Osteocytes and mechanical loading

The Wnt connection

Whitney A. Bullock, Fredrick Pavalko, Alexander Robling

Research output: Contribution to journalArticle

Abstract

Bone adapts to the mechanical forces that it experiences. Orthodontic tooth movement harnesses the cell- and tissue-level properties of mechanotransduction to achieve alignment and reorganization of the dentition. However, the mechanisms of action that permit bone resorption and formation in response to loads placed on the teeth are incompletely elucidated, though several mechanisms have been identified. Wnt/Lrp5 signalling in osteocytes is a key pathway that modulates bone tissue's response to load. Numerous mouse models that harbour knock-in, knockout and transgenic/overexpression alleles targeting genes related to Wnt signalling point to the necessity of Wnt/Lrp5, and its localization to osteocytes, for proper mechanotransduction in bone. Alveolar bone is rich in osteocytes and is a highly mechanoresponsive tissue in which components of the canonical Wnt signalling cascade have been identified. As Wnt-based agents become clinically available in the next several years, the major challenge that lies ahead will be to gain a more complete understanding of Wnt biology in alveolar bone so that improved/expedited tooth movement becomes a possibility.

Original languageEnglish (US)
Pages (from-to)175-179
Number of pages5
JournalOrthodontics and Craniofacial Research
Volume22
Issue numberS1
DOIs
StatePublished - May 1 2019

Fingerprint

Osteocytes
Bone and Bones
Tooth Movement Techniques
Dentition
Gene Targeting
Bone Resorption
Osteogenesis
Tooth
Alleles

Keywords

  • low-density lipoprotein receptor-related protein 5
  • Sclerostin
  • Sost
  • Wnt

ASJC Scopus subject areas

  • Orthodontics
  • Surgery
  • Oral Surgery
  • Otorhinolaryngology

Cite this

Osteocytes and mechanical loading : The Wnt connection. / Bullock, Whitney A.; Pavalko, Fredrick; Robling, Alexander.

In: Orthodontics and Craniofacial Research, Vol. 22, No. S1, 01.05.2019, p. 175-179.

Research output: Contribution to journalArticle

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