[Simulators and other tools in orthopedic-trauma surgery training]. / Simulatoren und andere Hilfsmittel in der orthopädisch-unfallchirurgischen Weiterbildung.

INTRODUCTION: The classic paradigm of "learning on the patient in the operating room" is more and more in conflict with the growing requirements of cost-efficient work and patient safety. With the technology available today for simulator systems, the accessibility of digital tools and the development of a metaverse as a digital meeting place result in various application scenarios and alternatives to classic orthopedic training. SIMULATORS: First VR-desktop simulations in orthopedics and traumatology were developed more than 20 years ago. VR-desktop simulators consist of a computer with a video screen and a joint model. Different instruments can be paired with this system and allow haptic feedback. With innovative software, numerous training programs can be selected, and the user receives precise feedback on their performance. Immersive VR simulators have also played an increasingly important role in recent years. OTHER DIGITAL TOOLS: The use of digital media such as audio and video podcasts as learning and information sources increased in the context of COVID-19. There is also an increasing number of orthopedic and trauma surgery topics on social media platforms. In all fields, however, there is a risk of the spread of misinformation. A quality standard must be maintained. EFFECTIVENESS AND UTILITY OF THE TRAINING: In order to evaluate simulators and their value as a training tool, it is important to comply with various validity criteria. Transfer validity plays an essential role for clinical application. Various studies demonstrate that the skills learned on simulators can also be successfully transferred to real clinical scenarios. DISCUSSION: A lack of availability, costs and high effort are limitations of classic training methods. In contrast, there are versatile use cases of VR-based simulations that are individually adapted to the trainees and cannot endanger patients. The still high acquisition costs, technical obstacles and the not yet widespread availability are limiting factors. The metaverse still offers unimaginable possibilities today to transfer VR-based applications to experimental learning methods.

rAAV-Mediated Human FGF-2 Gene Therapy Enhances Osteochondral Repair in a Clinically Relevant Large Animal Model Over Time In Vivo.

BACKGROUND: Osteochondral defects, if left untreated, do not heal and can potentially progress toward osteoarthritis. Direct gene transfer of basic fibroblast growth factor 2 (FGF-2) with the clinically adapted recombinant adeno-associated viral (rAAV) vectors is a powerful tool to durably activate osteochondral repair processes. PURPOSE: To examine the ability of an rAAV-FGF-2 construct to target the healing processes of focal osteochondral injury over time in a large translational model in vivo versus a control gene transfer condition. STUDY DESIGN: Controlled laboratory study. METHODS: Standardized osteochondral defects created in the knee joints of adult sheep were treated with an rAAV human FGF-2 (hFGF-2) vector by direct administration into the defect relative to control (reporter) rAAV-lacZ gene transfer. Osteochondral repair was monitored using macroscopic, histological, immunohistological, and biochemical methods and by micro-computed tomography after 6 months. RESULTS: Effective, localized prolonged FGF-2 overexpression was achieved for 6 months in vivo relative to the control condition without undesirable leakage of the vectors outside the defects. Such rAAV-mediated hFGF-2 overexpression significantly increased the individual histological parameter "percentage of new subchondral bone" versus lacZ treatment, reflected in a volume of mineralized bone per unit volume of the subchondral bone plate that was equal to a normal osteochondral unit. Also, rAAV-FGF-2 significantly improved the individual histological parameters "defect filling,""matrix staining," and "cellular morphology" and the overall cartilage repair score versus the lacZ treatment and led to significantly higher cell densities and significantly higher type II collagen deposition versus lacZ treatment. Likewise, rAAV-FGF-2 significantly decreased type I collagen expression within the cartilaginous repair tissue. CONCLUSION: The current work shows the potential of direct rAAV-mediated FGF-2 gene therapy to enhance osteochondral repair in a large, clinically relevant animal model over time in vivo. CLINICAL RELEVANCE: Delivery of therapeutic (hFGF-2) rAAV vectors in sites of focal injury may offer novel, convenient tools to enhance osteochondral repair in the near future.

Evaluation and analysis of graft hypertrophy by means of arthroscopy, biochemical MRI and osteochondral biopsies in a patient following autologous chondrocyte implantation for treatment of a full-thickness-cartilage defect of the knee.

Graft hypertrophy represents a characteristic complication following autologous chondrocyte implantation (ACI) for treatment of cartilage defects. Although some epidemiological data suggest that incidence is associated with first-generation ACI using autologous chondrocyte implantation, it has also been reported in other technical modifications of ACI using different biomaterials. Nevertheless, it has not been described in autologous, non-periosteum, implant-free associated ACI. In addition, little is known about histological and T2-relaxation appearance of graft hypertrophy. The present case report provides a rare case of extensive graft hypertrophy following ACI using an autologous spheres technique with clinical progression over time. Detailed clinical, MR tomographic and histological evaluation has been performed, which demonstrates a high quality of repair tissue within the hypertrophic as well as non-hypertrophic transplanted areas of the repair tissue. No expression of collagen type X (a sign of chondrocyte hypertrophy), only slight changes of the subchondral bone and a nearly normal cell-matrix ratio suggest that tissue within the hypertrophic area does not significantly differ from intact and high-quality repair tissue and therefore seems not to cause graft hypertrophy. This is in contrast to the assumption that histological hypertrophy might cause or contribute to an overwhelming growth of the repair tissue within the transplantation site. Data presented in this manuscript might contribute to further explain the etiology of graft hypertrophy following ACI.