Mechanism of Ligamentum Flavum Hypertrophy.
- Author:
Jae Ho YANG
1
;
Young Mi KANG
;
Chul Hyun KI
;
Sa Hyun SUNG
;
Hwan Mo LEE
;
Seong Hwan MOON
Author Information
1. Department of Orthopedic Surgery, Yonsei University College of Medicine, Korea. shmoon@yuhs.ac
- Publication Type:Review
- Keywords:
Ligamentum flacvum;
Hypertrophy;
Lumbar spinal stenosis;
Relaxin
- MeSH:
Aged;
Anti-Inflammatory Agents, Non-Steroidal;
Cell Death;
Collagen;
Cytokines;
Decompression;
Decompression, Surgical;
Fibroblasts;
Fibrosis;
Freezing;
Humans;
Hypertrophy*;
Intercellular Signaling Peptides and Proteins;
Ligaments;
Ligamentum Flavum*;
Pathology;
Relaxin;
Spinal Canal;
Spinal Stenosis;
Spine;
Zygapophyseal Joint
- From:Journal of Korean Orthopaedic Research Society
2015;18(1):25-32
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Ligamentum flavum (LF) is yellowish ligament tissue connecting the lamina of adjacent vertebra. Degenerative changes in the spine cause the hypertrophy of LF and facet joint and disc bulging and herniation. These changes results in a narrowing of the spinal canal. Neural decompression surgery by removing the hypertrophied lamina, LF and disc pathologies has been considered as successful treatment method in lumbar spinal stenosis. This surgery has showed relatively satisfactory clinical results and has increased life-expectancy in elderly patients. However, issues about post spinal surgery syndrome and re-stenosis after the surgery also have been reported. Because LF is one of the main mechanisms of spinal stenosis, accurate understanding about pathologic mechanism on the LF hypertrophy may suggest alternative treatment methods such as medical treatment or less invasive treatment than surgical decompression can be considered. Hypertrophy of the ligamentum flavum is generated from increase of collagen synthesis, fibroblast proliferation, and fibrosis caused by 1) the expression of growth factors (TGF-beta1 etc.) stimulated by the repeated mechanical tension, 2) inflammatory cytokines from spinal facet joint structure and LF 3) delayed cell death, and 4) inflammatory cytokine from hypertrophied and degenerated LF itself. After the middle ages, gradual and partial inhibition of LF hypertrophy can be expected by administration NSAIDs or selective cyclo-oxygenase-2 inhibitors because these drugs may cause reduction of the increased cytokines. Also, relaxin can be another new treatment material for spinal stenosis by the mechanism of melting hypertrophied LF and reducing synthesis of collagen.
