1993 Volume 56 Issue 5 Pages 426-440
Senescence accelerated mouse (SAM) show various signs of accelerated aging, including degenerative joint disease. To determine whether SAM can be an animal model of degenerative joint disease, we evaluated their craniofacial morphology and analyzed differences in age-related morphological changes between accelerated senescence prone mouse (SAMP) with accelerated senescence and accelerated senescence resistant mouse (SAMR) having normal senescence.
Forty-three male SAMP1//Odu were used as the experimental group, and 39 male SAMR1/Odu were the controls. The mice were periodically weighed. Lateral x-ray films of the head were obtained at 5, 9, 14, 21, 29 and 36 weeks of age, and analyzed by Persson's method.
Body weight rapidly increased until 9 weeks of age in both SAMP1//Odu and SAMR1/Odu, with no differences between the two.
The SAMP1//Odu showed significantly higher values (p<0.005) in Ba-So at age 5 weeks, N-A and PoBa/PoE at age 9 weeks, Ba-Pr, Ba-So and PoBa/PoE at age 14 weeks, Ba-Pr, Ba-So and PoBa/PoE at age 21 weeks, Ba-Pr at age 29 weeks and Ba-Pr, Ba-So, PoBa/PoE, AN/PoE and AN/SoE at 36 weeks of age.
These results suggest that morphological differences in the jaws, face and cranium between SAMP1//Odu and SAMR1/Odu are not associated with growth and development, but are due to changes in Ba position at 5 weeks of age. Thus, the two strains already had morphological differences at 5 weeks of age and showed no age-related differences as had been reported in SAMP3 and SAMR. No definite conclusions can be made since pathological examinations were not performed in this study. However, unlike SAMP3, SAMP1//Odu may not be suitable for an animal model of temporomandibular joint osteoarthritis.