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Related Concept Videos

Canonical Wnt Signaling Pathway02:54

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The gene encoding the main signaling molecules of the Wnt signaling pathways (the Wnt proteins) was discovered almost four decades ago by Nüsslein-Volhard and Wieschaus. They identified and originally named the gene "wingless" (wg) after a phenotype discovered during their landmark genetic screen in Drosophila for body pattern defects. At around the same time, another researcher named Harold Varmus found that a murine tumor virus activates the mammalian wg homolog, Int-1, which...
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Wnt is a zygotic effect gene that is expressed during very early embryonic development. It regulates various processes in animals starting from early development through the adult stage, such as organogenesis in the embryo and maintenance of neuronal and blood stem cells. Wnt proteins can induce a wide variety of intracellular pathways depending upon the specific abilities of different Wnt ligands to form a complex with shared and cognate receptors in the presence of different co-receptors. The...
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Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
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The Notch signaling pathway is a major intracellular signaling pathway that is highly conserved over a broad spectrum of metazoan species. It stands unique from other intracellular signaling mechanisms in animals because notch protein itself acts as the receptor as well as the primary signaling molecule.
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Induction of Periodontitis via a Combination of Ligature and Lipopolysaccharide Injection in a Rat Model
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Wnt signaling in periodontitis.

Zeliha Güney1,2, Şivge Kurgan3, Canan Önder1

  • 1Faculty of Dentistry Department of Periodontology, Ankara University, 06500-Cankaya, Ankara, Turkey.

Clinical Oral Investigations
|October 9, 2023
PubMed
Summary

Periodontitis disrupts the Wnt/β-catenin signaling pathway in gingival tissues, indicated by elevated Wnt protein levels and altered β-catenin localization. This disruption correlates with inflammation and tissue destruction in periodontal disease.

Keywords:
PeriodontitisWnt 10bWnt 3aWnt 5aβ-Catenin

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Area of Science:

  • Oral biology
  • Molecular biology
  • Immunology

Background:

  • The Wnt/β-catenin signaling pathway is crucial for tissue homeostasis and development.
  • Periodontitis is a chronic inflammatory disease leading to periodontal tissue destruction.

Purpose of the Study:

  • To investigate the activity of the Wnt/β-catenin signaling pathway in gingival tissues of periodontitis patients.
  • To correlate Wnt pathway alterations with the inflammatory state and tissue destruction in periodontitis.

Main Methods:

  • Quantitative PCR (Q-PCR) to measure Wnt 3a, Wnt 5a, Wnt 10b, and β-catenin gene expression.
  • Immunohistochemical analysis to determine the topographic localization of β-catenin, Wnt 5a, and Wnt 10b proteins.
  • Assessment of TNF-α for inflammatory status and Runx2 as a mediator of destruction.

Main Results:

  • Significantly higher expressions of Wnt 3a, Wnt 5a, and Wnt 10b in periodontitis tissues compared to controls (p < 0.05).
  • Intranuclear β-catenin staining observed in connective tissue of periodontitis patients, contrasting with intracytoplasmic staining in controls.
  • Elevated Wnt5a and Wnt10b protein levels in connective tissues of periodontitis patients, particularly in Stage III Grade C.

Conclusions:

  • Periodontal inflammation associated with periodontitis disrupts the Wnt/β-catenin signaling pathway.
  • Altered Wnt signaling contributes to tissue homeostasis disruption and host-induced tissue destruction in periodontitis pathogenesis.
  • Findings highlight the role of Wnt pathway dysregulation in the immunoinflammatory response during periodontal disease.