Cervical intervertebral disc degeneration induced by unbalanced dynamic and static forces: a novel in vivo rat model.

STUDY DESIGN: Establishment of a novel in vivo animal model of cervical spondylosis. OBJECTIVE: To investigate apoptotic, degenerative, and inflammatory changes occurring in the cervical intervertebral discs of rats. SUMMARY OF BACKGROUND DATA: Cervical degeneration occurs as the result of imbalance of both static and dynamic spinal stabilizers. The disc degeneration that occurs is characterized by increased local inflammation and increased apoptosis of intervertebral disc cells. METHODS: By excising the paraspinal musculature and posterior cervical spinal ligaments of rats, both static and dynamic cervical stabilizers were disrupted. The resultant biomechanical imbalance resulted in biochemical and histologic changes, which were characterized by light microscopy, electron microscopy, immunostaining, enzyme-linked immunosorbent assay, polymerase chain reaction, and in situ hybridization. RESULTS: Histologic analysis showed characteristic degenerative changes of the intervertebral discs and vertebral endplates following surgery. Ultrastructural examination revealed apoptotic changes, which were verified by immunostaining. Instability also resulted in significant up-regulation of inflammatory factors, as shown by enzyme-linked immunosorbent assay, polymerase chain reaction, and in situ hybridization. CONCLUSIONS: By creating static and dynamic posterior instability of the cervical spine, this novel model of cervical spondylosis results in rapid intervertebral disc degeneration characterized by increased apoptosis and local inflammation, such as that seen clinically.

Microfracture and changes in energy absorption to fracture of young vertebral cancellous bone following physiological fatigue loading.

STUDY DESIGN: Fifty-five human thoracolumbar vertebrae were randomly fatigue loaded and analyzed. OBJECTIVES: The purpose of this study was to explore the relationship between fatigue loading, trabecular microfracture, and energy absorption to fracture in human cadaveric thoracolumbar vertebrae. BACKGROUND: Although trabecular microfractures are found in vivo and have been produced by fatigue loading in vitro, the effect of the level of physiologic fatigue loading on microfracture and energy absorption has not been investigated. METHODS: Fifty-five human thoracolumbar vertebrae (T11-L4) were randomly divided into 5 groups: 1) control (no loading, n = 6); 2) axial compression to yield (n = 7); and 3-5) 20,000 cycles of fatigue loading at 2 Hz (each n = 14). The level of fatigue loading was determined as a proportion of the yield load of Group 2 as follows: 10% (Group 3), 20% (Group 4), and 30% (Group 5). Half of the specimens in groups 3 to 5 were used for radiographic and histomorphometric analysis to determine microfracture density and distribution, whereas the other half were tested to determine the energy absorption to yield failure. RESULTS: No radiographic evidence of gross fracture was found in any of the groups following fatigue loading. A mean 7.5% increase in stiffness was found in specimens subject to cyclic loading at 10% of yield stress (Group 3). Fatigue at 20% (Group 4) and 30% of yield stress (Group 5) caused significantly higher (P < 0.05) increases in mean stiffness of 23.6% and 24.2%, respectively. Microfracture density increased from 0.46/mm in Group 3 to 0.66/mm in Group 4 and 0.94/mm in Group 5 (P < 0.05). The energy absorbed to failure decreased from 21.9 J in Group 3 to 18.1 J and 19.6 J in Groups 4 and 5, respectively (P < 0.05). CONCLUSIONS: Fatigue loading at physiologic levels produced microfractures that are not detectable by radiography. Increased fatigue load results in an increase in microfracture density and decrease energy absorbed to fracture, indicating a reduced resistance to further fatigue loading.