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Background. Almost every sector in the health care is affected by the COVID-19 pandemic. Many studies already investigated the effect on different aspects in orthopedic and trauma care. However, the current literature lacks data regarding the consequence on daily surgical business. Thus, the aim of the present study was to analyze the development of knee-related pathologies and surgical procedures in a German university level-one trauma center during the lockdown phase and early lockdown phase to investigate the impact of the COVID-19 lockdown on orthopedic and trauma knee surgery. Material and Methods. The amount of knee joint surgeries performed during the high-peak COVID-19 crisis in the period of January to May 2020 was evaluated retrospectively and compared to the corresponding time periods of the previous years (2017-2019). Results. The COVID-19 lockdown led to a significant decrease in the number of knee injuries in March and April 2020 by 83.3%. Surgical procedures were reduced by 84.8% during the same period. In May 2020, the number of knee joint procedures returned to an almost prepandemic level. The distribution of urgent and elective knee surgery changed to predominantly acute trauma care at the beginning of the COVID-19 lockdown and persisted through to May 2020. Conclusion. The COVID-19 pandemic had a high impact on emergency and elective knee surgery in a level-one trauma center in Germany during the lockdown phase. It also showed that a level-one trauma center in the German healthcare system is able to handle urgent trauma and orthopedic operations during a worldwide medical crisis and to return to a prepandemic level within a short phase.

The transcription factor AP-2ε(activating enhancer-binding protein epsilon) is expressed in cartilage of humans and mice. However, knowledge about regulatory mechanisms influencing AP-2εexpression is limited. Using quantitative real time PCR, we detected a significant increase in AP-2εmRNA expression comparing initial and late stages of chondrogenic differentiation processesin vitroandin vivo. Interestingly, in these samples the expression pattern of the prominent hypoxia marker geneangiopoietin-like 4 (Angptl4)strongly correlated with that ofAP-2εsuggesting that hypoxia might represent an external regulator of AP-2εexpression in mammals. In order to show this, experiments directly targeting the activity of hypoxia-inducible factor-1 (HIF1), the complex mediating responses to oxygen deprivation, were performed. While the HIF1-activating compounds 2,2′-dipyridyl and desferrioxamine resulted in significantly enhanced mRNA concentration of AP-2ε, siRNA against HIF1αled to a significantly reduced expression rate ofAP-2ε. Additionally, we detected a significant upregulation of the AP-2εmRNA level after oxygen deprivation. In sum, these different experimental approaches revealed a novel role for the HIF1 complex in the regulation of theAP-2εgene in cartilaginous cells and underlined the important role of hypoxia as an important external regulatory stimulus during chondrogenic differentiation modulating the expression of downstream transcription factors.