Bone might be more solid than other tissues, but it is just as dynamic: maintenance of bone is a constant, balanced process of creation by osteoblast cells and destruction by osteoclast cells. With age, this balance breaks down, however. Osteoblasts accomplish proportionally less work, and osteoclasts accomplish more. As a result, bone becomes weakened, porous, and fragile, leading to the clinical condition of osteoporosis. This is a significant component of frailty and mortality, as fractures and breaks of bone in elderly individuals can happen with little provocation, and when they do, that trauma often marks the beginning of the final spiral downwards.
In seeking to understand osteoporosis, researchers are largely working backwards from the disease state, looking for mechanisms that change the balance of osteoblast and osteoclast cell populations and activity. There are a sizable number of plausible candidates. Chronic inflammation, for example, is thought to be a part of the problem, and it certainly disrupts many other important systems of cellular coordination related to regeneration and tissue maintenance. Senescent cells are a significant source of inflammation in older individuals, and researchers have demonstrated that removing them can partially reverse osteoporosis in mice.
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