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The role of the immune system in the pathophysiology of osteoporosis

Authors


* Dr Jackie Clowes
Mayo Clinic College of Medicine
Endocrine Research Unit
Joseph 5-194
St Mary's Hospital
Rochester, MN 55905
USA
Tel.: +1 507 2556788
Fax: +1 507 2554828
E-mail: clowes.jackie@mayo.edu

Abstract

Summary:  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.

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