Showing papers by "Patricia Dolan published in 2013"

Intervertebral disc decompression following endplate damage: implications for disc degeneration depend on spinal level and age.

Abstract: Study design Mechanical and morphological studies on cadaveric spines. Objective To explain how spinal level and age influence disc degeneration arising from endplate fracture. Summary of background data Disc degeneration can be initiated by damage to a vertebral body endplate, but it is unclear why endplate lesions, and patterns of disc degeneration, vary so much with spinal level and age. Methods One hundred seventy-four cadaveric motion segments, from T7-T8 to L5-S1 and aged 19 to 96 years, were subjected to controlled compressive overload to damage a vertebral body. Stress profilometry was performed before and after damage to quantify changes in intradiscal pressure, and compressive stresses in the annulus. Eighty-six of the undamaged vertebral bodies were then sectioned in the midsagittal plane, and the thickness of the central bony endplate was measured from microradiographs. Regression analysis was used to compare the relative influences of spinal level, age, disc degeneration, and sex on results obtained. Results Compressive overload caused endplate fracture at an average force of 3.4 kN, and reduced motion segment height by an average 1.88 mm. Pressure loss in the adjacent nucleus pulposus decreased from 93% at T8-T9 to 38% at L4-L5 (R = 22%, P Conclusion Endplate fracture creates abnormal stress distributions in the adjacent intervertebral disc, increasing the risk of internal disruption and degeneration. Effects are greatly reduced in the lower lumbar spine, and in young specimens, primarily because of differences in nucleus volume, and materials properties, respectively. Disc degeneration between L4 and S1 may often be unrelated to endplate fracture. Level of evidence N/A.

Do intervertebral discs degenerate before they herniate, or after?

Abstract: The belief that an intervertebral disc must degenerate before it can herniate has clinical and medicolegal significance, but lacks scientific validity. We hypothesised that tissue changes in herniated discs differ from those in discs that degenerate without herniation. Tissues were obtained at surgery from 21 herniated discs and 11 non-herniated discs of similar degeneration as assessed by the Pfirrmann grade. Thin sections were graded histologically, and certain features were quantified using immunofluorescence combined with confocal microscopy and image analysis. Herniated and degenerated tissues were compared separately for each tissue type: nucleus, inner annulus and outer annulus. Herniated tissues showed significantly greater proteoglycan loss (outer annulus), neovascularisation (annulus), innervation (annulus), cellularity/inflammation (annulus) and expression of matrix-degrading enzymes (inner annulus) than degenerated discs. No significant differences were seen in the nucleus tissue from herniated and degenerated discs. Degenerative changes start in the nucleus, so it seems unlikely that advanced degeneration caused herniation in 21 of these 32 discs. On the contrary, specific changes in the annulus can be interpreted as the consequences of herniation, when disruption allows local swelling, proteoglycan loss, and the ingrowth of blood vessels, nerves and inflammatory cells. In conclusion, it should not be assumed that degenerative changes always precede disc herniation. Cite this article: Bone Joint J 2013;95-B:1127–33.