Journal of Oral Biosciences最新文献

{"title":"Surfactin selectively suppresses acidogenicity in Streptococcus sobrinus without inhibiting growth or biofilm formation","authors":"Nobuhiro Wakamatsu ,&nbsp;Yoshie Yoshioka ,&nbsp;Manabu Habu ,&nbsp;Wataru Ariyoshi ,&nbsp;Ryota Yamasaki","doi":"10.1016/j.job.2026.100756","DOIUrl":"10.1016/j.job.2026.100756","url":null,"abstract":"<div><h3>Objectives</h3><div>Dental caries are caused by organic acids produced by cariogenic bacteria through carbohydrate metabolism. Suppression of acid production without disrupting the oral microbiome is a promising preventive strategy against dental caries. Surfactin, a naturally derived biosurfactant, has several biological activities. However, its effects on acid production by cariogenic bacteria remain unclear. In this study, the effects of surfactin on lactate production, growth, biofilm formation, and metabolic activity of <em>Streptococcus sobrinus</em>, were investigated.</div></div><div><h3>Methods</h3><div><em>In vitro</em> assays were performed to distinguish surfactin-mediated suppression of acidogenic metabolism from its effects on bacterial growth or biofilm formation, combined with molecular and enzymatic analyses to explore the underlying regulatory mechanisms.</div></div><div><h3>Results</h3><div>Surfactin significantly reduced lactate production in planktonic and biofilm-associated <em>S. sobrinus</em>, and it delayed environmental pH reduction in the presence of sucrose. Notably, these effects were observed without inhibition of bacterial growth or biofilm formation. There were no significant changes in the expression of lactate production-related genes, and lactate dehydrogenase activity was not inhibited by surfactin. In contrast, in the MTT assay, there was a transient reduction in metabolic activity, accompanied by delayed initiation of growth.</div></div><div><h3>Conclusion</h3><div>These findings indicate that surfactin selectively attenuates acidogenicity in <em>S. sobrinus</em>, without markedly affecting bacterial viability or biofilm architecture, which is consistent with an anti-virulence mode of action. Although further validation in more complex oral environments and comprehensive safety assessments are required, this study provides fundamental evidence supporting the potential of naturally derived biosurfactants as a basis for future preventive strategies for caries.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"68 2","pages":"Article 100756"},"PeriodicalIF":2.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146154364","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":"Roles of the aryl hydrocarbon receptor and its ligands in osteoclast differentiation and temporomandibular joint osteoarthritis","authors":"Takashi Izawa ,&nbsp;Islamy Rahma Hutami ,&nbsp;Yuri Yoshikawa ,&nbsp;Gohji Kozaki ,&nbsp;Yusaku Hamada ,&nbsp;Yuki Namba ,&nbsp;Misa Taguchi ,&nbsp;Jiamin Chen ,&nbsp;Janvier Habumugisha ,&nbsp;Hiroshi Kamioka","doi":"10.1016/j.job.2025.100726","DOIUrl":"10.1016/j.job.2025.100726","url":null,"abstract":"<div><h3>Background</h3><div>The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that plays an essential role in skeletal homeostasis. Increasing evidence indicates that AhR critically regulates osteoclast differentiation and activity, thereby influencing bone mass, bone resorption, and susceptibility to skeletal diseases. Although AhR has also been implicated in osteoblast-lineage cells, its regulatory roles in osteoclasts and immune cells are less well understood but are increasingly recognized as central to bone remodeling. In particular, AhR signaling modulates immune cell subsets relevant to bone metabolism and governs the differentiation of bone marrow-derived macrophages into osteoclasts.</div></div><div><h3>Highlight</h3><div>This review summarizes the recent findings regarding the regulation of osteoclast differentiation by AhR and its ligands under both physiological and pathological conditions. Special emphasis is placed on the interaction between AhR and the RANKL signaling axis in osteoclasts, as well as on how exogenous and endogenous ligands, including benzo[<em>a</em>]pyrene (B[<em>a</em>]P) and 6-formylindolo[3,2-<em>b</em>]carbazole (FICZ), modulate bone resorption and subchondral bone remodeling in temporomandibular joint osteoarthritis. Furthermore, the role of macrophages as osteoclast progenitors and immunomodulators has been highlighted, positioning AhR as a critical intermediary that links environmental exposure, inflammation, and skeletal metabolism.</div></div><div><h3>Conclusion</h3><div>In this review, we outlined the diverse functions of AhR signaling and its ligands in oral and temporomandibular joint osteoarthritis. AhR plays a central role in bone remodeling. The harmful exogenous ligand B[<em>a</em>]P generally promotes bone loss, whereas the endogenous ligand FICZ exerts protective actions. These insights highlight AhR as a key regulatory switch linking the skeletal and immune systems and as a promising therapeutic target for bone-destructive disorders.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"68 1","pages":"Article 100726"},"PeriodicalIF":2.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145839801","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":"Osteopontin deficiency disturbs dentin bridge formation after direct pulp capping with mineral trioxide aggregate","authors":"Risa Ohshima ,&nbsp;Angela Quispe-Salcedo ,&nbsp;Hayato Ohshima ,&nbsp;Nobuyuki Kawashima ,&nbsp;Takashi Okiji ,&nbsp;Yoshio Yahata","doi":"10.1016/j.job.2026.100740","DOIUrl":"10.1016/j.job.2026.100740","url":null,"abstract":"<div><h3>Objectives</h3><div>After direct pulp capping with mineral trioxide aggregate (MTA), osteopontin (OPN) deposition occurs beneath the exposed pulp before the differentiation of odontoblast-like cells. This study aims to determine whether OPN is directly required for dentin bridge formation following direct pulp capping.</div></div><div><h3>Methods</h3><div>Pulp exposures were made on the occlusal surface of maxillary first molars of five to six week-old, wild-type (WT) and <em>Opn</em> knockout (KO) mice. The cavity was filled with MTA and then with glass ionomer cement. One to 28 days (PODs 1–28), specimens were subjected to immunohistochemistry for evaluating nestin, OPN, Ki67, dentin matrix protein (DMP)-1, F4/80, and CD206; and quantitative real-time polymerase-chain reaction was performed for evaluating <em>nestin (Nes</em>), <em>dentin sialophosphoprotein</em> (<em>Dspp</em>), <em>Dmp-1</em>, <em>and Opn</em> mRNA.</div></div><div><h3>Results</h3><div>In WT mice, OPN was deposited just beneath the exposed pulp after odontoblast degeneration on POD 3, followed by an increase in <em>Nes</em> mRNA expression and CD206 immunoreactivity on POD 5. Nestin-positive odontoblast-like cells aligned on POD 14, resulting in dentin bridge formation on POD 28. Conversely, the arrangement of nestin-positive odontoblast-like cells was disrupted in <em>Opn</em> KO mice, with decreased expression levels of <em>Nes</em> mRNA, <em>Dspp</em> mRNA, and CD206-immunoreactivity on PODs 3–7. Eventually, dentin bridge formation was suppressed, resulting in pulp necrosis on POD 28.</div></div><div><h3>Conclusions</h3><div>Following direct pulp capping with MTA, <em>Opn</em> KO mice exhibited impaired arrangement of nestin-positive odontoblast-like cells and failed to form a dentin bridge, indicating that OPN contributes remarkably to these responses.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"68 1","pages":"Article 100740"},"PeriodicalIF":2.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146037232","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":"Microbiota-dependent transcriptional priming of lung innate immune cells in a mouse model of LPS-induced sepsis-associated lung injury","authors":"Kota Iioka ,&nbsp;Hirobumi Morisaki ,&nbsp;Tomoki Makiura ,&nbsp;Haruka Fukamachi ,&nbsp;Mie Kurosawa ,&nbsp;Armelia Sari Widyarman ,&nbsp;Ayako Sato ,&nbsp;Mariko Kikuchi ,&nbsp;Manami Hayashi ,&nbsp;Hiroki Ishikawa ,&nbsp;Masayuki Iyoda ,&nbsp;Rikuo Masuda ,&nbsp;Hirotaka Kuwata","doi":"10.1016/j.job.2026.100742","DOIUrl":"10.1016/j.job.2026.100742","url":null,"abstract":"<div><h3>Objectives</h3><div>While commensal microbiota are known to play essential roles in functional maturation of the innate immune system, the mechanisms by which microbial signals shape pulmonary immunity remain unclear. We performed single-cell RNA sequencing of lung immune cells from germ-free (GF) and conventional (CV) mice under normal physiological and LPS-induced septic conditions.</div></div><div><h3>Methods</h3><div>Lung immune cells were isolated from GF and CV mice exposed to normal or septic conditions. Single-cell RNA sequencing data were analyzed using standard pipelines with cell-type annotation and pathway profiling based on enrichment analyses.</div></div><div><h3>Results</h3><div>In GF mice, innate immune cell populations, including neutrophils, macrophages, and natural killer cells, exhibited an altered baseline transcriptional state characterized by reduced inflammatory readiness and a shift toward metabolic and stress-associated programs relative to these cell populations in CV mice. Neutrophils from GF mice exhibited a disrupted maturation trajectory with loss of transitional states and immature cell accumulation, suggesting that microbiota-derived cues are necessary to complete peripheral maturation and support a conserved systemic mechanism of microbiota-dependent innate immune differentiation. The lipopolysaccharide-responsive sub-cluster of macrophages exhibited high CCAAT enhancer-binding protein beta (<em>Cebpb</em>) expression in CV mice, which was linked to preferential engagement of inflammatory rather than homeostatic programs, whereas these macrophages in GF mice failed to induce <em>Cebpb</em>. During LPS-induced sepsis, lack of microbial priming results in blunted inflammatory responses and inadequate transcriptional network activation.</div></div><div><h3>Conclusions</h3><div>Commensal microbiota influence transcriptional activity and maturation of pulmonary innate immune cells under experimental conditions, thereby influencing susceptibility to LPS-induced lung injury. Targeting microbiota-guided immune training pathways may allow modulation of pulmonary host defenses.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"68 1","pages":"Article 100742"},"PeriodicalIF":2.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146037233","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":"Periodontitis induces bone formation around alveolar bone in mice","authors":"Shogo Kamikawa ,&nbsp;Akiko Karakawa ,&nbsp;Yuki Azetsu ,&nbsp;Masahiro Chatani ,&nbsp;Megumi Ikeda ,&nbsp;Matsuo Yamamoto ,&nbsp;Masamichi Takami","doi":"10.1016/j.job.2026.100745","DOIUrl":"10.1016/j.job.2026.100745","url":null,"abstract":"<div><h3>Objectives</h3><div>Periodontitis is a chronic inflammatory disease, characterized by alveolar bone resorption and mediated by osteoclast activation. Clinical reports and cone-beam computed tomography (CT) analyses have noted the presence of thickened bone structures, known as buttressing bone formation, around inflammatory lesions. However, clinical frequency, extent, and mechanisms of new bone formation have not been fully elucidated. To elucidate the inflammation-induced mechanisms of buttressing bone formation, a ligature-induced mouse model of periodontitis was examined.</div></div><div><h3>Methods</h3><div>Marginal periodontitis model mice were established by silk thread ligation around the right maxillary second molar, and an apical periodontitis model was established by removing the dental pulp, using eight-week-old male C57BL/6J mice. Subcutaneous anti-receptor activator of nuclear factor kappa B ligand (RANKL) antibody injections were performed on Days 0 and 7, then μCT, histological, and histomorphometric analyses were performed.</div></div><div><h3>Results</h3><div>The mice in both models had inflammation-induced bone resorption, accompanied by new bone formation along the outer surface of the alveolar bone. Newly-formed bone in the apical and buccal regions, and extensive osteoclastic and osteoblastic activities were observed throughout the alveolar bone. Inhibition of RANKL suppressed bone resorption and formation, whereas newly-formed bone maintained its structure and mass, even after suture had removed.</div></div><div><h3>Conclusions</h3><div>The regulation of inflammation-induced bone formation by RANKL-dependent osteoclast activity has been shown in a mouse model of periodontitis. This newly-reported mechanism of bone formation may be maintained by a combination of modelling-based bone apposition and remodelling-based coupling via osteoclasts and osteoblasts. The findings highlight the importance of three-dimensional analysis of bone morphology as part of routine periodontal diagnosis.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"68 1","pages":"Article 100745"},"PeriodicalIF":2.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146187304","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":"Dental plaque metabolites induce polymorphonuclear leukocyte death accompanying peptidyl arginine deiminase 4 and citrullinated protein release: Potential contribution to rheumatoid arthritis pathogenesis","authors":"Daichi Horikoshi ,&nbsp;Yoshikazu Mikami ,&nbsp;Taku Toriumi ,&nbsp;Muneaki Tamura ,&nbsp;Hiroshi Shiratsuchi ,&nbsp;Kazumichi Yonenaga ,&nbsp;Hiromasa Tsuda","doi":"10.1016/j.job.2026.100754","DOIUrl":"10.1016/j.job.2026.100754","url":null,"abstract":"<div><h3>Objectives</h3><div>Neutrophils form the front line of defense in the periodontal pocket. They release the web-like DNA structures, known as neutrophil extracellular traps (NETs). NETosis, a form of programmed cell death, is characterized by the release of NETs, peptidyl arginine deiminase (PAD), and citrullinated proteins. Plaque bacteria produce a variety of metabolites that can interact with neutrophils and potentially modulate its function. In this study, how these bacterial metabolites influence NETosis-like cell death in polymorphonuclear leukocytes (PMNL) was investigated.</div></div><div><h3>Methods</h3><div>SYTOX Green dye, which strongly fluoresces on binding to double-stranded DNA, was used to quantify and visualize NETosis-like cell death. The release of neutrophil elastase, PAD4, and citrullinated histone H3 were evaluated using western blotting.</div></div><div><h3>Results</h3><div>Culture supernatants of various oral pathogens induced NETosis-like cell death. As these supernatants were rich in short-chain fatty acids (SCFAs), each SCFA was tested individually, and they all induced cell death. Similarly, SCFA mixtures replicating the composition of the bacterial supernatant induced PMNL death. Interestingly, SCFA treatment enhanced the release of extracellular neutrophil elastase, PAD4, and citrullinated histone H3. These effects were significantly attenuated by ROS scavenging and PAD4 inhibition.</div></div><div><h3>Conclusions</h3><div>SCFAs produced by plaque bacteria trigger ROS- and PAD4-dependent NETosis-like cell death, leading to the release of PAD4 and citrullinated proteins. Given that protein citrullination plays a pivotal role in the generation of autoantibodies during the onset and progression of rheumatoid arthritis (RA), these findings indicate that bacterial SCFAs may substantially contribute to the initiation and exacerbation of RA.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"68 1","pages":"Article 100754"},"PeriodicalIF":2.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146187291","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":"Growing lesser horn of the hyoid in human fetuses with special references to muscles attaching to it","authors":"Jose Francisco Rodríguez-Vázquez ,&nbsp;Kenta Abe ,&nbsp;Kazuma Morita ,&nbsp;Yuki Yoshihashi ,&nbsp;Masahito Yamamoto ,&nbsp;Shin-ichi Abe","doi":"10.1016/j.job.2026.100733","DOIUrl":"10.1016/j.job.2026.100733","url":null,"abstract":"<div><h3>Objectives</h3><div>The hyoid lesser horn (LH) forms a transient joint with the greater horn in human fetuses. The chondroglossus muscle attaches to the LH; however, its morphology remains unclear. We hypothesized that the muscles involved in LH accelerate joint formation.</div><div>Methods: We examined 34 human fetuses with crown-rump length of 39–230 mm.</div></div><div><h3>Results</h3><div>The LH joint was bilaterally absent in eight fetuses; the largest specimen “without” joints was 110 mm crown-rump length, whereas the smallest specimen “with” joints was 55 mm. The chondroglossus was identified as oblique muscle fibers attached to the LH medial aspect (23/34). The chondroglossus, Adjacent to the transverse lingual muscle (TLM), the chondroglossus ran supero-antero-medially to join the genioglossus. The TLM (21/34) and middle pharyngeal constrictor (pars chondropharyngica; 21/34) originated from the LH. The latter ran posteriorly from the LH medial to the hypoglossal nerve, whereas the middle constrictor arose largely from the greater horn. Notably, without LH attachment, the anterior margin of the mylohyoideus muscle (MPCM) was connected to the TLM using thick fascia wrapped around the LH. Therefore, LH disrupts the muscular ring surrounding the oropharynx.</div></div><div><h3>Conclusions</h3><div>The variation in joint formation timing (9–16 weeks gestational age) suggests that the chondroglossus, TLM, and MPCM development do not require joint movement. Alternatively, an elongated greater horn may provide joint-like space.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"68 1","pages":"Article 100733"},"PeriodicalIF":2.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145976195","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":"Oral biosciences: The annual review 2025","authors":"Hayato Ohshima ,&nbsp;Kentaro Ono ,&nbsp;Kenji Mishima","doi":"10.1016/j.job.2026.100750","DOIUrl":"10.1016/j.job.2026.100750","url":null,"abstract":"<div><h3>Background</h3><div>The <em>Journal of Oral Biosciences</em> is dedicated to advancing and disseminating fundamental knowledge across the full spectrum of oral biosciences. This editorial features recently published review articles spanning key domains, including “craniofacial biology”; “bone, tooth, and mineral biology”; “periodontal and pulp biology”; “microbiology and immunology”; “pharmacology”; “biomaterials”; “oncology”; “salivary research”; and “regenerative medicine.”</div></div><div><h3>Highlight</h3><div>The featured review articles address a diverse range of topics, including buccal bifurcation cysts, mandibular prognathism, glucose metabolism, gingival overgrowth, dextrins, chemokine receptor 5, electrical stimulation, the tumor microenvironment, computer-aided diagnosis, adiponectin, myoepithelial cells, secretory granules, apoptosis, dental regenerative medicine, and three-dimensional <em>in vitro</em> models.</div></div><div><h3>Conclusion</h3><div>The review articles featured in the <em>Journal of Oral Biosciences</em> provide comprehensive insights into contemporary research themes and emerging concepts in oral biosciences. This editorial discusses their key findings and underscores their significance in advancing the understanding of oral health and disease.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"68 1","pages":"Article 100750"},"PeriodicalIF":2.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146229148","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":"Abaloparatide increases bone mass by increasing bone formation regardless of alendronate pretreatment in mice","authors":"Akito Makino ,&nbsp;Tomoka Hasegawa ,&nbsp;Tomomaya Yamamoto ,&nbsp;Hideko Takagi ,&nbsp;Takeshi Iijima ,&nbsp;Norio Amizuka","doi":"10.1016/j.job.2025.100708","DOIUrl":"10.1016/j.job.2025.100708","url":null,"abstract":"<div><div>The effects of bisphosphonate pretreatment on the bone anabolic effects of abaloparatide (ABL) in mice were investigated. Mice were administered alendronate (ALN) at different doses for 21 days, followed by 28 days of ABL. ABL increased femoral bone mineral density at all ALN doses, with effects equal to or greater than those observed in mice without ALN. Histological analysis demonstrated that ABL increased ALPase- and PHOSPHO1-positive osteoblasts, irrespective of ALN pretreatment. However, the increase in TRAP-positive osteoclasts by ABL was attenuated at higher ALN doses. These findings suggest that ABL promotes bone formation in mice, independently of ALN pretreatment.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"68 1","pages":"Article 100708"},"PeriodicalIF":2.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145580406","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":"Cross-disease transcriptomic screening identifies fibroblast-associated mediators shared across periodontitis and rheumatoid arthritis","authors":"Yuta Izumi ,&nbsp;Taisuke Hani ,&nbsp;Tomoo Kudo ,&nbsp;Yukihiro Numabe ,&nbsp;Yuuichi Soeno","doi":"10.1016/j.job.2026.100751","DOIUrl":"10.1016/j.job.2026.100751","url":null,"abstract":"<div><h3>Objectives</h3><div>Periodontitis and rheumatoid arthritis (RA) are chronic inflammatory diseases characterized by progressive tissue destruction, and numerous studies have suggested that they are linked. However, the molecular mechanisms underlying this association remain unclear. The aim of this study was to identify molecular pathways beyond classical inflammation and immunity that are commonly dysregulated in periodontitis and RA.</div></div><div><h3>Methods</h3><div>We performed <em>in silico</em> screening of publicly available transcriptomic datasets for periodontitis and RA. Next, we performed experimental validation of candidate molecules in an <em>in vitro</em> culture model designed to mimic periodontal tissue under RA-associated conditions.</div></div><div><h3>Results</h3><div>Comparative analyses of healthy controls identified 540 differentially expressed genes (DEGs) in periodontitis, 4019 DEGs in RA, and 117 commonly upregulated DEGs. Among these, <em>CHI3L2</em> and <em>MMP3</em> were selected for further investigation and were found to be prominently expressed in gingival fibroblasts. Quantitative real-time polymerase chain reaction analyses showed that both genes were significantly upregulated by lipopolysaccharide stimulation and by conditioned medium derived from RA synovial cells, with a synergistic enhancement observed when both stimuli were applied simultaneously. Co-culture and wound-healing assays showed that RA synovial cells impaired proliferation and migration of gingival fibroblasts.</div></div><div><h3>Conclusions</h3><div>RA-associated pathological factors may influence the responsiveness of periodontal tissue to inflammatory stimuli. Although periodontitis and RA are primarily driven by immune-mediated inflammation, tissue-level molecular expression and sensitivity to stimulus may also be altered, providing complementary insights into shared disease mechanisms and their potential relevance for clinical management.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"68 1","pages":"Article 100751"},"PeriodicalIF":2.3,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146187305","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}