ABC of Rheumatology: OSTEOPOROSISBMJ 1995; 310 doi: https://doi.org/10.1136/bmj.310.6985.989 (Published 15 April 1995) Cite this as: BMJ 1995;310:989
- Nicola Peel,
- Richard Eastell
Osteoporosis causes considerable morbidity and mortality, and there is evidence that the burden of this condition is increasing out of proportion to the changing demographic structure of populations in Western countries.
Osteoporosis may be defined as a disorder resulting from the combination of low bone mass (osteopenia) and low trauma fractures. Typical sites of osteoporotic fracture are the vertebral body, distal forearm, and proximal femur.
It is now possible to accurately determine individuals' risk of osteoporosis and to monitor their response to treatment by means of bone densitometry. Many cases of osteoporosis are preventable, and treatments are effective in reducing the number of further fractures in patients with established disease.
The human skeleton is composed of about 20% trabecular bone and 80% cortical bone. Bone undergoes a continual process of resorption and formation in discrete bone remodelling units. About 10% of the adult skeleton is remodelled each year. This turnover prevents fatigue damage and is important in maintaining calcium homoeostasis. Bone loss results from an imbalance between the rates of resorption and formation. Trabecular bone is more metabolically active, and osteoporotic fractures tend to occur at sites composed of more than 50% trabecular bone.
Bone loss leads to thinning, and in some cases perforation, of the trabecular plates. Trabecular perforation occurs in situations of increased bone turnover, and the resulting loss of normal architecture leads to a disproportionate loss of strength for the amount of bone lost.
Peak bone mass is achieved by age 30.
After skeletal maturity, bone is lost in both sexes at about 1% a year.
Women experience a phase of accelerated bone loss for five 10 years after the menopause.