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Cellular and Molecular Pathways Leading to External Root Resorption.

A Iglesias-Linares1, J K Hartsfield2

  • 11 Department of Orthodontics, School of Dentistry, Complutense University of Madrid, Madrid, Spain.

Journal of Dental Research
|November 5, 2016
PubMed
Summary
This summary is machine-generated.

Orthodontic treatment can cause external apical root resorption by activating specific cells. Understanding the molecular pathways and cellular balance, particularly macrophages, is key to managing root resorption and promoting repair.

Keywords:
dental cementumdentinmolecular mechanismsorthodonticsroot caries/resorptiontooth movement

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Area of Science:

  • Biomedical Science
  • Oral Biology
  • Orthodontics

Background:

  • External apical root resorption (EARR) is a complex biological process occurring during orthodontic treatment.
  • Molecular, genomic, and proteomic studies have shed light on the cellular and molecular mechanisms underlying EARR.
  • The balance between pro-resorptive and anti-resorptive cellular activities is crucial in EARR and root repair.

Purpose of the Study:

  • To review recent molecular mechanisms and developments in external apical root resorption.
  • To elucidate the role of different macrophage phenotypes (M1 and M2) in root resorption and repair.
  • To explore the molecular pathways involved in clastic cell adhesion, fusion, activation, and the regulation of root repair.

Main Methods:

  • Review of in vitro and in vivo molecular, genomic, and proteomic studies.
  • Analysis of cellular components, including macrophage phenotypes (M1 and M2) and mesenchymal dental pulp cells.
  • Examination of molecular pathways such as RANKL/RANK/OPG, ATP-P2RX7-IL1, and the roles of specific cytokines and proteins.

Main Results:

  • M1 macrophages (CD68+, iNOS+) are associated with root resorption, while M2 macrophages (CD68+, CD163+) are linked to root repair.
  • Key molecules involved include tumor necrosis factor, inducible nitric oxide synthase, interferon γ, interleukin 4, interleukin 10, and arginase I.
  • Molecular pathways regulating clastic cell adhesion (integrins, osteopontin) and fusion/activation (RANKL/RANK/OPG, ATP-P2RX7-IL1) are critical in EARR.

Conclusions:

  • The balance of macrophage polarization and specific molecular signaling pathways are central to external apical root resorption and repair during orthodontics.
  • Mesenchymal dental pulp cells play a role in attenuating dentin resorption.
  • Further understanding of these pathways can inform strategies to manage EARR and enhance root repair.