Washington, DC - Decreased bone-mineral density (BMD) is correlated with decreased arterial elasticity in healthy subjects, according to a new study presented here at the American Geriatrics Society 2008 Annual Meeting [1]. The study also found fewer endothelial progenitor cells (EPCs) in the peripheral blood of subjects with low BMD. The findings raise the possibility that BMD provides an indication of vascular function.

The study enrolled 61 healthy patients (34 men, 27 women) with a mean age of 48 years. All were assessed for BMD of the femoral neck (f-BMD) and the greater trochanter (t-BMD). Peripheral blood was drawn to determine cell counts of CD34+ cells and CD34+VEGF+ cells.

Lead author Frank E Corrigan III (Johns Hopkins University School of Medicine, Baltimore, MD) explained, "The CD34+ cell is a progenitor cell, and within that population there are [EPCs; the percentage] varies. We were actually characterizing them when we did the CD34+VEGF+ cells, because those are considered the cells that are the endothelial progenitor cells."

EPCs are thought to be recruited by the circulation to repair the endothelium. When atherosclerosis begins, the endothelium is damaged, and damaged endothelium may be manifested as increased arterial stiffness. A "wave" of blood is reflected when it strikes the point where an artery bifurcates, and the size of this reflected wave provides an index of elasticity or rigidity—the arterial augmentation index (AIx). A high AIx indicates arterial stiffness.

Statistical analysis found that f-BMD was positively correlated with the CD34+ cell count (r=0.321; p=0.022). t-BMD was negatively correlated with AIx (r=-0.311; p=0.020). These results suggest that high bone density accompanies a high progenitor-cell count and arterial elasticity. Corrigan commented: "One chart I showed [in the presentation] had the Framingham risk score. . . . The people who had higher EPCs had less Framingham risk. That's sort of like a clinical vignette of 'this is what's going on.' "

The data also indicated that progenitor-cell counts of subjects with low BMD (t-score <1) were significantly lower than those of subjects with normal BMD: CD34+ 2.1±0.9 vs 2.7±1.0 cells/L (p=0.040); the percentages of CD34+VEGF+ cells in the CD34+ population in patients with low BMD vs normal BMD were 41.7%±26.1% vs 55.8%±22.4% (p=0.042), respectively.

The data suggest a relationship between lower levels of EPCs and greater arterial stiffness in healthy individuals with low BMD. Subjects with low BMD also showed AIx increasing with age. This relationship was not seen in individuals with normal BMD.

"I worry that these two things covary with age," session moderator Dr George E Taffet (Baylor College of Medicine, Houston, TX) commented. "That is, bone density goes down with age, and arterial stiffness goes up with age. . . . There may not even be a common cause, just . . . two things [that] coexist in elderly people."

However, Taffet added, "The one [possibility] that I like is that cytokines cause osteoporosis, and cytokines also may promote atherosclerosis. So that might be a common link between the two."

Corrigan acknowledged the need for more research: "Animal studies would have to show that there is, in fact, osteoblastic and osteoclastic differentiation and regulation of the arterial calcium, in the sense that the same thing is going on in the bone. That's been characterized in some studies, but . . . it's not really known. The other thing is, this was just 61 people. Right now they're recruiting more and more people, so eventually we're hoping that as we get more people we'll be able to make a more definitive answer."