Scurvy Dentin

A. The patient exhibits the classic symptoms of scurvy, a deficiency in vitamin C. In addition to being an important biological antioxidant, ascorbic acid is required for the hydroxylation of proUne and lysine residues of procollagen in the synthesis of collagen. A deficiency leads to defects in collagen synthesis, which adversely affects the intercellular cement substances in connective tissue, bones, and dentin. 

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]. 

All intercellular substances of supporting tissues, bone, cartilage, fibrous connective tissue and dentine have a conunon sub-structure of collagen. By collagen we wish to indicate a number of compounds of similar, though not necessarily identical composition, which react similarly to staining technique. It is this protein sub-structure which in scurvy is either not produced or is produced in defective form. 

Observations that a deficiency of vitamin A induces scurvy-like alterations in teeth (Johnson et al., 1942, 1945) are also suspect, since it is well established that a deficiency of the vitamin leads to marked degenerative changes in the dentine and enamel of teeth, which cannot be cured by ascorbic acid, but only by vitamin A (Wolbach and Howe, 1933 Boyle, 1933 Mellanby, 1939). 

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