Researchers here provide evidence for the raised blood pressure of hypertension to accelerate the progression of osteoporosis, the loss of bone density characteristic of old age, leading to an earlier onset of the condition. They speculate that inflammation is the mechanism of interest, based on the differences in outcome following induced hypertension in old mice, already suffering the inflammation of aging, versus induced hypertension in young mice. There are already many good reasons to work to minimize both chronic inflammation and any increase in blood pressure with age; more evidence for just how bad these aspects of aging are just reinforces that call to action.
Researchers compared young mice with induced hypertension to older mice without hypertension to assess the potential relationship of hypertension to bone aging. A group of 12 young mice (4 months old) were given angiotensin II for six weeks, a hormone that leads to high blood pressure. A group of 11 older mice (16 months old) also received of angiotensin II for six weeks. Two control groups of 13 young mice and 9 old mice received a buffer solution that did not include angiotensin II, and these mice did not develop high blood pressure.
After six weeks, researchers analyzed the bones of mice from all four groups using micro-computed tomography. When compared to the young mice without hypertension, the young mice with induced hypertension had a significant 24% reduction in bone volume fraction, an 18% reduction in the thickness of the sponge-like trabecular bone located at the end of long bones, such as femurs and the spinal column, and a 34% reduction in estimated failure force, which is the ability of bones to withstand different types of force.
In contrast, the older mice who were given the angiotensin-II infusion did not exhibit similar bone loss. During the study, however, the old mice, with or without high blood pressure, exhibited a reduced bone quality similar to that of the hypertensive young mice. To assess the impact of inflammation on bone health of the mice, researchers analyzed the bone marrow using flow cytometry. This tool allowed researchers to identify individual cells and to sort out specific immune cells. In the hypertensive young mice, they found an increase in the number of inflammatory signaling molecules, indicating an increase in inflammation in the bones when compared to the young mice that did not receive angiotensin II.
"This increase in active immune cells tells us that the older mice are more inflamed overall, and that a continued state of inflammation, whether they had high blood pressure or not, may have an impact on bone health. It appeared that high blood pressure was adjusting the bone remodeling process toward bone loss, rather than bone gain or bone equilibrium, in the hypertensive young mice. As a result, bones will be weaker, leading to an increased risk for osteoporosis and fragility fracture. In humans, this might mean that we should screen for osteoporosis in people with high blood pressure."