120 7. Brooks, B. and Hillstrom, H. T. Effect of roentgen rays on bone growth and boneirradiation. Am. J. Surg. 20, 599-G14 (1933). . Bloom, W. and Bloom, M. A. Histological changes after irradiation. Radiation Biolegy, Ed. A. Hollaender, Me(Crraw-Hill Book Co., Inc., New York, 1954, pp. 10911114. . Kember, N. F. Ann vivo cell survival system based on the recovery of rat growth cartilage from radiation injury. Nature 207, 501-503 (1965}. 10. Kember, N. F. Cell survival and radiation damage in growth cartilage. Brit. J. Radzol, 40, 496-305 (1967). 11. Kember, N. F. Kinetics of population of bone forming eells in the normal and irradiated rat. Some Aspects of Internal Irradiation, Ed. T. F. Dougherty, W. 8.5. Jee, C. W. Mavs, and B. J. Stover. Pergamon Press, New York, 1962, pp. 309-316. 12. Regen, E. M. and Wilkins, W. E, The effect. of large doses of x-rays on the growth of young bone. J. Bone Jni. Surg. 18, 61-68 (1936). 13, Woodard, H. Q. and Spiers, F. W. Theeffect of x-rays of different qualities on the alkaline phosphatase of living mouse bone. Brit. J. Radiol, 26, 38-46 (1953). 14, Cairnie, A. B. Cell proliferation studies in the intestinal epithelium of the rat: Response to continuous irradia- tion. Radiat. Res. 32, 240-264 (1967}. 15. Lamerton, L. F. Cell proliferation under conti: irradiation. Radiat. Res. 27, 119-138 (1966). 16. Wimber, D. R. and Lamerton, L. F. Cell population st on the intestine of continuously irradiated rats. [tc Res. 18, 137-146 (1963). 17. Lamerton, L. F., Partifex, A. H., Blackett, N. M.. Adams, K. Effect of protracted irradiation on the } forming organs of the rat. Part 1. Continuous exp: Brit. J. Radiol. 33, 287-301 (1960). 18. Pybus, F. C. and Miller, E. W. The gross patholo; . spontaneous bone tumors in mice. Am. J. Cance 47 (1940). 19. Pybus, F. C. and Miller, E. W. The histology of spon ous bone tumors in mice. Am. J. Cancer 40, 54 (1920. Finkel, M. P., Bergstrand, P. J., and Biskis, B. 0. latent period, incidence, and growth of Sr®°-inc osteosarcomas in CF, and CBA mice. Radiology TT. 281 (1961). . Finkel, M. P., Lisco, H., and Brues, A. M. Toxic: Sr®9 in mice. Malignant bone tumors. Argonne Nat Laboratory Biological and Medical Research Div Quarterly Report, November and December 195+ January 1955. ANL-5378, p. 106. . Auerbach, H. and Brues, A. M. Total-body surface irradiator for mice. Radiat. Res. 27, 37-38 (1966). 23. Trueta, J. The role of the vessels in osteogenesis. J. Jnt. Surg. 45B, 402-418 (1963). THE DEVELOPMENT AND HEALING OF RICKETS IN RATS. Il, STUDIES WITH TRITIATED PROLINE* D. J. Simmons and A. S. KuninT One of the most dramatic modifications of skeletal mineralization occurs in rickets. The present investigation uses autoradiography of tritiated proline in rats in order to determine whether the failure of mineralization of cartilage in rachitic rats is related to change in the ability of cells to produce collagen. The results indicate that in bone the cellular production of collagen is normal, but that in cartilage the most maturecells do not producesignificant amountsof collagen. INTRODUCTION Rickets readily develops in the skeleton of young growing rats fed a low phosphate, vitamin D-ifree diet. The resultant morphology is characterized in part by widened growth plates composed predominantly of unresorbed hypertrophic cells. In rachitic cartilage, the chondrocytes appear to mature normally") and the ultrastructure of the matrix seems unremarkable'?); yet mineralization, a prerequisite for capillary invasion and cartilage resorption, fails to occur. *This study was supported by the U. 8. Atomic Energy Commission and a grant, AM-09632, awarded to Dr, Kunin from the National Institutes of Health. 7 Departments of Medicine and Orthopedic Surgery, University of Vermont College of Medicine, Burlington, Vermont. Biochemical: studies on this relatively avasc tissue have revealed that carbohydrate metabc in growth cartilage, as in bone, is predominantly colytic in character. However, when slices of rac cartilages are incubated in vittro, glyco is markedly increased over that of the normal. tary phosphate supplementation is probably b: able to reverse this abnormality than vitamin alone.'* #) Others © have also remarked that min D cannot by itself cure rickets in the rat conjunction with increased, glycolysis, the act: of the major glycolytic enzymes in rachitic carti is coordinately increased and can be coordin: reduced to normal levels by either dietary phosp or vitamin D,) Histochemical observations in allel studies with this model system‘are in gei accord with the biochemical data. The role of dietary phosphate and vitamin I the development and healing of rickets has also © investigated by high resolution autoradiographic t niques employing tritiated thymidine (7HTdR) marker for cells preparing to enter mitosis.'® results indicate that the rapidity with which h logic rickets occurs initially is due to enhanced