Type II osteoporosis

Type II osteoporosis is a purely age-related syndrome,
which affects men and women over 70 and is twice
as common in women as in men. Bone loss increases
gradually with aging, unlike the accelerated loss seen
in type I osteoporosis. In both sexes, cancellous bone
loss begins at about age 40 and continues into old age.
Cortical bone loss commences fi ve to ten years later
but slows or ceases later in life (Riggs & Melton, 1986).
In elderly women, type I and type II osteoporosis
overlap and result in a disproportionate loss of cancellous
bone. Type II osteoporotic fractures occur most
commonly in the proximal femur (hip) and the spinal
vertebrae. The vertebral fractures are of the compression
type causing the normally cube-shaped vertebrae
to become wedge-shaped. A severe consequence of
vertebral compression fractures is kyphosis, known
as ‘dowager’s hump’.
A number of age-related factors are implicated in
the aetiology of type II osteoporosis (Kassem et al.,
1996). Two important factors are (1) impaired bone
formation at the cellular level, where osteoblasts fail
to refi ll the resorption pits created by osteoclasts during
bone remodelling, and (2) secondary hyperparathyroidism,
which leads to increased bone turnover.
Impaired bone formation may be due to a decreased
production of osteoblasts or to their decreased
responsiveness to regulatory factors. Secondary
hyper parathyroidism could arise from an age-related
impairment of 25-hydroxyvitamin D conversion to
1,25-dihydroxyvitamin D in the kidneys. This would
lead to a decrease in the intestinal absorption of
calcium and the lowered blood calcium level would
trigger the release of parathyroid hormone. In the
presence of defective osteoblastic bone formation,
the parathyroid hormone-mediated increase in bone
turnover will result in a net increase in bone loss. Obviously,
a nutritional defi ciency of vitamin D will have
a similar outcome.