Journal of Dental Research最新文献

{"title":"Chewing-Activated TRPV4/PIEZO1–HIF-1α–Zn Axes in a Rat Periodontal Complex","authors":"Y. Wang, B.H. Lee, Z. Yang, T.J. Ho, H. Ci, B. Jackson, T. Pushon, B. Wang, J. Levy, S.P. Ho","doi":"10.1177/00220345241294001","DOIUrl":"https://doi.org/10.1177/00220345241294001","url":null,"abstract":"The upstream mechanobiological pathways that regulate the downstream mineralization rates in periodontal tissues are limitedly understood. Herein, we spatially colocalized and correlated compression and tension strain profiles with the expressions of mechanosensory ion channels (MS-ion) TRPV4 and PIEZO1, biometal zinc, mitochondrial function marker ( MFN2), cell senescence indicator ( p16), and oxygen status marker hypoxia-inducible factor-1α ( HIF-1α) in rats fed hard and soft foods. The observed zinc and related cellular homeostasis in vivo were ascertained by TRPV4 and PIEZO1 agonists and antagonists on human periodontal ligament fibroblasts ex vivo. Four-week-old male Sprague-Dawley rats were fed hard ( n = 3) or soft ( n = 3) foods for 4 wk (in vivo). Significant changes in alveolar socket and root shapes with decreased periodontal ligament space and increased cementum volume fraction were observed in maxillae on reduced loads (soft food). Reduced loads impaired distally localized compression-stimulated PIEZO1 and mesially localized tension-stimulated TRPV4, decreased mitochondrial function ( MFN2), and increased cell senescence in mesial and distal periodontal regions. The switch in HIF-1α from hard food–distal to soft food–mesial indicated a plausible effect of shear-regulated blood and oxygen flows in the periodontal complex. Blunting or activating TRPV4 or PIEZO1 MS-ion channels by channel-specific antagonists or agonists in human periodontal ligament fibroblast cultures (in vitro) indicated a positive correlation between zinc levels and zinc transporters but not with MS-ion channel expressions. The effects of reduced chewing loads in vivo were analogous to TRPV4 and PIEZO1 antagonists in vitro. Study results collectively illustrated that tension-induced TRPV4 and compression-induced PIEZO1 activations are necessary for cell metabolism. An increased hypoxic state with reduced functional loads can be a conducive environment for cementum growth. From a practical standpoint, dose rate–controlled loads can modulate tension and compression-specific MS-ion channel activation, cellular zinc, and HIF-1α transcription. These mechanobiochemical events indicate the plausible catalytic role of biometal zinc in mineralization, periodontal maintenance, and dentoalveolar joint function.","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":"76 1","pages":""},"PeriodicalIF":7.6,"publicationDate":"2025-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143056492","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dasatinib and Quercetin Limit Gingival Senescence, Inflammation, and Bone Loss","authors":"K. Rattanaprukskul, X.-J. Xia, M. Hysa, M. Jiang, M. Hung, S.F. Suslavich, S.E. Sahingur","doi":"10.1177/00220345241299789","DOIUrl":"https://doi.org/10.1177/00220345241299789","url":null,"abstract":"Cellular senescence has emerged as one of the central hallmarks of aging and drivers of chronic comorbidities, including periodontal diseases. Senescence can also occur in younger tissues and instigate metabolic alterations and dysfunction, culminating in accelerated aging and pathological consequences. Senotherapeutics, such as the combination of dasatinib and quercetin (DQ), are being increasingly used to improve the clinical outcomes of chronic disorders and promote a healthy life span through the reduction of senescent cell burden and senescence-associated secretory phenotype (SASP). Recent evidence suggests that senescent cells and SASP can contribute to the pathogenesis of periodontal diseases as well. In this study, we investigated the effect of DQ interventions on periodontal tissue health using preclinical models of aging. In vitro, DQ ameliorated biological signatures of senescence in human gingival keratinocytes upon persistent exposure to periodontal bacteria, Fusobacterium nucleatum, by modulating the levels of key senescence markers such as p16, SA-β-galactosidase, and lamin-B1 and inflammatory mediators associated with SASP including interleukin-8, matrix metalloproteinase (MMP)–1, and MMP-3. In vivo, the oral administration of DQ mitigated senescent cell burden and SASP in gingival tissues and reduced naturally progressing periodontal bone loss in aged mice. Collectively, our findings provide proof-of-concept evidence for translational studies and reveal that targeting gingival senescence and the senescence-associated secretome can be an effective strategy to improve periodontal health, particularly in vulnerable populations.","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":"31 1","pages":""},"PeriodicalIF":7.6,"publicationDate":"2025-01-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142961233","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolic Profiling of Individuals with Missing Teeth and Tooth Loss","authors":"A.M. Halme, A. Salminen, A.L. Suominen, A. Havulinna, P. Mäntylä, K. Buhlin, S. Paju, S. Männistö, V. Salomaa, W. Sattler, J. Sinisalo, P.J. Pussinen","doi":"10.1177/00220345241298219","DOIUrl":"https://doi.org/10.1177/00220345241298219","url":null,"abstract":"Missing teeth have been linked to incident cardiovascular disease, diabetes, and all-cause mortality. Our previous study revealed that signs of oral infections and inflammatory conditions (i.e., periodontal disease and dental caries) are associated with disadvantageous features of circulating metabolites. This study investigates whether missing teeth and tooth loss, the end points of these diseases, are associated with similar metabolic features. The 2 Finnish population-based studies Health-2000 ( n = 6,197) and FINRISK-97 ( n = 6,050) were included, as was Parogene ( n = 465), a cohort of patients with an indication for coronary angiography. The number of teeth was recorded in clinical examinations. Serum concentrations of 157 metabolites were determined by a nuclear magnetic resonance spectroscopy–based method. Health-2000 participants ( n = 3,371) provided follow-up serum samples, and 1,186 of them participated in a repeated oral examination 11 y after the baseline. Linear regression models adjusted for age, sex, smoking, body mass index, and diabetes were fitted to the number of teeth and metabolite measures. The results from the separate cohorts were combined in a fixed-effects meta-analysis. We also analyzed whether the number of teeth at baseline and tooth loss during follow-up were associated with changes in metabolite concentrations. Missing teeth were associated with increased very-low-density lipoprotein–related measures and triglyceride concentrations, as well as with decreased high-density lipoprotein parameters and small particle size. Missing teeth also had an association with low levels of unsaturated fatty acids (FAs), including omega-3 and omega-6 FAs, and elevated proportions of monounsaturated and saturated FAs. The number of teeth at baseline predicted changes in several concentrations, such as measures related to intermediate-density lipoprotein, low-density lipoprotein, and FAs, but no associations with tooth loss during the 11-y follow-up were observed. To conclude, missing teeth are associated with adverse metabolic features characterized by systemic inflammation and several risk factors for cardiometabolic diseases.","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":"83 1","pages":""},"PeriodicalIF":7.6,"publicationDate":"2025-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142925094","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Novel Dual Cross-linking Reagent for Dentin Bonding Interface Stability","authors":"Z.L. Tian, H.M. Wang, S.H. Yang, S.W. Qiao, X.Z. Han, S. Zhu, Z.S. Shi","doi":"10.1177/00220345241300263","DOIUrl":"https://doi.org/10.1177/00220345241300263","url":null,"abstract":"The cross-linking reagent has been proposed as a means of modifying dentin collagen, inhibiting matrix metalloproteinase activities, and enhancing bond durability during dentin bonding procedures. This study aimed to synthesize an operation-friendly dual cross-linking reagent—3-(4-formyphenoxy)-2-hydroxypropyl methacrylate (FPA)—to assess its ability to cross-link dentin collagen and reduce enzymatic activity at the bonding interface. Cytotoxicity was evaluated by a cell counting kit–8 test and calcein AM/propidium iodide assay. Attenuated total reflection–Fourier transform infrared spectroscopy, ultraviolet-visible spectroscopy, and molecular docking of FPA-collagen showed that FPA can mediate covalent bonding and hydrogen bonding. The hydroxyproline release test and thermogravimetric analysis demonstrated that FPA-collagen can resist exogenous proteases and thermolysis. The gelatin zymography and in situ zymography indicated that FPA can reduce enzymatic activity at the bonding interface. The bonded samples were subjected to microtensile bond strength analysis after 24 h and thermocycling. The bonding interface quality was evaluated by the water contact angle, confocal laser scanning microscope, field emission scanning electron microscopy, and nanoleakage assessment. This study demonstrated the effectiveness and significant clinical potential of the dual cross-linking reagent FPA in that it increases the longevity of resin-dentin bonds and reduces dentin matrix metalloproteinase activities at the bonding interface.","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":"34 1","pages":"220345241300263"},"PeriodicalIF":7.6,"publicationDate":"2024-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142887871","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Posteruptive Loss of Proteins in Porcine Enamel","authors":"H. Karaaslan, A.R. Walker, A. Gil-Bona, B. Depalle, F.B. Bidlack","doi":"10.1177/00220345241299382","DOIUrl":"https://doi.org/10.1177/00220345241299382","url":null,"abstract":"Tooth enamel maturation requires the removal of proteins from the mineralizing enamel matrix to allow for crystallite growth until full hardness is reached to meet the mechanical needs of mastication. While this process takes up to several years in humans before the tooth erupts, it is greatly accelerated in the faster-developing pigs. Pig teeth erupt with softer, protein-rich enamel that is similar to hypomineralized human enamel but continues to harden quickly after eruption. Proteins that bind to enamel crystals and prevent crystal growth and enamel hardening (e.g., albumin) have been suggested as a cause for hypomineralized human enamel. It is unclear whether fast posteruptive enamel hardening in pigs occurs despite the high protein content or requires facilitated protein loss for crystal growth. This study asked how the protein content in porcine enamel changes after eruption in relation to saliva. Given previous evidence of high albumin content in erupted porcine enamel, we hypothesized that enamel- and saliva-derived enzymes facilitate protein removal from porcine enamel after eruption. To test this, we analyzed the enamel of fourth primary premolars and the saliva proteome at 3 critical time points: at the time of tooth eruption and 2 and 6 weeks after eruption. We found a decrease in the number of proteins and their abundancy in enamel with posteruptive time, including a decrease in serum albumin within enamel. The rapid decrease within 2 weeks posteruption is consistent with the previously reported rapid increase in mineral density of porcine enamel after eruption. In addition to enamel proteases KLK-4 and MMP-20, we identified other serine-, cysteine-, aspartic-, and metalloproteases in enamel that are found in the porcine saliva. Our findings suggest that the fast posteruptive enamel maturation in the porcine model coincides with saliva exchange and influx of saliva enzymes into porous enamel.","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":"32 1","pages":"220345241299382"},"PeriodicalIF":7.6,"publicationDate":"2024-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142887905","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Schwann Cell–Secreted S100B Promotes Wound Healing via Paracrine Modulation","authors":"Y. Zhou, K. Li, Z. Ma, L. Wang, L. Chen, W. Li, Z. Wong, X. Wang, Z. Yang, Y. Liao, W. Chen, G. Fu, C. Ding, D. Zou","doi":"10.1177/00220345241296103","DOIUrl":"https://doi.org/10.1177/00220345241296103","url":null,"abstract":"As the supply source for gingival grafts, the palatal tissue possesses marked regenerative ability after repeated wounding over the buccal attached gingiva and skin. However, the intrinsic mechanisms are poorly understood. Schwann cells reportedly participate in wound repair of many tissues. Here, we investigate whether Schwann cells play an essential role in the wound healing of palatal mucosa. We performed multiomics analysis in nonhuman primates, integrating scRNA-seq and proteomics analysis, and built wound-healing models in the palatal mucosa and buccal attached gingiva and skin to compare the regeneration among different sites and explore the paracrine role of Schwann cells in the healing of palatal mucosa. With regard to in vivo validation, GelMA hydrogels loaded with conditional medium or exogenous protein were applied in rat and monkey skin. We revealed greater distributions and a lower differentiation state of Schwann cells in the palatal mucosa at baseline. Moreover, S100B levels were significantly greater in the wound healing of palatal mucosa than in the buccal attached gingiva, and Schwann cell–secreted S100B can promote the healing-related capabilities of fibroblasts via paracrine modulation with receptor of advanced glycation end products (RAGE), which activates the crosstalk between NF-κB and Notch signaling, leading to expedited wound closure in vivo. Our work shows that Schwann cells play a crucial role in the wound healing of the palatal mucosa through the S100B/RAGE/NF-κB/Notch paracrine axis. In addition, our data provide novel insights into the therapeutic effects of S100B protein on wound healing.","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":"32 1","pages":""},"PeriodicalIF":7.6,"publicationDate":"2024-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142874266","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Induction of Oral Lichen Planus–like Histopathology in Mice","authors":"V.T.-D. Phuc, M.G. Kang, H. Kim, Y.K. Ko, S. Acharya, E.B. Kim, J.-Y. Park, S.-H. Chang, H.-J. Kim, H.-J. Yoon, Y. Choi","doi":"10.1177/00220345241304760","DOIUrl":"https://doi.org/10.1177/00220345241304760","url":null,"abstract":"Oral lichen planus (OLP) is a chronic T cell–mediated inflammatory mucosal disease of unknown etiology. The lack of suitable animal models has hampered understanding of its etiopathogenesis. This study aimed to clarify the contribution of bacterial infection and zinc deficiency (ZD) in OLP pathogenesis by developing a murine model. Infection of human oral keratinocytes with OLP-isolated Escherichia coli 7.2 in the presence of a zinc chelator increased the intracellular survival of E. coli, likely due to the mitigation of zinc poisoning. C57BL/6 female mice were subjected to either a standard diet or a zinc-deficient diet for 1 mo. Their labial mucosa was then microdamaged through scratching, followed by oral administration of E. coli 7.2. Scratching alone triggered bacterial translocation to the epithelium and lamina propria, upregulated Mmp9, increased immune responses in the cervical lymph nodes, and amplified CD4<jats:sup>+</jats:sup> T-cell recruitment to labial mucosae. All these responses were intensified by E. coli infection, showing a strong synergism with ZD that shifted the Th cells infiltrating the labial mucosa in response to E. coli infection from Th1 to Th17 dominance. Repeated scratching plus E. coli infection amplified T-cell recruitment, even without ZD, leading to patchy lymphocytic infiltration, characterized by the presence of colloid bodies and disrupted basement membranes. Interestingly, Th1 blockade with anti-IFNγ and anti–IL-12 antibodies during E. coli infection hindered bacterial clearance in the epithelium and caused intense T-cell infiltration, epithelial degeneration and necrosis with colloid bodies, basement membrane destruction, and epithelial detachment, similar to erosive OLP lesions. This suggests that the Th1/IFNγ pathway may not be a suitable therapeutic target for OLP. In conclusion, OLP-like histopathology in the oral mucosa was induced through E. coli infection when combined with ZD, repeated epithelial microdamage, or Th1 blockade. This animal model provides a valuable platform for exploring specific hypotheses related to OLP pathogenesis and potential therapeutic targets.","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":"128 1","pages":""},"PeriodicalIF":7.6,"publicationDate":"2024-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142874267","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Masticatory Stress Maintains Mucosal Homeostasis via M2 Polarization","authors":"M.Z. Ning, X.T. Zhai, X. Wang, H. Liu, J.S. Wang, X.G. Wang, S.L. Wang, L. Hu","doi":"10.1177/00220345241290778","DOIUrl":"https://doi.org/10.1177/00220345241290778","url":null,"abstract":"In addition to breaking down food, mastication plays regulatory roles in tissue homeostasis. During mastication, the oral mucosa is subjected to masticatory stress, and the maintenance between mucosal damage and repair is a key process. Despite rapid healing in the oral mucosa during chewing, the molecular mechanisms underlying repair remain unclear. In this study, we investigated the impact of masticatory stress on masticatory mucosal wound healing. Our data showed that reduced masticatory stress on the oral mucosa in mice fed a soft food diet resulted in decelerated hard palate mucosal wound healing and decreased numbers of Ki67-positive cells as compared with the hard food diet group. An RNA sequencing analysis revealed lower expression levels of the mechanosensitive gene Piezo1 in the hard palate mucosa, as well as lower levels of transforming growth factor β1 ( Tgf-β1) and Tgf-β receptor 2 ( Tgf-βr2), in the soft food diet group than the hard food diet group. Immunofluorescence staining, flow cytometry, and polymerase chain reaction analyses demonstrated that masticatory stress induced M2 polarization of macrophages surrounding the wound in the hard food diet group, leading to increased Tgf-β1 secretion. The specific deletion of Piezo1 in macrophages ( Piezo1<jats:sup>DLysm</jats:sup>) attenuated masticatory stress–induced accelerated healing in mice. These findings reveal the crucial role of masticatory stress–induced Piezo1 expression in tissue repair, potentially influencing M2 polarization of mucosal macrophages and Tgf-β1 secretion. These findings underscore the pivotal role of physical stimulation in the immune response and tissue repair and may provide important insights into therapeutic interventions for tissue repair.","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":"1 1","pages":""},"PeriodicalIF":7.6,"publicationDate":"2024-12-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142869967","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Twist1 Acts Upstream of the Dlx5-Hand2 Pathway to Pattern the Mammalian Jaw","authors":"N. Adhikari, Z. Wu, Y. Huang, Y. Lan, R. Jiang","doi":"10.1177/00220345241291527","DOIUrl":"https://doi.org/10.1177/00220345241291527","url":null,"abstract":"Both the upper and lower jaws develop from cranial neural crest cells (CNCCs) populating the first pharyngeal arch in all gnathostomes. Previous studies showed that the Edn1/Ednra-Dlx5/Dlx6-Hand2 signaling pathway is necessary for lower jaw formation and that ectopic expression of Edn1 or Hand2 throughout the CNCCs partly transformed the upper jaw to lower jaw structures, but the molecular mechanisms regulating upper jaw development remain unclear. Here we show that the basic helix-loop-helix transcription factor Twist1 is required for upper jaw development. Whereas the Twist1<jats:sup>fl/fl</jats:sup>; Wnt1-Cre mouse embryos, with tissue-specific inactivation of Twist1 in premigratory CNCCs, exhibited aberrantly persistent expression of the key neuroglial lineage regulator Sox10 in the postmigratory CNCCs populating the facial primordia, we found that genetic inactivation of Sox10 did not rescue the defects in CNCC survival and patterning in Twist1<jats:sup>fl/fl</jats:sup>; Wnt1-Cre embryos. However, analysis of Sox10<jats:sup>fl/+</jats:sup>; Twist1<jats:sup>fl/fl</jats:sup>; Wnt1-Cre mice revealed duplicated mandibular structures, including ectopic Meckel’s cartilage, in place of the maxilla. Both Sox10<jats:sup>fl/+</jats:sup>; Twist1<jats:sup>fl/fl</jats:sup>; Wnt1-Cre and Sox10<jats:sup>fl/fl</jats:sup>; Twist1<jats:sup>fl/fl</jats:sup>; Wnt1-Cre embryos exhibited ectopic expression of Dlx5 and Hand2 in the developing maxillary processes at E10.5. Furthermore, we found that Twist1<jats:sup>fl/fl</jats:sup>; Wnt1-Cre embryos also expressed Dlx5 and Hand2 ectopically in the maxillary domain at E10.5 and subsequently developed Meckel’s cartilage–like cartilage rods bilaterally at the maxillary region. However, the expression of Edn1 was unaltered in the developing Twist1<jats:sup>fl/fl</jats:sup>; Wnt1-Cre embryos, indicating that Twist1 functions in the CNCC-derived facial mesenchyme to regulate the Dlx5-Hand2 pathway without affecting Edn1 expression in the epithelial and mesodermal compartments. We further show that Twist1 represses reporter gene activation driven by the Dlx5/Dlx6 intergenic enhancer known to drive Dlx5/Dlx6 expression in the developing mandibular arch. Together, these data identify a new role of Twist1 in patterning the regional identities of the CNCC-derived facial mesenchyme and provide novel insight into the pathogenic mechanisms underlying TWIST1-related craniofacial developmental disorders.","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":"22 1","pages":""},"PeriodicalIF":7.6,"publicationDate":"2024-12-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142869949","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Healthy Oral Microbiome: A Changing Ecosystem throughout the Human Lifespan","authors":"J.D. Corrêa, P.P.S. Carlos, G.A. Faria, L.C.R. Pacheco, V.S. da Costa, I.R.R. Mendes, A.B. de Oliveira, A.P.V. Colombo","doi":"10.1177/00220345241297583","DOIUrl":"https://doi.org/10.1177/00220345241297583","url":null,"abstract":"Microorganisms have co-evolved with a variety of plants and animals, developing complex symbiotic relationships with their hosts and the environment. The diversity of symbionts acquired over time help their hosts to adapt, survive, and evolve more rapidly and efficiently, improving fitness across the lifespan. Understanding these synergistic relationships between humans and their endogenous microbiota may provide valuable information on human physiology and on potential mechanisms associated with the onset of diseases. This review summarizes current data on the composition and functionality of the predominant taxa of the healthy oral microbiome across different ages and habitats within the oral cavity, critically pointing out the inconsistency of methodologies for microbiological analysis and what still needs to be validated. We discuss how early acquisition and establishment of the oral microbiome are influenced by factors such as delivery type and feeding practices, and how adolescence marks a phase of significant shifts in the oral taxa due to hormonal and behavioral transitions. During adulthood, the healthy oral microbiome may acquire multistable signatures, shaped by genetic and environmental factors, while minor changes in core microorganisms are observed in the healthy aging populations. Overall, evidence shows that the oral microbiome is a complex ecosystem, continuously modulated by several factors, since its early acquisition through adulthood and into old age. Fluctuations do happen, but a resilient core community will persist over time in most humans to maintain homeostasis. Future challenges of microbiome research will rely on our ability to define multiple age-related healthy oral microbiomes across populations, so that oral dysbiosis can be detected and managed in advance. In this context, standardization of data acquisition and analysis, as well as improvements in multidisciplinary clinical diagnosis of oral health, must be pursued for a better comprehension of the balanced host–microbiome interaction.","PeriodicalId":15596,"journal":{"name":"Journal of Dental Research","volume":"14 1","pages":""},"PeriodicalIF":7.6,"publicationDate":"2024-12-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142869950","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}