This disease occurs in children during the earlier periods of growth, and so far as the bones are concerned it is a disease of development, the normal process of ossification being interfered with. Cases have been observed of congenital rickets, but these are rare, and in the majority of cases it begins in the first or second year, its commencement being very rarely delayed beyond the fourth or fifth year. In a large proportion of cases its onset seems to be in the latter half of the first year or the first half of the second.
An endeavour has been made to make out that rickets is merely a manifestation of hereditary syphilis, but this view has not received acceptance in this country-It has been pointed out again and again that tickets is very common in cities where syphilis is uncommon. In the city of Glasgow, for instance, rickets is very common among the poorer classes, but syphilis is relatively uncommon. It is so also in Aberdeen, Edinburgh, Belfast, and elsewhere. We shall see afterwards that syphilis-produces changes in the bones in some respects analogous to rickets, and atrophy of the cranial bones, sometimes designated Craniotabes, although formerly'regarded as rachitic, is probably in most cases syphilitic; the two diseases, however, are essentially distinct.
Rickets occurs amongst children who are injudiciously fed and badly housed, and the disease in the bones is to be regarded as part of a general loss of health. The body is weakened, and, besides the bones, there are other parts that suffer. According to Macewen, it supervenes in a considerable number of cases on an attack of one of the acute fevers, as measles or scarlet fever, such an attack leaving the child in an ill-nourished condition. There are usually symptoms of indigestion and intestinal catarrh, sometimes with fever, and in a certain proportion of cases there is enlargement of the spleen and sometimes also of the liver and lymphatic glands. The bones, being the most actively growing parts at this period of life, are, however, specially affected.
Rickets, or a condition analogous to it, has been produced artificially in growing animals by feeding them with small doses of phosphorus, or by giving them lactic acid, by the mouth or subcutaneously. In both cases the diet must be deficient in lime salts. In the latter case it has been supposed that the lactic acid, being a ready solvent of lime, prevents its deposition in the bones, and it has been inferred that in the human subject gastric derangement causes the formation of an excess of lactic acid, which is the cause of the disease in the bones. There is, however, the objection to this view, that rickets is not always accompanied by any considerable gastric disorder, and such a view does not explain its occasional occurrence in the fœtus. Besides, the disease is clearly an error in development, and were it due merely to absence of the lime salts, we should expect the bony matrix to be formed without the lime salts. The very opposite frequently occurs: we have often an impregnation of the cartilage with lime salts, a calcification of the cartilage (see Fig. 267, b, b), while true ossification lingers, Rickets can, in most cases, be cured by supplying sufficient food and proper lodging, and this points to its origin in the opposite of these.