The role of the immune system in the pathophysiology of osteoporosis

Jackie A. Clowes, B. Lawrence Riggs, Sundeep Khosla

Research output: Contribution to journalArticle

231 Citations (Scopus)

Abstract

The role of the immune system in the development of senile osteoporosis, which arises primarily through the effects of estrogen deficiency and secondary hyperparathyroidism, is slowly being unraveled. This review focuses on our current understanding of how the components of this complex-interlinked system are regulated and how these fit with previous models of senile and postmenopausal osteoporosis. There is certainly substantial evidence that bone remodeling is a tightly regulated, finely balanced process influenced by subtle changes in proinflammatory and inhibitory cytokines as well as hormones and cellular components that act primarily but not exclusively through the receptor activator of nuclear factor-κB (RANK)/RANK ligand/ osteoprotegerin system. In addition, an acute or chronic imbalance in the system due to infection or inflammation could contribute to systemic (or local) bone loss and increase the risk of fracture. Although significant progress has been made, there remains much to be done in unraveling this complex interaction between the immune system and bone.

Original languageEnglish (US)
Pages (from-to)207-227
Number of pages21
JournalImmunological Reviews
Volume208
DOIs
StatePublished - Dec 2005

Fingerprint

Osteoporosis
Immune System
RANK Ligand
Osteoprotegerin
Bone and Bones
Postmenopausal Osteoporosis
Secondary Hyperparathyroidism
Bone Remodeling
Cytoplasmic and Nuclear Receptors
Estrogens
Hormones
Cytokines
Inflammation
Infection

ASJC Scopus subject areas

  • Immunology

Cite this

The role of the immune system in the pathophysiology of osteoporosis. / Clowes, Jackie A.; Riggs, B. Lawrence; Khosla, Sundeep.

In: Immunological Reviews, Vol. 208, 12.2005, p. 207-227.

Research output: Contribution to journalArticle

Clowes, Jackie A. ; Riggs, B. Lawrence ; Khosla, Sundeep. / The role of the immune system in the pathophysiology of osteoporosis. In: Immunological Reviews. 2005 ; Vol. 208. pp. 207-227.
@article{a9f75dfe8ea64e2bbaf111a8ee78df3a,
title = "The role of the immune system in the pathophysiology of osteoporosis",
abstract = "The role of the immune system in the development of senile osteoporosis, which arises primarily through the effects of estrogen deficiency and secondary hyperparathyroidism, is slowly being unraveled. This review focuses on our current understanding of how the components of this complex-interlinked system are regulated and how these fit with previous models of senile and postmenopausal osteoporosis. There is certainly substantial evidence that bone remodeling is a tightly regulated, finely balanced process influenced by subtle changes in proinflammatory and inhibitory cytokines as well as hormones and cellular components that act primarily but not exclusively through the receptor activator of nuclear factor-κB (RANK)/RANK ligand/ osteoprotegerin system. In addition, an acute or chronic imbalance in the system due to infection or inflammation could contribute to systemic (or local) bone loss and increase the risk of fracture. Although significant progress has been made, there remains much to be done in unraveling this complex interaction between the immune system and bone.",
author = "Clowes, {Jackie A.} and Riggs, {B. Lawrence} and Sundeep Khosla",
year = "2005",
month = "12",
doi = "10.1111/j.0105-2896.2005.00334.x",
language = "English (US)",
volume = "208",
pages = "207--227",
journal = "Immunological Reviews",
issn = "0105-2896",
publisher = "Wiley-Blackwell",

}

TY - JOUR

T1 - The role of the immune system in the pathophysiology of osteoporosis

AU - Clowes, Jackie A.

AU - Riggs, B. Lawrence

AU - Khosla, Sundeep

PY - 2005/12

Y1 - 2005/12

N2 - The role of the immune system in the development of senile osteoporosis, which arises primarily through the effects of estrogen deficiency and secondary hyperparathyroidism, is slowly being unraveled. This review focuses on our current understanding of how the components of this complex-interlinked system are regulated and how these fit with previous models of senile and postmenopausal osteoporosis. There is certainly substantial evidence that bone remodeling is a tightly regulated, finely balanced process influenced by subtle changes in proinflammatory and inhibitory cytokines as well as hormones and cellular components that act primarily but not exclusively through the receptor activator of nuclear factor-κB (RANK)/RANK ligand/ osteoprotegerin system. In addition, an acute or chronic imbalance in the system due to infection or inflammation could contribute to systemic (or local) bone loss and increase the risk of fracture. Although significant progress has been made, there remains much to be done in unraveling this complex interaction between the immune system and bone.

AB - The role of the immune system in the development of senile osteoporosis, which arises primarily through the effects of estrogen deficiency and secondary hyperparathyroidism, is slowly being unraveled. This review focuses on our current understanding of how the components of this complex-interlinked system are regulated and how these fit with previous models of senile and postmenopausal osteoporosis. There is certainly substantial evidence that bone remodeling is a tightly regulated, finely balanced process influenced by subtle changes in proinflammatory and inhibitory cytokines as well as hormones and cellular components that act primarily but not exclusively through the receptor activator of nuclear factor-κB (RANK)/RANK ligand/ osteoprotegerin system. In addition, an acute or chronic imbalance in the system due to infection or inflammation could contribute to systemic (or local) bone loss and increase the risk of fracture. Although significant progress has been made, there remains much to be done in unraveling this complex interaction between the immune system and bone.

UR - http://www.scopus.com/inward/record.url?scp=28544439444&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=28544439444&partnerID=8YFLogxK

U2 - 10.1111/j.0105-2896.2005.00334.x

DO - 10.1111/j.0105-2896.2005.00334.x

M3 - Article

C2 - 16313351

AN - SCOPUS:28544439444

VL - 208

SP - 207

EP - 227

JO - Immunological Reviews

JF - Immunological Reviews

SN - 0105-2896

ER -