Knotless suture in revision total joint arthroplasty: a prospective randomized controlled trial.

INTRODUCTION: The use of barbed sutures for wound closure in primary total joint arthroplasty (TJA) has been shown to be effective and safe. However, their effectiveness and safety in revision TJA procedures has not been thoroughly studied. This study aims to evaluate the efficacy and safety of using barbed suture closure in revision TJA setting. METHODS: A total of 80 patients undergoing revision TJA between September 2020 and November 2022 were included in this randomized controlled trial study. Following informed consent, patients were computer-randomized to the treatment arm (barbed suture wound closure) or to the control arm (conventional wound closure). Closure duration, closure rate, number of sutures used and wound related outcomes including complication rates and Patient and Observer Scar Assessment Scale (POSAS) score were compared between groups. RESULTS: The use of barbed sutures decreased closure time by 6 min (30.1 vs. 36.1 min, P = 0.008) with a higher wound closure rate (6.5 vs. 5.5 mm/minute, P = 0.013). Additionally, the number of sutures used for wound closure in the barbed group was significantly lower than in the control group (6.2 vs. 10.1, respectively, P < 0.001). There were no significant differences in the rate of postoperative wound complications (P = 0.556) or patient and observer POSAS scores (P = 0.211, P = 297, respectively) between the two groups at 3-month follow-up. CONCLUSION: Closure of revision TJA surgical wound utilizing barbed sutures reduced closure time and the number of needles handled by operative staff, with no significant increase in intra- or post-operative complications rate when compared to traditional closure technique. LEVEL OF EVIDENCE: I.

A CRISPR/Cas9-Engineered ARID1A-Deficient Human Gastric Cancer Organoid Model Reveals Essential and Nonessential Modes of Oncogenic Transformation.

Mutations in ARID1A rank among the most common molecular aberrations in human cancer. However, oncogenic consequences of ARID1A mutation in human cells remain poorly defined due to lack of forward genetic models. Here, CRISPR/Cas9-mediated ARID1A knockout (KO) in primary TP53-/- human gastric organoids induced morphologic dysplasia, tumorigenicity, and mucinous differentiation. Genetic WNT/ß-catenin activation rescued mucinous differentiation, but not hyperproliferation, suggesting alternative pathways of ARID1A KO-mediated transformation. ARID1A mutation induced transcriptional regulatory modules characteristic of microsatellite instability and Epstein-Barr virus-associated subtype human gastric cancer, including FOXM1-associated mitotic genes and BIRC5/survivin. Convergently, high-throughput compound screening indicated selective vulnerability of ARID1A-deficient organoids to inhibition of BIRC5/survivin, functionally implicating this pathway as an essential mediator of ARID1A KO-dependent early-stage gastric tumorigenesis. Overall, we define distinct pathways downstream of oncogenic ARID1A mutation, with nonessential WNT-inhibited mucinous differentiation in parallel with essential transcriptional FOXM1/BIRC5-stimulated proliferation, illustrating the general utility of organoid-based forward genetic cancer analysis in human cells. SIGNIFICANCE: We establish the first human forward genetic modeling of a commonly mutated tumor suppressor gene, ARID1A. Our study integrates diverse modalities including CRISPR/Cas9 genome editing, organoid culture, systems biology, and small-molecule screening to derive novel insights into early transformation mechanisms of ARID1A-deficient gastric cancers.See related commentary by Zafra and Dow, p. 1327.This article is highlighted in the In This Issue feature, p. 1307.