I suggest that before you read this, you read post 20.14.
In post 16.18, we saw that a cell is conventionally considered to be the smallest part of us that is alive. Bone contains four types of cell: osteoblasts, osteoclasts, osteocytes and endosteal cells. In this post we will consider only the first two.
Osteoblasts build the bone. (If you are taking a biology exam, remember that osteoBlasts Build!) Osteoclasts live on bone surfaces and absorb bone. The coexistence of osteoclasts and osteoblasts might seem futile – osteoblasts dig holes in the bone and osteoblasts fill them in again!
But the existence of these two cell types is important because they enable a bone to remodel – to adapt its size and shape to the mechanical forces that it needs to withstand during life. This ability of bone to adapt in response to mechanical loading is sometimes called Wolff’s law. Osteoblasts and osteoclasts are also involved in fracture repair – osteoclasts remove bone material and osteoblasts use it to make new bone at the fracture site. This is a very simplified description of all the events that take place during repair of a fracture. Fracture repair is more important than we often realise because tiny cracks can form in bone but our body can repair them before they lead to a more serious fracture.
Normally osteoblasts replace bone at the same rate that it is removed by osteoclasts.
But in osteoporosis, osteoclasts remove bone more rapidly than it can be replaced by osteoblasts. This imbalance in osteoblast and osteoclast function is usually associated with aging. Women suffer from osteoporosis more than men because the behaviour of their bone cells depends on the level of the female sex hormone oestrogen. After the menopause, the oestrogen level drops and this can lead to osteoporosis.
There are many ways of treating osteoporosis and the resulting bone fractures. One common treatment, for post-menopausal women, is hormone replacement therapy (HRT) which increases their oestrogen levels.
But how can we prevent osteoporosis? If we get a lot of exercise when we are young, our bones will increase in size to withstand the forces involved, according to Wolff’s law. Then, if things go wrong, we have more bone to lose and the effects of osteoporosis will not be so serious.
Remember that osteoclasts live on bone surfaces – this explains why osteoporosis affects cancellous bone more than cortical bone (post 20.14).
Let’s suppose that a trabecula in cancellous bone (post 20.14) is a cylinder of radius r, where r is about 0.5 mm. Since osteoclasts are on the surface of bone, the rate of removal of bone from a trabecula will depend on its surface area. For a length L of trabecula, this area is
At = 2πrL.
If we express this result as a fraction of the volume of bone in a trabecula, we get the result that
ft = (2πrL)/(πr2L) = 2/r.
So, if r = 0.2 mm, ft = 2/0.2 = 10 mm-1.
Now let’s think about the cylindrical cortical shell, surrounding the cancellous bone (post 20.14) of mean radius rc and thickness Δr, where Δr will be a few millimetres. Then its surface area will be
Ac = 2(2πrcL).
The first 2 arises because the cortical shell has an inner and an outer surface. The volume of the cortical shell is
Vc ≈ (2πrcL)Δr
So the area, from which bone is lost, expressed as a fraction of the mass of bone is
fc = (4πrcL)/(2πrcL.Δr) = 2/Δr.
If Δr = 2 mm, fc =2/2 = 1 mm-1.
So bone loss, as a fraction of total bone will be about ten times as fast for cancellous than for cortical bone. This may not seem a very big difference but remember that osteoblasts are still at work so that bone that is lost more slowly has a better chance of being replaced.
There is a lot more to learn about osteoporosis than I have covered here and in post 20.14. Because it is a very common disease, there is a lot of information about osteoporosis on the web and a lot of misinformation too! For further reliable information see: