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).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.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%.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.

Etiology

Joint arthroplasty

10.5435/jaaosglobal-d-22-00218

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Citations (6)

The mitochondrial calcium uniporter compensates for Complex I dysfunction

Research Square (Research Square) (2021)

Enrique Balderas David Eberhardt John M. Pleinis Salah Sommakia Anthony M. Balynas

Abstract Calcium (Ca2+) entering mitochondria potently stimulates ATP synthesis. Increases in Ca2+ preserve energy synthesis in cardiomyopathies caused by mitochondrial dysfunction, and occur due to enhanced activity of the mitochondrial Ca2+ 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 (ETC). 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 (CLIPT). 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 Ca2+ influx during Complex I impairment.

Uniporter

10.21203/rs.3.rs-378028/v1

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Erratum

New England Journal of Medicine (1939)

Frederick Scarborough Gray New Hampshire Allen Knapp C Stanley Walter Machaj

10.1056/nejm193910262211716

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Mitochondrial calcium uniporter stabilization preserves energetic homeostasis during Complex I impairment

Nature Communications (2022)

Enrique Balderas David Eberhardt Sandra Lee John M. Pleinis Salah Sommakia

Abstract 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.

Uniporter

Homeostasis

10.1038/s41467-022-30236-4

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Citations (33)

Aseptic Loosening in Single-Stage Revision Arthroplasty for Periprosthetic Joint Infection

Journal of Orthopaedic Experience & Innovation (2022)

Kranti V. Peddada Brandon M. Welcome Mitchell C. Parker Connor M. Delma Christopher T. Holland

We set out to more definitively understand, using a meta-analysis, where we tried to assess the reoperation rates secondary to infection and aseptic loosening in single-stage revision total hips and total knees. Secondarily, we looked at the overall reoperation rate, i.e., survivorship, other etiologies of reoperations and the overall mortality rate.

Aseptic processing

Infection rate

Etiology

Joint arthroplasty

10.60118/001c.32652

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