The well-controlled loading environment applied to the discs in this model provides a means of isolating the influence of joint-loading conditions on the response of the intervertebral disc. Results indicate that chronically applied compressive forces, in the absence of any disease process, caused changes in mechanical properties and composition of tail discs. These changes have similarities and differences in comparison with human spinal disc degeneration.
Sustained mechanical loading alters longitudinal growth of bones, and this growth sensitivity to load has been implicated in progression of skeletal deformities during growth. The objective of this study was to quantify the relationship between altered growth and different magnitudes of sustained altered stress in a diverse set of nonhuman growth plates. The sensitivity of endochondral growth to differing magnitudes of sustained compression or distraction stress was measured in growth plates of three species of immature animals (rats, rabbits, calves) at two anatomical locations (caudal vertebra and proximal tibia) with two different ages of rats and rabbits. An external loading apparatus was applied for 8 days, and growth was measured as the distance between fluorescent markers administered 24 and 48 h prior to euthanasia. An apparently linear relationship between stress and percentage growth modulation (percent difference between loaded and control growth plates) was found, with distraction accelerating growth and compression slowing growth. The growth-rate sensitivity to stress was between 9.2 and 23.9% per 0.1 MPa for different growth plates and averaged 17.1% per 0.1 MPa. The growth-rate sensitivity to stress differed between vertebrae and the proximal tibia (15 and 18.6% per 0.1 MPa, respectively). The range of control growth rates of different growth plates was large (30 microns/day for rat vertebrae to 366 microns/day for rabbit proximal tibia). The relatively small differences in growth-rate sensitivity to stress for a diverse set of growth plates suggest that these results might be generalized to other growth plates, including human. These data may be applicable to planning the management of progressive deformities in patients having residual growth. ß
Sustained mechanical load is known to modulate endochondral growth in the immature skeleton, but it is not known what causes this mechanical sensitivity. This study aimed to quantify alterations in parameters of growth plate performance associated with mechanically altered growth rate. Vertebral and proximal tibial growth plates of immature rats and cattle, and rabbit (proximal tibia only) were subjected to different magnitudes of sustained loading, which altered growth rates by up to 53%. The numbers of proliferative chondrocytes, their rate of proliferation, and the amount of chondrocytic enlargement occurring in the hypertrophic zone were quantified. It was found that reduced growth rate with compression and increased growth rate with distraction were associated with corresponding changes in the number of proliferative chondrocytes per unit width of growth plate, and in the final (maximum) chondrocytic height in the hypertrophic zone (overall correlation coefficients 0.38 and 0.56 respectively). According to multiple linear regression coefficients for these two variables (0.72 and 1.39 respectively), chondrocytic enlargement made a greater contribution to altered growth rates.
The findings confirm that vertebral growth is modulated by loading, according to the Hueter-Volkmann principle. The quantification of this relationship will permit more rational design of conservative treatment of spinal deformity during the adolescent growth spurt.
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