An immunohistochemical and monastral blue-vascular labelling study on the involvement of capsaicin-sensitive sensory innervation of the junctional epithelium in neurogenic plasma extravasation in the rat gingiva

Kondo, Teruyoshi; Kido, Mizuho A.; Kiyoshima, Tamotsu; Yamaza, Takayoshi; Takano, Teruo

doi:10.1016/0003-9969(95)00060-3

Cited by 28 publications

(29 citation statements)

References 34 publications

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“…Electron microscopy revealed TRPV2 immunoreactivity in thinly myelinated and unmyelinated axons in the submucosal layer, whereas very little immunoreactivity was observed in intraepithelial nerves. These TRPV2-immunopositive axons were fewer in number than nerves with calcitonin gene-related peptide or substance-P immunoreactivity observed in our previous studies of gingival tissue (Kondo et al 1995;Tanaka et al 1996). These results are consistent with the small number of TRPV2-immunopositive .…”

Section: Discussionsupporting

confidence: 94%

TRPV2 expression in rat oral mucosa

Shimohira

Kido

Danjo

et al. 2009

Histochem Cell Biol

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The oral mucosa is a highly specialised, stratified epithelium that confers protection from infection and physical, chemical and thermal stimuli. The non-keratinised junctional epithelium surrounds each tooth like a collar and is easily attacked by foreign substances from the oral sulcus. We found that TRPV2, a temperature-gated channel, is highly expressed in junctional epithelial cells, but not in oral sulcular epithelial cells or oral epithelial cells. Dual or triple immunolabelling with immunocompetent cell markers also revealed TRPV2 expression in Langerhans cells and in dendritic cells and macrophages. Electron microscopy disclosed TRPV2 immunoreactivity in the unmyelinated and thinly myelinated axons within the connective tissue underlying the epithelium. TRPV2 labelling was also observed in venule endothelial cells. The electron-dense immunoreaction in junctional epithelial cells, macrophages and neural axons occurred on the plasma membrane, on invaginations of the plasma membrane and in vesicular structures. Because TRPV2 has been shown to respond to temperature, hypotonicity and mechanical stimuli, gingival cells expressing TRPV2 may act as sensor cells, detecting changes in the physical and chemical environment, and may play a role in subsequent defence mechanisms.

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Section: Discussionsupporting

confidence: 94%

TRPV2 expression in rat oral mucosa

Shimohira

Kido

Danjo

et al. 2009

Histochem Cell Biol

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“…Substance P also plays a basic role in modulating blood vessels to increase blood flow and plasma leakage (Lembeck and Holzer 1979;Otsuka and Yoshida 1993). Kondo et al (1995) have shown that substance P causes vasodilation and plasma extravasation from post-capillary venules beneath the JE. Substance P released from nerves in the peri-implant mucosa may bind to the NK1 receptor of endothelial cells of blood vessels to modulate fluid flow in the peri-implant tissue as a defense mechanism.…”

Section: Discussionmentioning

confidence: 98%

“…Furthermore, we have demonstrated the dense innervation of the JE by nerve fibers derived from the trigeminal ganglion ) and by substance-P-containing nerves Kondo et al 1995;Tanaka et al 1996). Substance P is an undecapeptide that is mostly expressed in neurons, and that plays diverse roles (Nicoll et al 1980;Otsuka and Yoshida 1993).…”

Section: Introductionmentioning

confidence: 99%

Distribution of substance P and neurokinin-1 receptors in the peri-implant epithelium around titanium dental implants in rats

et al. 2008

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We examined the distribution of substance P and neurokinin-1 (NK1) receptors and substance-P-containing nerve fibers in the peri-implant mucosa around titanium dental implants in rats. Immunohistochemistry and immunocytochemistry revealed that substance-P-immunoreactive nerve fibers abundantly innervated the peri-implant epithelium (PIE) compared with other epithelia of the peri-implant mucosa. NK1 receptor mRNA and protein expression in the peri-implant mucosa were confirmed by reverse transcription with the polymerase chain reaction and immunoblotting. Immunoelectron microscopy revealed that NK1 receptor immunoreactivity was preferentially localized in peri-implant epithelial cells. NK1-receptor-positive products were found on the plasma membrane and in vesicles and granules in PIE cells. Neutrophils and intraepithelial nerve axons in the PIE were positive for the NK1 receptor. NK1 receptor immunoreactivity was also detected in endothelial cells, fibroblasts, and nerve fibers in the connective tissue beneath the PIE. These findings suggest that peri-implant tissue receives sensory information through regenerated nerves expressing substance P and the NK1 receptor. In the peri-implant mucosa, the substance P/NK1 receptor system may play a role in pain transmission, the endocytosis of neutrophils, the extravasation of crevicular fluid, and the migration of macrophages and neutrophils in response to neurogenic inflammation, as in healthy gingiva.

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“…Both neuropeptides induce vasodilation (16), local blood flow increase (15), vascular permeability enhancement (17), and pain (18,19), thus modulating inflammation (20,21). CGRP and SP are present in pulpal and gingival tissues (17,22,23) and are increased markedly in human teeth exposing pulp due to advanced caries and/or those with painful pulpitis (24,25), which suggests a modulation of pulpal inflammation by these peptides. CGRP and SP are released from neurons by activation of proteinase-activated receptors (PAR) (14), a family of four subtypes of seven transmembrane domain receptors coupled with G protein (26).…”

mentioning

confidence: 99%

Neuropeptide Release from Dental Pulp Cells by RgpB via Proteinase-Activated Receptor-2 Signaling

Tancharoen

Sarker

Imamura

et al. 2005

The Journal of Immunology

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Dental pulp inflammation often results from dissemination of periodontitis caused mostly by Porphyromonas gingivalis infection. Calcitonin gene-related peptide and substance P are proinflammatory neuropeptides that increase in inflamed pulp tissue. To study an involvement of the periodontitis pathogen and neuropeptides in pulp inflammation, we investigated human dental pulp cell neuropeptide release by arginine-specific cysteine protease (RgpB), a cysteine proteinase of P. gingivalis, and participating signaling pathways. RgpB induced neuropeptide release from cultured human pulp cells (HPCs) in a proteolytic activity-dependent manner at a range of 12.5–200 nM. HPCs expressed both mRNA and the products of calcitonin gene-related peptide, substance P, and proteinase-activated receptor-2 (PAR-2) that were also found in dental pulp fibroblast-like cells. The PAR-2 agonists, SLIGKV and trypsin, also induced neuropeptide release from HPCs, and HPC PAR-2 gene knockout by transfection of PAR-2 antisense oligonucleotides inhibited significantly the RgpB-elicited neuropeptide release. These results indicated that RgpB-induced neuropeptide release was dependent on PAR-2 activation. The kinase inhibitor profile on the RgpB-neuropeptide release from HPC revealed a new PAR-2 signaling pathway that was mediated by p38 MAPK and activated transcription factor-2 activation, in addition to the PAR-2-p44/42 p38MAPK and -AP-1 pathway. This new RgpB activity suggests a possible link between periodontitis and pulp inflammation, which may be modulated by neuropeptides released in the lesion.

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An immunohistochemical and monastral blue-vascular labelling study on the involvement of capsaicin-sensitive sensory innervation of the junctional epithelium in neurogenic plasma extravasation in the rat gingiva

Cited by 28 publications

References 34 publications

TRPV2 expression in rat oral mucosa

TRPV2 expression in rat oral mucosa

Distribution of substance P and neurokinin-1 receptors in the peri-implant epithelium around titanium dental implants in rats

Neuropeptide Release from Dental Pulp Cells by RgpB via Proteinase-Activated Receptor-2 Signaling

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