A new mouse study presented at an American Heart Association convention reveals that hypertension may cause bones to age faster.
A new study presented today at the American Heart Association’s Hypertension Scientific Sessions 2022 conference in San Diego shows that young mice with high blood pressure had the same bone loss and damage from osteoporosis as older mice.
Both hypertension and osteoporosis are common conditions, and individuals may have both at the same time. Researchers in this study looked at inflammation linked to high blood pressure in mice and discovered it might be related to osteoporosis.
“Bone marrow is where both new bone and new immune cells are produced,” says lead study author Elizabeth Maria Hennen.
They hypothesize that increased pro-inflammatory immune cells in the bone marrow may be contributing to bone injury and weakening the bone.
“By understanding how hypertension contributes to osteoporosis,” adds the lead author, “we may be able to reduce the risk of osteoporosis and better protect people later in life from having fragility fractures and a lower quality of life.”
In order to examine the potential link between hypertension and bone aging, researchers in the study compared young mice with artificially generated hypertension against older mice without hypertension. According to Hennen, the human age equivalent for the young mice was around 20-30 years old and 47-56 years old for the elder mice. Twelve young (4 months old) mice were administered angiotensin II, a hormone that causes elevated blood pressure. For six weeks, the young mice were given 490 nanograms/kilogram of angiotensin II. Angiotensin II at a dose of 490 nanograms per kilogram was also administered for six weeks to a group of 11 older mice (16 months old). A buffer solution without angiotensin II was administered to two control groups of 13 young and 9 old mice, and these mice did not develop elevated blood pressure.
After six weeks, scientists used micro-computed tomography, a sophisticated imaging method, to examine the bones of mice from all four groups. Bone strength and density were used to assess bone health. The probable impacts of hypertension and aging on the mice’s bone’s microstructure and strength were calculated using mathematical techniques.
Compared to young mice without hypertension, young mice with induced hypertension had a significant 24% decrease in bone volume fraction, an 18% decrease in the thickness of the sponge-like trabecular bone at the end of long bones like the femurs and the spinal column, and a 34% decrease in estimated failure force, which is the ability of bones to withstand different types of force.
“Failure force,” explains Hennen, “translates into weaker bones. In the spine, bone weakness can lead to vertebral fractures later in life.”
However, similar bone loss was not present in the older mice that received the angiotensin-II infusion. However, during the investigation, the aged mice, whether they had high blood pressure or not, showed deteriorated bone quality comparable to that of the young hypertension animals.
“In these mice, being hypertensive at a younger age essentially aged bones as if they were 15-25 human years older,” Hennen adds.
Researchers used flow cytometry to examine bone marrow samples to see how inflammation affected the mice’s bone health. Researchers were able to distinguish between distinct immune cells and identify individual cells using this method. When compared to young mice who did not receive angiotensin II, the hypertensive young mice had an increase in the amount of inflammatory signaling molecules, which suggested an increase in bone inflammation.
Whether the older mice had high blood pressure or not, an ongoing state of inflammation may have an effect on bone health, according to Hennen.
“This increase in active immune cells tells us that the older mice are more inflamed overall,” she added.
“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.”
Hennen says that these results may help researchers find the immune cells and processes that are important to the health of human bones. This breadth of knowledge might inspire fresh ideas for preventing osteoporosis in young adults.
Due to the study’s limitations, which include the fact that it is just descriptive, more research is required to determine precisely how the various immune cell types may contribute to bone loss.
Furthermore, it is unknown whether a comparable link occurs in humans, thus similar study in humans is required to corroborate these findings.
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