Bone metabolism dysfunction mediated by the increase of proinflammatory cytokines in chronic HIV infection.

Despite the efficacy of antiretroviral therapy (ART) on the control of viral replication, the current challenge is to decrease the chronic inflammatory status and toxicity of the antiretroviral drugs that contribute to increase the risk of metabolic complications. To verify the influence of proinflammatory cytokines on bone metabolism mediated by chronic HIV infection, a cross-sectional study was conducted with 50 HIV-infected adult men treated or not treated with ART. Dual energy X-ray absorptiometry (DXA) was performed to assess bone mineral density. Biochemical analysis were performed of IL-6, TNF-α, osteocalcin, PTH, 25-OH-D, total calcium, albumin, 24 h urinary calcium, and urinary deoxypyridinoline. The participants not treated with ART exhibited higher values of IL-6 and TNF-α than the participants treated with ART for more than 2 years. The TNF-α values were higher in the participants treated with ART for <2 years than in participants treated with ART for more than 2 years (p < 0.05). The increased values of urinary deoxypyridinoline indicated a high reabsorptive activity of bone tissue in all groups, with a significant difference between the participants not treated with ART and the participants treated with ART for <2 years. Through the DXA we found a bone mass reduction in all bone sites in each group. The increase in production of proinflammatory cytokines, most notably in the viremic group, demonstrated the ability to stimulate osteoclast activity and subsequently affect bone mass. The reduction of bone mineral density was observed in all bone sites, principally for the groups receiving antiretroviral treatment.