Morphology and TGF-beta1 Concentration Analysis of Ligamentum Flavum in Patients with Lumbar Canal Stenosis and Lumbar Disc Herniation.

The most common spinal disorder in elderly patients is lumbar spinal canal stenosis, causing low back and leg pain and paresis. The aetiology of degenerative changes occurring in lumbar stenosis remain unclear: some authors hypothesize hyperplasia and others hypertrophy of the LF. The change in LF is known to be related to degenerative changes secondary to the aging process or mechanical instability. This study aimed to analyse the ligamentum flavum (LF) of patients with lumbar canal stenosis and lumbar disc herniation to evaluate the morphology and concentration of the Transforming Growth Factor-beta 1 (TGF-beta 1). The study was undertaken in three phases: A) Measurement of the thickness of the ligamentum flavum in patients with lumbar stenosis and/or herniated lumbar disc through axial T1 weighted lumbo-sacral MR images; B) Removal of ligamentum flavum in patients undergoing intervention for lumbar stenosis and lumbar disc herniation (control group); C) Optical microscopy study of the morphology of degenerated ligamentum and immunohistochemical analysis to assess the concentration of TGF-beta 1 in the LF. Morphological analysis of the LF (i.e. the increase in the number of fibres or distension and relaxation of the same as a result of degenerative processes) and the presence or absence of a high concentration of TGF-beta1 (then more fibroblasts involved in the degenerative process) can be important to establish whether there is hypertrophy or hyperplasia of the LF in lumbar canal stenosis. The current study showed that decreased elasticity of the LF in the elderly is due to a loss of elastic fibres that are degenerated and a concomitant increase in collagenous fibres (hypertrophy). TGF-beta1 concentrations of the LF were higher in lumbar spinal stenosis than in disc herniations. This suggest that LF of lumbar canal stenosis is hypertrophic: LF hypertrophy could be due to thickening of the normal elastic layer and the abnormal collagenous layer and to higher expression of TGF-beta 1 by fibroblasts.