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Biomechanical, radiologic, and histopathologic correlations in the pathogenesis of experimental intervertebral disc
B H Ziran1, S Pineda, H Pokharna
1Department of Orthopaedic Surgery, University Hospitals of Cleveland, Case Western Reserve University, Ohio.
Study Design:
The desert sand rat, an animal model for spinal degenerative disc disease, was studied for biomechanical, histologic, and radiographic characteristics. Load deformation curves with peak force and force decay, hematoxylin-eosin-stained sections, and lateral radiographs were correlated.
Objectives:
The hypothesis that the subchondral bone response preceded or contributed to the degenerative disc disease seen in the desert sand rat was tested.
Summary Of Background Data:
Intervertebral disc disease spontaneously develops in the desert sand rat during its lifetime. Approximately 50% will have significant disc disease by age 18 months. Previous studies have found metabolic and histologic changes associated with intervertebral disc degeneration in the sand rat.
Methods:
Desert sand rats were killed at 3-, 9-, 15-, and 18-month intervals and tested in Rheometrics Solid Analyzer with nondestructive step strain loading to obtain a load deformation curve. Radiographs and histologic sections of each animal were compared. Peak force and force decay were analyzed by level and by age. Analysis of variance and Tukey's methods were applied to data.
Results:
There were no statistically significant differences in biomechanical data. No histologic changes were noted in the study groups up to 18 months of age. Radiographic differences characterized by subchondral bony sclerosis were noted by 18 months of age. No trends were noted when radiographic grades were compared with force data.
Conclusions:
The absence of biomechanical histologic changes in the intervertebral disc per se from 3 through 18 months, with radiographic changes in the subchondral bone, supports the hypothesis that the earliest changes in intervertebral disc disease in this animal model are related to the subchondral bone response.