Cited by 76Oral microbiology and periodontitis researchNeutrophil, Myeloperoxidase and Oxidative MechanismsPeriodontal Regeneration and Treatments

Interactions Between Neutrophils and Periodontal Pathogens in Late-Onset Periodontitis

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Jiang, Qingsong, Zhao, Yuxi, Shui, Yusen, Zhou, Xuedong, Cheng, Lei, Ren, Biao, Chen, Zhu, Li, Mingyun·2021·Frontiers in Cellular and Infection Microbiology

Abstract

Late-onset periodontitis is associated with a series of inflammatory reactions induced by periodontal pathogens, such as Porphyromonas gingivalis , a keystone pathogen involved in periodontitis. Neutrophils are the most abundant leukocytes in the periodontal pocket/gingival crevice and inflamed periodontal tissues. They form a “wall” between the dental plaque and the junctional epithelium, preventing microbial invasion. The balance between neutrophils and the microbial community is essential to periodontal homeostasis. Excessive activation of neutrophils in response to periodontal pathogens can induce tissue damage and lead to periodontitis persistence. Therefore, illuminating the interactions between neutrophils and periodontal pathogens is critical for progress in the field of periodontitis. The present review aimed to summarize the interactions between neutrophils and periodontal pathogens in late-onset periodontitis, including neutrophil recruitment, neutrophil mechanisms to clear the pathogens, and pathogen strategies to evade neutrophil-mediated elimination of bacteria. The recruitment is a multi-step process, including tethering and rolling, adhesion, crawling, and transmigration. Neutrophils clear the pathogens mainly by phagocytosis, respiratory burst responses, degranulation, and neutrophil extracellular trap (NET) formation. The mechanisms that pathogens activate to evade neutrophil-mediated killing include impairing neutrophil recruitment, preventing phagocytosis, uncoupling killing from inflammation, and resistance to ROS, degranulation products, and NETs.

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Crossref · 10.3389/fcimb.2021.627328

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  • The relationship between BOP and oral inflammation is inconsistent and appears to rely on the microbial nature of the biofilm.

    “Nonetheless, the presence of BOP might be indicative of underlying inflammation; however, the relationship between BOP and oral inflammation is inconsistent and appears to rely on the microbial nature of the biofilm. 25 , 38 , 39”

    From Prognostic utility of oral neutrophil counts in high-risk periodontitis: A retrospective study (2025) · cites this paper as [39]

    The Introduction (page not specified) says the oral microbial community can induce inflammation and that dysbiosis and inflammation promote each other. But the paper does not address bleeding on probing (searched: BOP, bleeding on probing) or establish that its relationship with inflammation is inconsistent or depends on biofilm composition. (LLM, conf=0.78)

    Experimental — accuracy not yet measured
  • oPMN accumulate within the gingivocrevicular fluid alongside biofilms rich in periodontal pathogens and tend to be associated with patients at risk of future disease progression.

    “oPMN accumulate within the gingivocrevicular fluid (GCF), alongside biofilms rich in periodontal pathogens including Porphyromonas gingivalis (Pg), Treponema denticola (Td), Tannerella forsythia (Tf), Aggregatibacter actinomycetemcomitans (Aa), and Prevotella intermedia (Pi), and tend to be associated with patients who are at risk of future disease progression. 37 , 39”

    From Prognostic utility of oral neutrophil counts in high-risk periodontitis: A retrospective study (2025) · cites this paper as [39]

    The Introduction (page unavailable) places oral neutrophils in crevicular fluid and periodontal pockets and identifies several listed bacteria as periodontitis-associated pathogens. The NET Formation section says neutrophils are attracted toward dental biofilms. The paper does not establish that oPMN accumulation identifies patients at risk of future disease progression, and the retrieved passages do not substantiate the full five-species list in that setting. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

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Authors
Jiang, Q., Zhao, Y., Shui, Y., Zhou, X., Cheng, L., Ren, B., Chen, Z., & Li, M.
Affiliations
Sichuan University (CN)
Corresponding author
  • Chen, Zhu
  • Li, Mingyun
Venue
Frontiers in Cellular and Infection Microbiology
Published
2021-03-12
Volume
11
Pages
627328-627328
ISSN
2235-2988 (ISSN-L)
OpenAlex
W3138697958
Cited by
76
References
127
Citations by year
2026: 12 · 2025: 23 · 2024: 19 · 2023: 15 · 2022: 6 · 2021: 1
FWCI
1.76
Type
journal article
Language
en
Open access
Locations
  • Frontiers in Cellular and Infection Microbiology (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • National Natural Science Foundation of China (2016YFC1102700, 2017JQ0028, 81870759, 2021YFH0188, 81430011, 81400501)
  • Department of Science and Technology of Sichuan Province (2021YFH0188, 2017JQ0028, 81400501)
  • National Key Research and Development Program of China (2016YFC1102700)
Topics
  • Health Sciences › Dentistry › Periodontics › Oral microbiology and periodontitis research
  • Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Health Sciences › Medicine › Urology › Periodontal Regeneration and Treatments
Keywords
neutrophils, periodontitis, periodontal pathogens, Porphyromonas gingivalis, neutrophil recruitment, neutrophil transmigration, phagocytosis, respiratory burst, neutrophil extracellular traps, degranulation, periodontal homeostasis, periodontal pockets
MeSH terms
Humans, Neutrophils, Periodontitis, Phagocytosis, Porphyromonas gingivalis, Extracellular Traps

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