Survivorship and Etiologies of Failure in Single-stage Revision Arthroplasty for Periprosthetic Joint Infection: A Meta-analysis.

INTRODUCTION: Single-stage revision arthroplasty for periprosthetic joint infection (PJI) may yield comparable infection-free survivorship with two-stage revision arthroplasty. It is unclear if the most common mode of failure of single-stage revision arthroplasty is infection or aseptic loosening. In this meta-analysis, we sought to (1) determine survivorship and (2) compare rates of different etiologies of failure of single-stage revision total hip arthroplasty (THA) and total knee arthroplasty (TKA). METHODS: Preferred Reporting Items for Systematic Review and Meta-analyses guidelines search was done using search terms for "single stage revision," "exchange arthroplasty," "periprosthetic infection," "PJI," and "single stage." Patient demographics such as age, body mass index, and mean follow-up time were recorded. Overall survivorship and rates of revision surgery were aggregated using a random-effects model. Comparison of septic and aseptic loosening rates was done by risk difference and associated 95% confidence interval (CI) calculation. RESULTS: Twenty-four studies were identified with 2,062 and 147 single-stage revision THA and TKA procedures performed between 1984 and 2019, respectively. The weighted mean follow-up and age were 69.8 months and 66.3 years, respectively, with 55% men overall. The all-cause revision surgery rate was 11.1% and 11.8% for THA and TKA, respectively. The revision surgery rate secondary to infection and aseptic loosening and associated 95% CI for the risk difference for THA and TKA was 5.5% and 3.3% (-1.7% to 5.0%), and 3% and 8.8% (-11.4% to 2.3%), respectively. Revision surgeries due to instability and fracture combined and mortality rate were both less than 3%. DISCUSSION: Single-stage revision THA and TKA for PJI demonstrated overall high rates of survivorship, low mortality, and revision surgeries secondary to infection and aseptic loosening to be equivalent. Aseptic loosening after single-stage revision TKA might be higher than in primary TKA. As implant survivorship from infection improves in PJI, surgeons should be aware of aseptic loosening as an equally common mode of failure.

Harvest of All-Soft Tissue Quadriceps Tendon Autograft for Anterior Cruciate Ligament Reconstruction With or Without Closure of Resulting Defect Has No Effect on Patellar Height.

Purpose: To evaluate the radiographic effect of quadriceps tendon harvest on patellar height and to determine whether closure of a quadriceps graft harvest defect resulted in a significant change in patellar height compared to nonclosure. Methods: We conducted a retrospective review of prospectively enrolled patients. The institutional database was queried and all patients who underwent quadriceps autograft anterior cruciate ligament reconstruction between 2015 and March 2020 were included. Graft harvest length in millimeters and final graft diameter after preparation for implantation were obtained from the operative record and demographic data were obtained from the medical record. Radiographic analysis was performed of eligible patients using standard ratios of patellar height: Insall-Salvati (IS), Blackburn-Peele (BP), and Caton-Deschamps (CD). Measurements were performed using digital calipers on a digital imaging system by 2 postgraduate fellow surgeons. Preoperative and postoperative radiographs were performed at 0° according to a standard protocol. Postoperative radiographs were performed 6 weeks postoperatively in all cases. Preoperative patellar height ratios were compared with postoperative patellar height ratios for all patients using t-tests. Subanalysis was then performed to compare the effect of closure of with nonclosure on patellar height ratios using repeated-measures analysis of variance. Interrater reliability between the 2 reviewers was assessed using an intraclass correlation coefficient calculation. Results: In total, 70 patients met final inclusion criteria. There were no statistically significant changes from pre- to postoperative values for either reviewer for IS (reviewer 1, P = .47; reviewer 2, P = .353), BP (reviewer 1, P = .98; reviewer 2, P = .907), or CD (reviewer 1, P = .107; reviewer, 2 P = .188). The closure and nonclosure groups were adequately powered and no statistically significant demographic differences between the closure and nonclosure groups was identified for sex (P = .066), age (P = .343), weight (P = .881), height (P = .42), laterality (P = 1), meniscal repair (P = .332), graft diameter (P = .068), or graft length (P = .183). According to the repeated measures analysis of variance, closure of the quadriceps defect had no significant impact on any of the knee ratios. However, reviewer identity had a significant influence on the CD ratio. Intraclass correlation coefficient analysis revealed excellent agreement between reviewers for the IS (0.982) and BP (0.954) ratios, but only moderate-to-good agreement for the CD (0.751) ratio. Conclusions: Harvest of quadriceps tendon graft does not result in radiographic changes in patellar height. Furthermore, closure of the quadriceps defect does not appear to result in radiographic changes in patellar height. Level of Evidence: III, retrospective comparative trial.

Mitochondrial calcium uniporter stabilization preserves energetic homeostasis during Complex I impairment.

Calcium entering mitochondria potently stimulates ATP synthesis. Increases in calcium preserve energy synthesis in cardiomyopathies caused by mitochondrial dysfunction, and occur due to enhanced activity of the mitochondrial calcium uniporter channel. The signaling mechanism that mediates this compensatory increase remains unknown. Here, we find that increases in the uniporter are due to impairment in Complex I of the electron transport chain. In normal physiology, Complex I promotes uniporter degradation via an interaction with the uniporter pore-forming subunit, a process we term Complex I-induced protein turnover. When Complex I dysfunction ensues, contact with the uniporter is inhibited, preventing degradation, and leading to a build-up in functional channels. Preventing uniporter activity leads to early demise in Complex I-deficient animals. Conversely, enhancing uniporter stability rescues survival and function in Complex I deficiency. Taken together, our data identify a fundamental pathway producing compensatory increases in calcium influx during Complex I impairment.