This communication advances the proposal that all the diverse manifestations of scurvy can be attributed to depolymerisation of ground substance glycosaminoglycans brought about by exposure to uninhibited cellular hyaluronidase. It suggests that ascorbic acid exerts its prime biological function indirectly by incorporation into a glycosaminoglycan residue to form the physiological hyaluronidase inhibitor. The therapeutic implications of this working hypothesis are briefly discussed.