IBMS BoneKEy | Perspective

HIV and low bone density: Responsible party, or guilty by association?

Mark J Bolland
Andrew Grey

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DOI:10.1138/20110486

Abstract

Infection with HIV has been associated with low bone mineral density (BMD), and recent guidelines have recommended regular monitoring of BMD every 1-2 years. Preclinical data suggest that HIV can infect bone cells, and alter bone metabolism potentially causing low BMD. A transgenic rat model of HIV exhibited markedly reduced BMD, with increased bone resorption and osteoclastogenesis, attributable in part to dysfunctional B cell-derived RANK signaling. These results are consistent with data from clinical studies of humans with HIV infection, which have reported a high prevalence of low BMD, and suggest that the immune dysfunction characteristic of untreated HIV infection may contribute to the skeletal phenotype. However, HIV-infected patients commonly have classical risk factors for low BMD such as low body weight, cigarette smoking, and excess alcohol use, which may largely account for the observed low BMD. Furthermore, most HIV-infected people in developed/first-world countries receive anti-retroviral therapy, with consequent marked improvements in general health and nutrition. The available clinical evidence suggests that BMD is stable or improves in HIV-infected people receiving long-term combination anti-retroviral therapy (originally termed HAART), and that if fracture risk is increased, it is largely attributable to a higher prevalence of classical risk factors for low BMD and fracture. Consequently, we suggest that management of skeletal health in HIV-infected people be undertaken according to guidelines for the general population. Future research on BMD or fractures and HIV should consider traditional risk factors for low BMD or fracture in HIV-infected cohorts before concentrating on specific HIV-related factors.

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