[Boric acid produced malformations of the posterior extremities of chicken embryos and their histogenesis].

Malformations of the legs of chicken embryos which are typical of the boric-acid produced syndrome were examined histologically and an attempt was made to interpret the mechanism leading to the genesis of the bend. These malformations of the legs appear most clearly in the tarsometatarsus which is bent backwards and severly shortened. Bends in the tibiotarsus were also observed. They may, however, be turned backwards or forward. A histologic examination showed that the bend of the tarsometatarsus is established on the 8th day of breeding at the proximal part of the osseous covering of the cartilage, while the cartilage cells show no alteration. Severe histologic changes do not become visible until the individual has grown further. Their effect on 13 day old embryos is described.A comparison with similar malformations produced by other agents (Insulin and Aristamid) suggests that both malformations result from a disturbance of the Stemmkörpereffect of the growing cartilage. As they show a dissimilar histogenesis this disturbance must be due to different causes. One of these causes may be the deswelling capacity of boric acid, which affects the cartilage cells and the cartilage matrix, thus weakening the Stemmkörpereffect. Secondly, there are several observations suggesting that boric acid interferes with the process of extension of the collagen fibres, especially of the sinews, and by this produces the malformation. It may also be induced by deswelling. The histologic effects described agree with this hypothesis.