Coracoclavicular Ligament Reconstruction Using TightRope for Delayed Grade III Acromioclavicular Joint Injury After Ipsilateral Diaphyseal Clavicle Fracture Fixation: Surgical Technique and Review of Current Literature.

Athletes commonly sustain high-energy direct impact injuries to the shoulder, with acromioclavicular joint (ACJ) injuries accounting for over half. Ipsilateral ACJ injury and diaphyseal clavicle fracture occur nearly 7% of the time. There is limited literature offering treatment suggestions for this unique injury pattern and limited evidence providing guidance to suggest which injury patterns should be treated operatively or nonoperatively. Here, we present successful treatment of a high-level athlete utilizing a Knotless TightRope XP placed through a superior clavicle plate with successful return to full activity at 6 months postoperation. The TightRope technique offers the ability to augment through a preexisting superior clavicular plate in a low-profile manner and promote easy suture tensioning to obtain and maintain reduction of the injured ACJ.

Does shoulder stability differ with or without subscapularis repair after primary reverse total shoulder arthroplasty? A systematic review.

The use of reverse total shoulder arthroplasty (RTSA) has expanded from its original indication as a rotator cuff arthropathy treatment to include a large variety of pathologies. A frequently reported complication with this surgery is postoperative shoulder instability with reported incidence varying widely from 2.3 to 38%. The etiology for this instability is broad and includes prosthesis design, mechanical impingement, surgical technique, and axillary/deltoid function. A PROSPERO-registered systematic review was performed utilizing PRISMA guidelines using Cochrane, PUBMED, Embase, and Eline. Of the 1442 studies initially identified, 7 studies met all inclusion criteria, all of which were level III or IV evidence. All 7 studies evaluated postoperative instability, but no study reported a statistically significant difference in instability rates between the groups. Dislocations occurred in 5 patients (5/679, 0.7%) with subscapularis repair and 8 patients (8/527, 1.5%) without repair. A nonsignificant difference in the risk of instability for surgeries with repair compared to surgeries without repair was found (overall risk difference: 0.01, random effects 95% confidence interval: -0.00 to 0.02, P = .11). This review suggests no difference in postoperative shoulder instability rates between patients that underwent primary RTSA with or without subsequent repair of the subscapularis tendon. Interestingly, one study comparing implants with a medialized or nonlateralized implant showed a significantly increased rate of dislocation with the medialized group compared to the lateralized group. When these groups were then stratified based on subscapularis repair status, there was no increased risk with a nonrepaired tendon. This study suggests that implant design may have more influence on the stability of RTSA than subscapularis status. However, overall, there does appear to be a trend suggesting improved postoperative clinical outcomes and active range of motion for patients with a subscapularis repair vs. without a repair. Further research is needed to better elucidate the ideal combination of surgical technique and implant design to minimize postoperative glenohumeral joint instability while optimizing postoperative clinical outcomes and range of motion after primary RTSA.

Increasing Stress to Induce Apoptosis in Pancreatic Cancer via the Unfolded Protein Response (UPR).

High rates of cell proliferation and protein synthesis in pancreatic cancer are among many factors leading to endoplasmic reticulum (ER) stress. To restore cellular homeostasis, the unfolded protein response (UPR) activates as an adaptive mechanism through either the IRE1α, PERK, or ATF6 pathways to reduce the translational load and process unfolded proteins, thus enabling tumor cells to proliferate. Under severe and prolonged ER stress, however, the UPR may promote adaptation, senescence, or apoptosis under these same pathways if homeostasis is not restored. In this review, we present evidence that high levels of ER stress and UPR activation are present in pancreatic cancer. We detail the mechanisms by which compounds activate one or many of the three arms of the UPR and effectuate downstream apoptosis and examine available data on the pre-clinical and clinical-phase ER stress inducers with the potential for anti-tumor efficacy in pancreatic cancer. Finally, we hypothesize a potential new approach to targeting pancreatic cancer by increasing levels of ER stress and UPR activation to incite apoptotic cell death.