Osteocyte-driven bone remodeling

Research output: Contribution to journalReview article

144 Citations (Scopus)

Abstract

Osteocytes, the most abundant cells in bone, have been long postulated to detect and respond to mechanical and hormonal stimuli and to coordinate the function of osteoblasts and osteoclasts. The discovery that the inhibitor of bone formation sclerostin is primarily expressed in osteocytes in bone and downregulated by anabolic stimuli provided a mechanism by which osteocytes influence the activity of osteoblasts. Advances of the last few years provided experimental evidence demonstrating that osteocytes also participate in the recruitment of osteoclasts and the initiation of bone remodeling. Apoptotic osteocytes trigger yet-to-be-identified signals that attract osteoclast precursors to specific areas of bone, which in turn differentiate to mature, bone-resorbing osteoclasts. Osteocytes are also the source of molecules that regulate the generation and activity of osteoclasts, such as OPG and RANKL; and genetic manipulations of the mouse genome leading to loss or gain of function or to altered expression of either molecule in osteocytes markedly affect bone resorption. This review highlights these investigations and discusses how the novel concept of osteocyte-driven bone resorption and formation impacts our understanding of the mechanisms by which current therapies control bone remodeling.

Original languageEnglish (US)
Pages (from-to)25-34
Number of pages10
JournalCalcified Tissue International
Volume94
Issue number1
DOIs
StatePublished - Jan 1 2014

Fingerprint

Osteocytes
Bone Remodeling
Osteoclasts
Bone and Bones
Bone Resorption
Osteoblasts
Osteogenesis
Down-Regulation
Genome

Keywords

  • Bone remodeling
  • OPG
  • Osteoblast
  • Osteoclast
  • Osteocyte
  • RANKL
  • Sost

ASJC Scopus subject areas

  • Orthopedics and Sports Medicine
  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

Cite this

Osteocyte-driven bone remodeling. / Bellido, Teresita.

In: Calcified Tissue International, Vol. 94, No. 1, 01.01.2014, p. 25-34.

Research output: Contribution to journalReview article

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