubMedWoSScopu

Thymosin β4 and its degradation product, Ac-SDKP, are novel reparative factors in renal fibrosis

Previously we found thymosin β4 (Tβ4) is up-regulated in glomerulosclerosis and required for angiotensin II-induced expression of plasminogen activator inhibitor-1 (PAI-1) in glomerular endothelial cells. Tβ4 has beneficial effects in dermal and corneal wound healing and heart disease yet its effects in kidney disease are unknown. Here we studied renal fibrosis in wild type and PAI-1 knockout mice following unilateral ureteral obstruction to explore the impact of Tβ4 and its prolyl oligopeptidase tetrapeptide degradation product, Ac-SDKP, in renal fibrosis. Additionally, we explored interactions of Tβ4 with PAI-1. Treatment with Ac-SDKP significantly decreased fibrosis in both wild type and PAI-1 knockout mice, as observed by decreased collagen and fibronectin deposition, fewer myofibroblasts and macrophages, and suppressed pro-fibrotic factors. In contrast, Tβ4 plus a prolyl oligopeptidase inhibitor significantly increased fibrosis in wild type mice. Tβ4 alone also promoted repair and reduced late fibrosis in wild type mice. Importantly, both pro-fibrotic effects of Tβ4 plus the prolyl oligopeptidase inhibitor, and late reparative effects of Tβ4 alone, were absent in PAI-1 knockout mice. Thus, Tβ4 combined with prolyl oligopeptidase inhibition, is consistently pro-fibrotic, but by itself, has anti-fibrotic effects in late stage fibrosis, while Ac-SDKP has consistent anti-fibrotic effects in both early and late stages of kidney injury. These effects of Tβ4 are dependent on PAI-1