The nature of the injury to the calcifying mechanism in rickets due to strontium

Abstract

WHEN young rats are fed on diets containing strontium carbonate they become rachitic. The bones of these animals are characterised by a markedly diminished calcifying mechanism [Sobel et al. 1934]. At present, the nature of the alteration in the bone cell causing this variation is quite obscure. In fact, the entire problem of the factors operating locally in the bone cell is still unsolved. Whilst there are a number of theories as to what constitutes the "local factor", the bone "phosphatase mechanism" is the only one supported by satisfactory experimental evidence [Robison, 1932; Robison and Rosenheim, 1934; Niven and Robison, 1934; Fell and Robison, 1934]. Even this enzyme is known not to be the only factor involved as was confirmed in our studies of strontium rickets [Sobel et al., 1935]. A further study of strontium rickets is therefore of importance because of the information that may be revealed regarding the factors responsible for calcification at the site of deposition. The present experi- ments seem to point to a "competitive retardation" of Sr++ upon the action of a constituent of the bone cell whose concentration is a factor in calcification. This experimental evidence is discussed below.