Scurvy Fibroblasts

The striking increases in the formation of tritiated water and tritiated hydroxyproline on in vitro addition of ascorbate are consistent with a function of this vitamin in hydroxylation—probably at step 3. The present results do not support a systemic ascorbic acid-mediated effect, the belief that ascorbic acid functions in the maintenance of collagen, or acts by stimulating maturation of the fibroblasts in the system under study here. The present data do not support the possibility that intermediates containing hydroxyproline accumulate in scurvy. The proposal that ascorbic acid is involved in the hydroxylation reaction itself is consistent with studies on the nonenzymatic hydroxylation of proline (4) and on enzymatic hydroxylation of other compounds (5, 20, 21, 44, 51). 

Ross, R.. and Benditt, E. P. Wound healing and collagen formation. IV. Distortion of ribosomal patterns of fibroblasts in scurvy. J. Cell Biol., 304 22 365-389,1964. 

The typical injury of scurvy consists of an incapacity of the mesenchymal cells—such as fibroblasts, osteoblasts, or odontoblasts—to produce their normal fundamental substance. In other words, the cell can proliferate, but it cannot form collagen, osteoid, or dentin. This basic alteration is responsible for increased fragility of the capillaries, retarded wound healing, abnormal bone growth, and eventually abnormal tooth growth [78]. 

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