Immune checkpoint blockade (ICB) therapy has recently shown promise in treating several malignancies. However, only a limited number of patients respond to this treatment, partially because of the “immune cold” condition of the tumor immune microenvironment. Pyroptosis is a type of gasdermin-mediated programmed cell death that often leads to inflammation and immune responses. Many studies on the mechanism and function of pyroptosis have led to increasing recognition of the role of pyroptosis in malignant progression and immune therapy. Pyroptosis has the potential to alter the tumor immune microenvironment by releasing tumor-associated antigens, damage-associated molecular patterns, and proinflammatory cytokines, thus leading to intratumoral inflammatory responses, stimulation of tumor-specific cytotoxic T cell infiltration, conversion of “cold” to “hot” tumors, and ultimately improving the efficacy of ICB therapy. Some cancer treatments have been shown to restore anticancer immunosurveillance through the induction of pyroptosis. Therapy promoting pyroptosis and ICB therapy may have synergistic effects in cancer treatment. This review summarizes the mechanisms and roles of pyroptosis in the tumor microenvironment and combination treatment strategies. An improved understanding of the roles of pyroptosis in tumorigenesis, immune evasion, and treatment would aid in the development of therapeutic strategies for malignancies.

Inflammatory bone diseases include osteoarthritis (OA) and rheumatoid arthritis (RA), which can cause severe bone damage in a chronic inflammation state, putting tremendous pressure on the patients' families and government agencies regarding medical costs. In addition, the complexity of osteoimmunology makes research on these diseases difficult. Hence, it is urgent to determine the potential mechanisms and find effective drugs to target inflammatory bone diseases to reduce the negative effects of these diseases. Recently, pyroptosis, a gasdermininduced necrotic cell death featuring secretion of pro-inflammatory cytokines and lysis, has become widely known. Based on the effect of pyroptosis on immunity, this process has gradually emerged as a vital component in the etiopathogenesis of inflammatory bone diseases. Herein, we review the characteristics and mechanisms of pyroptosis and then focus on its clinical significance in inflammatory How to cite this article: Zhang R-N, Sun Z-J, Zhang L. Pyroptosis in inflammatory bone diseases: Molecular insights and targeting strategies. The

Background/Aim Abstracts of randomized controlled trials (RCTs) provide a summary of the entire trial report. Their transparent, detailed, and accurate reporting is essential for clinical decision‐making and evidence‐based dental practice. The aim of this study was to assess the reporting quality and prevalence of spin in abstracts of RCTs in the field of dentofacial trauma. Materials and Methods The PubMed database was searched to identify RCT reports published between 2017 and 2021 in the field of dentofacial trauma. The reporting quality of abstracts was assessed according to the 16‐item CONSORT for Abstracts checklist and measured with an overall quality score (OQS, range: 0–16). Linear regression analyses were used to identify factors associated with reporting quality. Among the included RCTs, parallel‐group RCTs with non‐significant primary outcomes were selected for spin assessment using predefined spin strategies. Results One hundred and twelve eligible abstracts were identified and included. The mean OQS was 4.51 (SD, 1.35; 95% CI, 4.26–4.76). Abstracts with more than 250 words (p = .004) and a structured format (p = .032) had significantly better reporting quality. Of the 30 abstracts that were eligible for spin assessment, spin was identified in 23 (76.7%). Among these, spin was observed in the Conclusions sections of 22 abstracts (73.3%) and the Results sections of 9 abstracts (30.0%). Conclusions Among RCT abstracts in the field of dentofacial trauma, the reporting quality was sub‐optimal and the prevalence of spin was relatively high. Strict adherence to the CONSORT for Abstracts guidelines is needed to ensure complete and transparent reporting. Relevant stakeholders need to make concerted efforts to avoid spin.

Macroautophagy/autophagy is critically involved in the process of salivary gland (SG) diseases such as xerostomia, which has a serious impact on quality of life. KRT14 + progenitor cells are found to be the main progenitors for maintaining the ductal homeostasis of the submandibular SGs. In this study, we investigated the role of ATG5 in SG KRT14 + cells in mice and humans. Human labial salivary glands (LSG) from primary Sjogren's syndrome (pSS) and non-pSS patients (normal), and submandibular glands (SMG) from Atg5 flox/flox ; Krt14-Cre (cKO) mice were used. ATG5 + KRT14 + and p62 + KRT14 + cells were detected by immunofluorescence staining in LSG. TUNEL, immunofluorescence, immunohistochemistry, and western blot were performed to detect cell death in SMG. Saliva was collected in 12-week-old (12 W) and 32-week-old (32 W) mice, then the concentration of calcium and buffering capacity were detected to analyze the function of SG. We found that LSG from pSS patients showed increased p62 and decreased ATG5 in KRT14 + cells. We further revealed that in 32 W, (1) the function of salivary glands was significantly impaired in cKO mice, (2) cell death increased in cKO mice, but cl-Caspase 3 was not significantly changed, and (3) cleaved gasdermin D increased and was highly expressed in KRT14 + cells of cKO mice. After applying a pyroptosis inhibitor to 32 W mice, the reduced saliva flow rate was rescued. In