During ageing, bones become more fragile and more likely to break, and also take longer to heal. Furthermore, age puts us at greater risk of two debilitating conditions: osteoporosis and osteoarthritis.
The age-related decline in bone mass is primarily due to the loss of calcium, making bones more fragile. This is why elderly people can suffer fractures after relatively minor falls. Changes in the structure of proteins within the bone can also reduce its ability to absorb shocks, further increasing the likelihood of fractures.
Osteoporosis is a severe weakening of the bones that leads to frequent fractures and therefore potentially chronic pain. Women are more susceptible to this disease, as their bone mass declines more rapidly on average after reaching its peak.
Ageing also increases the risk of osteoarthritis, which will be covered in more detail in a later article. Within the joints, cartilage that protects the ends of the two bones can degenerate. With the loss of this protective cartilage, the bone beneath is exposed and begins to be eroded as well.
Bone tissue is continually remodelled throughout life, as it frequently suffers microscopic damage. Cells called osteoclasts resorb (reabsorb) damaged bone, which is replaced with new tissue by osteoblasts. Stem cells within the bone marrow have the ability to become osteoblasts – the bone-building cells – or to become fat cells. With age, they begin to produce more fat cells and fewer osteoblasts. This causes resorption to outstrip production, which leads to the weakening of the bone structure.
Calcium and vitamin D appear to be important for preventing bone fragility. Both are required for bone formation, and vitamin D enhances calcium absorption. Insufficient intake of either increases the production of parathyroid hormone, which stimulates osteoclast activity. This is exacerbated by the fact that we are less able to absorb vitamins (and consequently, calcium) as we grow older.
Exercise is also preventative against bone fragility, as mechanical loading stimulates osteoblasts, while lack of exercise raises the level of inflammatory molecules within the bone, which stimulates resorption.
Current drugs for osteoporosis aim to reduce osteoclast activity in favour of osteoblasts. This is achieved either by targeting signalling molecules within the bone, or by targeting age-related hormonal changes that influence osteoclast activity – particularly the post menopausal decline of oestrogen in women.
We previously mentioned how stem cells developing into fat cells instead of osteoblasts lead to bone weakening. It may be possible to target the molecules controlling this process in order to maintain bone production.
Aging and bone loss: new insights for the clinician: doi: 10.1177/1759720X11430858
Aging and Bone: doi: 10.1177/0022034510377791
Cbfβ governs osteoblast-adipocyte lineage commitment through enhancing β-catenin signaling and suppressing adipogenesis gene expression: doi: 10.1073/pnas.1619294114
Stem cells in Osteoporosis: From Biology to New Therapeutic Approaches: doi: 10.1155/2019/1730978
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