Role
of Nutrition in Bone Growth
There
are two major cells involved with bone biology - osteoclasts
and osteoblasts.
Osteoclasts
are responsible for breaking down old bone. They have many
nuclei, and sit on the surface of trabecular bone (the spongy
inner bone). Osteoclasts use villi to resorb old bone matrix
such as collagen, protein and minerals, and spits them out
behind it - often releasing growth factors stored within
the bone.
Osteoblasts
are responsible for building up new bone, particularly in
areas where the osteoclasts have eaten old bone away. They
have one nucleus and lay down new bone matrix. Sometimes
osteoblasts become stuck inside the bone, but they continue
to function and become osteosites.
The
cellular events in bone turnover are fairly straight-forward.
Very simply, bone turnover occurs when osteoclasts eat the
old bone and osteoblasts build the new bone. This new bone
is first laid down as unmineralised bone, and then the osteoblast
mineralises it. It takes approximately 3 months to turnover
one Bone Modelling Unit. In the first 20 years of life,
bone formation exceeds bone resorption - this is where the
majority of bone modelling is achieved. In the next 30 years,
bone is maintained and reformed through resorption. This
is known as bone remodelling. After about 50 years, resorption
exceeds formation, and this is where bone loss occurs. Bone
turnover is regulated by circulating hormones, local growth
factors produced by bone cells and other cells, and stored
in bone matrix, and cell to cell contact of rank-rank ligand-OPG
which controls osteoclast development and activation.
After
menopause estrogen levels drop, and as this hormone has
been regulating bone turnover, bone density weakens. Calcium
is also drawn out of the bones so the matrix has less mineralization.
As the matrix becomes weaker, when the osteoclasts break
down old trabecular bone, sometimes the trabeculae holding
the matrix together may perforate and cause microfractures.
This causes bone density weakness and is further exacerbated
by inefficient osteoblast activity - the buildup of new
bone can not keep up with the breaking down of old bone,
and while the remaining trabeculae are thickened as they
are repaired, the bridge between trebecular gaps are not
able to be rebuilt. This leads to postmenopausal osteoporosis
which is a syndrome of having too little bone in the bone.
Steroids accelerate osteoporosis, and in older women often
these are used. Genetics plays a 70% role in determining
osteoporosis, and it seems having a higher peak bone mass
earlier in life affects how much bone is lost before osteoporosis
occurs.
Calcium
is a nutritional aspect that impacts on bone metabolism.
About 99% of calcium in the body is stored in the bones,
so maintaining this level is important for strong bones.
The recommended daily intake for women (the most common
sufferers of osteoporosis) is between 1200-1500mg calcium.
It is fairly difficult to achieve this quantity from diet
alone - you would have to eat a lot of dairy products, green
leafy vegetables and soy - so supplementation is a good
idea in addition to eating high-calcium foods.
Calcium
helps to strengthen bone mass, and achieving a higher peak
mass in your 20's ensures adequate bone mass at menopause
so that as it drops, the chance of developing osteoporosis
or fractures is delayed a number of years. It is better
to increase calcium in the diet earlier rather than later,
although many studies show calcium supplementing beginning
after menopause has some effect. One NZ study has determined
a difference in BMD of 1SD is associated with a twofold
difference in fracture risk. NZ has a very high level of
osteoporosis, so an effective method of reducing this development
would be a great health interest.
Calcium
is mineralised in the trabecular bone where it plays its
more important bone strengthening roles, and has only minimal
effects on the cortical bone (the hard outer layers of bone).
Summarised
from lecture notes from Jill Cornish, University of Auckland
Medical School, July 2003
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