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Increased Young’s Modulus and Hardness of Col1a2^oim Dentin

¹ Endocrinology Section, Department of Medicine, University of Wisconsin, H4/556 CSC (5148), 600 Highland Ave., Madison, WI 53792, USA;
³ Research Division, Hospital for Special Surgery, 535 East 70th St., New York, NY, 10021, USA;
⁴ Department of Materials Science & Engineering, 1509 University Ave., Madison, WI 53706, USA;
⁵ Geriatrics Research, Education, and Clinical Center, William S. Middleton VAMC, 2500 Overlook Terrace, Madison, WI 53705, USA; and
⁶ Osteoporosis Research and Clinical Center, 2870 Marshall Ct., Madison, WI 53705, USA

^* corresponding author, rdb{at}medicine.wisc.edu

Mice harboring the Col1a2^oim mutation (oim) express dentinogenesis imperfecta. To determine the effect of Col1a2 genotype on tissue mechanical properties, we compared Young’s modulus and hardness of dentin in the 3 Col1a2 genotypes. Upper incisors were tested by nanoindentation. Genotype had a significant effect on Young’s modulus, but there was not a simple mutant allele dosage relationship. The effect of genotype on hardness did not reach significance. Hardness and Young’s modulus were greater near the dento-enamel junction than near the pulp chamber. Greater hardness and Young’s modulus values near the dento-enamel junction reflected continued mineralization of the dentin following its initial synthesis. Analysis showed the mechanical data to be consistent with Fourier transform infrared and backscattered electron microscopy studies that revealed increased mineralization in oim bone. Analysis of the data suggests that clinical fragility of teeth in oim mice is not due to deficiencies of hardness or Young’s modulus, but may be due to defects in post-yield behavior or resistance to fatigue damage.

KEY WORDS: collagen type I • dentinogenesis imperfecta • osteogenesis imperfecta • biomechanics • tooth calcification