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A dysbiotic microbiome triggers T H 17 cells to mediate oral mucosal immunopathology in mice and humans
Open accessAbstract
Combined patient and animal model studies implicate microbiota-triggered T H 17 cells as disease drivers and therapeutic targets in periodontitis.
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“Studies using germ‐free mice have also been employed in the context of the oral microbiome, demonstrating the role of diabetes in disrupting the equilibrium of the oral microbiota50 and confirming the role of the oral microbiota in periodontal disease pathogenesis.51, 52”
From The oral microbiome: Role of key organisms and complex networks in oral health and disease (2021) · cites this paper as [52]
In the citing paper
“In line with the role of oral mucosa as a physiological barrier, the functions of immune networks within this mucosa reflect the site‐specific challenges faced within the oral cavity. For example, they contribute to homeostasis in response to masticatory forces and trigger immune responses to the development of pathologic microbial communities.52, 53”
From The oral microbiome: Role of key organisms and complex networks in oral health and disease (2021) · cites this paper as [52]
In the citing paper
“Microbial dysbiosis is also necessary for additional inflammatory responses characteristic of periodontal disease, including local expansion of pathologic interleukin‐17+/CD4+ T‐helper (T‐helper 17) cells.52”
From The oral microbiome: Role of key organisms and complex networks in oral health and disease (2021) · cites this paper as [52]
In the citing paper
“The importance of commensal species to pathogenesis is further demonstrated by the requirement for commensal microbial communities in the instigation of disease by periodontal pathogens.51, 52”
From The oral microbiome: Role of key organisms and complex networks in oral health and disease (2021) · cites this paper as [52]
In the citing paper
“homeostatic T‐helper 17 cells were found to be induced by mechanical stimuli in a microbiome‐independent manner, whereas periodontitis‐associated T‐helper 17 cells were found to accumulate in a microbiome‐dependent manner and to require both interleukin‐6 and interleukin‐23.”
From The oral microbiome: Role of key organisms and complex networks in oral health and disease (2021) · cites this paper as [52]
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Citations
Cites
Induction of Intestinal Th17 Cells by Segmented Filamentous Bacteria
Ivanov, I. I., Atarashi, K., Manel, N., Brodie, E. L., Shima, T., Karaoz, U., Wei, D., Goldfarb, K. C., Santee, C. A., Lynch, S. V., et al. (2009) · Cell · doi:10.1016/j.cell.2009.09.033 · Cited by 4,554 · cited 1×
“Microbial induction of TH17 cells has been well documented at various other barrier sites, including the lower GI (32) and skin (33).”
Periodontitis: from microbial immune subversion to systemic inflammation
Hajishengallis, G. (2015) · Nature Reviews Immunology · doi:10.1038/nri3785 · Cited by 3,046 · cited 2×
“To date, the pathogenic drivers of exaggerated destructive inflammation are incompletely understood, and treatment largely aims at reduction of microbial stimulation rather than at targeting of specific immune pathways through hostmodulation therapies (2).”
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“DISCUSSION At mucosal barrier sites, the local immune system is tasked with the delicate act of maintaining a dynamic balance between host and environmental stimuli (26).”
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“In human lesions of periodontitis, we document an expansion of TH17 cells that secrete cytokines associated with pathogenic activity (10, 30) and are predominantly resident memory TH17 cells (31).”
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Spatial scale in analysis of the dental plaque microbiome
Borisy, G. G., & Valm, A. M. (2021) · Periodontology 2000 · doi:10.1111/prd.12364 · Cited by 54
C3-targeted therapy in periodontal disease: moving closer to the clinic
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“The same study [33] showed that C3 deficiency inhibited the production of cytokines that drive inflammatory bone loss in periodontitis, such as interleukin (IL)-23 and IL-17, which are derived from mainly antigen-presenting cells [34] and Th17 cells [35], respectively.”
BackgroundSelf-citationNeutrophils and neutrophil extracellular traps in oral health and disease
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The Interrelationship Between Diabetes, IL-17 and Bone Loss
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The DEL-1/β3 integrin axis promotes regulatory T cell responses during inflammation resolution
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Self-citationPros and cons of causative association between periodontitis and rheumatoid arthritis
Kozieł, J., & Potempa, J. (2022) · Periodontology 2000 · doi:10.1111/prd.12432 · Cited by 47
Periodontitis: a newly identified comorbidity in psoriasis and psoriatic arthritis
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“Theoretically, antipsoriatic therapies inhibiting the IL-17 pathway may thus provide therapeutic benefit for periodontal disease, as shown recently [62].”
BackgroundIlluminating the oral microbiome and its host interactions: animal models of disease
Hajishengallis, G. (2023) · FEMS Microbiology Reviews · doi:10.1093/femsre/fuad018 · Cited by 49
“Ligature placement in conventional mice causes an increase in bacterial biomass and compositional changes in the microbial community of ligated sites (r elativ e to unligated/healthy sites) and these alter ations ar e associated with inflammatory bone loss (Dutzan et al. 2018 ).”
InfluentialSelf-citationMonasterio, G., Budini, V., Fernández, B., Castillo, F. A., Rojas, C., Álvarez, C., Cafferata, E. A., Vicencio, E., Cortés, B. I., Cortéz, C., et al. (2019) · Journal of Periodontal Research · doi:10.1111/jre.12654 · Cited by 45
Inflammatory and Immunological Basis of Periodontal Diseases
Baima, G., Arce, M., Romandini, M., & Dyke, T. E. V. (2025) · Journal of Periodontal Research · doi:10.1111/jre.70040 · Cited by 53
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Zidar, A., Kristl, J., Kocbek, P., & Zupančič, Š. (2021) · Expert Opinion on Drug Delivery · doi:10.1080/17425247.2021.1908260 · Cited by 45
Probiotics and probiotic-based vaccines: A novel approach for improving vaccine efficacy
Kazemifard, N., Dehkohneh, A., & Ghavami, S. B. (2022) · Frontiers in Medicine · doi:10.3389/fmed.2022.940454 · Cited by 48
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Gut-Bone Axis: A Non-Negligible Contributor to Periodontitis
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“Th17 lymphocytes express the following master-switch transcription factors: signal transducer and activator of transcription (STAT)-3 and retinoic acid receptor-related orphan nuclear receptor-γt (RORγt) RORC2 in humans [49,50].”
BackgroundConnection between oral health and chronic diseases
Fu, D., Shu, X., Zhou, G., Ji, M., Liao, G., & Zou, L. (2025) · MedComm · doi:10.1002/mco2.70052 · Cited by 67
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“Majority of people with diabetes fall into two broad pathogenetic categories, type 1 or type 2 diabetes [23,35].”
Backgroundγδ T Cells Differentially Regulate Bone Loss in Periodontitis Models
Barel, O., Aizenbud, Y., Tabib, Y., Jaber, Y., Leibovich, A., Horev, Y., Zubeidat, K., Saba, Y., Eli‐Berchoer, L., Heyman, O., et al. (2021) · Journal of Dental Research · doi:10.1177/00220345211042830 · Cited by 40
“Upon ligature placement, Th17 cells, which differentiate rapidly and locally from Foxp3+ Treg cells in a microbiotadependent manner, were shown to mediate the periodontal damage (Dutzan et al. 2018; Tsukasaki et al. 2018).”
BackgroundInfluentialImmunopathogenesis and distinct role of Th17 in periodontitis: A review
Kini, V. V., Mohanty, I. R., Telang, G., & Vyas, N. (2022) · Journal of Oral Biosciences · doi:10.1016/j.job.2022.04.005 · Cited by 40
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Microbial Reconstitution Improves Aging-Driven Lacrimal Gland Circadian Dysfunction
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Osteoimmunology in periodontitis; a paradigm for Th17/IL-17 inflammatory bone loss
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Self-citationSocial networking at the microbiome-host interface
Lamont, R. J., Hajishengallis, G., & Koo, H. (2023) · Infection and Immunity · doi:10.1128/iai.00124-23 · Cited by 39
Self-citationPeriodontal disease as a model to study chronic inflammation in aging
Bertolini, M., & Clark, D. R. (2023) · GeroScience · doi:10.1007/s11357-023-00835-0 · Cited by 43
“Tregs activity in the peri-odontium has been shown to downregulate the osteo-lytic processes in periodontal disease [132].”
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Is the oral microbiome a source to enhance mucosal immunity against infectious diseases?
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“Furthermore, animal model studies [5] show that periodontal bacteria and local inflammatory markers can disseminate and cause a systemic response and therefore, by causing a low-grade systemic inflammation, might influence the development of comorbidities [6].”
BackgroundOsteocyte RANKL Drives Bone Resorption in Mouse Ligature-Induced Periodontitis
Kittaka, M., Yoshimoto, T., Levitan, M. E., Urata, R., Choi, R. B., Teno, Y., Xie, Y., Kitase, Y., Prideaux, M., Dallas, S. L., et al. (2023) · Journal of Bone and Mineral Research · doi:10.1002/jbmr.4897 · Cited by 37
“(7,11,12,14,17) As a result, the use of 3D BV analysis in the LIP model has been limited and uncommon.”
MethodResultPersonalizing Nutrition Strategies: Bridging Research and Public Health
Clemente‐Suárez, V. J., Peris-Ramos, H. C., Redondo-Flórez, L., Beltrán-Velasco, A. I., Martín-Rodríguez, A., David-Fernandez, S., Sepulveda, R. A. Y., & Tornero-Aguilera, J. F. (2024) · Journal of Personalized Medicine · doi:10.3390/jpm14030305 · Cited by 38
“Evidence indicates that macronutrients and micronutrients can modulate pro-inflammatory and anti-inflammatory cascades, thus influencing the host’s microflora [318].”
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“Taken together, these data indicate that ligature-induced periodontitis is associated with upregulation of a number of proinflammatory genes that seem to be inhibited by LP17, which predominantly targets IL-17A expression, a signature cytokine of Th17 cells that were shown to drive inflammatory bone loss in mice and h…”
BackgroundSelf-citationAngiotensin-Converting Enzyme 2 as a Possible Correlation between COVID-19 and Periodontal Disease
Mancini, L., Quinzi, V., Mummolo, S., Marzo, G., & Marchetti, E. (2020) · Applied Sciences · doi:10.3390/app10186224 · Cited by 35
“IL-17 and a dysbiotic microbiome might promote each other, leading to the enhancement of both microbiome pathogenicity and mucosal immunopathology [40,41].”
BackgroundBhaskaran, N., Faddoul, F., da Silva, A. P., Jayaraman, S., Schneider, E., Mamileti, P., Weinberg, A., & Pandiyan, P. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2020.595936 · Cited by 35
Pacheco, C. M. D. F., Maltos, K. L. M., Shehabeldin, M., Thomas, L. L., Zhuang, Z., Yoshizawa, S., Verdelis, K., Gaffen, S. L., Garlet, G. P., Little, S. R., et al. (2021) · The Journal of Immunology · doi:10.4049/jimmunol.2001432 · Cited by 35
Human and herpesvirus microRNAs in periodontal disease
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The dual role of IL-17 in periodontitis regulating immunity and bone homeostasis
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Advances in the application and mechanism of bioactive peptides in the treatment of inflammation
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“47].”
Erythromycin inhibits neutrophilic inflammation and mucosal disease by upregulating DEL-1
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“This oral disease is driven by IL-17 in both mice and humans (17, 28), and DEL-1 is a strong inhibitor of IL-17–driven immunopathology in periodontitis and other disease models in mice as well as nonhuman primates (17, 18, 21, 47).”
BackgroundSelf-citationRecognition of Candida albicans and Role of Innate Type 17 Immunity in Oral Candidiasis
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Periodontitis Salivary Microbiota Aggravates Ischemic Stroke Through IL-17A
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“IL-17A plays a vital role in the process of periodontitis because of its close association Frontiers in Neuroscience | www.frontiersin.org 12 May 2022 | Volume 16 | Article 876582 with periodontal bacteria (Dutzan et al., 2018).”
BackgroundLim, Y., Kim, H. Y., An, S., & Choi, B. (2022) · Journal of Oral Microbiology · doi:10.1080/20002297.2022.2123550 · Cited by 35
Development and Function of γδT Cells in the Oral Mucosa
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“As mentioned earlier, ablation of Vγ6+ γδT17 cells results in recruitment of IL-17-producing αβT cells (likely Th17 cells; Wilharm et al. 2019) that promote alveolar bone loss (Dutzan et al. 2018; Tsukasaki et al. 2018).”
BackgroundA 16S rRNA Gene and Draft Genome Database for the Murine Oral Bacterial Community
Joseph, S., Aduse‐Opoku, J., Hashim, A., Hanski, E., Streich, R., Knowles, S. C. L., Pedersen, A. B., Wade, W. G., & Curtis, M. A. (2021) · mSystems · doi:10.1128/msystems.01222-20 · Cited by 32
“Despite this inherent simplicity of the mouse oral microbiome, it has significant relevance as a model to investigate and understand the mechanisms of human oral diseases such as periodontitis (7, 9, 10).”
BackgroundMucosal Vaccination Against Periodontal Disease: Current Status and Opportunities
Vaernewyck, V., Arzi, B., Sanders, N. N., Cox, E., & Devriendt, B. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.768397 · Cited by 32
Oral Microbiome and Gingival Transcriptome Profiles of Ligature-Induced Periodontitis
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“The findings are consistent with altered cellular immune response capacity at the level of gene expression and immune pathway functions in progressing periodontitis that have been reported in rodent models (Han et al. 2007) and humans (Abusleme and Moutsopoulos 2017; Dutzan et al. 2018).”
BackgroundVaried Composition and Underlying Mechanisms of Gut Microbiome in Neuroinflammation
Farooq, R. K., Alamoudi, W., Alhibshi, A., Rehman, S., Sharma, A. R., & Abdulla, F. A. (2022) · Microorganisms · doi:10.3390/microorganisms10040705 · Cited by 31
Increased STAT3 Activation in Periodontitis Drives Inflammatory Bone Loss
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“It is well documented that STAT3 tightly regulates T helper (Th)17 differentiation and IL-17A expression (Durant et al. 2010), both critical for tissue destruction in periodontitis (Dutzan et al. 2018).”
BackgroundMethodInfluentialSelf-citationDesign of probiotic delivery systems and their therapeutic effects on targeted tissues
Xu, C., Guo, J., Chang, B., Zhang, Y., Tan, Z., Tian, Z., Duan, X., Ma, J., Jiang, Z., & Hou, J. (2024) · Journal of Controlled Release · doi:10.1016/j.jconrel.2024.08.037 · Cited by 32
Comparative study on the pathogenesis of Crohn’s disease and ulcerative colitis
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“Microbial infections cause inflammation directly or indirectly by a damaged intestinal mucosal barrier, imbalance of microbial homeostasis, as well as altering immune system in IBD[47].”
InfluentialmTOR Signaling in the Regulation of CD4+ T Cell Subsets in Periodontal Diseases
Jiang, Q., Huang, X., Yu, W., Huang, R., Zhao, X., & Chen, C. (2022) · Frontiers in Immunology · doi:10.3389/fimmu.2022.827461 · Cited by 28
The oral-gut axis: a missing piece in the IBD puzzle
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Cellular Mechanisms of Inflammaging and Periodontal Disease
Clark, D. L., Radaic, A., & Kapila, Y. L. (2022) · Frontiers in Dental Medicine · doi:10.3389/fdmed.2022.844865 · Cited by 28
“Expansion of Th17 cell populations and the associated increase in IL-17 expression are characteristic of the pathogenic response in periodontal disease (84, 85).”
BackgroundInfluentialLi, Y., He, X., Luo, G., Zhao, J., Bai, G., & Xu, D. (2025) · Frontiers in Cellular and Infection Microbiology · doi:10.3389/fcimb.2025.1556688 · Cited by 26
Core–shell microneedles with MMP/pH-triggered release for periodontitis bone repair
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“The periodontitis microenvironment is characterized by pathogenic bacterial overgrowth, disrupted macrophage polarization equilibrium, hyperse-cretion of inflammatory mediators, dysregulated matrix metalloproteinase (MMP) activity, and localized pH dysregulation [7–9].”
Indigenous Microbiota Protects against Inflammation-Induced Osteonecrosis
Williams, D. W., Vuong, H. E., Kim, S., Lenon, A., Ho, K., Hsiao, E. Y., SUNG, E. C., & Kim, R. H. (2020) · Journal of Dental Research · doi:10.1177/0022034520908594 · Cited by 26
“2018) or absolute (Dutzan et al. 2018) quantification of 16S rDNA copies (Fig.”
BackgroundMethodResultInfluentialThe role of Th17 cells: explanation of relationship between periodontitis and COPD?
Liu, J., Ouyang, Y., Zhang, Z., Wen, S., Pi, Y., Chen, D., Su, Z., Liang, Z., Guo, L., & Wang, Y. (2022) · Inflammation Research · doi:10.1007/s00011-022-01602-1 · Cited by 27
“The concentration of IL-23 is directly proportional to the amount of tissue damage in the GCF of periodontitis patients [110] and directly associated with IL-17 expression [72, 111].”
BackgroundKondo, T., Okawa, H., Hokugo, A., Shokeen, B., Sundberg, O., Zheng, Y., McKenna, C. E., Lux, R., & Nishimura, I. (2022) · Communications Biology · doi:10.1038/s42003-022-03896-7 · Cited by 23
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“Another study discovered neutrophil depletion ameliorated experimental periodontitis, while unrestrained recruitment aggravated it ( Dutzan et al., 2018 ).”
BackgroundNiche Specific Microbiota-Dependent and Independent Bone Loss around Dental Implants and Teeth
Heyman, O., Horev, Y., Koren, N., Barel, O., Aizenbud, I., Aizenbud, Y., Brandwein, M., Shapira, L., Hovav, A., & Wilensky, A. (2020) · Journal of Dental Research · doi:10.1177/0022034520920577 · Cited by 24
“Destruction of alveolar bone due to a dysbiotic microbiome was reported in experimental and human periodontitis and was mediated by expansion of IL-17–producing T cells (Th17) and recruitment of neutrophils (Dutzan et al. 2018).”
BackgroundInfluence of Vitamin D on Periodontal Inflammation: A Review
Meghil, M. M., & Cutler, C. W. (2023) · Pathogens · doi:10.3390/pathogens12091180 · Cited by 25
“DCs can shape Th17/Treg balance towards Th17 to eradicate invading bacteria, but Th17/Treg imbalance promotes osteoclast-mediated alveolar bone loss [28,29].”
BackgroundKajikawa, T., Wang, B., Li, X., Wang, H., Chavakis, T., Moutsopoulos, N. M., & Hajishengallis, G. (2020) · Journal of Leukocyte Biology · doi:10.1002/jlb.5hi0420-648r · Cited by 24
Self-citationA review of T helper 17 cell-related cytokines in serum and saliva in periodontitis
Medara, N., Lenzo, J. C., Walsh, K. A., Reynolds, E. C., Darby, I. B., & O’brien-simpson, N. M. (2020) · Cytokine · doi:10.1016/j.cyto.2020.155340 · Cited by 27
Complement Is Required for Microbe-Driven Induction of Th17 and Periodontitis
Wang, H., Ideguchi, H., Kajikawa, T., Mastellos, D. C., Lambris, J. D., & Hajishengallis, G. (2022) · The Journal of Immunology · doi:10.4049/jimmunol.2200338 · Cited by 25
Self-citationNi, Q., Li, G., Chen, Y., Bao, C., Wang, T., Li, Y.-Y., Ruan, X., Wang, H., & Sun, W. S. (2024) · Mucosal Immunology · doi:10.1016/j.mucimm.2024.05.003 · Cited by 23
Zhang, B., Gong, G., He, Y., Liu, J., Wang, B., Li, Y., Fang, J., Zhao, Z., & Guo, J. (2024) · Biomaterials · doi:10.1016/j.biomaterials.2024.122961 · Cited by 23
Shaped by the epithelium – postnatal immune mechanisms of oral homeostasis
Zubeidat, K., & Hovav, A. (2021) · Trends in Immunology · doi:10.1016/j.it.2021.05.006 · Cited by 21
Charalambous, E. G., Mériaux, S. B., Guébels, P., Muller, C. P., Leenen, F. A. D., Elwenspoek, M. M. C., Thiele, I., Hertel, J., & Turner, J. D. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms222312682 · Cited by 23
“This is directly induced by microbial dysbiosis [92].”
BackgroundInterleukin-17 promotes osteoclastogenesis and periodontal damage via autophagy in vitro and in vivo
Zhong, J., Wang, Z., Yuan, W., Shen, Y., & Chen, L. (2022) · International Immunopharmacology · doi:10.1016/j.intimp.2022.108631 · Cited by 24
Moreno, C. M., Bybee, E., Freitas, C. M. T., Pickett, B. E., & Weber, K. S. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23105580 · Cited by 21
“Evidence suggests that T helper 17 (Th17) cells are drivers of periodontitis pathogenesis and that they are recruited to periodontal lesions by IL-6 and interleukin 23 (IL-23) [23].”
BackgroundEngineered Human Dendritic Cell Exosomes as Effective Delivery System for Immune Modulation
Elsayed, R., Elashiry, M., Tran, C., Yang, T., Carroll, A., Liu, Y., Hamrick, M. W., & Cutler, C. W. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms241411306 · Cited by 23
“DCs can shape the Th17:T regulatory cell (Treg) balance toward Th17 to eradicate invading bacteria, but Th17:Treg imbalance promotes osteoclast-mediated alveolar bone loss [3,22].”
BackgroundCurrent Understanding of Osteoimmunology in Certain Osteoimmune Diseases
Zhou, A., Wu, B., Yu, H., Tang, Y., Liu, J., Jia, Y., Yang, X., & Xiang, L. (2021) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2021.698068 · Cited by 22
“Activated by IL-1β, IL-6, and IL-23, TH17 cells produce IL-17 family cytokines including IL-17A, which is demonstrated to be the primary mediator of immunopathology in the context of periodontitis and periodontitis-related systemic diseases (Moutsopoulos et al., 2012; Dutzan et al., 2018; Samuel et al., 2019), while I…”
BackgroundByrne, S., Chang, D. H. C., Adams, G. G., Butler, C. A., Reynolds, E. C., Darby, I. B., & Dashper, S. G. (2022) · Journal of Oral Microbiology · doi:10.1080/20002297.2022.2043595 · Cited by 22
“community composition rather than the total microbial load being associated with periodontitis [22,51].”
BackgroundOral microbiota–host interaction: the chief culprit of alveolar bone resorption
Xu, J., Yu, L., Ye, S., Ye, Z., Yang, L., & Xu, X. (2024) · Frontiers in Immunology · doi:10.3389/fimmu.2024.1254516 · Cited by 22
Th17-to-Tfh plasticity during periodontitis limits disease pathology
McClure, F. A., Wemyss, K., Cox, J. R., Bridgeman, H. M., Prise, I. E., King, J. I., Jaigirdar, S. A., Whelan, A., Jones, G. W., Grainger, J. R., et al. (2024) · The Journal of Experimental Medicine · doi:10.1084/jem.20232015 · Cited by 24
“…disease that results in impaired Th17 cell development (Autosomal Dominant Hyper-IgE Syndrome; patients with loss-of-function Stat3 mutations) exhibit not only limited gingival Th17 cells but reduced periodontal inflammation compared with age-matched healthy controls (Dutzan et al., 2018).”
BackgroundInfluentialAct Locally, Act Globally—Microbiota, Barriers, and Cytokines in Atherosclerosis
Kurilenko, N., Fatkhullina, A. R., Mazitova, A., & Koltsova, E. K. (2021) · Cells · doi:10.3390/cells10020348 · Cited by 22
Distinct spatial organization governs oral mucosal immunity
Theofilou, V. I., FRASER, D. D., Kanasi, E., Brenchley, L., Greenwell‐Wild, T., Adade, E. E., Valm, A. M., Douagi, I., Belkaid, Y., Tran, D. T., et al. (2026) · Nature Immunology · doi:10.1038/s41590-025-02398-y · Cited by 22
Self-citationCalprotectin (S100A8/A9) Is an Innate Immune Effector in Experimental Periodontitis
Johnstone, K. F., Wei, Y., Bittner‐Eddy, P. D., Vreeman, G. W., Stone, I. A., Clayton, J. B., Reilly, C., Walbon, T. B., Wright, E. N., Hoops, S., et al. (2021) · Infection and Immunity · doi:10.1128/iai.00122-21 · Cited by 22
“have not been identified and lesions result from the development of dysbiosis (5, 69).”
BackgroundIrie, K., Azuma, T., Tomofuji, T., & Yamamoto, T. (2023) · Dentistry Journal · doi:10.3390/dj11080194 · Cited by 24
“Imbalanced homeostasis between Th17 and Treg has been attributed to periodontitis [76], thereby necessitating a harmonious balance between Th17 effector cells and Treg to maintain functional immunity and host health [77].”
BackgroundApplication of Nanomaterials Targeting Immune Cells in the Treatment of Chronic Inflammation
Ci, Z., Wang, H., Luo, J., Wei, C., Chen, J., Wang, D., & Zhou, Y. (2024) · International Journal of Nanomedicine · doi:10.2147/ijn.s497590 · Cited by 23
“31 The research team led by Fang Fuchun identified a neutrophil subpopulation associated with NETs in gingival tissues using single-cell technology for the first time.”
Systemic, Lifestyle and Environmental Modifying Factors in the Pathogenesis of Periodontitis
Groeger, S. E., Yuxi, Z., Yong, J., Wang, L., Ruf, S., & Meyle, J. (2025) · Journal of Periodontal Research · doi:10.1111/jre.70003 · Cited by 26
Williams, D. W., Ho, K., Lenon, A., Kim, S., Kim, T., Gwack, Y., & Kim, R. H. (2020) · Journal of Bone and Mineral Research · doi:10.1002/jbmr.4614 · Cited by 20
““Type 17” cells are a subset of CD3 T cells that ubiquitously express IL23R,((24)) have been shown to drive the pathologic bone loss in periodontal disease,((25)) and have been implicated in a multiple myeloma model of BRONJ.”
BackgroundNair, V., Grover, V., Arora, S., Das, G., Ahmad, I. S., Ohri, A., Sainudeen, S., Saluja, P., & Saha, A. (2022) · Medicina · doi:10.3390/medicina58081042 · Cited by 22
“The IL-17 family consists of six family members, IL-17A to IL-17F, and it has been reported that IL-17 and a dysbiotic microbiome mutually promote each other, thus increasing the microbiome pathogenicity and mucosal immunopathology [42,43].”
BackgroundHathaway‐Schrader, J. D., Aartun, J. D., Poulides, N. A., Kuhn, M. B., McCormick, B. E., Chew, M. E., Huang, E., Darveau, R. P., Westwater, C., & Novince, C. M. (2022) · JCI Insight · doi:10.1172/jci.insight.140738 · Cited by 19
Shi, Z., Lü, J., Zhang, Q., Sun, L., Wang, X., Qin, X., & Xia, Y. (2022) · Bioengineering & Translational Medicine · doi:10.1002/btm2.10466 · Cited by 19
“Enhanced periodontal regeneration by PDLSCs implantation has been achieved with and without a scaffold.(29,30) The underlying mechanisms are attributed to the osteo/dentinogenic differentiation poten-”
BackgroundPeriodontitis and COVID-19: Immunological Characteristics, Related Pathways, and Association
Qi, M., Sun, W., Wang, K., Li, W., Lin, J., Gong, J., & Wang, L. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24033012 · Cited by 22
“Conversely, patients with autosomal dominant hyper-immunoglobulin E syndrome with defective differentiation of TH17 cells were not susceptible to periodontal disease and had significantly reduced periodontal inflammation and bone loss [85].”
BackgroundCorral, M. A. T., Daza, E. H., Jimenez, N. A., Vera, D. Z. M., Porras, J. V., Uriza, C. L., Arregocés, F. M. E., Martínez, P. H., Cortés, M. E., Otero, L., et al. (2023) · Heliyon · doi:10.1016/j.heliyon.2023.e14340 · Cited by 25
Metronidazole may display anti‐inflammatory features in periodontitis treatment: A scoping review
Suárez, L. J., Arce, R. M., Gonçalves, C., Furquim, C. P., dos Santos, N. C. C., Retamal‐Valdes, B., & Feres, M. (2024) · Molecular Oral Microbiology · doi:10.1111/omi.12459 · Cited by 19
Bittner‐Eddy, P. D., Fischer, L. A., & Costalonga, M. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2020.00677 · Cited by 19
Lee, J. S., Chowdhury, N., Roberts, J. S., & Yilmaz, Ö. (2020) · Virulence · doi:10.1080/21505594.2020.1763061 · Cited by 19
Multifunctional role of oral bacteria in the progression of non-alcoholic fatty liver disease
Mei, E., Yao, C. H., Chen, Y.-N., Nan, S.-X., & Qi, S.-C. (2024) · World Journal of Hepatology · doi:10.4254/wjh.v16.i5.688 · Cited by 19
Rozenblum, G., Ait‐Aissa, K., Zahran, G. E. D., Alipour, M., Sahyoun, A. M., Munkhsaikhan, U., Kassan, A., Ishrat, T., Wang, Q., Abidi, A. H., et al. (2025) · Alzheimer s & Dementia · doi:10.1002/alz.71011 · Cited by 19
Succession of the oral microbiome with the increasing severity of periodontitis
Mi, J., Zhi, M., Kang, W., Liang, Q., Tang, D., Wang, T., Song, W., Sun, T., Li, M., Shao, J., et al. (2024) · Open Research (University of Surrey) · doi:10.1002/viw.20230118 · Cited by 18
Monasterio, G., Castillo, F. A., Astorga, J., Hoare, A., Terraza‐Aguirre, C., Cafferata, E. A., Villablanca, E. J., & Vernal, R. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2020.591240 · Cited by 18
“Nonetheless, alveolar bone resorption during periodontitis is mainly mediated by the Th17type of immune response, which is central in the periodontal osteo-immune network crosstalk (50).”
BackgroundThe Microbiome in Hidradenitis Suppurativa Tunnels: A Systematic Review
Soto‐Moreno, A., Haselgruber, S., León‐Pérez, F. J., García‐Moronta, C., Cuenca‐Barrales, C., Arias‐Santiago, S., & Molina‐Leyva, A. (2025) · International Journal of Dermatology · doi:10.1111/ijd.17892 · Cited by 17
Regulatory T cells showed characteristics of T helper‐17(Th17) cells in mice periodontitis model
Kou, Y., Jiang, Y., Liu, S., Yang, P., Lu, Y., Liu, H., & Li, M. (2021) · Oral Diseases · doi:10.1111/odi.14072 · Cited by 17
Jiang, L., Zhang, J., Fang, M., Qin, Y., Huang, Y., & Tao, R. (2022) · Frontiers in Microbiology · doi:10.3389/fmicb.2022.939608 · Cited by 17
Metadata
- Authors
- Dutzan, N., Kajikawa, T., Abusleme, L., Greenwell-Wild, T., Zuazo, C. E., Ikeuchi, T., Brenchley, L., Abe, T., Hurabielle, C., Martin, D., Morell, R. J., Freeman, A. F., Lazarevic, V., Trinchieri, G., Diaz, P. I., Holland, S. M., Belkaid, Y., Hajishengallis, G., & Moutsopoulos, N. M.
- Affiliations
- Oral Immunity and Inflammation Unit, NIDCR, NIH, Bethesda, MD 20892, USA.
- University of Pennsylvania (US)
- National Institutes of Health (US)
- Genomics and Computational Biology Core, NIDCD, NIH, Bethesda, MD 20892, USA.
- UConn Health (US)
- Corresponding author
- Moutsopoulos, Niki M.
- ORCID
- Dutzan, Nicolas
- Kajikawa, Tetsuhiro
- Abusleme, Loreto
- Zuazo, Carlos E.
- Ikeuchi, Tomoko
- Brenchley, Laurie
- Abe, Toshiharu
- Hurabielle, Charlotte
- Martin, Daniel
- Morell, Robert J.
- Freeman, Alexandra F.
- Lazarevic, Vanja
- Trinchieri, Giorgio
- Diaz, Patricia I.
- Holland, Steven M.
- Belkaid, Yasmine
- Hajishengallis, George
- Moutsopoulos, Niki M.
- Venue
- Science Translational Medicine
- Published
- 2018-10-17
- Volume
- 10
- Issue
- 463
- ISSN
- 1946-6234 (ISSN-L)
- 1946-6242
- PMC
- PMC6330016
- OpenAlex
- W2896857921
- Cited by
- 382
- References
- 58
- Citations by year
- 2026: 38 · 2025: 46 · 2024: 49 · 2023: 46 · 2022: 47 · 2021: 70 · 2020: 57 · 2019: 28 · 2018: 1
- FWCI
- 44.82
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science Translational Medicine (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Fondation pour la Recherche Médicale
- NIAID (IRP)
- NIDCR (Intramural, DE024153, DE026152)
- NCI Intramural
- La Roche-Posay
- CEDEF
- Philippe Foundation
- fondation groupe pasteur mutualité
- Société Française de Dermatologie
- Topics
- Health Sciences › Dentistry › Periodontics › Oral microbiology and periodontitis research
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- dysbiosis, oral microbiota, Th17 cells, oral inflammation, periodontitis, oral immunity, targeted therapy
- MeSH terms
- Animals, Bacteria, Bone Resorption, Cell Differentiation, Humans, Inflammation, Mouth Mucosa, Neutrophils, Periodontitis, Interleukin-6, Mice, Interleukin-23, Nuclear Receptor Subfamily 1, Group F, Member 3, Th17 Cells, Microbiota, Dysbiosis
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