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Related Concept Videos

Notch Signaling Pathway03:14

Notch Signaling Pathway

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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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Nitric oxide (NO), an inorganic gas, acts as a potent second messenger in most animal and plant tissues. NO diffuses out of the cells that produce it and enters the neighboring cells to generate a downstream response. NO synthase (NOS) catalyzes NO production by the deamination of the amino acid arginine. There are three isoforms of NOS. Endothelial cells have endothelial NOS (eNOS), nerve and muscle cells have neuronal NOS (nNOS), and macrophages produce inducible NOS (iNOS) upon exposure...
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Related Experiment Video

Updated: Jun 7, 2025

Isolation, Processing and Analysis of Murine Gingival Cells
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CCN2: A potential contributor to gingival overgrowth.

Asmaa Fadl1, Andrew Leask1

  • 1College of Dentistry, University of Saskatchewan, 105 Wiggins Rd, Saskatoon, SK, S7H 2E5, Canada.

Journal of Oral Biosciences
|November 9, 2024
PubMed
Summary

Gingival overgrowth (GO) involves hyperproliferation, not scarring. Matricellular protein CCN2 is implicated in GO development and recurrence, suggesting it as a potential therapeutic target for non-invasive treatment.

Keywords:
CCNExtracellular matrixFibrosisGingival fibroblastsGingival overgrowth

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Area of Science:

  • Oral biology
  • Fibrosis research
  • Cellular signaling

Background:

  • Gingival overgrowth (GO) presents as hyperproliferative fibrotic responses, distinct from typical scar tissue.
  • GO can be drug-induced or genetic, often recurs post-surgery, necessitating non-invasive treatments.
  • Matricellular protein CCN2 is a known factor in other fibrotic conditions but is understudied in GO.

Purpose of the Study:

  • To review the current understanding of CCN2 expression in gingival overgrowth.
  • To explore the potential role of CCN2 as a therapeutic target for gingival overgrowth.

Main Methods:

  • Literature review of studies on CCN2 expression in gingival fibroblasts and GO.
  • Analysis of factors known to induce fibrogenesis and GO in relation to CCN2.

Main Results:

  • CCN2 expression is induced by transforming growth factor-β, a promoter of oral fibrogenesis.
  • Specific drugs causing GO, including cyclosporine, nifedipine, and phenytoin, also induce CCN2.

Conclusions:

  • CCN2 expression correlates with gingival overgrowth and its recurrence.
  • Further research into CCN2's function in GO is warranted to develop novel therapeutic strategies.