Vitamin D and Health

one with a mesh structure. Different bones and skeletal sites have different ratios of cortical to
trabecular bone but, overall, the human skeleton comprises 80% cortical bone and 20% trabecular
bone (Eriksen et al., 1994).
6.13 During the lifespan, bone undergoes processes of growth, modelling and remodelling (Clarke, 2008).
Longitudinal and radial growth of bone occurs during childhood and adolescence. At maturity, bone
stops growing in length but continues to grow in width and change shape in response to physiological
influences or mechanical forces in a process known as modelling. Bone remodelling is a continuous
lifelong process of replacement and repair, in which old bone is broken down (resorption) and new
bone formed (formation or ossification), and which adapts the skeleton to physical stress (related to
physical activity and load bearing) and to release ionised calcium and phosphate as required.
6.14 Bone cells involved in bone modelling and remodelling are osteocytes, osteoclasts and osteoblasts.
Osteoblasts and osteoclasts, which originate in the bone marrow, are responsible for the processes of
new bone formation and bone resorption, respectively. Osteoblasts synthesise osteoid (uncalcified
pre-bone tissue) and facilitate its calcification; osteoclasts are phagocytic cells which remove bone
tissue; and osteocytes, which are derived from osteoblasts and constitute over 90% of adult bone
cells, play a role in activation of bone formation and resorption (Datta et al., 2008). The activation
process is regulated by mechanical forces, bone cell turnover, hormones (e.g., PTH), cytokines and
local factors.
6.15 Bone mass accrual is rapid in the fetus and infant. It continues to increase during childhood at a
slower rate until the adolescent growth spurt when it again undergoes rapid growth. During these
periods of growth, bone turnover is very high and formation exceeds resorption leading to a net gain
in bone mass. Peak bone mass is reached, typically, in the early 20s. In the young adult skeleton,
bone formation and resorption is in approximate balance. With increasing age, the process of bone
resorption predominates over bone formation leading to a net loss of bone mass. Bone mass later in
life depends on peak bone mass reached at skeletal maturity and the subsequent rate of bone loss.
The rate of bone loss is initially slow but, in women, accelerates rapidly in the first 4-8 years following
menopause and then at a slower continuous rate throughout the rest of life (Riggs et al., 2002). The
accelerated rate of bone loss is caused by the sudden decline in oestrogen production by the ovaries
at menopause. For men, bone loss is slow and continual; therefore, women generally lose more bone
than men.
6.16 Bone strength depends primarily on bone mass which accounts for about 50-70% of bone strength
(Pocock et al., 1987). Bone strength is also affected by bone geometry, cortical thickness and porosity
and trabecular bone morphology. The main determinant of bone mass is genotype; however,
hormones (calcium regulating hormones and sex hormones) and lifestyle factors (such as diet and
physical activity) can also influence bone mass. Nutritional deficiencies, particularly of calcium,
vitamin D and phosphorus can lead to formation of weak, poorly mineralised bone.
Skeletal disorders
6.17 Insufficient vitamin D during growth leads to the development of rickets (vitamin D deficiency rickets).
If diagnosed early, vitamin D supplementation can reverse the skeletal changes but if the skeletal
deformities are widespread and significant, and growth plates have begun to mature, as in puberty,
then it cannot. In the UK, a serum 25(OH)D concentration < 25 nmol/L has been the threshold
adopted to define increased risk of rickets (DH, 1998). Other causes of rickets include inadequate
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