Purpose Total knee arthroplasty (TKA) rates have increased substantially in the recent decades worldwide, with Germany being one of the leading countries in the prevalence of TKA. The aim of this study was to provide an overview of treatment changes during the last decade and to project the expected burden of primary and revision TKA (rTKA) for the next 30 years. Methods Comprehensive nationwide data from Germany was used to quantify primary and revision TKA rates as a function of age and gender. Projections were performed with use of a Poisson regression models and a combination of exponential smoothing and autoregressive integrated moving average models on historical procedure rates in relation to official population projections from 2020 to 2050. Results The incidence rate of primary TKAs is projected to increase by around 43% to 299 per 100,000 inhabitants [95% CI 231-368], leading to a projected total number of 225,957 primary TKAs in 2050 (95% CI 178,804-276,442). This increase has been related to a growing number of TKA performed in male patients, with the highest increase modelled in patients between 50 and 65 years of age. At the same time, the annual total number of revision procedures is forecast to increase even more rapidly by almost 90%, accounting for 47,313 (95% CI 15,741-78,885; IR = 62.7 per 100,000, 95% CI 20.8-104.5) procedures by 2050. Those numbers are primarily associated with a rising number of rTKAs secondary to periprosthetic joint infection (PJI). Conclusions Using this country-specific forecast approach, a rising number of primary TKA and an even more rapidly growing number of rTKA, especially for PJI, has been projected until 2050, which will inevitably provide a huge challenge for the future health care system. As many other industrialized nations will face similar demographic and procedure-specific developments, these forecasts should be alarming for many health care systems worldwide and emphasize the tremendous need for an appropriate financial and human resource management in the future. Level of evidence Level III, prognostic study, economic and decision analysis.
Despite the success of treating rheumatic disorders with biologic therapies, joint replacement surgery still remains the final treatment option in many cases. Approximately 1.5 million joint arthroplastic operations are performed annually worldwide. Implant failure due to massive bone loss and aseptic loosening of prostheses, however, is a major complication of joint replacement, which can lead to high socioeconomic burdens both for the individual patient and for health-care systems. To date, there is no approved drug therapy to prevent or inhibit periprosthetic osteolysis, and aseptic loosening of prostheses can only be overcome by surgical revision. Research during the past decade, however, has unravelled much of the pathogenesis of aseptic prosthesis loosening and preclinical studies have identified potential targets for pharmaceutical treatments. This article highlights the importance of a cooperative interaction between rheumatologists and orthopedic surgeons, and presents novel insights into the molecular mechanisms behind aseptic loosening of prostheses. In addition, we outline potential perspectives for the development of future therapeutic strategies for this devastating complication.
BackgroundRecent clinical and animal studies have shown that extracorporeal shock wave therapy has a promoting influence on the healing process of musculoskeletal disorders. However, the underlying biological effects of extracorporeal shock wave therapy on human skeletal muscle cells have not yet been investigated.MethodsIn this study, we investigated human skeletal muscle cells after exposure to radial extracorporeal shock waves in a standardized in vitro setup. Cells were isolated from muscle specimens taken from adult patients undergoing spine surgery. Primary muscle cells were exposed once or twice to radial extracorporeal shock waves in vitro with different energy flux densities. Cell viability and gene expression of the paired box protein 7 (Pax7), neural cell adhesion molecule (NCAM), and myogenic factor 5 (Myf5) and MyoD as muscle cell markers were compared to non-treated muscle cells that served as controls.ResultsIsolated muscle cells were positive for the hallmark protein of satellite cells, Pax7, as well as for the muscle cell markers NCAM, MyoD, and Myf5. Exposure to radial extracorporeal shock waves at low energy flux densities enhanced cell viability, whereas higher energy flux densities had no further significant impact. Gene expression analyses of muscle specific genes (Pax7, NCAM, Myf5, and MyoD) demonstrated a significant increase after single exposure to the highest EFD (4 bar, 0.19 mJ/mm2) and after double exposure with the medium EFDs (2 and 3 bar; 0.09 and 0.14 mJ/mm2, respectively). Double exposure of the highest EFD, however, results in a significant down-regulation when compared to single exposure with this EFD.ConclusionsThis is the first study demonstrating that radial extracorporal shock wave therapy has the potential to modulate the biological function of human skeletal muscle cells. Based on our experimental findings, we hypothesize that radial extracorporal shock wave therapy could be a promising therapeutic modality to improve the healing process of sports-related structural muscle injuries.
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