After that, infantile scurvy was not reported for another 200 years. In 1912, Holst and Frolisch induced and cured scurvy in guinea pigs through dietary modification. The typical pathological manifestations of vitamin C deficiency are noted in dentine, osteoid, and capillary vessel wall tissues. Defective collagen synthesis leads to defective dentine formation, hemorrhaging into the gums, and loss of teeth. Hemorrhaging is a hallmark feature of scurvy and can occur in any organ.
Hair follicles are one of the common sites of cutaneous bleeding.
Bone involvement is typical for infantile scurvy. The bony changes occur at the junction between the end of the diaphysis and growth cartilage. Calcification of the growth cartilage at the end of the long bones continues, leading to the thickening of the growth plate. The typical invasion of the growth cartilage by the capillaries does not occur. Preexisting bone becomes brittle and undergoes resorption at a normal rate, resulting in microscopic fractures of the spicules between the shaft and calcified cartilage.