Aim Recent reports of potential harmful effects of nonsteroidal anti‐inflammatory drugs (NSAIDs) in treating patients with coronavirus disease 2019 (COVID‐19) have raised great concern. Methods We searched the PubMed, EMBASE, Cochrane Library and MedRxiv databases to examine the prevalence of NSAID use and associated COVID‐19 risk, outcomes and safety. Results Twenty‐five studies with a total of 101 215 COVID‐19 patients were included. Prevalence of NSAID use among COVID‐19 patients was 19% (95% confidence interval [CI] 14‐23%, no. of studies [n] = 22) and NSAID use prior to admission or diagnosis of COVID‐19 was not associated with an increased risk of COVID‐19 (adjusted odds ratio [aOR] = 0.93, 95% CI 0.82‐1.06, I 2 = 34%, n = 3), hospitalization (aOR = 1.06, 95% CI 0.76‐1.48, I 2 = 81%, n = 5), mechanical ventilation (aOR = 0.71, 95% CI 0.47‐1.06, I 2 = 38%, n = 4) or length of hospital stay. Moreover, prior use of NSAIDs was associated with a decreased risk of severe COVID‐19 (aOR = 0.79, 95% CI 0.71‐0.89, I 2 = 0%, n = 7) and death (aOR = 0.68, 95% CI 0.52‐0.89, I 2 = 85%, n = 10). Prior NSAID administration might also be associated with an increased risk of stroke (aOR = 2.32, 95% CI 1.04‐5.2, I 2 = 0%, n = 2), but not myocardial infarction (aOR = 1.49, 95% CI 0.25‐8.92, I 2 = 0, n = 2) and composite thrombotic events (aOR = 1.56, 95% CI 0.66‐3.69, I 2 = 52%, n = 2). Conclusion Based on current evidence, NSAID use prior to admission or diagnosis of COVID‐19 was not linked with increased odds or exacerbation of COVID‐19. NSAIDs might provide a survival benefit, although they might potentially increase the risk of stroke. Controlled trials are still required to further assess the clinical benefit and safety (e.g., stroke and acute renal failure) of NSAIDs in treating patients with COVID‐19.

Cell aggregates that mimic in vivo cell–cell interactions are promising and powerful tools for tissue engineering. This study isolated a new, easily obtained, population of mesenchymal stem cells (MSCs) from rat hard palates named hard palatal‐derived mesenchymal stem cells (PMSCs). The PMSCs were positive for CD90, CD44, and CD29 and negative for CD34, CD45, and CD146. They exhibited clonogenicity, self‐renewal, migration, and multipotent differentiation capacities. Furthermore, this study fabricated scaffold‐free 3D aggregates using light‐controlled cell sheet technology and a serum‐free method. PMSC aggregates were successfully constructed with good viability. Transplantation of the PMSC aggregates and the PMSC aggregate‐implant complexes significantly enhanced bone formation and implant osseointegration in vivo, respectively. This new cell resource is easy to obtain and provides an alternative strategy for tissue engineering and regenerative medicine.

Short root anomaly (SRA) is a dental disorder that presents an abnormal root morphology with short and blunt dental roots. In this situation, many dental treatments face a difficult challenge, especially orthodontic and prosthodontic treatments.Therefore, an understanding of how SRA develops is urgently needed. Here we describe that the abnormal expression of nuclear factor I C-type (Nfic), osterix (Osx), hedgehog (Hh), bone morphogenetic proteins (BMPs), transforming growth factor-β (TGF-β), Smad, Wnt, β-catenin, and dickkopf-related protein 1 (DKK1) leads to SRA.These factors interact with each other and constitute complicated signaling network in tooth formation. Specifically, BMP signaling inhibits the activity of Wnt/β-catenin directly or by inducing Osx via Runx2-dependent and Runx2-independent pathways. And Osx is a main inhibitor of Wnt/β-catenin signaling. In return, Wnt/β-catenin signaling has an antagonistic action of BMP pathway and a stimulation of Runx2. We highlight the importance of Wnt/β-catenin signaling in the pathological mechanisms.Either suppression or overactivation of this signaling influences the normal odontogenesis. Finally, we list rescue experiments on animal models, which have been reported to restore the interrupted cell differentiation and impaired tooth formation.We hope to find potential treatments for SRA based on these evidences in the future.