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Osteoporosis is defined as “low bone mass and microarchitectural deterioration of bone tissue, leading to enhanced bone fragility and consequent increase in fracture risk.”1 It is a major public health concern, with 50 000 hip and an estimated 50 000 vertebral osteoporosis related fractures occurring annually in the United Kingdom, with an annual cost of more than £500 million.2 Until recently the condition was widely seen as an inevitable and untreatable consequence of aging. However, the introduction of dual energy xray absorptiometry (DXA) scanning as an investigative tool, and the emergence of effective treatments have led to an explosion of clinical, academic, and commercial interest in the field. This editorial reviews its relevance within neurology and presents recent guidelines for the management of steroid induced osteoporosis.
Overview
To date there have been no prospective case-control studies of fracture risk in neurological conditions. However, there are good reasons why some neurological patients may be at particular risk of osteoporosis and fracture. Although the aetiology of osteoporosis is multifactorial (with genetic factors accounting for 70% of the variability in bone density) exposure to high dose corticosteroids and poor mobility are two important potential causes. In addition, epileptics are a separate group at particular risk of fracture.
Bone physiology
Some knowledge of bone physiology is useful in the understanding of osteoporosis and its treatment. To adapt to stress and to maintain calcium homeostasis bone undergoes a constant process of remodelling. In this process “remodelling units”, of which around a million are active at any one time within the skeleton, remove and replace bone in a coordinated manner via osteoclasts and osteoblasts. Net bone loss occurs when there is increased osteoclastic activity or decreased osteoblastic activity. In normal subjects bone density declines slowly from around the age of 30 years at a rate of …