Comparison Between Powered and Manual Toothbrushes Effectiveness for Maintaining an Optimal Oral Health Status.

This integrative literature review evaluates the effectiveness of power toothbrushes (PTBs) compared to manual toothbrushes (MTBs) across various populations, focusing on plaque removal, gingival health, calculus reduction, and stain removal. PTBs equipped with advanced technologies such as oscillating-rotating and high-frequency sonic mechanisms have been examined for their potential to enhance oral hygiene. Special attention is given to vulnerable groups, including the elderly and individuals with intellectual disabilities, to assess how PTBs meet their specific oral health needs. A comprehensive literature search was conducted in databases including PubMed, Cochrane Library, Embase, and Google Scholar using keywords such as "power toothbrush", "electric toothbrush", "manual toothbrush", "plaque removal", "gingivitis", "calculus", "dental stains", "oral hygiene", "elderly", and "intellectual disabilities". Studies published between 2000 and 2024 were selected based on their relevance to the PTB and MTB comparison, with an emphasis on outcomes related to oral hygiene efficacy. As this review is narrative rather than systematic, it focuses on synthesizing existing knowledge without applying strict inclusion or exclusion criteria. The results indicate that PTBs generally outperform MTBs in reducing plaque, gingivitis, and stains, though the benefits for special populations are less pronounced but still significant. However, practical issues such as user experience and mechanical reliability of PTBs warrant further investigation. In conclusion, this review enhances the understanding of PTB effectiveness, guides consumer choices, and informs future technological advancements in dental care practices.

Mir221- and Mir222-enriched adsc-exosomes mitigate PM exposure-exacerbated cardiac ischemia-reperfusion injury through the modulation of the BNIP3-MAP1LC3B-BBC3/PUMA pathway.

Epidemiology has shown a strong relationship between fine particulate matter (PM) exposure and cardiovascular disease. However, it remains unknown whether PM aggravates myocardial ischemia-reperfusion (I/R) injury, and the related mechanisms are unclear. Our previous study has shown that adipose stem cell-derived exosomes (ADSC-Exos) contain high levels of Mir221 and Mir222. The present study investigated the effects of PM exposure on I/R-induced cardiac injury through mitophagy and apoptosis, as well as the potential role of Mir221 and Mir222 in ADSC-Exos. Wild-type, mir221- and mir222-knockout (KO), and Mir221- and Mir222-overexpressing transgenic (TG) mice were intratracheally injected with PM (10 mg/kg). After 24 h, mice underwent left coronary artery ligation for 30 min, followed by 3 h of reperfusion (I/R). H9c2 cardiomyocytes were cultured under 1% O2 for 6 h, then reoxygenated for 12 h (hypoxia-reoxygenation [H/R]). PM aggravated I/R (or H/R) cardiac injury by increasing ROS levels and causing mitochondrial dysfunction, which increased the expression of mitochondrial fission-related proteins (DNM1L/Drp1 and MFF) and mitophagy-related proteins (BNIP3 and MAP1LC3B/LC3B) in vivo and in vitro. Treatment with ADSC-Exos or Mir221- and Mir222-mimics significantly reduced PM+I/R-induced cardiac injury. Importantly, ADSC-Exos contain Mir221 and Mir222, which directly targets BNIP3, MAP1LC3B/LC3B, and BBC3/PUMA, decreasing their expression and ultimately reducing cardiomyocyte mitophagy and apoptosis. The present data showed that ADSC-Exos treatment regulated mitophagy and apoptosis through the Mir221 and Mir222-BNIP3-MAP1LC3B-BBC3/PUMA pathway and significantly reduced the cardiac damage caused by PM+I/R. The present study revealed the novel therapeutic potential of ADSC-Exos in alleviating PM-induced exacerbation of myocardial I/R injury.Abbreviation: ADSC-Exos: adipose-derived stem cell exosomes; AL: autolysosome; ATP: adenosine triphosphate; BBC3/PUMA: BCL2 binding component 3; BNIP3: BCL2/adenovirus E1B interacting protein 3; CASP3: caspase 3; CASP9: caspase 9; CDKN1B/p27: cyclin dependent kinase inhibitor 1B; CVD: cardiovascular disease; DCFH-DA: 2',7'-dichlorodihydrofluorescein diacetate; DHE: dihydroethidium; DNM1L/Drp1: dynamin 1-like; EF: ejection fraction; FS: fractional shortening; H/R: hypoxia-reoxygenation; I/R: ischemia-reperfusion; LDH: lactate dehydrogenase; MAP1LC3B/LC3B: microtubule-associated protein 1 light chain 3 beta; MFF: mitochondrial fission factor; miRNA: microRNA; NAC: N-acetylcysteine; OCR: oxygen consumption rate; PIK3C3/Vps34: phosphatidylinositol 3-kinase catalytic subunit type 3; PM: particulate matter; PRKAA1/AMPK: protein kinase AMP-activated catalytic subunit alpha 1; ROS: reactive oxygen species; SQSTM1/p62: sequestosome 1; TEM: transmission electron microscopy; TRP53/p53: transformation related protein 53; TUNEL: terminal deoxynucleotidyl transferase dUTP nick end labeling.

Polycaprolactone in Bone Tissue Engineering: A Comprehensive Review of Innovations in Scaffold Fabrication and Surface Modifications.

Bone tissue engineering has seen significant advancements with innovative scaffold fabrication techniques such as 3D printing. This review focuses on enhancing polycaprolactone (PCL) scaffold properties through structural modifications, including surface treatments, pore architecture adjustments, and the incorporation of biomaterials like hydroxyapatite (HA). These modifications aim to improve scaffold conformation, cellular behavior, and mechanical performance, with particular emphasis on the role of mesenchymal stem cells (MSCs) in bone regeneration. The review also explores the potential of integrating nanomaterials and graphene oxide (GO) to further enhance the mechanical and biological properties of PCL scaffolds. Future directions involve optimizing scaffold structures and compositions for improved bone tissue regeneration outcomes.

Effects of handheld nonthermal plasma on the biological responses, mineralization, and inflammatory reactions of polyaryletherketone implant materials.

Background/purpose: The handheld nonthermal plasma (HNP) treatment may alter the surface properties, bone metabolism, and inflammatory reactions of polyaryletherketone (PAEK) dental implant materials. This study tested whether the HNP treatment might increase the biocompatibility, surface hydrophilicity, surface free energies (SFEs), and the cell adhesion and mineralization capability of PAEK materials. Materials and methods: Disk-shaped samples of titanium (Ti), zirconia (Zr), polyetheretherketone (PEEK [PE]), and polyetherketoneketone (PEKK [PK]) were subjected to HNP treatment and termed as TiPL, ZrPL, PEPL, and PKPL, respectively. Water-surface reactions were examined using a goniometer. MG-63 cells were cultured on all samples to assess the cell viability, cytotoxicity, cell attachment, and mineralization characteristics. The expression of pro-inflammatory cytokines (tumor necrosis factor-alpha and interleukin-6) and key mineralization markers (alkaline phosphatase [ALKP], osteopontin [OPN], and dentin matrix protein 1 [DMP1]) was measured using enzyme-linked immunosorbent assay kits. Results: The HNP-treated samples exhibited significantly enhanced surface hydrophilicities and SFEs compared to the untreated samples. The cell viability remained high across all samples, indicating no cytotoxic effects. The HNP treatment significantly enhanced MG-63 cell adherence and proliferation. Elevated levels of ALKP and OPN were observed for the plasma-treated PEPL and PKPL specimens, while DMP1 levels increased significantly only in the PKPL specimen. Pro-inflammatory cytokine levels were low across all samples, suggesting no inflammatory response. Conclusion: The HNP-treated PAEKs have enhanced the surface hydrophilicity and SFEs as well as superior cell adhesion and mineralization capability, and thus may be good clinical dental implant materials.

A Narrative Review: Repurposing Metformin as a Potential Therapeutic Agent for Oral Cancer.

Oral cancer, particularly oral squamous cell carcinoma (OSCC), is a significant global health challenge because of its high incidence and limited treatment options. Major risk factors, including tobacco use, alcohol consumption, and specific microbiota, contribute to the disease's prevalence. Recently, a compelling association between diabetes mellitus (DM) and oral cancer has been identified, with metformin, a widely used antidiabetic drug, emerging as a potential therapeutic agent across various cancers, including OSCC. This review explores both preclinical and clinical studies to understand the mechanisms by which metformin may exert its anticancer effects, such as inhibiting cancer cell proliferation, inducing apoptosis, and enhancing the efficacy of existing treatments. Preclinical studies demonstrate that metformin modulates crucial metabolic pathways, reduces inflammation, and impacts cellular proliferation, thereby potentially lowering cancer risk and improving patient outcomes. Additionally, metformin's ability to reverse epithelial-to-mesenchymal transition (EMT), regulate the LIN28/let-7 axis, and its therapeutic role in head and neck squamous cell carcinoma (HNSCC) are examined through experimental models. In clinical contexts, metformin shows promise in enhancing therapeutic outcomes and reducing recurrence rates, although challenges such as drug interactions, complex dosing regimens, and risks such as vitamin B12 deficiency remain. Future research should focus on optimizing metformin's application, investigating its synergistic effects with other therapies, and conducting rigorous clinical trials to validate its efficacy in OSCC treatment. This dual exploration underscores metformin's potential to play a transformative role in both diabetes management and cancer care, potentially revolutionizing oral cancer treatment strategies.

The crosstalk between copper-induced oxidative stress and cuproptosis: a novel potential anticancer paradigm.

Copper is a crucial trace element that plays a role in various pathophysiological processes in the human body. Copper also acts as a transition metal involved in redox reactions, contributing to the generation of reactive oxygen species (ROS). Under prolonged and increased ROS levels, oxidative stress occurs, which has been implicated in different types of regulated cell death. The recent discovery of cuproptosis, a copper-dependent regulated cell death pathway that is distinct from other known regulated cell death forms, has raised interest to researchers in the field of cancer therapy. Herein, the present work aims to outline the current understanding of cuproptosis, with an emphasis on its anticancer activities through the interplay with copper-induced oxidative stress, thereby providing new ideas for therapeutic approaches targeting modes of cell death in the future.

Unlocking the Future of Periodontal Regeneration: An Interdisciplinary Approach to Tissue Engineering and Advanced Therapeutics.

Periodontal defects present a significant challenge in dentistry, necessitating innovative solutions for comprehensive regeneration. Traditional restoration methods have inherent limitations in achieving complete and functional periodontal tissue reconstruction. Tissue engineering, a multidisciplinary approach integrating cells, biomaterials, and bioactive factors, holds tremendous promise in addressing this challenge. Central to tissue engineering strategies are scaffolds, pivotal in supporting cell behavior and orchestrating tissue regeneration. Natural and synthetic materials have been extensively explored, each offering unique advantages in terms of biocompatibility and tunable properties. The integration of growth factors and stem cells further amplifies the regenerative potential, contributing to enhanced tissue healing and functional restoration. Despite significant progress, challenges persist. Achieving the seamless integration of regenerated tissues, establishing proper vascularization, and developing biomimetic scaffolds that faithfully replicate the natural periodontal environment are ongoing research endeavors. Collaborative efforts across diverse scientific disciplines are essential to overcoming these hurdles. This comprehensive review underscores the critical need for continued research and development in tissue engineering strategies for periodontal regeneration. By addressing current challenges and fostering interdisciplinary collaborations, we can unlock the full regenerative potential, paving the way for transformative advancements in periodontal care. This research not only enhances our understanding of periodontal tissues but also offers innovative approaches that can revolutionize dental therapies, improving patient outcomes and reshaping the future of periodontal treatments.

Ribonucleic Acid Sequencing Reveals the Upregulation and Resolution of Inflammation and Extracellular Matrix Remodeling in Lidocaine-Treated Human Acute Monocytic Leukemia Cell Line THP-1.

Lidocaine, a local anesthetic widely used in dentistry, is esteemed for its efficacy and safety. Recent research reveals its additional role in modulating the immune system, and particularly in reducing inflammation crucial for protecting tooth-supporting tissues. Notably, monocytes and macrophages, essential cellular components overseeing various physiological and pathological processes, stand as potential mediators of lidocaine's effects. Therefore, this study aimed to investigate how lidocaine influences cell behavior using RNA sequencing. To investigate the effect of lidocaine on THP-1 cells' behavior, we performed an MTT assay and RNA-Seq along with qPCR analyses to evaluate the transcriptomic and proteomic changes in THP-1 cells. Our results showed that a high dose of lidocaine (>1 mM) had a significant cytotoxic effect on THP-1 cells. However, a lidocaine dose lower than 0.5 mM induced a mixed anti-inflammatory profile by significantly upregulating tissue remodeling (GDF15, FGF7, HGF, COL4A3, COL8A2, LAMB2, LAMC2, PDGFRA, and VEGFA) and through the resolution of inflammation (Cpeb4, Socs1, Socs2, Socs3, Dusp1, Tnfaip3, and Gata3) gene cassettes. This study explores the effect of lidocaine on the THP-1 in the M2-like healing phenotype and provides potential applications of lidocaine's therapeutic effectiveness in dental tissue repair.

Harnessing peroxisome proliferator-activated receptor γ agonists to induce Heme Oxygenase-1: a promising approach for pulmonary inflammatory disorders.

The activation of peroxisome proliferator-activated receptor (PPAR)-γ has been extensively shown to attenuate inflammatory responses in conditions such as asthma, acute lung injury, and acute respiratory distress syndrome, as demonstrated in animal studies. However, the precise molecular mechanisms underlying these inhibitory effects remain largely unknown. The upregulation of heme oxygenase-1 (HO-1) has been shown to confer protective effects, including antioxidant, antiapoptotic, and immunomodulatory effects in vitro and in vivo. PPARγ is highly expressed not only in adipose tissues but also in various other tissues, including the pulmonary system. Thiazolidinediones (TZDs) are highly selective agonists for PPARγ and are used as antihyperglycemic medications. These observations suggest that PPARγ agonists could modulate metabolism and inflammation. Several studies have indicated that PPARγ agonists may serve as potential therapeutic candidates in inflammation-related diseases by upregulating HO-1, which in turn modulates inflammatory responses. In the respiratory system, exposure to external insults triggers the expression of inflammatory molecules, such as cytokines, chemokines, adhesion molecules, matrix metalloproteinases, and reactive oxygen species, leading to the development of pulmonary inflammatory diseases. Previous studies have demonstrated that the upregulation of HO-1 protects tissues and cells from external insults, indicating that the induction of HO-1 by PPARγ agonists could exert protective effects by inhibiting inflammatory signaling pathways and attenuating the development of pulmonary inflammatory diseases. However, the mechanisms underlying TZD-induced HO-1 expression are not well understood. This review aimed to elucidate the molecular mechanisms through which PPARγ agonists induce the expression of HO-1 and explore how they protect against inflammatory and oxidative responses.

Silica Nanoparticles Shed Light on Intriguing Cellular Pathways in Human Tracheal Smooth Muscle Cells: Revealing COX-2/PGE2 Production through the EGFR/Pyk2 Signaling Axis.

The use of manufactured silica nanoparticles (SiNPs) has become widespread in everyday life, household products, and various industrial applications. While the harmful effects of crystalline silica on the lungs, known as silicosis or chronic pulmonary diseases, are well understood, the impact of SiNPs on the airway is not fully explored. This study aimed to investigate the potential effects of SiNPs on human tracheal smooth muscle cells (HTSMCs). Our findings revealed that SiNPs induced the expression of cyclooxygenase-2 (COX-2) mRNA/protein and the production of prostaglandin E2 (PGE2) without causing cytotoxicity. This induction was transcription-dependent, as confirmed by cell viability assays and COX-2 luciferase reporter assays. Further analysis, including Western blot with pharmacological inhibitors and siRNA interference, showed the involvement of receptor tyrosine kinase (RTK) EGF receptor (EGFR), non-RTK Pyk2, protein kinase Cα (PKCα), and p42/p44 MAPK in the induction process. Notably, EGFR activation initiated cellular signaling that led to NF-κB p65 phosphorylation and translocation into the cell nucleus, where it bound and stimulated COX-2 gene transcription. The resulting COX-2 protein triggered PGE2 production and secretion into the extracellular space. Our study demonstrated that SiNPs mediate COX-2 up-regulation and PGE2 secretion in HTSMCs through the sequential activation of the EGFR/Pyk2/PKCα/p42/p44MAPKs-dependent NF-κB signaling pathway. Since PGE2 can have both physiological bronchodilatory and anti-inflammatory effects, as well as pathological pro-inflammatory effects, the increased PGE2 production in the airway might act as a protective compensatory mechanism and/or a contributing factor during airway exposure to SiNPs.

Evaluation of shade correspondence between high-translucency pre-colored zirconia and shade tab by considering the influence of cement shade and substrate materials.

Statement of problem: The relation between cement color and abutment substrate material and the corresponding effect on the color accuracy of high-transparency pre-colored zirconia (HT-Zr) remains unclear. Purpose: This in-vitro study aimed to investigate the difference in color accuracy when the HT-Zr is bonded to different materials-based substrates with differently colored resin cement. Materials and methods: Vita A1 shade HT-Zr with 1 mm thickness was used as the testing sample. The samples were first placed on zirconia (ZR), tooth color resin (CR), and metallic (MT) abutment substrates. Subsequently, four differently colored cements (translucent (TR), bleach, opaque, and A2 shade (A2)) were used for bonding HT-Zr onto the substrate, and the non-bonded group was used as the control group (CG). There were 15 groups in total (n = 10 per group). A digital colorimeter was used to obtain Commission Internationale de l'Eclairage (CIELab) color parameters. The translucency parameter (TP00) of the substrate and sample, as well as color difference (ΔE00) and chroma (C) between the different groups were calculated. Additionally, the ΔE00 and TP00 were compared with the moderately unacceptable match of ΔE00 = 3.6. The statistical analysis was conducted using ANOVA and Tukey HSD post-hoc test (α = 0.05). Results: HT-Zr exhibited high translucency (TP00 = 11.02 ± 0.18), and the mean ΔE00 of the testing samples ranged between 2.18 ± 0.20 and 13.14 ± 0.31. The ZR-CG and MT-A2 groups showed the highest and lowest lightness separately. The CR-CG group exhibited the highest C, and the ΔE00 was lower than that of 3.6. The MT-TR group showed the lowest C and the highest ΔE00. The inter-group comparison revealed that the ΔE00 for different cement is mostly lower than the acceptable color match of 1.0; moreover, the ΔE00 for all the substrates, excluding the CG group, is higher than 3.6. Conclusions: The abutment substrate materials and the cement color should be considered with caution when using HT-Zr, with the effect of abutment substrate materials being more apparent in color accuracy. HT-Zr restorations are not recommended for discolored or bleached abutments but only for natural-colored abutments to achieve the optimal color appearance.

High-density lipoprotein protects vascular endothelial cells from indoxyl sulfate insults through its antioxidant ability.

Chronic kidney disease (CKD) patients have a high risk of cardiovascular disease. Indoxyl sulfate (IS) is a uremic toxin that has been shown to inhibit nitric oxide production and cause cell senescence by inducing oxidative stress. High-density lipoprotein (HDL) has a protective effect on the cardiovascular system; however, its impacts on IS-damaged endothelial cells are still unknown. This study aimed to explore the effects of exogenous supplement of HDL on vascular endothelial cells in a uremia-mimic environment. Tube formation, migration, adhesion, and senescence assays were used to evaluate the cell function of human aortic endothelial cells (HAECs). Reactive oxygen species generation was measured by using Amplex red assay. L-NAME and MCI186 were used as a nitric oxide synthase inhibitor and a free radical scavenger, respectively. HDL exerted anti-inflammatory and antioxidant effects via HIF-1α/HO-1 activation and IL-1ß/TNF-α/IL-6 inhibition in IS-stimulated HAECs. HDL improved angiogenesis ability through upregulating Akt/eNOS/VEGF/SDF-1 in IS-stimulated HAECs. HDL decreased endothelial adhesiveness via downregulating VCAM-1 and ICAM-1 in IS-stimulated HAECs. Furthermore, HDL reduced cellular senescence via upregulating SIRT1 and downregulating p53 in IS-stimulated HAECs. Importantly, the above beneficial effects of HDL were mainly due to its antioxidant ability. In conclusion, HDL exerted a comprehensive protective effect on vascular endothelial cells against damage from IS through its antioxidant ability. The results of this study might provide a theoretical basis for potential HDL supplementation in CKD patients with endothelial damage.

Rhamnetin Prevents Bradykinin-Induced Expression of Matrix Metalloproteinase-9 in Rat Brain Astrocytes by Suppressing Protein Kinase-Dependent AP-1 Activation.

Bradykinin (BK) has been recognized as a stimulant for matrix metalloproteinase (MMP)-9 expression, contributing to neuroinflammation. Modulating the BK/MMP-9 pathway offers potential in the treatment of neuroinflammatory disorders. Rhamnetin (RNT), a flavonoid compound known for its antioxidant and anti-inflammatory effects, has shown promise. However, the specific mechanisms through which RNT inhibits BK-induced MMP-9 expression remain unclear. Therefore, this study aims to delve into the intricate mechanisms underlying this process. Here, we initially demonstrated that RNT effectively attenuated BK-induced MMP-9 expression and its associated cell migration in rat brain astrocyte-1 (RBA-1) cells. Further investigation revealed that BK-driven MMP-9 protein, mRNA, and promoter activity linked to cell migration relied on c-Src, Pyk2, EGFR, PDGFR, PI3K/Akt, JNK1/2, and c-Jun. This was validated by the inhibition of these effects through specific inhibitors, a finding substantiated by the introduction of siRNAs targeting these signaling molecules. Notably, the phosphorylated levels of these signaling components induced by BK were significantly reduced by their respective inhibitors and RNT, underscoring the inhibitory role of RNT in this process. These findings indicate that, in RBA-1 cells, RNT diminishes the heightened induction of MMP-9 triggered by BK through the inhibition of c-Src/Pyk2/PDGFR and EGFR/PI3K/Akt/JNK1/2-dependent AP-1 activation. This suggests that RNT holds promise as a potential therapeutic approach for addressing neuroinflammation in the brain.

Bisphosphonates and Their Connection to Dental Procedures: Exploring Bisphosphonate-Related Osteonecrosis of the Jaws.

Bisphosphonates are widely used to treat osteoporosis and malignant tumors due to their effectiveness in increasing bone density and inhibiting bone resorption. However, their association with bisphosphonate-related osteonecrosis of the jaws (BRONJ) following invasive dental procedures poses a significant challenge. This review explores the functions, mechanisms, and side effects of bisphosphonates, emphasizing their impact on dental procedures. Dental patients receiving bisphosphonate treatment are at higher risk of BRONJ, necessitating dentists' awareness of these risks. Topical bisphosphonate applications enhance dental implant success, by promoting osseointegration and preventing osteoclast apoptosis, and is effective in periodontal treatment. Yet, systemic administration (intravenous or intraoral) significantly increases the risk of BRONJ following dental procedures, particularly in inflamed conditions. Prevention and management of BRONJ involve maintaining oral health, considering alternative treatments, and careful pre-operative and post-operative follow-ups. Future research could focus on finding bisphosphonate alternatives with fewer side effects or developing combinations that reduce BRONJ risk. This review underscores the need for further exploration of bisphosphonates and their implications in dental procedures.

Optimizing Dental Bond Strength: Insights from Comprehensive Literature Review and Future Implications for Clinical Practice.

This review examines the modifying factors affecting bond strength in various bonding scenarios, particularly their relevance to the longevity of dental restorations. Understanding these factors is crucial for improving clinical outcomes in dentistry. Data were gathered from the PubMed database, ResearchGate, and Google Scholar resources, covering studies from 1992 to 2022. The findings suggest that for dentin-resin bonds, minimizing smear layers and utilizing MMP inhibitors to prevent hybrid layer degradation are essential. In the case of resin-resin bonds, reversing blood contamination is possible, but preventing saliva contamination is more challenging, underscoring its critical importance during clinical procedures. Additionally, while pretreatment on ceramics has minimal impact on bond strength, the influence of specific colorings should be carefully considered in treatment planning. This comprehensive review highlights that although established practices recognize significant bond strength factors, ongoing research provides valuable insights to enhance the clinical experience for patients. Once confirmed through rigorous experimentation, these emerging findings should be swiftly integrated into dental practice to improve patient outcomes.

Exploring Possible Diagnostic Precancerous Biomarkers for Oral Submucous Fibrosis: A Narrative Review.

Oral submucous fibrosis (OSF) stands as a progressive oral ailment, designated as a potentially malignant disorder. OSF has gained widespread recognition as a significant precursor to malignant transformation. In the pursuit of dependable, straightforward, and non-invasive diagnostic measures for the early detection of oral malignant progression, research has delved into potential diagnostic biomarkers of OSF. This comprehensive review delves into current investigations that explore the correlation between various biomarkers and OSF. The molecular biomarkers of OSF are categorized based on cytology and sampling methods. Moreover, this review encompasses pertinent studies detailing how these biomarkers are acquired and processed. Within this scope, we scrutinize four potential biomarkers that hold the promise of facilitating the development of diagnostic tools for detecting early-stage OSF.

Reactive Oxygen Species-Dependent Activation of EGFR/Akt/p38 Mitogen-Activated Protein Kinase and JNK1/2/FoxO1 and AP-1 Pathways in Human Pulmonary Alveolar Epithelial Cells Leads to Up-Regulation of COX-2/PGE2 Induced by Silica Nanoparticles.

The risk of lung exposure to silica nanoparticles (SiNPs) and related lung inflammatory injury is increasing with the wide application of SiNPs in a variety of industries. A growing body of research has revealed that cyclooxygenase (COX)-2/prostaglandin E2 (PGE2) up-regulated by SiNP toxicity has a role during pulmonary inflammation. The detailed mechanisms underlying SiNP-induced COX-2 expression and PGE2 synthesis remain unknown. The present study aims to dissect the molecular components involved in COX-2/PGE2 up-regulated by SiNPs in human pulmonary alveolar epithelial cells (HPAEpiCs) which are one of the major targets while SiNPs are inhaled. In the present study, we demonstrated that SiNPs induced COX-2 expression and PGE2 release, which were inhibited by pretreatment with a reactive oxygen species (ROS) scavenger (edaravone) or the inhibitors of proline-rich tyrosine kinase 2 (Pyk2, PF-431396), epidermal growth factor receptor (EGFR, AG1478), phosphatidylinositol 3-kinase (PI3K, LY294002), protein kinase B (Akt, Akt inhibitor VIII), p38 mitogen-activated protein kinase (MAPK) (p38 MAPK inhibitor VIII), c-Jun N-terminal kinases (JNK)1/2 (SP600125), Forkhead Box O1 (FoxO1, AS1842856), and activator protein 1 (AP-1, Tanshinone IIA). In addition, we also found that SiNPs induced ROS-dependent Pyk2, EGFR, Akt, p38 MAPK, and JNK1/2 activation in these cells. These signaling pathways induced by SiNPs could further cause c-Jun and FoxO1 activation and translocation from the cytosol to the nucleus. AP-1 and FoxO1 activation could increase COX-2 and PGE2 levels induced by SiNPs. Finally, the COX-2/PGE2 axis might promote the inflammatory responses in HPAEpiCs. In conclusion, we suggested that SiNPs induced COX-2 expression accompanied by PGE2 synthesis mediated via ROS/Pyk2/EGFR/PI3K/Akt/p38 MAPK- and JNK1/2-dependent FoxO1 and AP-1 activation in HPAEpiCs.

Unraveling the Link between Periodontitis and Coronavirus Disease 2019: Exploring Pathogenic Pathways and Clinical Implications.

Periodontitis involves the inflammation of the periodontal tissue, leading to tissue loss, while coronavirus disease 2019 (COVID-19) is a highly transmissible respiratory disease caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which is amplified by poor systemic health. Key facilitators of SARS-CoV-2's entry into host cells are angiotensin-converting enzyme 2 (ACE2) and transmembrane serine protease 2 (TMPRSS2). This review reveals that periodontal pockets can serve as a hotspot for virus accumulation, rendering surrounding epithelia more susceptible to infection. Given that ACE2 is expressed in oral mucosa, it is reasonable to suggest that poor periodontal health could increase the risk of COVID-19 infection. However, recent studies have not provided sufficient evidence to imply a significant effect of COVID-19 on periodontal health, necessitating further and more long-term investigations. Nevertheless, there are hypotheses linking the mechanisms of the two diseases, such as the involvement of interleukin-17 (IL-17). Elevated IL-17 levels are observed in both COVID-19 and periodontitis, leading to increased osteoclast activity and bone resorption. Lastly, bidirectional relationships between periodontitis and systemic diseases like diabetes are acknowledged. Given that COVID-19 symptoms may worsen with these conditions, maintaining good oral health and managing systemic diseases are suggested as potential ways to protect against COVID-19.

Thrombin-Induced COX-2 Expression and PGE2 Synthesis in Human Tracheal Smooth Muscle Cells: Role of PKCδ/Pyk2-Dependent AP-1 Pathway Modulation.

In this study, we confirmed that thrombin significantly increases the production of COX-2 and PGE2 in human tracheal smooth muscle cells (HTSMCs), leading to inflammation in the airways and lungs. These molecules are well-known contributors to various inflammatory diseases. Here, we investigated in detail the involved signaling pathways using specific inhibitors and small interfering RNAs (siRNAs). Our results demonstrated that inhibitors targeting proteins such as protein kinase C (PKC)δ, proline-rich tyrosine kinase 2 (Pyk2), c-Src, epidermal growth factor receptor (EGFR), phosphatidylinositol 3-kinase (PI3K), or activator protein-1 (AP-1) effectively reduced thrombin-induced COX-2 and PGE2 production. Additionally, transfection with siRNAs against PKCδ, Pyk2, c-Src, EGFR, protein kinase B (Akt), or c-Jun mitigated these responses. Furthermore, our observations revealed that thrombin stimulated the phosphorylation of key components of the signaling cascade, including PKCδ, Pyk2, c-Src, EGFR, Akt, and c-Jun. Thrombin activated COX-2 promoter activity through AP-1 activation, a process that was disrupted by a point-mutated AP-1 site within the COX-2 promoter. Finally, resveratrol (one of the most researched natural polyphenols) was found to effectively inhibit thrombin-induced COX-2 expression and PGE2 release in HTSMCs through blocking the activation of Pyk2, c-Src, EGFR, Akt, and c-Jun. In summary, our findings demonstrate that thrombin-induced COX-2 and PGE2 generation involves a PKCδ/Pyk2/c-Src/EGFR/PI3K/Akt-dependent AP-1 activation pathway. This study also suggests the potential use of resveratrol as an intervention for managing airway inflammation.

Enhancing Dental Cement Bond Strength with Autofocus-Laser-Cutter-Generated Grooves on Polyetheretherketone Surfaces.

Polyetheretherketone (PEEK) is widely used in dentistry owing to its exceptional properties, including its natural appearance; however, existing surface treatment methods for bonding PEEK have limitations. Autofocus laser cutters, known for their precise engraving and cutting capabilities, offer potential for surface treatment of PEEK; thus, the objective of this study was to investigate the creation of laser groove structures on PEEK to enhance its bonding capability with dental resin cement. A dental computer-aided design and manufacturing system was used to fabricate PEEK samples, and three groove patterns (circle, line, and grid) were generated on PEEK surfaces, with air-abrasion used as the control group. The surface characteristics, cell viability, and bond strength were evaluated, and the data were statistically analyzed using one-way analysis of variance and post hoc Tukey's tests (α = 0.05). Laser-treated PEEK exhibited a uniform texture with a groove depth of approximately 39.4 µm, hydrophobic properties with a contact angle exceeding 90°, a surface roughness of 7.3-12.4 µm, consistent topography, and comparable cell viability compared with untreated PEEK. Despite a decrease in bond strength after thermal cycling, no significant intergroup differences were observed, except for the line-shaped laser pattern. These findings indicate that the autofocus laser cutter effectively enhances the surface characteristics of PEEK by creating a uniform texture and grooves, showing promise in improving bonding properties, even considering the impact of thermal cycling effects.