Beryllium “Rickets”

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Abstract
By replacing the calcium carbonate in Steenbock's rachitogenic diet 2965 with an equivalent amount of beryllium carbonate, or by adding small quantities of this substance to the normal stock diet (Bills'), bone lesions which have certain similarities to rickets may readily be produced in young rats, the severity of the lesions bearing an approximate relationship to the amount of the beryllium salt in the diet. The percentage of ash in the bones is much diminished. Both x-ray photographs and histological sections reveal almost complete failure of mineral deposition in the metaphysis, even immediately proximal to the epiphyseal disc, and reduced amounts of mineral salts in the trabeculae and cortex of the tibia. Other long bones are similarly affected. The depth of the metaphysis is comparable to that exhibited in severe Steenbock rickets. The maintenance of the columnar arrangement of the cartilage cells in the metaphysis is distinctive of beryllium “rickets” in the rat. The inorganic phosphorus content of the blood plasma is very much reduced, and the acid-soluble phosphoric esters of the liver are diminished in quantity. The phosphatase content of the kidney is markedly lowered. Beryllium does not appear to be deposited in appreciable quantities in the bones. This type of bone lesion is not preventable by cod liver oil nor by irradiated ergosterol administration, nor is it amenable to the anti-rachitic influence of ultraviolet light.

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