Journal of Oral Biosciences最新文献

{"title":"Creating 3D constructs with cranial neural crest-derived cell lines using a bio-3D printer","authors":"Masahide Taguchi ,&nbsp;Shohei Yoshimoto ,&nbsp;Kanako Suyama ,&nbsp;Satoko Sumi ,&nbsp;Shirabe Ohki ,&nbsp;Kayoko Ogata ,&nbsp;Ryota Fujimoto ,&nbsp;Daiki Murata ,&nbsp;Koichi Nakayama ,&nbsp;Kyoko Oka","doi":"10.1016/j.job.2024.05.005","DOIUrl":"10.1016/j.job.2024.05.005","url":null,"abstract":"<div><h3>Objectives</h3><p>The development of bio-three-dimensional (bio-3D) printers has led to significant advances in regenerative medicine. Three-dimensional constructs, including spheroids, are maintained by extracellular matrix proteins secreted by cells so that the cells can be cultured in conditions closer to the physiological environment. This study aimed to create a useful 3D construct as a model of the dentin-pulp complex.</p></div><div><h3>Methods</h3><p>We examined the expression patterns of extracellular matrix proteins and cell proliferation areas in a 3D construct created using O9-1 cells derived from cranial neural crest cells of mice. The 3D construct was created by sticking the spheroid cultures onto a needle array using a bio-3D printer.</p></div><div><h3>Results</h3><p>Cell proliferation areas along with characteristic expression of tenascin C and DMP1 were evaluated. The expression of tenascin C and DMP1 was significantly enhanced in the spheroids compared to that in two-dimensional cultures. Moreover, cell proliferation regions and tenascin C expression were confirmed in the outer layer of spheroids in the embryonic stem cell medium, with insignificant DMP1 expression being observed. Interestingly, in a 3D construct cultured in calcification-induction medium, DMP1 expression was promoted, and DMP1-positive cells existed in the outermost layer without overlapping with tenascin C expression.</p></div><div><h3>Conclusions</h3><p>The extracellular matrix proteins, tenascin C and DMP1, were expressed in a polarized manner in spheroids and 3D constructs, similar to the findings in the dental papilla. Therefore, these 3D constructs show potential as artificial models for studying odontogenesis.</p></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"66 2","pages":"Pages 339-348"},"PeriodicalIF":2.4,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1349007924000884/pdfft?md5=8f885124196ccc1de6d2898988bc6099&pid=1-s2.0-S1349007924000884-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140945462","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Remineralizing potential of Calcium Sucrose Phosphate in white spot lesions: A Systematic Review","authors":"Tanisha Rout,&nbsp;Amol Patil,&nbsp;Sonakashee Deshmukh,&nbsp;Sonakshi Sharma","doi":"10.1016/j.job.2024.04.005","DOIUrl":"10.1016/j.job.2024.04.005","url":null,"abstract":"<div><h3>Background</h3><p>This systematic review aimedto evaluate the remineralizing efficacy of calcium sucrose phosphate (CaSP) for the treatment of white spot lesions (WSLs) that commonly occur after orthodontic treatment with fixed appliances using various randomized controlled trials (RCTs) available in the literature todate.</p></div><div><h3>Highlights</h3><p>Adhering to the Preferred Reporting Items for Systematic Reviews and Meta-Analyzes (PRISMA) guidelines, RCTs that assessed the efficacious remineralizing potential of CaSP on WSLs and demineralized enamel and compared it with either no intervention or other remineralizing agents wereselected. The methodological rigor of the included studies was subjected to the Risk of Bias tool-2 (ROB-2) and Grading of Recommendations, Assessment, Development and Evaluation (GRADE) tools. Furthermore, a Begg's Funnel Plot was used to assess publication bias. The qualitative analysis encompassed a corpus of 36 studies. The remineralization potential of CaSP was investigated using an array of parameters, including surface microhardness, surface morphology, surface roughness, mineral content, and lesion size and depth. Based on the ROB-2 tool, most of the included studies were judged to be high risk, largely attributable to the presence of attrition bias. Using the GRADE framework, the certainty of evidence was determined to be moderate.</p></div><div><h3>Conclusion</h3><p>This systematic review reveals that CaSP yields favorableoutcomes in terms of increased surface microhardness and calcium-phosphate content, reduced demineralized area and surface roughness, and enhanced surface topography</p></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"66 2","pages":"Pages 261-271"},"PeriodicalIF":2.4,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140762573","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Peroxiredoxin 1 promotes proliferation and inhibits differentiation of MC3T3-E1 cells via AKT1 / NF-κB signaling pathway","authors":"Juan Du ,&nbsp;Wei Zhou ,&nbsp;Zhe Sun ,&nbsp;Weilong Zhang ,&nbsp;Wei Luo ,&nbsp;Shanshan Liu","doi":"10.1016/j.job.2024.04.007","DOIUrl":"10.1016/j.job.2024.04.007","url":null,"abstract":"<div><h3>Objectives</h3><p>Osteoporosis is the most common metabolic bone disease worldwide. The decrease in bone mass is primarily accompanied by a decrease in the number and activity of osteoblasts. Peroxiredoxins (PRDXs) are proteins that detect extremely low peroxide levels and act as sensors that regulate oxidation signals, thereby regulating various cellular functions. This study aimed to evaluate the effects of PRDX1 and estrogen on the biological behavior of osteoblasts, including their proliferation and differentiation.</p></div><div><h3>Methods</h3><p>Ovariectomized (OVX) mice were used to establish a model of osteoporosis and perform morphological and immunohistochemical analyses. <em>Prdx1</em> gene knockout and overexpression were performed in mouse MC3T3-E1 pre-osteoblasts to assess proliferation and osteogenic differentiation using the cell counting kit-8, quantitative reverse transcription polymerase chain reaction, western blotting (WB), Alizarin Red S staining, etc.</p></div><div><h3>Results</h3><p>The OVX mice exhibited osteoporosis and PRDX1 expression increased. <em>In vitro</em> experiments showed that during the osteogenic differentiation of osteoblasts, PRDX1 expression decreased, while the expression of COL1 and RUNX2 increased. After <em>Prdx1</em> knockout, the proliferation of osteoblasts decreased; expression of Runx2, ALP, and COL1 increased; and mineralization increased. However, after <em>Prdx1</em> overexpression, osteoblast proliferation was enhanced, whereas osteogenic differentiation and mineralization were inhibited. Estrogen inhibits the H₂O₂-induced decrease in osteoblastic differentiation and increase in PRDX1 expression. WB revealed that when LY294002 inhibited the AKT signaling pathway, the levels of <em>p</em>-AKT1, p-P65, and PRDX1 protein in MC3T3-E1 cells decreased. However, when pyrrolidine dithiocarbamate (PDTC) inhibited the NF-κB signaling pathway, the expression of <em>p</em>-AKT1 and PRDX1 did not change except for a significant reduction of p-P65 expression. Furthermore, PDTC reversed the decreased expression of RUNX2, ALP, and COL1 caused by PRDX1 overexpression.</p></div><div><h3>Conclusions</h3><p>PRDX1 promotes the proliferation of osteoblasts and inhibits osteogenic differentiation. Estrogen regulated osteoblastic differentiation by affecting the expression of PRDX1 in osteoblasts, and the effect is related to the AKT1/NF-κB signaling pathway.</p></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"66 2","pages":"Pages 403-411"},"PeriodicalIF":2.4,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140768176","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Muscarinic acetylcholine receptor-mediated phosphorylation of extracellular signal-regulated kinase in HSY salivary ductal cells involves distinct signaling pathways","authors":"Rezon Yanuar,&nbsp;Shingo Semba,&nbsp;Akihiro Nezu,&nbsp;Akihiko Tanimura","doi":"10.1016/j.job.2024.02.002","DOIUrl":"10.1016/j.job.2024.02.002","url":null,"abstract":"<div><h3>Objectives</h3><p>Typical agonists of G protein-coupled receptors (GPCRs), including muscarinic acetylcholine receptors (mAChRs), activate both G-protein and β-arrestin signaling systems, and are termed balanced agonists. In contrast, biased agonists selectively activate a single pathway, thereby offering therapeutic potential for the specific activation of that pathway. The mAChR agonists carbachol and pilocarpine are known to induce phosphorylation of extracellular signal-regulated kinase-1/2 (ERK1/2) <em>via</em> G-protein-dependent and -independent pathways, respectively. We investigated the involvement of β-arrestin and its downstream mechanisms in the ERK1/2 phosphorylation induced by carbachol and pilocarpine in the human salivary ductal cell line, HSY cells.</p></div><div><h3>Methods</h3><p>HSY cells were stimulated with pilocarpine or carbachol, with or without various inhibitors. The cell lysates were analyzed by western blotting using the antibodies p44/p42^MAPK and phosphor-p44/p42^MAPK.</p></div><div><h3>Results</h3><p>Western blot analysis revealed that carbachol elicited greater stimulation of ERK1/2 phosphorylation compared to pilocarpine. ERK1/2 phosphorylation was inhibited by atropine and gefitinib, suggesting that mAChR activation induces transactivation of epidermal growth factor receptors (EGFR). Moreover, inhibition of carbachol-mediated ERK1/2 phosphorylation was achieved by GF-109203X (a PKC inhibitor), a βARK1/GRK2 inhibitor, barbadin (a β-arrestin inhibitor), pitstop 2 (a clathrin inhibitor), and dynole 34-2 (a dynamin inhibitor). In contrast, pilocarpine-mediated ERK1/2 phosphorylation was only inhibited by barbadin (a β-arrestin inhibitor) and PP2 (a Src inhibitor).</p></div><div><h3>Conclusion</h3><p>Carbachol activates both G-protein and β-arrestin pathways, whereas pilocarpine exclusively activates the β-arrestin pathway. Additionally, downstream of β-arrestin, carbachol activates clathrin-dependent internalization, while pilocarpine activates Src.</p></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"66 2","pages":"Pages 447-455"},"PeriodicalIF":2.4,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139713228","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Development and establishment of oral microbiota in early life","authors":"Shinya Kageyama,&nbsp;Toru Takeshita","doi":"10.1016/j.job.2024.05.001","DOIUrl":"10.1016/j.job.2024.05.001","url":null,"abstract":"<div><h3>Background</h3><p>The oral microbiota has recently attracted attention owing to its association with oral and systemic diseases. Accordingly, gaining an understanding of oral microbiota development and the factors influencing it can contribute to preventing the establishment of dysbiotic oral microbiota and, eventually, oral microbiota-related diseases.</p></div><div><h3>Highlight</h3><p>In this review, we highlight the results of a longitudinal project focusing on oral microbiota development during early life. At 4 months of age, the oral microbiota of infants was found to differ considerably from the maternal oral microbiota, even though infants acquire oral bacteria from their mothers. At 18 months, although the infant microbiota is still not completely comparable with that of adults, from 4 to 18 months, there is a rapid phase of development, during which the microbial composition undergoes considerable change to a profile more similar to that in adults. During this development, the infant oral microbiota converges into two different profiles with adult-like traits, namely, <em>Streptococcus salivarius</em>- and <em>Neisseria</em>-dominant profiles. This divergence is strongly influenced by dietary habits, with a frequent intake of sweetened beverages being associated with an <em>S. salivarius</em>-dominant profile, which is suspected to be implicated in oral and systemic diseases.</p></div><div><h3>Conclusion</h3><p>The foundation of the adult oral microbiota may be established by 18 months of age, and the developmental period from 4 to 18 months may be an appropriate period during which to modify the microbial balance to obtain a desirable healthy state. In particular, dietary habits during this period warrant close attention.</p></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"66 2","pages":"Pages 300-303"},"PeriodicalIF":2.4,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1349007924000847/pdfft?md5=93be854326af0429ffeac77531dfcef4&pid=1-s2.0-S1349007924000847-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140866411","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tacrolimus, FK506, promotes bone formation in bone defect mouse model","authors":"Satoko Nishida ,&nbsp;Yuki Azetsu ,&nbsp;Masahiro Chatani ,&nbsp;Akiko Karakawa ,&nbsp;Kai Otake ,&nbsp;Hidemitsu Sugiki ,&nbsp;Nobuhiro Sakai ,&nbsp;Yasubumi Maruoka ,&nbsp;Mie Myers ,&nbsp;Masamichi Takami","doi":"10.1016/j.job.2024.02.003","DOIUrl":"10.1016/j.job.2024.02.003","url":null,"abstract":"<div><h3>Objectives</h3><p>Some studies have reported that tacrolimus (FK506), an immunosuppressant, may have positive effects on bone formation. However, the precise effects of FK506 on bone repair or osteoblasts remain inadequately elucidated, and limited research has explored the outcomes of its use in an <em>in vivo</em> mouse model. This study aims to examine the effects of FK506 on bone repair and osteoblast functions using bone defect and BMP-2-induced ectopic ossification mouse models, as well as cultured primary mouse osteoblasts treated with FK506.</p></div><div><h3>Methods</h3><p>We established mouse models of femur bone defect and BMP-2-induced ectopic ossification to evaluate the effect of FK506 on new bone formation, respectively. Additionally, primary mouse osteoblasts were cultured with FK506 and examined for gene expressions related to osteoblast differentiation.</p></div><div><h3>Results</h3><p>While FK506 promoted the repair of bone defect areas in the femur of the bone defect mouse model, it also led to widespread abnormal bone formation outside the intended area. Additionally, following the implantation of a collagen sponge containing BMP-2 into mouse muscle tissue, FK506 was found to promote ectopic ossification and enhance BMP-2-induced osteoblast differentiation <em>in vitro</em>. Our findings also revealed that FK506 increased the number of immature osteoblasts in the absence of BMP-2 without affecting osteoblast differentiation. <span>Furthermore</span>, direct effects were observed, reducing the ability of osteoblasts to support osteoclastogenesis.</p></div><div><h3>Conclusions</h3><p>These results indicate that FK506 increases new bone formation during bone repair and influences the proliferation of immature osteoblasts, as well as osteoblast-supported osteoclastogenesis.</p></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"66 2","pages":"Pages 391-402"},"PeriodicalIF":2.4,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139742292","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Areca nut-induced oral fibrosis – Reassessing the biology of oral submucous fibrosis","authors":"Mohit Sharma ,&nbsp;Sachin C. Sarode ,&nbsp;Gargi Sarode ,&nbsp;Raghu Radhakrishnan","doi":"10.1016/j.job.2024.02.005","DOIUrl":"10.1016/j.job.2024.02.005","url":null,"abstract":"<div><h3>Background</h3><p>Oral submucous fibrosis (OSF) is a pathological condition characterized by excessive tissue healing resulting from physical, chemical, or mechanical trauma. Notably, areca nut consumption significantly contributes to the development of oral fibrosis. The current definition of OSF, recognizing its potential for malignant transformation, necessitates a more comprehensive understanding of its pathophysiology and etiology.</p></div><div><h3>Highlights</h3><p>Areca nut induces fibrotic pathways by upregulating inflammatory cytokines such as TGF-β and expressing additional cytokines. Moreover, it triggers the conversion of fibroblasts to myofibroblasts, characterized by α-SMA and γSMA expression, resulting in accelerated collagen production. Arecoline, a component of areca nut, has been shown to elevate levels of reactive oxygen species, upregulate the expression of various cytokines, and activate specific signaling pathways (MEK, COX2, PI3K), all contributing to fibrosis. Therefore, we propose redefining OSF as “Areca nut-induced oral fibrosis” (AIOF) to align with current epistemology, emphasizing its distinctive association with areca nut consumption. The refined definition enhances our ability to develop targeted interventions, thus contributing to more effective prevention and treatment strategies for oral submucous fibrosis worldwide.</p></div><div><h3>Conclusion</h3><p>Arecoline plays a crucial role as a mediator in fibrosis development, contributing to extracellular matrix accumulation in OSF. The re-evaluation of OSF as AIOF offers a more accurate representation of the condition. This nuanced perspective is essential for distinguishing AIOF from other forms of oral fibrosis and advancing our understanding of the disease's pathophysiology.</p></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"66 2","pages":"Pages 320-328"},"PeriodicalIF":2.4,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1349007924000185/pdfft?md5=7f4a4bc5bf67a446810c21e59ff7f0f0&pid=1-s2.0-S1349007924000185-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139940902","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Stem cells in regenerative dentistry: Current understanding and future directions","authors":"Pooja Shah ,&nbsp;Marziyeh Aghazadeh ,&nbsp;Sheeja Rajasingh ,&nbsp;Douglas Dixon ,&nbsp;Vinay Jain ,&nbsp;Johnson Rajasingh","doi":"10.1016/j.job.2024.02.006","DOIUrl":"10.1016/j.job.2024.02.006","url":null,"abstract":"<div><h3>Background</h3><p>Regenerative dentistry aims to enhance the structure and function of oral tissues and organs. Modern tissue engineering harnesses cell and gene-based therapies to advance traditional treatment approaches. Studies have demonstrated the potential of mesenchymal stem cells (MSCs) in regenerative dentistry, with some progressing to clinical trials. This review comprehensively examines animal studies that have utilized MSCs for various therapeutic applications. Additionally, it seeks to bridge the gap between related findings and the practical implementation of MSC therapies, offering insights into the challenges and translational aspects involved in transitioning from preclinical research to clinical applications.</p></div><div><h3>Highlights</h3><p>To achieve this objective, we have focused on the protocols and achievements related to pulp-dentin, alveolar bone, and periodontal regeneration using dental-derived MSCs in both animal and clinical studies. Various types of MSCs, including dental-derived cells, bone-marrow stem cells, and umbilical cord stem cells, have been employed in root canals, periodontal defects, socket preservation, and sinus lift procedures. Results of such include significant hard tissue reconstruction, functional pulp regeneration, root elongation, periodontal ligament formation, and cementum deposition. However, cell-based treatments for tooth and periodontium regeneration are still in early stages. The increasing demand for stem cell therapies in personalized medicine underscores the need for scientists and responsible organizations to develop standardized treatment protocols that adhere to good manufacturing practices, ensuring high reproducibility, safety, and cost-efficiency.</p></div><div><h3>Conclusion</h3><p>Cell therapy in regenerative dentistry represents a growing industry with substantial benefits and unique challenges as it strives to establish sustainable, long-term, and effective oral tissue regeneration solutions.</p></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"66 2","pages":"Pages 288-299"},"PeriodicalIF":2.4,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139973942","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nanoscale osseointegration of zirconia evaluated from the interfacial structure between ceria-stabilized tetragonal zirconia and cell-induced hydroxyapatite","authors":"Mari M. Saito,&nbsp;Kazuo Onuma,&nbsp;Yasuo Yamakoshi","doi":"10.1016/j.job.2024.05.003","DOIUrl":"10.1016/j.job.2024.05.003","url":null,"abstract":"<div><h3>Background</h3><p>The osseointegration of zirconia implants has been evaluated based on their implant fixture bonding with the alveolar bone at the optical microscopic level. Achieving nano-level bonding between zirconia and bone apatite is crucial for superior osseointegration; however, only a few studies have investigated nanoscale bonding. This review outlines zirconia osseointegration, including surface modification, and presents an evaluation of nanoscale zirconia-apatite bonding and its structure.</p></div><div><h3>Highlight</h3><p>Assuming osseointegration, the cells produced calcium salts on a ceria-stabilized zirconia substrate. We analyzed the interface between calcium salts and zirconia substrates using transmission electron microscopy and found that 1) the cell-induced calcium salts were bone-like apatite and 2) direct nanoscale bonding was observed between the bone-like apatite and zirconia crystals without any special modifications of the zirconia surface.</p></div><div><h3>Conclusion</h3><p>Structural affinity exists between bone apatite and zirconia crystals. Apatite formation can be induced by the zirconia surface. Zirconia bonds directly with apatite, indicating superior osseointegration <em>in vivo</em>.</p></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"66 2","pages":"Pages 281-287"},"PeriodicalIF":2.4,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140899407","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Local anesthetics inhibit muscarinic acetylcholine receptor-mediated calcium responses and the recruitment of β-arrestin in HSY human parotid cells","authors":"Mari Shimatani ,&nbsp;Takao Morita ,&nbsp;Rezon Yanuar ,&nbsp;Akihiro Nezu ,&nbsp;Akihiko Tanimura","doi":"10.1016/j.job.2024.04.002","DOIUrl":"10.1016/j.job.2024.04.002","url":null,"abstract":"<div><h3>Objectives</h3><p>Local anesthetics act on G protein-coupled receptors (GPCRs); thus, their potential as allosteric modulators of GPCRs has attracted attention. Intracellular signaling via GPCRs involves both G-protein- and β-arrestin-mediated pathways. To determine the effects of local anesthetics on muscarinic acetylcholine receptors (mAChR), a family of GPCRs, we analyzed the effects of local anesthetics on mAChR-mediated Ca²⁺ responses and formation of receptor–β-arrestin complexes in the HSY human parotid cell line.</p></div><div><h3>Methods</h3><p>Ca²⁺ responses were monitored by fura-2 spectrofluorimetry. Ligand-induced interactions between mAChR and β-arrestin were examined using a β-arrestin GPCR assay kit.</p></div><div><h3>Results</h3><p>Lidocaine reduced mAChR-mediated Ca²⁺ responses but did not change the intracellular Ca²⁺ concentration in non-stimulated cells. The membrane-impermeant lidocaine analog QX314 and procaine inhibited mAChR-mediated Ca²⁺ responses, with EC₅₀ values of 48.0 and 20.4 μM, respectively, for 50 μM carbachol-stimulated Ca²⁺ responses. In the absence of extracellular Ca²⁺, the pretreatment of cells with QX314 reduced carbachol-induced Ca²⁺ release, indicating that QX314 reduced Ca²⁺ release from intracellular stores. Lidocaine and QX314 did not affect store-operated Ca²⁺ entry as they did not alter the thapsigargin-induced Ca²⁺ response. QX314 and procaine reduced the carbachol-mediated recruitment of β-arrestin, and administration of procaine suppressed pilocarpine-induced salivary secretion in mice.</p></div><div><h3>Conclusion</h3><p>Local anesthetics, including QX314, act on mAChR to reduce carbachol-induced Ca²⁺ release from intracellular stores and the recruitment of β-arrestin. These findings support the notion that local anesthetics and their derivatives are starting points for the development of functional allosteric modulators of mAChR.</p></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"66 2","pages":"Pages 465-472"},"PeriodicalIF":2.4,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140772904","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}