ABSTRACT
Studies of scorbutic guinea pigs by S. B. Wolbach and P. R. Howe demonstrated that the histological basis of the failure of wounds to heal in scurvy lies in the inability of the fibroblasts, osteoblasts, and odontoblasts to produce and maintain the intercellular supporting substances — collagen, bone, and dentin. In studies of the force required to cause dehiscence of experimental skin wounds in the forearms of volunteers, E. Lindstedt and P. Sandblom observed that patients with serum protein levels below 6.5 g/100 ml had weaker wounds at 5 days than did those with higher protein levels. Working at the Children's and Infants' Hospital in Boston, T. H. Lanman and T. H. Ingalls reported that plasma analysis disclosed a much higher incidence of asymptomatic scurvy than could be recognized by clinical examination. They reported wound dehiscence, 3 days after a second operation and congenital atresia of the bowel, in a 6-week-old infant.
