Loss of Aβ-nerve endings associated with the Merkel cell-neurite complex in the lesional oral mucosa epithelium of lichen planus and hyperkeratosis
Identifieur interne : 000818 ( Pmc/Curation ); précédent : 000817; suivant : 000819Loss of Aβ-nerve endings associated with the Merkel cell-neurite complex in the lesional oral mucosa epithelium of lichen planus and hyperkeratosis
Auteurs : Daniela Calder N Carri N [Allemagne] ; Yüksel Korkmaz [Allemagne] ; Britta Cho [Allemagne] ; Marion Kopp [Allemagne] ; Wilhelm Bloch [Allemagne] ; Klaus Addicks [Allemagne] ; Wilhelm Niedermeier [Allemagne]Source :
- International Journal of Oral Science [ 1674-2818 ] ; 2015.
Abstract
The Merkel cell-neurite complex initiates the perception of touch and mediates Aβ slowly adapting type I responses. Lichen planus is a chronic inflammatory autoimmune disease with T-cell-mediated inflammation, whereas hyperkeratosis is characterized with or without epithelial dysplasia in the oral mucosa. To determine the effects of lichen planus and hyperkeratosis on the Merkel cell-neurite complex, healthy oral mucosal epithelium and lesional oral mucosal epithelium of lichen planus and hyperkeratosis patients were stained by immunohistochemistry (the avidin-biotin-peroxidase complex and double immunofluorescence methods) using pan cytokeratin, cytokeratin 20 (K20, a Merkel cell marker), and neurofilament 200 (NF200, a myelinated Aβ- and Aδ-nerve fibre marker) antibodies. NF200-immunoreactive (ir) nerve fibres in healthy tissues and in the lesional oral mucosa epithelium of lichen planus and hyperkeratosis were counted and statistically analysed. In the healthy oral mucosa, K20-positive Merkel cells with and without close association to the intraepithelial NF200-ir nerve fibres were detected. In the lesional oral mucosa of lichen planus and hyperkeratosis patients, extremely rare NF200-ir nerve fibres were detected only in the lamina propria. Compared with healthy tissues, lichen planus and hyperkeratosis tissues had significantly decreased numbers of NF200-ir nerve fibres in the oral mucosal epithelium. Lichen planus and hyperkeratosis were associated with the absence of Aβ-nerve endings in the oral mucosal epithelium. Thus, we conclude that mechanosensation mediated by the Merkel cell-neurite complex in the oral mucosal epithelium is impaired in lichen planus and hyperkeratosis.
Url:
DOI: 10.1038/ijos.2015.31
PubMed: 27025263
PubMed Central: 4822177
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<front><div type="abstract" xml:lang="en"><p>The Merkel cell-neurite complex initiates the perception of touch and mediates Aβ slowly adapting type I responses. Lichen planus is a chronic inflammatory autoimmune disease with T-cell-mediated inflammation, whereas hyperkeratosis is characterized with or without epithelial dysplasia in the oral mucosa. To determine the effects of lichen planus and hyperkeratosis on the Merkel cell-neurite complex, healthy oral mucosal epithelium and lesional oral mucosal epithelium of lichen planus and hyperkeratosis patients were stained by immunohistochemistry (the avidin-biotin-peroxidase complex and double immunofluorescence methods) using pan cytokeratin, cytokeratin 20 (K20, a Merkel cell marker), and neurofilament 200 (NF200, a myelinated Aβ- and Aδ-nerve fibre marker) antibodies. NF200-immunoreactive (ir) nerve fibres in healthy tissues and in the lesional oral mucosa epithelium of lichen planus and hyperkeratosis were counted and statistically analysed. In the healthy oral mucosa, K20-positive Merkel cells with and without close association to the intraepithelial NF200-ir nerve fibres were detected. In the lesional oral mucosa of lichen planus and hyperkeratosis patients, extremely rare NF200-ir nerve fibres were detected only in the lamina propria. Compared with healthy tissues, lichen planus and hyperkeratosis tissues had significantly decreased numbers of NF200-ir nerve fibres in the oral mucosal epithelium. Lichen planus and hyperkeratosis were associated with the absence of Aβ-nerve endings in the oral mucosal epithelium. Thus, we conclude that mechanosensation mediated by the Merkel cell-neurite complex in the oral mucosal epithelium is impaired in lichen planus and hyperkeratosis.</p>
</div>
</front>
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<front><journal-meta><journal-id journal-id-type="nlm-ta">Int J Oral Sci</journal-id>
<journal-id journal-id-type="iso-abbrev">Int J Oral Sci</journal-id>
<journal-title-group><journal-title>International Journal of Oral Science</journal-title>
</journal-title-group>
<issn pub-type="ppub">1674-2818</issn>
<issn pub-type="epub">2049-3169</issn>
<publisher><publisher-name>Nature Publishing Group</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">27025263</article-id>
<article-id pub-id-type="pmc">4822177</article-id>
<article-id pub-id-type="pii">ijos201531</article-id>
<article-id pub-id-type="doi">10.1038/ijos.2015.31</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Original Article</subject>
</subj-group>
</article-categories>
<title-group><article-title>Loss of A<italic>β</italic>
-nerve endings associated with the Merkel cell-neurite complex in the lesional oral mucosa epithelium of lichen planus and hyperkeratosis</article-title>
<alt-title alt-title-type="running">Merkel cell-neurite complex in health and disease</alt-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Carrión</surname>
<given-names>Daniela Calderón</given-names>
</name>
<xref ref-type="aff" rid="aff1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Korkmaz</surname>
<given-names>Yüksel</given-names>
</name>
<xref ref-type="aff" rid="aff1">1</xref>
<xref ref-type="aff" rid="aff2">2</xref>
<xref ref-type="aff" rid="aff3">3</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Cho</surname>
<given-names>Britta</given-names>
</name>
<xref ref-type="aff" rid="aff2">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Kopp</surname>
<given-names>Marion</given-names>
</name>
<xref ref-type="aff" rid="aff1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Bloch</surname>
<given-names>Wilhelm</given-names>
</name>
<xref ref-type="aff" rid="aff4">4</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Addicks</surname>
<given-names>Klaus</given-names>
</name>
<xref ref-type="aff" rid="aff3">3</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Niedermeier</surname>
<given-names>Wilhelm</given-names>
</name>
<xref ref-type="aff" rid="aff1">1</xref>
</contrib>
<aff id="aff1"><label>1</label>
<institution>Department of Prosthetic Dentistry, Dental School, University of Cologne</institution>
, Cologne,<country>Germany</country>
</aff>
<aff id="aff2"><label>2</label>
<institution>Center for Biochemistry, Institute for Experimental Dental Research and Oral Musculoskeletal Biology, Medical Faculty, University of Cologne</institution>
, Cologne,<country>Germany</country>
</aff>
<aff id="aff3"><label>3</label>
<institution>Department of Anatomy, University of Cologne</institution>
, Cologne,<country>Germany</country>
</aff>
<aff id="aff4"><label>4</label>
<institution>Department of Molecular and Cellular Sport Medicine, German Sport University</institution>
, Cologne,<country>Germany</country>
</aff>
</contrib-group>
<author-notes><corresp id="caf1"><label>*</label>
<institution>Center for Biochemistry, Institute for Dental Research and Oral Musculoskeletal Biology, Medical Faculty, University of Cologne</institution>
, Kerpener-Street 32, Cologne 50931, <country>Germany</country>
E-mail: <email>yueksel.korkmaz@uk-koeln.de</email>
</corresp>
</author-notes>
<pub-date pub-type="ppub"><month>03</month>
<year>2016</year>
</pub-date>
<pub-date pub-type="epub"><day>23</day>
<month>10</month>
<year>2015</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>1</day>
<month>3</month>
<year>2016</year>
</pub-date>
<volume>8</volume>
<issue>1</issue>
<fpage>32</fpage>
<lpage>38</lpage>
<history><date date-type="accepted"><day>15</day>
<month>07</month>
<year>2015</year>
</date>
</history>
<permissions><copyright-statement>Copyright © 2015 West China School of Stomatology</copyright-statement>
<copyright-year>2015</copyright-year>
<copyright-holder>West China School of Stomatology</copyright-holder>
<license license-type="open-access" xlink:href="http://creativecommons.org/licenses/by-nc-nd/4.0/"><pmc-comment>author-paid</pmc-comment>
<license-p>This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 Unported License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit <ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by-nc-nd/4.0/">http://creativecommons.org/licenses/by-nc-nd/4.0/</ext-link>
</license-p>
</license>
</permissions>
<abstract><p>The Merkel cell-neurite complex initiates the perception of touch and mediates Aβ slowly adapting type I responses. Lichen planus is a chronic inflammatory autoimmune disease with T-cell-mediated inflammation, whereas hyperkeratosis is characterized with or without epithelial dysplasia in the oral mucosa. To determine the effects of lichen planus and hyperkeratosis on the Merkel cell-neurite complex, healthy oral mucosal epithelium and lesional oral mucosal epithelium of lichen planus and hyperkeratosis patients were stained by immunohistochemistry (the avidin-biotin-peroxidase complex and double immunofluorescence methods) using pan cytokeratin, cytokeratin 20 (K20, a Merkel cell marker), and neurofilament 200 (NF200, a myelinated Aβ- and Aδ-nerve fibre marker) antibodies. NF200-immunoreactive (ir) nerve fibres in healthy tissues and in the lesional oral mucosa epithelium of lichen planus and hyperkeratosis were counted and statistically analysed. In the healthy oral mucosa, K20-positive Merkel cells with and without close association to the intraepithelial NF200-ir nerve fibres were detected. In the lesional oral mucosa of lichen planus and hyperkeratosis patients, extremely rare NF200-ir nerve fibres were detected only in the lamina propria. Compared with healthy tissues, lichen planus and hyperkeratosis tissues had significantly decreased numbers of NF200-ir nerve fibres in the oral mucosal epithelium. Lichen planus and hyperkeratosis were associated with the absence of Aβ-nerve endings in the oral mucosal epithelium. Thus, we conclude that mechanosensation mediated by the Merkel cell-neurite complex in the oral mucosal epithelium is impaired in lichen planus and hyperkeratosis.</p>
</abstract>
<kwd-group><kwd>Aβ-nerve fibres</kwd>
<kwd>hyperkeratosis</kwd>
<kwd>lichen planus</kwd>
<kwd>mechanosensation</kwd>
<kwd>Merkel cell-neurite complex</kwd>
</kwd-group>
</article-meta>
</front>
<floats-group><fig id="fig1"><label>Figure 1</label>
<caption><p><bold>The expression of pK in keratinocytes and K20 in Merkel cells and the localization of NF200 in nerve fibres of healthy human oral mucosa.</bold>
(<bold>a</bold>
) In the healthy oral mucosal epithelium, pK is detected with different staining intensities (dependent on the epithelial layer) in keratinocytes and in Merkel cells of the oral mucosal epithelium. (<bold>b</bold>
) K20 is identified only in Merkel cells located at the basal layer of the epithelium. (<bold>c</bold>
and <bold>d</bold>
) NF200 is located in nerve fibres and nerve endings distributed in the intraepithelial area (one asterisk), in the basal layer of the epithelium (two asterisks) and in the lamina propria of the healthy oral mucosa. (<bold>e</bold>
) DRAQ5 (chromosome marker) is identified in cell nuclei of the keratinocytes (blue). Intraepithelial NF200-ir nerve fibres (green) are detected in association (yellow) with the K20-ir Merkel (red) cells at the basal layer of the epithelium. Note that some intraepithelial NF200-ir nerve fibres are not associated with the Merkel cells (arrows). Bars: a–d = 50 µm; e = 10 µm. bl, basal layer; ir, immunoreactive; K20, cytokeratin 20; lp, lamina propria; NF200, neurofilament 200; ome, oral mucosal epithelium; pK, pan cytokeratin.</p>
</caption>
<graphic xlink:href="ijos201531f1"></graphic>
</fig>
<fig id="fig2"><label>Figure 2</label>
<caption><p><bold>The expression of pK in keratinocytes and K20 in Merkel cells and the localization of NF200 in nerve fibres of the lesional human oral mucosa of lichen planus.</bold>
(<bold>a</bold>
) In lichen planus, the epithelium is thin, and rete pegs are not identified by H&E staining. (<bold>b</bold>
) The basal layer is not intact, and there are numerous lymphocytes with chronic inflammation in the lamina propria (detail of the squared area in <bold>a</bold>
). (<bold>c</bold>
) Keratinocytes are moderately positive for pK. Merkel cells are strongly positive for pK. (<bold>d</bold>
) Only Merkel cells located at the basal layer are positive for K20. (<bold>e</bold>
and <bold>f</bold>
) Compared with the healthy oral mucosa, the lesional oral mucosa of lichen planus is associated with a significantly decreased number of NF200-ir nerve fibres distributed in the lamina propria (asterisks). (<bold>g</bold>
) DRAQ5 is detected in the nuclei of cells of the diseased lichen planus tissue section. NF200-ir nerve fibres and nerve endings associated with the K20-ir Merkel cells are not detected. (<bold>h</bold>
) The lesional oral mucosa of lichen planus is associated with a significantly decreased number of NF200-ir nerve fibres compared with the healthy oral mucosa. Bar: a = 1 mm; b-f = 50 μm; g = 20 µm. bl, basal layer; H&E, hematoxylin and eosin; ir, immunoreactive; K20, cytokeratin 20; lp, lamina propria; NF200, neurofilament 200; ome, oral mucosal epithelium; pK, pan cytokeratin.</p>
</caption>
<graphic xlink:href="ijos201531f2"></graphic>
</fig>
<fig id="fig3"><label>Figure 3</label>
<caption><p><bold>The expression of pK in keratinocytes and K20 in Merkel cells and the localization of NF200 in nerve fibres of the lesional human oral mucosa of hyperkeratosis.</bold>
(<bold>a</bold>
and <bold>b</bold>
) In hyperkeratosis, the numerous great oval basal epithelial cell extensions at the basal cell layer are identified by H&E staining (<bold>b</bold>
= detail of the squared area in <bold>a</bold>
). (<bold>c</bold>
) Except for in the basal layer, keratinocytes and Merkel cells stain positively for pK. (<bold>d</bold>
) Merkel cells distributed in the basal layer are strongly ir for K20. (<bold>e</bold>
) NF200-ir is not detectable in the nerve fibres of the lesional epithelium of hyperkeratosis. (<bold>f</bold>
) NF200 is identified only in single nerve fibres in the lamina propria (asterisks). (<bold>g</bold>
) NF200-ir nerve fibres and nerve endings are not detected in relation to K20-ir Merkel cells of the lesional oral mucosal epithelium of hyperkeratosis. (<bold>h</bold>
) Compared with healthy oral mucosa, lesional oral mucosa of hyperkeratosis is associated with a significantly decreased number of NF200-ir nerve fibres. Bars: a = 1 mm; b–f = 50 µm, g = 20 µm. bl, basal layer; H&E, hematoxylin and eosin; ir, immunoreactive; K20, cytokeratin 20; lp, lamina propria; NF200, neurofilament 200; ome, oral mucosal epithelium; pK, pan cytokeratin.</p>
</caption>
<graphic xlink:href="ijos201531f3"></graphic>
</fig>
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