Comprehensive analysis of gene expression in the junctional epithelium by laser microdissection and microarray analysis

Hayashi, Yasunori; Mutoh, T.; Yamamoto, Gou; Nishii, K; Usui, Michihiko; Yamamoto, Masahide; Tachikawa, Tetsuhiko

doi:10.1111/j.1600-0765.2010.01276.x

Cited by 35 publications

(43 citation statements)

References 34 publications

(39 reference statements)

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“…Superficially the sulcus or pocket opens into the oral cavity, whereas the base of the trough is bounded by a thin, modified epithelium (junctional epithelium), which ends where the connective tissue bundles attach to the cementum surface of the root [46]. The sulcular and junctional epithelia are immunologically active sensors of the proximal dental plaque biofilm, expressing Toll-like receptors and other pathogen recognition receptors (PRR) on the lining stratified squamous, keratin-17-positive epithelial cells [47]. The keratinocytes of the gingival epithelium connect to one another through desmosomes and cell adhesion molecules such as CEACAM1 [46].…”

Section: Characteristics Of Different Oral Ecological Nichesmentioning

confidence: 99%

“…The keratinocytes of the gingival epithelium connect to one another through desmosomes and cell adhesion molecules such as CEACAM1 [46]. The junctional and sulcular epithelia release chemotactic molecules such as IL-8 (CXCL8) MCP-1 [48], CCL28, secretory leukocyte protease inhibitor (SLPI) [47,49] and RANTES [50]. These cytokines and chemokines signal neutrophils and monocytes to transmigrate through the epithelium into the sulcus or pocket [51].…”

Section: Characteristics Of Different Oral Ecological Nichesmentioning

confidence: 99%

“…These cytokines and chemokines signal neutrophils and monocytes to transmigrate through the epithelium into the sulcus or pocket [51]. Microbe-associated molecular patterns (MAMPs) from the biofilm activate the epithelium, increasing the proliferative rate, expression of adhesion molecules [47], and production of IL-1β [52] and antimicrobial proteins and peptides such as calprotectin and defensins [53] (reviewed in [54]). This mixture of immune and inflammatory mediators and white cells is contained in the gingival crevicular fluid (Fig.…”

Section: Characteristics Of Different Oral Ecological Nichesmentioning

confidence: 99%

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The oral microbiome and the immunobiology of periodontal disease and caries

2014

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The composition of the oral microbiome differs from one intraoral site to another, reflecting in part the host response and immune capacity at each site. By focusing on two major oral infections, periodontal disease and caries, new principles of disease emerge. Periodontal disease affects the soft tissues and bone that support the teeth. Caries is a unique infection of the dental hard tissues. The initiation of both diseases is marked by an increase in the complexity of the microbiome. In periodontitis, pathobionts and keystone pathogens such as Porphyromonas gingivalis appear in greater proportion than in health. As a keystone pathogen, P. gingivalis impairs host immune responses and appears necessary but not sufficient to cause periodontitis. Historically, dental caries had been causally linked to Streptococcus mutans. Contemporary microbiome studies now indicate that singular pathogens are not obvious in either caries or periodontitis. Both diseases appear to result from a perturbation among relatively minor constituents in local microbial communities resulting in dysbiosis. Emergent consortia of the minor members of the respective microbiomes act synergistically to stress the ability of the host to respond and protect. In periodontal disease, host protection first occurs at the level of innate gingival epithelial immunity. Secretory IgA antibody and other salivary antimicrobial systems also act against periodontopathic and cariogenic consortia. When the gingival immune response is impaired, periodontal tissue pathology results when matrix metalloproteinases are released from neutrophils and T cells mediate alveolar bone loss. In caries, several species are acidogenic and aciduric and appear to work synergistically to promote demineralization of the enamel and dentin. Whereas technically possible, particularly for caries, vaccines are unlikely to be commercialized in the near future because of the low morbidity of caries and periodontitis.

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Section: Characteristics Of Different Oral Ecological Nichesmentioning

confidence: 99%

Section: Characteristics Of Different Oral Ecological Nichesmentioning

confidence: 99%

Section: Characteristics Of Different Oral Ecological Nichesmentioning

confidence: 99%

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The oral microbiome and the immunobiology of periodontal disease and caries

2014

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“…For example, we previously reported that secretory leukocyte protease inhibitor (SLPI) and S100A8 are characteristically expressed in the JE. SLPI protects the intestinal epithelium from proteases secreted as part of the inflammatory response and is associated with the maintenance of tissue integrity7. S100A8 and S100A9 form a heterodimeric complex and constitute calprotectin, an antimicrobial peptide8.…”

mentioning

confidence: 99%

The junctional epithelium originates from the odontogenic epithelium of an erupted tooth

Yajima-Himuro

Oshima

Yamamoto

et al. 2014

Sci Rep

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The junctional epithelium (JE) is an epithelial component that is directly attached to the tooth surface and has a protective function against periodontal diseases. In this study, we determined the origin of the JE using a bioengineered tooth technique. We transplanted the bioengineered tooth germ into the alveolar bone with an epithelial component that expressed green fluorescence protein. The reduced enamel epithelium from the bioengineered tooth fused with the oral epithelium, and the JE was apparently formed around the bioengineered tooth 50 days after transplantation. Importantly, the JE exhibited green fluorescence for at least 140 days after transplantation, suggesting that the JE was not replaced by oral epithelium. Therefore, our results demonstrated that the origin of the JE was the odontogenic epithelium, and odontogenic epithelium-derived JE was maintained for a relatively long period.

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“…Le système de défense est différent dans l' épithélium de recouvrement et dans l' épithélium de jonction. Ce dernier se multiplie beaucoup plus rapidement que l' épithélium gingival car il possède une protéine Slpi (Secretory Leucocyte Protease Inhibitor) produite sous l' effet de 5 gènes particuliers, dans une quantité 100 fois supérieure à celle trouvée dans l' épithélium gingival, ce qui lui fournit une importante défense immunitaire [13]. Le système de défense est donc différent dans l' épithélium de recouvrement et dans l' épithélium de jonction.…”

Section: éPithélium Gingivalunclassified

Les cellules souches

Benoît¹

2014

Actual. Odonto-Stomatol.

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RésuméChez l'Homme, au stade du bouton embryonnaire, dans certaines conditions, les cellules de ce dernier peuvent se différencier en toutes cellules constituant un organisme : elles sont dites totipotentes. Chez l'adulte, une sub-population de cellules participe, in vivo, à l'homéostasie de chacun des tissus constitutifs du territoire oro-facial et se différencie en cellules spécifiques dans chacun de ces tissus. Ces cellules reçoivent le nom de cellules souches pluripotentes. Des recherches actuelles sont entreprises, in vitro

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Comprehensive analysis of gene expression in the junctional epithelium by laser microdissection and microarray analysis

Cited by 35 publications

References 34 publications

The oral microbiome and the immunobiology of periodontal disease and caries

The oral microbiome and the immunobiology of periodontal disease and caries

The junctional epithelium originates from the odontogenic epithelium of an erupted tooth

Les cellules souches

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