Skeletal maturation in cerebral palsy

Abstract

Skeletal health in children is made up of a number of factors including the overall pattern of the skeleton, the appropriate size and shape of individual bones, bone mass and internal architecture of both tubular and plate-like bones, and bone metabolism and turnover. Where among this group of attributes does skeletal maturity fit in? Skeletal maturity has been assessed either alone or in association with the variables indicated above for many years. A markedly advanced or delayed skeletal maturity may raise questions as to hormonal or other systemic disturbances that require further investigation in the individual patient. Such disturbances are often associated with other effects on bone that require attention. For example, corticosteroid-induced delay in skeletal maturation may be associated with bone loss, microarchitectural deterioration, and increased fracture risk. Altered skeletal maturity does not of itself, however, appear to confer any particular risk in terms of immediate harm to the skeleton. There have been concerns that delayed bone age might result in a reduced final height and bone mass. Some of the results obtained in other studies of delayed bone age and adult bone mass might reflect the uncritical use of bone density measurements by dual energy X-ray absorptiometry (DXA). Studies in which measurements are adjusted for bone size indicate that volumetric bone density is probably normal.1 The study in this issue of DMCN 2 also used DXA to assess bone density and, as the authors acknowledge, the results obtained are a reflection both of bone mass and bone size. The correlation of reduced skeletal maturity with reduced height and bone density is not surprising. An alternative interpretation of the data would be that the reduction in bone density is more a reflection of the small bone size. A well-reported feature of reduced muscle activity is reduced bone size; reduced stature and overall bone dimensions in cerebral palsy (CP) would, therefore, be expected. One element of the overall picture that is unclear to me is the extent to which reduced bone density might impact on the assessment of skeletal maturation using the Fels method. The use of anticonvulsant medication, as indicated by the authors, is associated with a reduction in bone mass in children who are not ambulant. Anticonvulsant medication may accelerate the metabolism of vitamin D, and vitamin D intake from diet and sunlight exposure may be reduced in this population, increasing the risk of fracture.3 Assessing vitamin D status in children who are immobilized with CP should be a routine event with appropriate supplements being given to all affected children. The American Academy of Paediatrics recently suggested that all members of the population should receive 200IU/day of vitamin D, irrespective of race or age.4 Such a dose would be unlikely to