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Author Notes:

Corresponding author: M. Neale Weitzmann, Ph.D. (mweitzm@emory.edu) or Ighovwerha Ofotokun, M.D., M.Sc. (iofotok@emory.edu).

Subject:

Research Funding:

The authors gratefully acknowledge financial support by NIAMS (AR059364) to M.N.W. and I.O. M.N.W. is also supported by NIAMS grants AR056090 and AR053607 and by the Biomedical Laboratory Research & Development Service of the VA Office of Research and Development (5I01BX000105). I.O. is also supported in part by K23 (A1073119) from NIAID. The author’s research activities are also supported in part by Atlanta Clinical and Translational Science Institute (UL1 RR025008) and Emory Center for AIDS Research (P30 AI050409).

HIV and Bone Metabolism

Tools:

Journal Title:

Discovery Medicine

Volume:

Volume 11, Number 60

Publisher:

, Pages 385-393

Type of Work:

Article | Post-print: After Peer Review

Abstract:

The skeleton is an organ whose integrity is maintained by constant lifelong renewal involving coordinated removal of worn bone by osteoclasts and resynthesis of new bone by osteoblasts. In young adult humans and animals this process is homeostatic with no net gain or loss of bone mass. With natural aging and exacerbated by numerous pathological conditions, bone removal exceeds bone formation, disrupting homeostasis and resulting in bone loss. Over time, skeletal decline reaches clinical significance with development of osteopenia and eventually osteoporosis, conditions that dramatically increase bone fragility and the risk of fracture. Bone fractures can be devastating with significant morbidity and mortality. Over the last decade, it has become clear that skeletal renewal is strongly influenced by the immune system, a consequence of deep integration and centralization of common cell types and cytokine mediators, which we have termed the “immuno-skeletal interface.” Consequently, dysregulated skeletal renewal and bone loss is a common feature of inflammatory conditions associated with immune activation. Interestingly, bone loss is also associated with conditions of immunodeficiency, including infection by the human immunodeficiency virus (HIV) that leads to acquired immunodeficiency syndrome (AIDS). Disruptions to the immuno-skeletal interface drive skeletal deterioration contributing to a high rate of bone fracture in HIV infection. This review examines current knowledge concerning the prevalence and etiology of skeletal complications in HIV infection, the effect of antiretroviral therapies (ART) on the skeleton, and how disruption of the immuno-skeletal interface may underlie bone loss in HIV infection and ART.

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© Discovery Medicine. All rights reserved.

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