Article
The putative role of inflammatory infiltrates in the hypertrophied ligamentum flavum
Die Rolle inflammatorischer Infiltrate im hypertrophierten Ligamentum flavum
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Published: | May 4, 2005 |
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Outline
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Objective
Hypertrophy of the ligamentum flavum (HLF) and its encroachment into the spinal canal play a major role in the pathogenesis of neurogenic claudication. The exact mechanisms underlying HLF are still unknown. Whereas the alterations in the architecture of the extracellular matrix components in HLF were well characterized in previous studies, there is no detailed information about the changes in the cellular composition.
Methods
Specimens of hypertrophied ligamenta flava were obtained at operation from 20 patients with lumbar osteoligamentous spinal canal stenosis. All samples were taken from the ligamentous insertion at the inferior articular process where it blends with the fibrous joint capsule and has contact with the nerve root. Paraffin sections were stained with hematoxylin and eosin and Elastica van Giesson. Immunohistochemistry was performed on 4μm paraffin sections using an ABC-method for demonstration of CD68, leucocyte common antigen, CD3 and CD20. For comparative reasons, sections of 5 normal ligamenta flava were examined in the same manner.
Results
The hypertrophied ligamenta flava were characterized by a relative increase in collagen fibers that were obviously disordered, sometimes interspersed with calcium crystal deposition or ossification of the extracellular matrix. Apart from an increment of fibroblasts, all specimen showed regions of neovascularization and perivascular inflammatory infiltrates, composed mainly of macrophages and T-lymphocytes. The extent of vascular proliferation and cellular infiltrates was correlated to the degree of hypertrophy, being moderate and peripherally arranged in moderate HLF and distinctive and scattered throughout the whole specimen in the advanced stages.
Conclusions
Hypertrophy of the ligamantum flavum is accompanied by a chronic inflammatory reaction, that might promote the proliferative process and contribute to nerve root injury. Although the etiology of this phenomenon remains obscure, our findings offer the potential therapeutic strategy of decelerating the process of HLF by the local application of anti-inflammatory agents.