As commercial space travel becomes a reality, the oral health of space tourists presents a new area of concern. The space environment, characterized by microgravity, altered atmospheric pressure, and exposure to cosmic radiation, may exacerbate pre-existing dental conditions and increase the risk of pain or complications. This review outlines current knowledge regarding the effects of spaceflight on oral health and proposes preliminary guidelines for managing dental conditions in space tourists. Emphasis is placed on identifying dental risks, screening protocols, and emergency management strategies to support the safe participation of individuals in space tourism.

Recently, several reports have described that the accuracy of intraoral scanners is equal to or greater than that of conventional methods using silicone rubber impressions. However, it is unclear whether intraoral scanners are applicable to patients with more than three missing teeth or edentulous jaws. A computer numerical control coordinate-measuring machine was employed to measure the reference models as a control. Subsequently, two types of intraoral scanners, TRIOS3 (TR3) and PrimeScan (PS), were examined to estimate the trueness and precision of the distance using image analysis software. In this study, the accuracy of the new high-end model of the intraoral scanner and the popular model were examined to verify their range of application to oral implant treatment. Regarding the error in trueness, no significant differences were observed between the scanners when short distances were measured, whereas the error in TR3 was significantly larger when a long distance was measured. No significant difference in precision error was observed between the two scanners, even when long-distance scanning was performed. When measured using TR3, the errors in both trueness and precision were significantly larger when long distances were scanned. In contrast, when using PS, the error in trueness was significantly larger when long distances were scanned; however, there was no significant difference in the error in precision between long- and short-distance scanning. The results of our study suggest that the errors tend to increase with an increase in the scanned distance. In addition, these results suggest that the accuracy was equivalent between the PS and TR, when the scanning distance was short. Optical impressions obtained using an intraoral scanner could be clinically applicable to implant treatment in the case of a small number of missing teeth. A newly provided high-performance scanner might be applicable to cases with a larger number of missing teeth.

Implant restoration is widely adopted for addressing dentition defects, but the failure rate due to insufficient bone integration remains high. This is often attributed to the low osteogenic efficiency and prolonged osseointegration periods associated with pure titanium (Ti) implants that lack surface treatments. Enhancing the surface of these implants could potentially improve their integration. This study aims to investigate the effects of non-thermal atmospheric pressure plasma (NTAP) in immobilizing bone morphogenetic protein-2 (BMP-2) onto Ti nanotubes (TNTs), examining its osteoinductive capabilities through the immune response pathway. Ti nanotubes (TNTs) were fabricated on the surface of Ti discs using a secondary anodic oxidation process. The capability of NTAP to facilitate the immobilization of BMP-2 on TNTs was assessed. The study further evaluated the influence of different Ti substrates on the polarization of macrophages and the osteogenic differentiation of bone marrow mesenchymal stem cells (BMMSCs), particularly through macrophage-induced polarization. The application of TNTs/NTAP/BMP-2 substantially reduced the presence of M1 macrophages while promoting M2 macrophages. The secreted products from macrophages treated with TNTs/NTAP/BMP-2 enhanced the migration and osteogenic differentiation of BMMSCs, as evidenced by increased cell migration, higher alkaline phosphatase activity, more mineralized nodules, and the up-regulation of osteogenesis-related genes and proteins. NTAP treatment effectively promotes the immobilization of BMP-2 on TNTs. This surface-modified Ti substrate significantly enhances the osteogenic differentiation of BMMSCs by modulating macrophage polarization. This approach could lead to improved outcomes in implant restoration by fostering better bone integration. This study provides new ideas and theoretical basis for the design of novel bone implant materials, which is expected to enhance the speed and strength of implant osseointegration, thus increasing the success rate of dental implants in the clinic.

We aimed to assess the effects of diode laser plus subgingival scaling and root planing (SRP) on secreted frizzled-related protein 1 (SFRP1) and β-catenin in children with periodontitis. A retrospective analysis was conducted on the clinical data of ninety-eight children with periodontitis hospitalized between May 2022 and May 2024. These children were assigned into a control group (n=49, treated with SRP) and a study group (n=49, provided with diode laser plus SRP) based on different therapeutic regimens. After 8 weeks and 12 weeks of treatment, the pocket probing depth, clinical attachment level, plaque index, gingival index and gingival sulcus bleeding index dropped in the two groups compared with those before treatment, and they were lower in the study group than in the control group (P<0.05). At 12 weeks after treatment, decreased prostaglandin E₂, interleukin (IL)-1β, hypersensitive C-reactive protein, IL-6, SFRP1 and β-catenin levels were observed in gingival crevicular fluid in the two groups compared to those before treatment, and these levels were lower in the study group than in the control group (P<0.05). Diode laser plus SRP can effectively improve the periodontal indexes and occlusal function, relieve periodontal pain and inflammatory responses, and decrease the expression levels of SFRP1 and β-catenin in the gingival tissues of children with periodontitis.

Osteosarcoma is the most prevalent primary bone cancer in both children and adolescents. One of the major clinical challenges in osteosarcoma treatment is chemoresistance, particularly resistance to cisplatin. Therefore, identifying novel biomarkers and underlying mechanisms of cisplatin resistance in osteosarcoma is imperative. In this study, we investigated the role and potential mechanisms of kinesin family member 20A (KIF20A) in cisplatin resistance in osteosarcoma. Publicly available clinical datasets were analyzed to assess the expression of KIF20A in osteosarcoma patients. Additionally, we examined the expression of KIF20A in osteosarcoma cell lines, and evaluated its functional role in cell proliferation, invasion, and cisplatin resistance in vitro. Finally, we explored the regulatory effect of KIF20A on the JAK/STAT3 signaling pathway. Our findings suggest that KIF20A is a potential regulator of osteosarcomaprogression and cisplatin resistance. Knockout of KIF20A significantly reduced the proliferation and invasion ability of osteosarcoma cells, and suppressed their resistance to cisplatin. Moreover, KIF20A was shown to regulate the oncogenic JAK/STAT3 signaling pathway. Elevated KIF20A expression enhanced osteosarcoma cell proliferation, invasion, and cisplatin resistance. This, in addition to serving as a novel biomarker for cisplatin resistance, KIF20A may represent a promising therapeutic target in osteosarcoma.

Bone marrow mesenchymal stem cells (BMSCs) play a pivotal role in skeletal regeneration. However, their osteogenic potential can be compromised under inflammatory conditions through interleukin-1β (IL-1β)-mediated activation of nuclear factor kappa B (NF-κB) signaling pathway. This study investigated the protective effects of diallyl disulfide (DADS) against IL-1β/NF-κB-induced impairment of osteogenic differentiation in BMSCs and explored the underlying mechanisms. Human BMSCs were characterized by morphology, tri-lineage differentiation capacity, and surface marker expression. Cells were treated with IL-1β with or without DADS. Assays were conducted to evaluate cell viability, osteogenic gene expression, matrix mineralization, oxidative stress markers, and the expression levels of proteins involved in the NF-κB and AMP-activated protein kinase (AMPK) signaling pathways. The role of AMPK was further examined by co-treatment with the AMPK inhibitor Compound C. IL-1β suppressed osteogenic differentiation and induced oxidative stress in a concentration-dependent manner via activation of the NF-κB signaling pathway. DADS reversed these effects by restoring the expression levels of osteogenic markers (RUNX2, OSX, and OCN), enhancing matrix mineralization, reducing reactive oxygen species (ROS) and malondialdehyde MDA levels, increasing glutathione peroxidase (GSH-PX) activity, and promoting AMPK phosphorylation. The protective effects of DADS were abolished by AMPK inhibition, indicating that its regulatory action is AMPK-dependent. These findings suggest that DADS could alleviate IL-1β-induced osteogenic dysfunction in BMSCs by modulating redox homeostasis and inhibiting NF-κB signaling through AMPK activation. These findings highlighted the therapeutic potential of DADS for inflammation-related bone diseases.

α-Smooth muscle actin (SMA) has been found in the pericytes of blood vessels. In addition, it has recently been reported that α-SMA-positive cells also appear during tissue repair, suggesting that this protein is a marker for undifferentiated cells. In this study, to analyze the involvement of α-SMA-positive cells in bone regeneration, the localization of α-SMA and osteoblast differentiation markers, including runt-related transcription factor 2 (Runx2) and osterix (Osx), was examined using an experimental animal model of rib bone fracture. Twenty-five Wister rats were used. The ribs were cut vertically and were collected on day 0 (Day 0) (before fracture) and days 4 (Day 4), 8 (Day 8), 12 (Day 12), and 28 (Day 28) (after fracture); α-SMA-positive reactions were observed around the fractured bone, except for the perivascular area at Day 4. At Day 8, α-SMA-positive cells were localized around the cartilage tissue at the fracture site. This localization pattern was similar to those of Runx2 and Osx. At Day 12, α-SMA-, Runx2-, and Osx-positive cells were localized on the surface of the new bone. At Day 28, few α-SMA-positive cells were found in the bone marrow or on the cortical bone surface. These findings suggest that α-SMA is related to the early stages of osteoblast differentiation and could be involved in new bone formation in endochondral ossification.

Diallyl disulfide (DADS) holds anti-inflammatory, anti-oxidant, and immunomodulatory properties and represses nuclear factor-κB (NF-κB)-dependent activation of NLRP3 inflammasomes. However, whether DADS alleviates chondrocyte injury by modulating NF-κB-dependent activation of the NLRP3 inflammasome remains unclear. In this study, lipopolysaccharide (LPS)-stimulated chondrocytes were used as an in vitro model of osteoarthritis (OA) to investigate the effects of DADS. Effects of DADS treatment on cell viability, apoptosis, extracellular matrix (ECM) degradation, and inflammation in chondrocytes were determined via several experiments. Western blot analysis was employed to examine the expression levels of NLRP3 inflammasome components and NF-κB signaling molecules. To determine whether DADS could act through the NF-κB pathway, caffeic acid phenethyl ester (CAPE), a specific NF-κB inhibitor, was used as a comparator. DADS treatment impaired LPS-induced chondrocyte apoptosis, ECM degeneration, and inflammation in a concentration-dependent manner. This was accompanied by a marked reduction in phosphorylated p65 level and downregulation of NLRP3, ASC, and Caspase-1 protein expression levels. Notably, CAPE exerted similar protective effects as DADS, reducing LPS-induced apoptosis, ECM degeneration, inflammatory cytokine production, and NLRP3 inflammasome activation. However, in the presence of CAPE, DADS did not confer additional benefits in LPS-stimulated chondrocytes, suggesting that its effects are primarily mediated through the NF-κB/NLRP3 signaling pathway. In conclusion, DADS alleviates LPS-induced chondrocyte apoptosis, ECM degeneration, and inflammatory response by repressing the NF-κB/NLRP3 signaling pathway, providing a scientific basis for formulating DADS-based treatment strategies for OA.