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Introduction: The number of surgical extractions performed in hospitals in England remains unclear. This study reports the volume of surgical extractions conducted in hospitals and change in activity during the COVID-19 pandemic.Methods: We conducted a nationwide observational cohort study using Hospital Episode Statistics (HES) in England for patients undergoing surgical removal of a tooth (defined using OPSC-4 code F09) between April 1, 2015, and December 31, 2020. Procedures were stratified by age, gender, and urgency (elective or nonelective), reported using descriptive statistics, number, and percentage. We conducted post hoc modeling to predict surgical activity to December 2023. In addition, we contrasted this with aggregate national data on simple dental extraction procedures and drainage of dental abscesses in hospital as well as dental activity in general practice.Results: We identified a total of 569,938 episodes for the surgical removal of a tooth (females 57%). Of these, 493,056/569,938 (87%) were for adults and 76,882/569,938 (13%) children ≤18 years. Surgical extractions were most frequent in adult females. Elective cases accounted for 96% (n= 548,805/569,938) of procedures. The median number of procedures carried out per quarter was 27,256, dropping to 12,003 during the COVID-19 pandemic, representing a 56% reduction in activity. This amounted to around 61,058 cancelled procedures. Modeling predicts that this activity has not returned to prepandemic levels.Conclusions: The number of surgical extractions taking place in hospitals during the pandemic fell by 56%. The true impact of this reduction is unknown, but delayed treatment increases the risk of complications, including life-threatening infections.Knowledge Transfer Statement: The result of this study provides an evidence-based overview of the trends relating to surgical extractions of teeth in England taking place in hospitals. This information can be used to inform service and workforce planning to meet the needs of patients requiring surgical extractions. The data also provide an insight into the oral health needs of the population in England.

Endoglin is an accessory receptor for TGF-β signaling and is required for normal hemangioblast, early hematopoietic, and vascular development. We have previously shown that an upstream enhancer, Eng−8, together with the promoter region, mediates robust endothelial expression yet is inactive in blood. To identify hematopoietic regulatory elements, we used array-based methods to determine chromatin accessibility across the entire locus. Subsequent transgenic analysis of candidate elements showed that an endothelial enhancer at Eng+9 when combined with an element at Eng+7 functions as a strong hemato-endothelial enhancer. Chromatin immunoprecipitation (ChIP)–chip analysis demonstrated specific binding of Ets factors to the promoter as well as to the −8, +7+9 enhancers in both blood and endothelial cells. By contrast Pu.1, an Ets factor specific to the blood lineage, and Gata2 binding was only detected in blood. Gata2 was bound only at +7 and GATA motifs were required for hematopoietic activity. This modular assembly of regulators gives blood and endothelial cells the regulatory freedom to independently fine-tune gene expression and emphasizes the role of regulatory divergence in driving functional divergence.

Transcription factors are key regulators of hematopoietic stem cells (HSCs), yet the molecular mechanisms that control their expression are largely unknown. Previously, we demonstrated that expression of Scl/Tal1, a transcription factor required for the specification of HSCs, is controlled by Ets and GATA factors. Here we characterize the molecular mechanisms controlling expression of Lyl1, a paralog of Sclalso required for HSC function. Two closely spaced promoters directed expression to hematopoietic progenitor, megakaryocytic, and endothelial cells in transgenic mice. Conserved binding sites required for promoter activity were bound in vivo by GATA-2 and the Ets factors Fli1, Elf1, Erg, and PU.1. However, despite coregulation of Scland Lyl1by the same Ets and GATA factors, Sclexpression was initiated prior to Lyl1in embryonic stem (ES) cell differentiation assays. Moreover, ectopic expression of Sclbut not Lyl1rescued hematopoietic differentiation in Scl−/−ES cells, thus providing a molecular explanation for the vastly different phenotypes of Scl−/−and Lyl1−/−mouse embryos. Furthermore, coregulation of Scland Lyl1later during development may explain the mild phenotype of Scl−/−adult HSCs.