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Author Notes:

Address Correspondence to: Ighovwerha Ofotokun, Infectious Diseases, Emory University School of Medicine, 49 Jesse Hill Jr Drive, Atlanta, GA 30303; Tel: (404) 616-0659; Fax: (404) 616 0592; iofotok@emory.edu

Human and Animal Rights and Informed Consent: This article does not contain any new studies with human or animal involvement performed by the authors.

Conflicts of Interest: Dr. Caitlin A. Moran, Dr., M. Neale Weitzmann, and Dr. Ighovwerha Ofotokun declare no conflicts of interest.


Research Funding:

The authors’ research activities are supported by the National Institute on Aging (NIA) under Award Number R01AG040013 and the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) under Award Numbers R01AR059364, R01AR068157 and R01AR070091 to M.N.W. and I.O. M.N.W. is also supported by a grant from the Biomedical Laboratory Research & Development Service of the VA Office of Research and Development (5I01BX000105).

C.A.M. is supported by National Center for Advancing Translational Sciences of the National Institutes of Health under Award Number UL1TR000454.

The authors gratefully acknowledge services provided by the Emory Center for AIDS Research (CFAR) funded though NIAID (P30AI050409) and the Atlanta Clinical and Translational Science Institute (ACTSI), funded though the National Center for Advancing Translational Sciences (UL1TR000454).


  • HIV
  • bisphosphonates
  • combination antiretroviral therapy
  • immune reconstitution
  • osteopenia
  • osteoporosis

Bone Loss in HIV Infection.


Journal Title:

Current Treatment Options in Infectious Diseases


Volume 9, Number 1


, Pages 52-67

Type of Work:

Article | Post-print: After Peer Review


Human immunodeficiency virus (HIV) infection is an established risk factor for low bone mineral density (BMD) and subsequent fracture, and treatment with combination antiretroviral therapy (cART) leads to additional BMD loss, particularly in the first 1-2 years of therapy. The prevalence of low BMD and fragility fracture is expected to increase as the HIV-infected population ages with successful treatment with cART. Mechanisms of bone loss in the setting of HIV infection are likely multifactorial, and include viral, host, and immune effects, as well as direct and indirect effects of cART, particularly tenofovir disoproxil fumarate (TDF) and the protease inhibitors (PIs). Emerging data indicate that BMD loss following cART initiation can be mitigated by prophylaxis with either long-acting bisphosphonates or vitamin D and calcium supplementation. In addition, newer antiretrovirals, particularly the integrase strand transfer inhibitors and tenofovir alafenamide (TAF), are associated with less intense bone loss than PIs and TDF. However, further studies are needed to establish optimal bone sparing cART regimens, appropriate screening intervals, and preventive measures to address the rising prevalence of fragility bone disease in the HIV population.

Copyright information:

© Springer Science+Business Media New York 2017

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