Hypertrophy of the ligamentum flavum in lumbar spinal canal stenosis is associated with abnormal accumulation of specific lipids

AbstractLigamentum flavum hypertrophy (HLF) is the most important component of lumbar spinal canal stenosis (LSCS). Analysis of hypertrophied ligamentum flavum (HLF) samples from patients with LSCS can be an important que. The current study analyzed the surgical samples of HLF samples in patients with LCSC using quantitative and qualitative high performance-liquid chromatography and mass spectrometry. We collected ligamentum flavum (LF) tissue from twelve patients with LSCS and from four patients with lumbar disk herniation (LDH). We defined LF from LSCS patients as HLF and that from LDH patients as non-hypertrophied ligamentum flavum (NHLF). Total lipids were extracted from the LF samples and evaluated for quantity and quality using liquid chromatography and mass spectrometry. The total lipid amount of the HLF group was 3.6 times higher than that of the NHLF group. Phosphatidylcholines (PCs), ceramides (Cers), O-acyl-ω-hydroxy fatty acids (OAHFAs), and triglycerides (TGs) in the HLF group were more than 32 times higher than those of the NHLF group. PC(26:0)+H+, PC(25:0)+H+, and PC(23:0)+H+ increased in all patients in the HLF group compared to the NHLF group. The thickness of the LF correlated significantly with PC(26:0)+H+ in HLF. We identified the enriched specific PCs, Cers, OAHFAs, and TGs in HLF.

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Hypertrophy of the Ligamentum Flavum in Lumbar Spinal Canal Stenosis is Associated with Abnormal Accumulation of Specific Lipids

10.21203/rs.3.rs-644646/v1 ◽

2021 ◽

Author(s):

Tomohiro Yamada ◽

Makoto Horikawa ◽

Tomohito Sato ◽

Tomoaki Kahyo ◽

Yusuke Takanashi ◽

...

Keyword(s):

Mass Spectrometry ◽

Liquid Chromatography ◽

Spinal Canal ◽

Ligamentum Flavum ◽

Spinal Canal Stenosis ◽

Lumbar Spinal Canal Stenosis ◽

Lumbar Disk Herniation ◽

Canal Stenosis ◽

Lumbar Spinal Canal ◽

Lumbar Spinal

Abstract Purpose. Ligamentum flavum hypertrophy (HLF) is the most important component of lumbar spinal canal stenosis (LSCS). Analysis of hypertrophied ligamentum flavum (HLF) samples from patients with LSCS can be an important que. The current study analyzed the surgical samples of HLF samples in patients with LCSC using quantitative and qualitative high performance-liquid chromatography and mass spectrometry.Methods. We collected ligamentum flavum (LF) tissue from twelve patients with LSCS and from four patients with lumbar disk herniation (LDH). We defined LF from LSCS patients as HLF and that from LDH patients as non-hypertrophied ligamentum flavum (NHLF). Total lipids were extracted from the LF samples and evaluated for quantity and quality using liquid chromatography and mass spectrometry.Results. The total lipid amount of the HLF group was 3.6 times higher than that of the NHLF group. Phosphatidylcholines (PCs), ceramides (Cers), O-acyl-ω-hydroxy fatty acids (OAHFAs), and triglycerides (TGs) in the HLF group were more than 32 times higher than those of the NHLF group. PC(26:0)+H+, PC(25:0)+H+, and PC(23:0)+H+ increased in all patients in the HLF group compared to the NHLF group. The thickness of the LF correlated significantly with PC(26:0)+H+ in HLF. Conclusion. We identified the enriched specific PCs, Cers, OAHFAs, and TGs in HLF.

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Pathomechanism of Loss of Elasticity and Hypertrophy of Lumbar Ligamentum Flavum in Elderly Patients With Lumbar Spinal Canal Stenosis

Spine ◽

10.1097/brs.0b013e31815b650f ◽

2007 ◽

Vol 32 (25) ◽

pp. 2805-2811 ◽

Cited By ~ 77

Author(s):

Hirofumi Kosaka ◽

Koichi Sairyo ◽

Ashok Biyani ◽

Douglas Leaman ◽

Richard Yeasting ◽

...

Keyword(s):

Elderly Patients ◽

Spinal Canal ◽

Ligamentum Flavum ◽

Spinal Canal Stenosis ◽

Lumbar Spinal Canal Stenosis ◽

Canal Stenosis ◽

Lumbar Spinal Canal ◽

Lumbar Spinal

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Decreased elastic fibers and increased proteoglycans in the ligamentum flavum of patients with lumbar spinal canal stenosis

Journal of Orthopaedic Research® ◽

10.1002/jor.23130 ◽

2015 ◽

Vol 34 (7) ◽

pp. 1241-1247 ◽

Cited By ~ 7

Author(s):

Yutaka Yabe ◽

Yoshihiro Hagiwara ◽

Masahiro Tsuchiya ◽

Masahito Honda ◽

Kouki Hatori ◽

...

Keyword(s):

Spinal Canal ◽

Ligamentum Flavum ◽

Spinal Canal Stenosis ◽

Elastic Fibers ◽

Lumbar Spinal Canal Stenosis ◽

Canal Stenosis ◽

Lumbar Spinal Canal ◽

Lumbar Spinal

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Leptin-induced inflammation by activating IL-6 expression contributes to the fibrosis and hypertrophy of ligamentum flavum in lumbar spinal canal stenosis

Bioscience Reports ◽

10.1042/bsr20171214 ◽

2018 ◽

Vol 38 (2) ◽

Cited By ~ 7

Author(s):

Chao Sun ◽

Zhen Wang ◽

Ji-Wei Tian ◽

Yun-Hao Wang

Keyword(s):

Spinal Canal ◽

Ligamentum Flavum ◽

Spinal Canal Stenosis ◽

Collagen I ◽

Inflammatory Factor ◽

Fibrosis Score ◽

Lumbar Spinal Canal Stenosis ◽

Canal Stenosis ◽

Lumbar Spinal Canal ◽

Lumbar Spinal

The ongoing chronic inflammation and subsequent fibrosis play an important role in ligamentum flavum (LF) fibrosis and hypertrophy in patients with lumbar spinal canal stenosis (LSCS). Leptin is a chronic inflammatory mediator and involved in the fibrotic process in multiple organ systems. The present study aimed to investigate the role of leptin in LF fibrosis and its related regulatory mechanisms. The LF specimens were obtained during the surgery from 12 patients with LSCS (LSCS group) and 12 control patients with lumbar disc herniation (LDH) group. The morphologic changes and fibrosis score of LF were assessed by Hematoxylin and eosin (H&E) and Masson’s trichrome staining respectively. The location and expression of leptin in LF tissues were determined. Then, the LF cells were cultured and exposed to recombinant human leptin (rhleptin). Collagen I and III were used as fibrosis markers and IL-6 was used as the inflammatory factor. As a result, the LF thickness and fibrosis score in the LSCS group were significantly higher than those in the LDH group (P<0.05). Leptin was detected in the hypertrophied LF and its expression was substantially increased in the LSCS group and positively correlated with LF thickness and fibrosis score (P<0.05). Moreover, our in vitro experiments revealed that rhleptin treated LF cells elevated the expression of collagen I and III. Finally, leptin administration induced IL-6 expression via nuclear factor-κB (NF-κB) pathway in LF cell (P<0.05). Our study demonstrated novel molecular events for leptin-induced inflammation in LF tissue by promoting IL-6 expression and thus might have potential implications for clarifying the mechanism underlying LF fibrosis and hypertrophy.

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