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Cited by 712Oral microbiology and periodontitis researchPeriodontal Regeneration and TreatmentsBacterial biofilms and quorum sensing

Molecular aspects of the pathogenesis of periodontitis

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Meyle, Joerg, Chapple, Iain·2015·Periodontology 2000
DOI 10.1111/prd.12104
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Abstract

The past decade of basic research in periodontology has driven radical changes in our understanding and perceptions of the pathogenic processes that drive periodontal tissue destruction. The core elements of the classical model of disease pathogenesis, developed by Page & Kornman in 1997, remain pertinent today; however, our understanding of the dynamic interactions between the various microbial and host factors has changed significantly. The molecular era has unraveled aspects of genetics, epigenetics, lifestyle and environmental factors that, in combination, influence biofilm composition and the host's inflammatory immune response, creating a heterogenic biological phenotype that we label as ‘periodontitis’. In this volume of Periodontology 2000 , experts in their respective fields discuss these emerging concepts, such as a health‐promoting biofilm being essential for periodontal stability, involving a true symbiosis between resident microbial species and each other and also with the host response to that biofilm. Rather like the gut microbiome, changes in the local environment, which may include inflammatory response mediators or viruses, conspire to drive dysbiosis and create a biofilm that supports pathogenic species capable of propagating disease. The host response is now recognized as the major contributor to periodontal tissue damage in what becomes a dysfunctional, poorly targeted and nonresolving inflammation that only serves to nourish and sustain the dysbiosis. The role of epithelial cells in signaling to the immune system is becoming clearer, as is the role of dendritic cells as transporters of periodontal pathogens to distant sites within the body, namely metastatic infection. The involvement of nontraditional immune cells, such as natural killer cells, is being recognized, and the simple balance between T‐helper 1‐ and T‐helper 2‐type T‐cell populations has become less clear with the emergence of T‐regulatory cells, T‐helper 17 cells and follicular helper cells. The dominance of the neutrophil has emerged, not only as a potential destructor when poorly regulated but as an equally unpredictable effector cell for specific B‐cell immunity. The latter has emerged, in part, from the realization that neutrophils live for 5.4 days in the circulation, rather than for 24 h, and are also schizophrenic in nature, being powerful synthesizers of proinflammatory cytokines but also responding to prostaglandin signals to trigger a switch to a pro‐resolving phenotype that appears capable of regenerating the structure and function of healthy tissue. Key to these outcomes are the molecular signaling pathways that dominate at any one time, but even these are influenced by microRNAs capable of ‘silencing’ certain inflammatory genes. This volume of Periodontology 2000 tries to draw these complex new learnings into a contemporary model of disease pathogenesis, in which inflammation and dysbiosis impact upon whether the outcome is driven toward acute resolution and stability, chronic resolution and repair, or failed resolution and ongoing periodontal tissue destruction.

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  • Accumulation of subgingival biofilms initiates development of clinical signs of gingivitis.

    “Accumulation of subgingival biofilms initiates development of clinical signs of gingivitis”

    From The dental plaque biofilm matrix (2021) · cites this paper as [279]

  • As a result of complex interactions between subgingival biofilms and the host immune response, gingivitis can further develop to periodontitis with concomitant loss of periodontal supportive tissues.

    “As a result of complex interactions between subgingival biofilms and the host immune response, gingivitis can further develop to periodontitis with concomitant loss of periodontal supportive tissues (Figure 7B).239,278,279”

    From The dental plaque biofilm matrix (2021) · cites this paper as [279]

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Authors
Meyle, J., & Chapple, I.
ORCID
Venue
Periodontology 2000
Publisher
Wiley
Published
2015-08-07
Volume
69
Issue
1
Pages
7-17
ISSN
  • 0906-6713 (ISSN-L)
  • 1600-0757
DOI
10.1111/prd.12104
OpenAlex
W1762827693
Cited by
705
References
83
Citations by year
2026: 52 · 2025: 86 · 2024: 98 · 2023: 92 · 2022: 73 · 2021: 108 · 2020: 57 · 2019: 48 · 2018: 34 · 2017: 37 · 2016: 16 · 2015: 2
FWCI
40.12
Type
journal article
Language
en
Open access
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations
  • Periodontology 2000 (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Dentistry › Periodontics › Oral microbiology and periodontitis research
  • Health Sciences › Medicine › Urology › Periodontal Regeneration and Treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bacterial biofilms and quorum sensing
Keywords
periodontitis, periodontal disease pathogenesis, periodontal biofilm, dysbiosis, host immune response, nonresolving inflammation, epithelial cells, dendritic cells, natural killer cells, regulatory T cells, Th17 cells, neutrophils, B-cell immunity, prostaglandins, microRNA, epigenetics
MeSH terms
Epithelial Cells, Humans, Mouth Mucosa, Periodontitis, Symbiosis, Cytokines, Biofilms, Host-Pathogen Interactions, Dysbiosis

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