The distribution and expression of <scp>S</scp>100<scp>A</scp>8 and <scp>S</scp>100<scp>A</scp>9 in gingival epithelium of mice

Nishii, K; Usui, Michihiko; Yamamoto, Gou; Yajima, Shugo; Y, Tsukamoto; Tanaka, Junichi; Tachikawa, Tetsuhiko; Yamamoto, Masahide

doi:10.1111/jre.12000

Cited by 24 publications

(21 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Thus, it is inferred that S100A9 is the proinflammatory subunit of calprotectin in periodontal fibroblasts. Interestingly, Nishii et al 37 found that the expression intensity of S100A9 was strongly upregulated in the presence of microorganisms, yet S100A8 remained unchanged. Therefore, the two subunits of calprotectin may exert different effects in the development and progression of periodontitis.…”

Section: Discussionmentioning

confidence: 99%

Proinflammatory effects and mechanisms of calprotectin on human gingival fibroblasts

Gao

Hou

Meng

et al. 2017

J of Periodontal Research

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 99%

Proinflammatory effects and mechanisms of calprotectin on human gingival fibroblasts

Gao

Hou

Meng

et al. 2017

J of Periodontal Research

View full text Add to dashboard Cite

show abstract

“…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. Furthermore, we reported the constitutive expression of chemokines and cytokines, such as keratinocyte-derived chemokine, macrophage inflammatory protein-2, and interleukin-1β, in the JE9.…”

mentioning

confidence: 86%

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

Yajima-Himuro

Oshima

Yamamoto

et al. 2014

Sci Rep

View full text Add to dashboard Cite

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.

show abstract

“…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%

The oral microbiome and the immunobiology of periodontal disease and caries

2014

View full text Add to dashboard Cite

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.

show abstract

The distribution and expression of S100A8 and S100A9 in gingival epithelium of mice

Cited by 24 publications

References 35 publications

Proinflammatory effects and mechanisms of calprotectin on human gingival fibroblasts

Proinflammatory effects and mechanisms of calprotectin on human gingival fibroblasts

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

The oral microbiome and the immunobiology of periodontal disease and caries

Contact Info

Product

Resources

About