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. 2007 Apr;16(4):547-55.
doi: 10.1007/s00586-006-0213-x. Epub 2006 Sep 1.

Temporo-spatial distribution of blood vessels in human lumbar intervertebral discs

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Temporo-spatial distribution of blood vessels in human lumbar intervertebral discs

Andreas G Nerlich et al. Eur Spine J. 2007 Apr.

Abstract

While there is consensus in the literature that blood vessels are confined to the outer anulus fibrosus of normal adult intervertebral disc, debate continues whether there is a vascular in-growths into inner parts of the intervertebral disc during degeneration. We therefore tested the hypothesis that vascular in-growth is not a distinct feature of disc degeneration. The specific endothelial cell marker CD 31 (PECAM) was used to immunohistochemically investigate 42 paraffin-embedded complete mid-sagittal human intervertebral disc sections of various ages (0-86 years) and varying extent of histomorphological degeneration. Additionally, 20 surgical disc samples from individuals (26-69 years) were included in this study. In discs of fetal to infantile age, blood vessels perforated the cartilaginous end plate and extended into the inner and outer anulus fibrosus, but not into the nucleus pulposus. In adolescents and adults, no blood vessels were seen except for the outer zone of the anulus fibrosus adjacent to the insertion to ligaments. The cartilaginous end plate remained free of vessels, except for areas with circumscribed destruction of the end plate. In advanced disc degeneration, no vessels were observed except for those few cases with complete, scar-like disc destruction. However, some rim lesions and occasionally major clefts were surrounded by a small network of capillary blood vessels extending into deeper zones of the anulus fibrosus. A subsequent morphometric analysis, revealed slightly "deeper" blood vessel extension in juvenile/adolescent discs when compared to young, mature and senile adult individuals with significantly "deeper" extension in the posterior than anterior anulus. The analysis of the surgical specimens showed that only sparse capillary blood vessels which did not extend into the nucleus pulposus even in major disc disruption. Our results show that vascular invasion deeper than the periphery was not observed during disc degeneration, which supports the hypothesis that vascular in-growth is not a distinct feature of disc degeneration.

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Figures

Fig. 1
Fig. 1
Vascular supply in postnatal intervertebral discs intervertebral disc using the vascular cell marker CD-31. The disc is invaded by large, often ectatic and thin-walled blood vessels that seem to form large vascular arcades within the disc cartilage. Vergrößerung: Original magnification a ×100; b ×250
Fig. 2
Fig. 2
Infantile intervertebral discs (2 years) reveal a focal obliteration of vascular channels (a H&E, b CD31 staining). The previous vascular channels seem to show some fibrosis, possibly the very first signs of vascular regression (b). Original magnification a ×250; b ×250
Fig. 3
Fig. 3
Adolescent intervertebral discs (16 years) are free of blood vessels (staining with CD31). There are only some vessels in the outer AF close to the ligaments. Original magnification: ×400
Fig. 4
Fig. 4
Young adult intervertebral discs (25 years) are also free of vessels (staining for CD31). There are some vascular arcades at the interface between the outer anulus fibrosus and the ligaments (arrow). Original magnification: ×400
Fig. 5
Fig. 5
Discs of older individuals (37 years) without major degeneration reveal some small blood vessels in the OAF, that extend significantly deeper into this zone as in the young adult group. Original magnification: ×400
Fig. 6
Fig. 6
Severely disturbed intervertebral discs of an elderly individual (77 years) show a focal ingrowth of blood vessels adjacent to degenerative lesions, sometimes in a granulation like pattern. An annular tear is associated with granulation tissue formation, which in turn contains small blood vessels (a). Small vascular invasion of the outer anulus fibrosus in the presence of a cleft formation (b). Original magnification: a ×400; b ×400

References

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