Journal of Oral Biosciences最新文献

{"title":"Effect of short-term gravitational changes on the human minor salivary gland stem cell characteristics","authors":"Jeong Mi Kim ,&nbsp;Tri Ho Minh ,&nbsp;Eun Jeong Jeon ,&nbsp;Jin Mi Park ,&nbsp;Sungryeal Kim ,&nbsp;Jeong-Seok Choi","doi":"10.1016/j.job.2025.100625","DOIUrl":"10.1016/j.job.2025.100625","url":null,"abstract":"<div><h3>Objectives</h3><div>Human minor salivary gland stem cells (huMSGSCs) are promising in regenerative medicine. Their multipotent capabilities enable tissue regeneration and offer treatment potential for various diseases. The effects of hypergravity (HyperG) and microgravity (MicroG) on stemness and therapeutic potential are not well explored. Therefore, this study investigated the effects of short-term HyperG and MicroG exposure on huMSGSC stemness and differentiation potential for treating salivary gland dysfunction.</div><div>Methods: huMSGSCs were exposed to 1G, MicroG, and HyperG. Cell morphology, proliferation, sphere formation, and differentiation potential were analyzed. Stem cell and tight junction markers were evaluated using flow cytometry, real-time PCR, Western blot, and immunofluorescence analysis.</div></div><div><h3>Results</h3><div>huMSGSCs showed fibroblast-like morphology and robust proliferation up to passage 10. Differentiation into adipocytes, chondrocytes, and osteocytes was successful, despite enhanced lineage-specific marker expression. HyperG significantly increased proliferation at 48 and 72 h, MicroG-exposed cells formed more numerous and smaller spheres, and HyperG-exposed cells produced larger spheres. HyperG elevated stem cell marker (CD90, LGR5, SOX2) expression levels, and the expression of tight junction protein expressions (ZO-1, ZO-2) was higher under HyperG treatment.</div></div><div><h3>Conclusions</h3><div>Short-term HyperG and MicroG exposure differentially influenced huMSGSC stemness and differentiation potential. HyperG enhanced proliferation, stem cell marker expression, and differentiation capacity. These findings suggest the potential of optimizing huMSGSCs for regenerative therapies that target salivary gland dysfunction and other tissue regeneration applications.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"67 1","pages":"Article 100625"},"PeriodicalIF":2.6,"publicationDate":"2025-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143366201","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":"Comparison of the structural features between chicken quadratomandibular joint and rat temporomandibular joint with reference to ligament and articular meniscus/disc","authors":"Masami Takahashi ,&nbsp;Shunichi Shibata ,&nbsp;Toru Shibui ,&nbsp;Masaki Takechi ,&nbsp;Kazuharu Irie","doi":"10.1016/j.job.2025.100623","DOIUrl":"10.1016/j.job.2025.100623","url":null,"abstract":"<div><h3>Objectives</h3><div>The new jaw joint of mammals evolved between the squamosal and the dentary. We investigated the structural features of the chicken quadratomandibular joint (QMJ) (primary jaw joint) and the rat temporomandibular joint (TMJ) (new jaw joint) to determine whether these structures reflect their putative movements from macroscopic and histological perspectives.</div></div><div><h3>Methods</h3><div>Chicken QMJ and rat TMJ were dissected, and their joint apparatuses, including ligaments and meniscus/disc, were analyzed macroscopically. Microscopic analysis, incorporating immunohistochemistry and in situ hybridization, was conducted to investigate protein localization and gene expression within the extracellular matrix of cartilage and bone.</div></div><div><h3>Results</h3><div>The chicken QMJ contained the jugomandibular ligament, running laterally and posteriorly to the QMJ, tightly bound to the articular meniscus. These features suggest a role in supporting and controlling quadrate bone movements. The rat TMJ lacked a lateral ligament, and the mandibular head had an elongated oval shape along the anterior–posterior axis. This morphology indicates that lateral mandibular movements are rare, with jaw motion predominantly occurring in the anterior–posterior direction. The chicken QMJ meniscus contained distinct cartilaginous tissues, whereas the rat TMJ articular disc acquired cartilaginous characteristics after occlusion was established (5 weeks postnatally), suggesting that the meniscus/disc properties are closely associated with mastication.</div></div><div><h3>Conclusions</h3><div>The structural features of chicken and rat jaw joints, including their joint apparatuses, appropriately reflect their respective functions, such as movement dynamics and resistance to mastication pressure.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"67 1","pages":"Article 100623"},"PeriodicalIF":2.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143081053","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":"Lipocalin 2 inhibits the expressions of interleukin-8 and macrophage inflammatory protein-1α in human neutrophil-like cells","authors":"Rie Kido ,&nbsp;Yuka Hiroshima ,&nbsp;Jun-ichi Kido ,&nbsp;Mika Bando ,&nbsp;Kaya Yoshida ,&nbsp;Yuji Inagaki ,&nbsp;Hiromichi Yumoto","doi":"10.1016/j.job.2025.100624","DOIUrl":"10.1016/j.job.2025.100624","url":null,"abstract":"<div><h3>Objectives</h3><div>Lipocalin 2 (LCN2) is a glycoprotein with multiple functions, including antimicrobial activity, inflammatory response modulation, and cell migration. LCN2 is expressed in some cells, such as epithelial cells and neutrophils, and its levels are increased in inflammatory diseases. This study investigated the presence of LCN2 receptor (24p3R) in cells around periodontal tissues and function of LCN2 in cells with a receptor to explore the role of LCN2 in periodontal diseases.</div></div><div><h3>Methods</h3><div>The presence of 24p3R was examined in periodontal cells, including human gingival fibroblasts, periodontal ligament fibroblasts, human oral epithelial cells (HOECs), and neutrophil-like cells (HL-60), by Western blotting. Changes in periodontal disease-associated proteins in the presence of recombinant LCN2 (rLCN2) were examined using a protein array in differentiated HL-60 (dHL-60) cells. Interleukin-8 (IL-8) and macrophage inflammatory protein-1α (MIP-1α) mRNA expressions were analyzed by qRT-PCR, and IL-8 and MIP-1α levels in dHL-60 cells treated with rLCN2 or <em>Porphyromonas gingivalis</em>-lipopolysaccaharide (<em>P.g</em>-LPS) were determined by enzyme-linked immunosorbent assay.</div></div><div><h3>Results</h3><div>We detected 24p3R in dHL-60 cells. IL-8 was highly expressed and MIP-1α was weakly expressed in dHL-60 cells using a protein array. rLCN2 significantly decreased IL-8 mRNA and protein levels and suppressed <em>P.g</em>-LPS-induced IL-8 production in dHL-60 cells. As dHL-60 cells were co-cultured with HOECs in which LCN2 was knocked down, IL-8 mRNA expression increased in dHL-60 cells. Furthermore, rLCN2 inhibited MIP-1α production in dHL-60 cells.</div></div><div><h3>Conclusion</h3><div>LCN2 suppresses inflammatory responses by regulating IL-8 and MIP-1α expression in periodontal diseases.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"67 1","pages":"Article 100624"},"PeriodicalIF":2.6,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143075651","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":"Aspirin promotes odontogenic differentiation via a mechanism involving FOXC1, RUNX2, and MCAM expression","authors":"Naoki Miyasaka ,&nbsp;Daisuke Torii ,&nbsp;Takafumi Satomi ,&nbsp;Kenichi Sakurai ,&nbsp;Taka Nakahara ,&nbsp;Takeo W. Tsutsui","doi":"10.1016/j.job.2025.100622","DOIUrl":"10.1016/j.job.2025.100622","url":null,"abstract":"<div><h3>Objectives</h3><div>This study aimed to investigate the effects of aspirin on the early stages of odontogenic differentiation. The roles of <em>FOXC1</em>, <em>RUNX2</em>, and <em>MCAM</em> gene expression in the mechanism of odontogenic differentiation were evaluated by examining the effects of downregulated <em>FOXC1</em> or <em>RUNX2</em> expression using small interfering RNAs (siRNAs).</div></div><div><h3>Methods</h3><div>Dental pulp cells were treated with aspirin (0, 2.5, 50, 100 μg/ml) to assess its impact on mineralization. The gene expression levels of <em>FOXC1</em>, <em>RUNX2</em>, and <em>MCAM</em> were measured using digital polymerase chain reaction, and the effects of siRNA-mediated knockdown of <em>FOXC1</em> and <em>RUNX2</em> were analyzed. The mineralization potential was quantitatively assessed using Alizarin Red S staining and a calcium assay.</div></div><div><h3>Results</h3><div>Analysis of cell growth curves and doubling times indicated that aspirin did not affect cell proliferation at 2.5 μg/ml and 50 μg/ml; however, 50 μg/ml aspirin promoted mineralization. In the <em>FOXC1</em> and <em>RUNX2</em> knockdown experiments, fluctuations in <em>FOXC1</em>, <em>RUNX2</em>, and <em>MCAM</em> gene expression were observed in the aspirin-treated group, suggesting the involvement of these genes in mineralization. Alizarin red S staining and calcium assays further demonstrated that aspirin enhanced mineralization.</div></div><div><h3>Conclusions</h3><div>These findings indicate that aspirin promotes odontogenic differentiation and regulates the expression of <em>FOXC1</em>, <em>RUNX2</em>, and <em>MCAM</em>. This suggests that aspirin may serve as a promising new therapeutic agent in dental pulp regenerative medicine.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"67 1","pages":"Article 100622"},"PeriodicalIF":2.6,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143075455","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":"Exploring the therapeutic potential of small extracellular vesicles derived from induced pluripotent stem cell in periodontal regeneration","authors":"Tingting Xu ,&nbsp;Yi Peng ,&nbsp;Yanan Xu ,&nbsp;Jing Zhu ,&nbsp;Qiao Yang ,&nbsp;Yali Liu ,&nbsp;Hefeng Yang","doi":"10.1016/j.job.2025.100621","DOIUrl":"10.1016/j.job.2025.100621","url":null,"abstract":"<div><h3>Objectives</h3><div>To investigate the role of small extracellular vesicles derived from induced pluripotent stem cells (iPSC-sEVs) in periodontal tissue regeneration, elucidate their potential molecular mechanisms, and provide theoretical guidance for the clinical application of iPSC-sEVs as a cell-free therapeutic strategy for periodontal tissue regeneration.</div></div><div><h3>Methods</h3><div>We investigated the effects of iPSC-sEVs on the proliferation, migration, and osteogenic differentiation of periodontal ligament stem cells (PDLSCs) in vitro. The regenerative potential of iPSC-sEVs was evaluated in vivo, using a periodontal defect model. Bulk RNA sequencing was performed to elucidate the underlying molecular mechanisms.</div></div><div><h3>Results</h3><div>iPSC-sEVs were isolated, characterized, and systemically evaluated for regenerative potential. The results revealed that treatment with iPSC-sEVs significantly enhanced the proliferation, migration, and osteogenic differentiation of PDLSCs. In situ treatment with iPSC-sEVs loaded onto collagen sponges was performed in a rat model of periodontal defects. Micro-CT and histological analyses indicated that iPSC-sEV treatment markedly promoted alveolar bone repair and periodontal ligament regeneration. Mechanistically, the analysis of bulk RNA sequencing data coupled with experimental validation revealed that iPSC-sEV treatment significantly activated the mitogen-activated protein kinase (MAPK) signaling pathway in PDLSCs. Further investigation showed that the inhibition of this pathway completely abolished the proliferative effects of iPSC-sEVs on PDLSCs.</div></div><div><h3>Conclusions</h3><div>iPSC-sEVs promote PDLSC proliferation through MAPK signaling pathway activation, while also enhancing PDLSC migratory and osteogenic differentiation capacities, facilitates the repair and regeneration of damaged periodontal tissue and presents a potential novel therapeutic strategy for clinical periodontal tissue regeneration.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"67 1","pages":"Article 100621"},"PeriodicalIF":2.6,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143075629","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":"Effects of thread design on soft and hard tissue healing around implants in lipopolysaccharide-induced peri-implantitis-like lesions in rat maxillae","authors":"Tomohiro Ishizaki ,&nbsp;Yusuke Uto ,&nbsp;Nao Inaba ,&nbsp;Fumika Tsuda ,&nbsp;Shinichiro Kuroshima ,&nbsp;Takashi Sawase","doi":"10.1016/j.job.2025.100620","DOIUrl":"10.1016/j.job.2025.100620","url":null,"abstract":"<div><h3>Objectives</h3><div>This study investigated the effects of thread design on the soft and hard tissues around implants in rat maxillary peri-implantitis-like lesions.</div></div><div><h3>Methods</h3><div>Fourteen, 9-week-old, female Wistar rats were used in this study. Two types of grade IV titanium tissue-level implants with a standard V-shape and buttress threads were prepared (control and test implants, respectively). The control and test implants were randomly placed into healed left or right sides four weeks after first molar extraction. Daily administration of lipopolysaccharide (LPS) into the peri-implant mucosal sulcus was performed in combination with Freund's incomplete and complete adjuvants. The maxillae were harvested 16 days after LPS administration for quantitative and qualitative analyses.</div></div><div><h3>Results</h3><div>LPS administration induced significant marginal bone loss, with increases in osteoclasts and polymorphonuclear cells around control implants. LPS administration did not change cell numbers around nor alter bone quality inside the buttress threads of the test implants, but resulted in a significant deterioration of bone quality, defined as the preferential alignment of collagen fibers inside the V-shaped threads of the control implant. LPS administration also significantly increased calprotectin production in the epithelium around the test implants and significantly increased calprotectin production in the connective tissue around both the control and test implants.</div></div><div><h3>Conclusions</h3><div>Buttress threads at specific angles provided resistance to LPS-induced inflammation in rats with LPS-induced peri-implantitis-like lesions. The upregulated production of calprotectin induced by LPS administration in the epithelium and connective tissues around the test implants may facilitate inflammation control around implants.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"67 1","pages":"Article 100620"},"PeriodicalIF":2.6,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143041431","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":"Factors secreted from the stem cells of human exfoliated deciduous teeth inhibit osteoclastogenesis through the activation of the endogenous antioxidant system","authors":"Cheng Ding ,&nbsp;Noboru Hashimoto ,&nbsp;Fumiya Kano ,&nbsp;Hirofumi Tenshin ,&nbsp;Takahiro Arai ,&nbsp;Linze Xia ,&nbsp;Yang Xu ,&nbsp;Houjun Lao ,&nbsp;Yifei Wang ,&nbsp;Tomonori Iwasaki ,&nbsp;Hideharu Hibi ,&nbsp;Akihito Yamamoto","doi":"10.1016/j.job.2025.100618","DOIUrl":"10.1016/j.job.2025.100618","url":null,"abstract":"<div><h3>Objectives</h3><div>Systemic administration of conditioned medium (CM) from stem cells derived from human exfoliated deciduous teeth (SHED-CM) in mouse models of rheumatoid arthritis, osteoporosis, and osteoarthritis suppresses excessive osteoclast activity and restores bone integrity. However, the mechanism through which SHED-CM regulates osteoclastogenesis remains largely unknown. In the present study, we examined the anti-osteoclastogenic mechanism of SHED-CM in vitro.</div></div><div><h3>Methods</h3><div>Bone marrow macrophages and RAW264.7 cells were treated with receptor activator of nuclear factor kappa-Β ligand (RANKL) in the presence of SHED-CM or CM from bone marrow mesenchymal stem cells (BMSC-CM). Osteoclast differentiation was assessed using tartrate-resistant acid phosphatase staining, actin ring formation, and expression of osteoclast-specific markers. RANKL-induced reactive oxygen species (ROS) production was analyzed as a critical mediator of osteoclastogenesis. The activation of endogenous antioxidant gene expression was examined using reverse transcription quantitative PCR. Liquid chromatography with tandem mass spectrometry (LC-MS) was used to identify proteins enriched in SHED-CM, and neutralizing antibodies were used to evaluate their functional roles.</div></div><div><h3>Results</h3><div>Compared to BMSC-CM, SHED-CM effectively inhibited RANKL-induced early osteoclast differentiation and late maturation. Notably, SHED-CM but not BMSC-CM suppressed RANKL-induced ROS production. SHED-CM increased the expression of genes encoding antioxidant enzymes. The LC-MS analysis identified seven proteins uniquely enriched in SHED-CM that activated the endogenous antioxidant system. Neutralizing antibodies against some of these proteins restore RANKL-induced ROS production and osteoclast differentiation.</div></div><div><h3>Conclusions</h3><div>SHED-CM inhibited osteoclastogenesis, partially through the activation of multiple antioxidant enzymes in osteoclast precursors, highlighting its potential for treating bone-destructive diseases.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"67 1","pages":"Article 100618"},"PeriodicalIF":2.6,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143041438","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":"Synergistic effects of estrogen deficiency and articular disk derangement on condylar bone loss","authors":"Kazuhiro Shibusaka ,&nbsp;Soichiro Negishi ,&nbsp;Nobuhiro Sakai ,&nbsp;Youngkwan Kim ,&nbsp;Hiroyuki Okada ,&nbsp;Fumiko Yano","doi":"10.1016/j.job.2025.100616","DOIUrl":"10.1016/j.job.2025.100616","url":null,"abstract":"<div><h3>Objectives</h3><div>Temporomandibular joint osteoarthritis (TMJ-OA) with condylar resorption is a multifactorial condition involving hormonal imbalance and articular disk dysfunction, often leading to severe TMJ degeneration. This study investigated the combined effects of estrogen deficiency and anterior articular disk derangement (ADD) on condylar bone resorption in a mouse model.</div></div><div><h3>Methods</h3><div>Female C57BL/6J mice underwent ovariectomy (OVX) to induce estrogen deficiency and ADD was surgically induced for stress. The animals were divided into the control, OVX, ADD, and OVX + ADD groups. Microcomputed tomography and histological analyses were conducted to evaluate condylar bone structure, trabecular architecture, and osteoclast activity.</div></div><div><h3>Results</h3><div>OVX and ADD caused significant condylar bone loss, characterized by reduced bone volume per tissue volume (BV/TV) and abnormal trabecular architecture. The OVX + ADD group exhibited exacerbated bone resorption, with decreased BV/TV and increased trabecular separation compared to OVX or ADD alone. Histological analyses revealed increased osteoclast activity in the OVX + ADD group, suggesting a synergistic effect of estrogen deficiency and ADD on condylar degradation.</div></div><div><h3>Conclusion</h3><div>Estrogen deficiency amplifies the bone-resorptive and inflammatory effects of ADD, accelerates temporomandibular joint (TMJ) degeneration, and underscores the interplay between hormone imbalance and articular disk dysfunction in the pathophysiology of TMJ-OA. There is a need for integrated treatment strategies, such as effective hormone replacement therapy and articular disk repositioning, to effectively manage temporomandibular joint disorders, particularly in postmenopausal women or those with hormonal imbalances. Further research is required to elucidate these molecular pathways and evaluate long-term therapeutic interventions.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"67 1","pages":"Article 100616"},"PeriodicalIF":2.6,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143041514","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":"Enhancement of differentiation and mineralization of human dental pulp stem cells via TGF-β signaling in low-level laser therapy using Er:YAG lasers","authors":"Ryo Yoshida ,&nbsp;Kazuyuki Kobayashi ,&nbsp;Kazuo Onuma ,&nbsp;Ryuji Yamamoto ,&nbsp;Risako Chiba-Ohkuma ,&nbsp;Takeo Karakida ,&nbsp;Shunjiro Yamakawa ,&nbsp;Noriyasu Hosoya ,&nbsp;Yasushi Yamazaki ,&nbsp;Yasuo Yamakoshi","doi":"10.1016/j.job.2025.100617","DOIUrl":"10.1016/j.job.2025.100617","url":null,"abstract":"<div><h3>Objectives</h3><div>Low-level laser therapy (LLLT) using an erbium-doped yttrium aluminum garnet (Er:YAG) laser provides a non-invasive approach applicable to various dental treatments. Here, we investigated the effects of Er:YAG laser irradiation on human dental pulp stem cells (hDPSCs) in an <em>in vitro</em> experiment.</div></div><div><h3>Methods</h3><div>The hDPSCs were categorized into four groups: laser-irradiated with activators (VLT: activated vitamin D₃, bone morphogenetic protein receptor inhibitor, and transforming growth factor-beta (TGF-β)) (LLLT(+)VLT), laser-irradiated without activators (LLLT(+)-only), non-irradiated with activators (LLLT(−)VLT), and non-irradiated without activators (control). Cell proliferation, hard tissue differentiation, TGF-β signaling pathway activity, mineralization induction, and gene expression levels were assessed using several approaches, including cell proliferation assays, ALP assays, western blotting, Alizarin Red S staining, X-ray diffraction, and quantitative polymerase chain reaction.</div></div><div><h3>Results</h3><div>Cell proliferation was similar between the LLLT(+)-only and control groups. The ALP activity was significantly higher in LLLT(+)VLT group than in LLLT(−)VLT group (<em>p</em> &lt; 0.05); however, it was suppressed by TGF-β signaling inhibitors. Western blotting showed enhanced SMAD3 phosphorylation in the LLLT(+)VLT group. The mineralization nodules and mRNA levels of matrix vesicle marker genes were significantly higher in LLLT(+)VLT group, and the nodules were partially composed of hydroxyapatite. The hard tissue formation marker gene expression in LLLT(+)VLT group was significantly higher (<em>p</em> &lt; 0.05) than that in the LLLT(+)-only and control groups; however, it was unchanged or suppressed compared with that in LLLT(−)VLT group.</div></div><div><h3>Conclusions</h3><div>LLLT using an Er:YAG laser, combined with VLT, may promote the differentiation of hDPSCs into hard tissue-forming cells and enhance mineralization.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"67 1","pages":"Article 100617"},"PeriodicalIF":2.6,"publicationDate":"2025-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143013839","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":"β1 Integrin/FAK signaling regulates interleukin-8 production in human gingival epithelial Ca9-22 cells","authors":"Meili Mu ,&nbsp;Hiroshi Inoue ,&nbsp;Dan Mao ,&nbsp;Nagako Sougawa ,&nbsp;Seiji Goda","doi":"10.1016/j.job.2025.100615","DOIUrl":"10.1016/j.job.2025.100615","url":null,"abstract":"<div><h3>Objectives</h3><div>Interleukin-8 (IL-8), a proinflammatory factor in human tissues, plays an important role in inflammation. Type IV collagen, a key component of the basement membrane, interacts with integrins, which are primary receptors in the extracellular matrix (ECM). Integrins are essential for the regulation of various cellular behaviors and signal transduction pathways. However, the relationship between type IV collagen, β1 integrin, and gingival epithelial cells is poorly understood. The aim in this study was to elucidate the effect of the interaction between type IV collagen and β1 integrin on IL-8 secretion in human gingival epithelial cells (Ca9-22).</div></div><div><h3>Methods</h3><div>Ca9-22 cells were treated with or without type IV collagen, and IL-8 production was assessed using an enzyme-linked immunosorbent assay (ELISA). The role of β1 integrin was investigated using a β1 integrin-neutralizing antibody. Western blotting was performed to measure the phosphorylation levels of the relevant proteins. The effects of the focal adhesion kinase (FAK) inhibitor Y15 and the MEK inhibitor U0126 on β1 integrin/FAK and Erk1/2 MAPK pathways in IL-8 production were evaluated to explore the involvement of these signaling pathways.</div></div><div><h3>Results</h3><div>β1 integrin induced IL-8 secretion in the Ca9-22 cells by regulating FAK, Erk1/2, and p130Cas proteins. p130Cas was independent of FAK, whereas Erk1/2 functioned downstream of FAK. Inhibition of FAK or Erk1/2 substantially reduced IL-8 secretion, highlighting their pivotal roles in this signaling pathway.</div></div><div><h3>Conclusion</h3><div>β1 integrin promotes IL-8 secretion in Ca9-22 cells via the β1 integrin/FAK/Erk1/2 signaling pathway. These findings elucidate the pathogenesis of periodontitis and provide a foundation for the development of targeted therapeutic strategies.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"67 1","pages":"Article 100615"},"PeriodicalIF":2.6,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143013845","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}