HIV: Inflammation and Bone

• Type of Material: Article
• Authors: Igho Ofotokun, Emory University; Emily McIntosh, Emory University; M Neale Weitzmann, Emory University
• Language: English
• Date: 2012-03
• Publisher: Springer (part of Springer Nature): Springer Open Choice Hybrid Journals
• Publication Version: Author Accepted Manuscript (After Peer Review)
• Copyright Statement: © Springer Science+Business Media, LLC 2011
• Final Published Version (URL): http://link.springer.com/article/10.1007%2Fs11904-011-0099-z
• Title of Journal or Parent Work: Current HIV/AIDS Reports
• ISSN: 1548-3568
• Volume: 9
• Issue: 1
• Start Page: 16
• End Page: 25
• Grant/Funding Information: Authors’ translational research activities are also supported in part by the Emory Center for AIDS Research CFAR, NIH Grant P30 AI050409, and the Atlanta Clinical and Translational Science Institute (ACTSI), NIH Grant MO1RR00039.; IO and MNW research is supported by NIAMS grant AR059364 and NIA grant AG040013.; MNW is also supported by the Biomedical Laboratory Research and Development Service of the VA Office of Research and Development (5I01BX000105) and by NIAMS grants AR056090 and AR053607.; IO is also supported in part by K23 A1073119 from NIAID.
• Keywords: AIDS; inflammation; HIV; immune-skeletal interface; osteoporosis
• Research Categories: Health Sciences, Pathology

Abstract

HIV infection and antiretroviral therapy (ART) are now established independent risk factors for osteoporosis. With a spate of recent studies reporting significant elevations in fracture prevalence in HIV patients, and a rapidly aging demographic, defining the mechanisms underlying HIV/ART-induced skeletal decline has become imperative. The recent emergence of the field of “osteoimmunology” has provided a conceptual framework to explain how the immune and skeletal systems interact. Furthermore, it is becoming clear that inflammatory states leading to perturbations in the immuno-skeletal interface, a convergence of common cells and cytokine mediators that regulate both immune and skeletal systems, conspire to imbalance bone turnover and induce osteoporosis. In this review we examine the role of inflammation in the bone loss associated with diverse inflammatory conditions and new concepts into how the underlying mechanisms by which inflammation and immune dysregulation impact bone turnover may be pertinent to the mechanisms involved in HIV/ART-induced bone loss.