Mechanical signaling for bone modeling and remodeling

Alexander Robling, Charles H. Turner

Research output: Contribution to journalArticle

129 Citations (Scopus)

Abstract

Proper development of the skeleton in utero and during growth requires mechanical stimulation. Loading results in adaptive changes in bone that strengthen bone structure. Bone's adaptive response is regulated by the ability of resident bone cells to perceive and translate mechanical energy into a cascade of structural and biochemical changes within the cells a process known as mechanotransduction. Mechanotransduction pathways are among the most anabolic in bone, and consequently, there is great interest in elucidating how mechanical loading produces its observed effects, including increased bone formation, reduced bone loss, changes in bone cell differentiation and lifespan, among others. A molecular understanding of these processes is developing, and with it comes a profound new insight into the biology of bone. In this article, we review the nature of the physical stimulus to which bone cells mount an adaptive response, including the identity of the sensor cells, their attributes and physical environment, and putative mechanoreceptors they express. Particular attention is allotted to the focal adhesion and Wnt signaling, in light of their emerging role in bone mechanotransduction. Te cellular mechanisms for increased bone loss during disuse, and reduced bone loss during loading are considered. Finally, we summarize the published data on bone cell accommodation, whereby bone cells stop responding to mechanical signaling events. Collectively, these data highlight the complex yet finely orchestrated process of mechanically regulated bone homeostasis.

Original languageEnglish
Pages (from-to)319-338
Number of pages20
JournalCritical Reviews in Eukaryotic Gene Expression
Volume19
Issue number4
StatePublished - 2009

Fingerprint

Bone Remodeling
Bone and Bones
Mechanoreceptors
Focal Adhesions
Osteogenesis
Skeleton
Cell Differentiation

Keywords

  • Adaptation
  • Bone mechanotransduction
  • Bone modeling
  • Bone strength
  • Bone turnover
  • Desensitization
  • Focal adhesion
  • Mechanical loading
  • Nitric oxide
  • Osteoblasts
  • Osteocytes
  • Prostaglandin
  • Wnt signaling

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics

Cite this

Mechanical signaling for bone modeling and remodeling. / Robling, Alexander; Turner, Charles H.

In: Critical Reviews in Eukaryotic Gene Expression, Vol. 19, No. 4, 2009, p. 319-338.

Research output: Contribution to journalArticle

@article{c9328fbd255f4ae3975706209aa6f88e,
title = "Mechanical signaling for bone modeling and remodeling",
abstract = "Proper development of the skeleton in utero and during growth requires mechanical stimulation. Loading results in adaptive changes in bone that strengthen bone structure. Bone's adaptive response is regulated by the ability of resident bone cells to perceive and translate mechanical energy into a cascade of structural and biochemical changes within the cells a process known as mechanotransduction. Mechanotransduction pathways are among the most anabolic in bone, and consequently, there is great interest in elucidating how mechanical loading produces its observed effects, including increased bone formation, reduced bone loss, changes in bone cell differentiation and lifespan, among others. A molecular understanding of these processes is developing, and with it comes a profound new insight into the biology of bone. In this article, we review the nature of the physical stimulus to which bone cells mount an adaptive response, including the identity of the sensor cells, their attributes and physical environment, and putative mechanoreceptors they express. Particular attention is allotted to the focal adhesion and Wnt signaling, in light of their emerging role in bone mechanotransduction. Te cellular mechanisms for increased bone loss during disuse, and reduced bone loss during loading are considered. Finally, we summarize the published data on bone cell accommodation, whereby bone cells stop responding to mechanical signaling events. Collectively, these data highlight the complex yet finely orchestrated process of mechanically regulated bone homeostasis.",
keywords = "Adaptation, Bone mechanotransduction, Bone modeling, Bone strength, Bone turnover, Desensitization, Focal adhesion, Mechanical loading, Nitric oxide, Osteoblasts, Osteocytes, Prostaglandin, Wnt signaling",
author = "Alexander Robling and Turner, {Charles H.}",
year = "2009",
language = "English",
volume = "19",
pages = "319--338",
journal = "Critical Reviews in Eukaryotic Gene Expression",
issn = "1045-4403",
publisher = "Begell House Inc.",
number = "4",

}

TY - JOUR

T1 - Mechanical signaling for bone modeling and remodeling

AU - Robling, Alexander

AU - Turner, Charles H.

PY - 2009

Y1 - 2009

N2 - Proper development of the skeleton in utero and during growth requires mechanical stimulation. Loading results in adaptive changes in bone that strengthen bone structure. Bone's adaptive response is regulated by the ability of resident bone cells to perceive and translate mechanical energy into a cascade of structural and biochemical changes within the cells a process known as mechanotransduction. Mechanotransduction pathways are among the most anabolic in bone, and consequently, there is great interest in elucidating how mechanical loading produces its observed effects, including increased bone formation, reduced bone loss, changes in bone cell differentiation and lifespan, among others. A molecular understanding of these processes is developing, and with it comes a profound new insight into the biology of bone. In this article, we review the nature of the physical stimulus to which bone cells mount an adaptive response, including the identity of the sensor cells, their attributes and physical environment, and putative mechanoreceptors they express. Particular attention is allotted to the focal adhesion and Wnt signaling, in light of their emerging role in bone mechanotransduction. Te cellular mechanisms for increased bone loss during disuse, and reduced bone loss during loading are considered. Finally, we summarize the published data on bone cell accommodation, whereby bone cells stop responding to mechanical signaling events. Collectively, these data highlight the complex yet finely orchestrated process of mechanically regulated bone homeostasis.

AB - Proper development of the skeleton in utero and during growth requires mechanical stimulation. Loading results in adaptive changes in bone that strengthen bone structure. Bone's adaptive response is regulated by the ability of resident bone cells to perceive and translate mechanical energy into a cascade of structural and biochemical changes within the cells a process known as mechanotransduction. Mechanotransduction pathways are among the most anabolic in bone, and consequently, there is great interest in elucidating how mechanical loading produces its observed effects, including increased bone formation, reduced bone loss, changes in bone cell differentiation and lifespan, among others. A molecular understanding of these processes is developing, and with it comes a profound new insight into the biology of bone. In this article, we review the nature of the physical stimulus to which bone cells mount an adaptive response, including the identity of the sensor cells, their attributes and physical environment, and putative mechanoreceptors they express. Particular attention is allotted to the focal adhesion and Wnt signaling, in light of their emerging role in bone mechanotransduction. Te cellular mechanisms for increased bone loss during disuse, and reduced bone loss during loading are considered. Finally, we summarize the published data on bone cell accommodation, whereby bone cells stop responding to mechanical signaling events. Collectively, these data highlight the complex yet finely orchestrated process of mechanically regulated bone homeostasis.

KW - Adaptation

KW - Bone mechanotransduction

KW - Bone modeling

KW - Bone strength

KW - Bone turnover

KW - Desensitization

KW - Focal adhesion

KW - Mechanical loading

KW - Nitric oxide

KW - Osteoblasts

KW - Osteocytes

KW - Prostaglandin

KW - Wnt signaling

UR - http://www.scopus.com/inward/record.url?scp=70349974398&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=70349974398&partnerID=8YFLogxK

M3 - Article

C2 - 19817708

AN - SCOPUS:70349974398

VL - 19

SP - 319

EP - 338

JO - Critical Reviews in Eukaryotic Gene Expression

JF - Critical Reviews in Eukaryotic Gene Expression

SN - 1045-4403

IS - 4

ER -