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The Junctional Epithelium: from Health to Disease
Abstract
The junctional epithelium is located at a strategically important interface between the gingival sulcus, populated with bacteria, and the periodontal soft and mineralized connective tissues that need protection from becoming exposed to bacteria and their products. Its unique structural and functional adaptation enables the junctional epithelium to control the constant microbiological challenge. The antimicrobial defense mechanisms of the junctional epithelium, however, do not preclude the development of gingival and periodontal lesions. The conversion of the junctional to pocket epithelium, which is regarded as a hallmark in disease initiation, has been the focus of intense research in recent years. Research has shown that the junctional epithelial cells may play a much more active role in the innate defense mechanisms than previously assumed. They synthesize a variety of molecules directly involved in the combat against bacteria and their products. In addition, they express molecules that mediate the migration of polymorphonuclear leukocytes toward the bottom of the gingival sulcus. Periodontopathogens—such as Actinobacillus actinomycetemcomitans or, in particular, Porphyromonas gingivalis—have developed sophisticated methods to perturb the structural and functional integrity of the junctional epithelium. Research has focused on the direct effects of gingipains, cysteine proteinases produced by Porphyromonas gingivalis, on junctional epithelial cells. These virulence factors may specifically degrade components of the cell-to-cell contacts. This review will focus on the unique structural organization of the junctional epithelium, on the nature and functions of the various molecules expressed by its cells, and on how gingipains may attenuate the junctional epithelium’s structural and functional integrity.
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“BOP is the result of ulceration of the sulcular epithelium caused by manipulation of these tissues, normally by a periodontal probe, in the presence of pathogenic bacteria. 35 , 36 , 37”
From Prognostic utility of oral neutrophil counts in high-risk periodontitis: A retrospective study (2025) · cites this paper as [36]
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“These extravascular metabolic products can enhance systemic inflammatory cytokines (34) and may lead to disruptive effects on the blood vessel's endothelium, including the reduced ability for the endothelium to produce nitric oxide (6, 7, 30, 31).”
From Oral inflammatory load predicts vascular function in a young adult population: a pilot study (2023) · cites this paper as [30]
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Metadata
- Authors
- Bosshardt, D. D., & Lang, N. P.
- Affiliations
- University of Bern (CH)
- Venue
- Journal of Dental Research
- Publisher
- SAGE Publications
- Published
- 2005-01
- Volume
- 84
- Issue
- 1
- Pages
- 9-20
- ISSN
- 0022-0345 (ISSN-L)
- 1544-0591
- OpenAlex
- W1970638674
- Cited by
- 388
- References
- 128
- Citations by year
- 2026: 18 · 2025: 30 · 2024: 15 · 2023: 21 · 2022: 24 · 2021: 17 · 2020: 24 · 2019: 24 · 2018: 21 · 2017: 30 · 2016: 21 · 2015: 18 · 2014: 26 · 2013: 12 · 2012: 19
- FWCI
- 1.80
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Dental Research (publishedVersion)
- PubMed (publishedVersion)
- The HKU Scholars Hub (University of Hong Kong) (submittedVersion)
- Topics
- Health Sciences › Dentistry › Periodontics › Oral microbiology and periodontitis research
- Health Sciences › Dentistry › Periodontics › Oral and gingival health research
- Health Sciences › Dentistry › Periodontics › Periodontal Regeneration and Treatments
- Keywords
- junctional epithelium, periodontal disease, gingival lesions, innate immunity, antimicrobial defense, leukocyte migration, Porphyromonas gingivalis, gingipains, cysteine protease, Aggregatibacter actinomycetemcomitans, periodontal pathogens, cell-cell contact, gingival sulcus
- MeSH terms
- Gingipain Cysteine Endopeptidases, Animals, Cell Communication, Cysteine Endopeptidases, Epithelial Attachment, Hemagglutinins, Humans, Periodontal Pocket, Cell Adhesion Molecules, Cytokines, Porphyromonas gingivalis, Adhesins, Bacterial
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