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 ≥ 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 ≥ 40 years. METHODS: We conducted a retrospective chart review of all patients aged ≥ 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 ≥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 < .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 ≥ 40 years. Rotator cuff tears should be suspected and repaired in patients with anterior instability, especially those aged ≥ 50 years.

Early radiographic failure of reverse total shoulder arthroplasty with structural bone graft for glenoid bone loss.

INTRODUCTION: Structural glenoid bone grafting in reverse total shoulder arthroplasty (RSA) has previously been reported to have good functional outcomes and low complication rates. We have observed different complication rates and hypothesized that baseplate fixation and severity of deformity may be predictors of early failure. METHODS: We retrospectively identified 44 patients who underwent RSA with structural bone grafting for glenoid bone defects. All patients had preoperative and postoperative (Grashey and axillary) radiographs at a minimum of 1 year after surgery and within 3 months of surgery for evaluation of implant and graft positioning. Clinical data and outcome scores were collected at the same intervals. RESULTS: There were 61% females and 39% males, with an average age of 74 ± 8 years at the time of surgery. The median final radiographic follow-up was 20 months, with 37 primary RSA and 7 revision RSA. Graft resorption was found in 11 of 44 patients (25%), and radiographic failure was found in 11 of 44 patients (25%) at a median of 8 months (range 3-51 months). Forward elevation, American Shoulder and Elbow Surgeons Standardized Shoulder Assessment Form, Single Assessment Numeric Evaluation (SANE), and Simple Shoulder Test (SST) scores all significantly improved postoperatively (P < .0001). Radiographic baseplate failure was associated with graft resorption (P = .002), more retroversion correction (P = .02), and worse SANE scores at final follow-up (P = .01). DISCUSSION/CONCLUSION: RSA with structural bone graft improved range of motion and function, but there was a larger than previously reported baseplate loosening rate. This early radiographic loosening appeared to be associated with graft resorption, retroversion correction, and worse outcome scores.

The effect of an orthopedic specialty hospital on operating room efficiency in shoulder arthroplasty.

BACKGROUND: Operating room (OR) time is a major cost to the health care system. Therefore, increasing OR efficiency to save time may be a cost-saving tool. This study analyzed OR efficiency in shoulder arthroplasty at an orthopedic specialty hospital (OSH) and a tertiary referral center (TRC). METHODS: All primary shoulder arthroplasties performed at our OSH and TRC were identified (2013-2015). Manually matched cohorts from the OSH and TRC were compared for OR times. Three times (minutes) were recorded: anesthesia preparation time (APT; patient in room to skin incision), surgical time (ST; skin incision to skin closed), conclusion time (CT; skin closed to patient out of room). RESULTS: There were 136 primary shoulder arthroplasties performed at the OSH and matched with 136 at the TRC. OSH and TRC patients were similar in age (P = .95), body mass index (P = .97), Charlson Comorbidity Index (P = 1.000), sex (P = 1.000), procedure (P = 1.000), insurance status (P = .714), discharge destination (P = .287), and diagnoses (P = .354). These matched populations had similar ST (OSH: 110.0 ± 26.6 minutes, TRC: 113.4 ± 28.7 minutes; P = .307). APT (39.2 ± 8.0 minutes) and CT (7.6 ± 3.8 minutes) were shorter in the OSH patients than APT (46.3 ± 8.8 minutes; P < .001) and CT (11.2 ± 4.7 minutes; P < .001) in TRC patients. Total nonoperative time (sum of APT and CT) at the OSH (46.8 ± 8.9 minutes) was shorter than at the TRC (57.5 ± 10.4 minutes; P < .001). CONCLUSIONS: Despite similar patient populations and case complexity, the OR efficiency at an OSH was superior to a TRC. Further analysis is needed to determine the financial implications of this superior OR efficiency.

Distinct GAB2 signaling pathways are essential for myeloid and lymphoid transformation and leukemogenesis by BCR-ABL1.

Tyrosine kinase inhibitors (TKIs) directed against BCR-ABL1, the product of the Philadelphia (Ph) chromosome, have revolutionized treatment of patients with chronic myeloid leukemia (CML). However, acquired resistance to TKIs is a significant clinical problem in CML, and TKI therapy is much less effective against Ph(+)B-cell acute lymphoblastic leukemia (B-ALL). BCR-ABL1, via phosphorylated Tyr177, recruits the adapter GRB2-associated binding protein 2 (GAB2) as part of a GRB2/GAB2 complex. We showed previously that GAB2 is essential for BCR-ABL1-evoked myeloid transformation in vitro. Using a genetic strategy and mouse models of CML and B-ALL, we show here that GAB2 is essential for myeloid and lymphoid leukemogenesis by BCR-ABL1. In the mouse model, recipients of BCR-ABL1-transducedGab2(-/-)bone marrow failed to develop CML-like myeloproliferative neoplasia. Leukemogenesis was restored by expression of GAB2 but not by GAB2 mutants lacking binding sites for its effectors phosphatidylinositol 3-kinase (PI3K) or SRC homology 2-containing phosphotyrosine phosphatase 2 (SHP2). GAB2 deficiency also attenuated BCR-ABL1-induced B-ALL, but only the SHP2 binding site was required. The SHP2 and PI3K binding sites were differentially required for signaling downstream of GAB2. Hence, GAB2 transmits critical transforming signals from Tyr177 to PI3K and SHP2 for CML pathogenesis, whereas only the GAB2-SHP2 pathway is essential for lymphoid leukemogenesis. Given that GAB2 is dispensable for normal hematopoiesis, GAB2 and its effectors PI3K and SHP2 represent promising targets for therapy in Ph(+)hematologic neoplasms.

Conformational control inhibition of the BCR-ABL1 tyrosine kinase, including the gatekeeper T315I mutant, by the switch-control inhibitor DCC-2036.

Acquired resistance to ABL1 tyrosine kinase inhibitors (TKIs) through ABL1 kinase domain mutations, particularly the gatekeeper mutant T315I, is a significant problem for patients with chronic myeloid leukemia (CML). Using structure-based drug design, we developed compounds that bind to residues (Arg386/Glu282) ABL1 uses to switch between inactive and active conformations. The lead "switch-control" inhibitor, DCC-2036, potently inhibits both unphosphorylated and phosphorylated ABL1 by inducing a type II inactive conformation, and retains efficacy against the majority of clinically relevant CML-resistance mutants, including T315I. DCC-2036 inhibits BCR-ABL1(T315I)-expressing cell lines, prolongs survival in mouse models of T315I mutant CML and B-lymphoblastic leukemia, and inhibits primary patient leukemia cells expressing T315I in vitro and in vivo, supporting its clinical development in TKI-resistant Ph(+) leukemia.