Soft Stenosis of the Lumbar Spine: Thickness vs Hypertrophy of the Ligamentum Flavum. A Pathogenetic and Molecular Point of View
|Alessandro Landi* and Roberto Delfini|
|Department of Neurology and Psychiatry, Division of Neurosurgery, University of Rome Sapienza, Italy|
|Corresponding Author :||Alessandro Landi
Department of Neurology and Psychiatry
Division of Neurosurgery, University of Rome Sapienza
Viale del Policlinico 155, 00181, Rome, Italy
E-mail: [email protected]
|Received November 12, 2013; Accepted November 14, 2013; Published November 17, 2013|
|Citation: Landi A, Delfini R (2013) Soft Stenosis of the Lumbar Spine: Thickness vs Hypertrophy of the Ligamentum Flavum. A Pathogenetic and Molecular Point of View. J Spine 2:e111. doi:10.4172/2165-7939.1000e111|
|Copyright: © 2013 Landi A, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.|
In the literature, there is no longer agreement neither on the real existence neither on the pathogenicmechanism that causes ligamentous lumbar stenosis or “soft stenosis”. In particular, the main questions are: 1 – is it caused by the hypertrophy of the ligamentum flavum or by its withdrawal into the spinal canal due to the loss of elasticity and the disc collapse? 2 - is there a molecular substrate that can explain the hypertrophy of the ligamentum flavum? Lately, the identification of the fractalkine’s overexpression demonstrated a fundamental role of the metameric instability and of the joint inflammation in the pathogenesis of hypertrophy of the ligamentum flavum, thus making clear the association between joint hypermobility and soft spinal stenosis.
The study of this association is worthy of more clinical and instrumental findings, even if recent studies have shown growing evidence that the soft stenosis is a clinic-pathological well-defined entity. Its primum movens seems to be the vertebral instability and its molecular substrate seem to be the overexpression of fractalkine, going to place in the unstable phase of the degenerative cascade of the lumbar spine.