The Angiogenic Capacity From Ligamentum Flavum Subsequent to Inflammation

Moon, Hong Joo; Park, Youn Kwan; Ryu, Young-Joon; Kim, Jong Hyun; Kwon, Taek Hyun; Chung, Hung Seob; Kim, Joo Han

doi:10.1097/brs.0b013e3182269b19

Cited by 32 publications

(19 citation statements)

References 43 publications

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“…Attention has recently focused on angiogenesis, a pivotal component of scarring and the tissue repair process. Moon et al [40] reported that LF cells interact with macrophage-like cells to produce angiogenesis-related factors, with the exception of transforming growth factor β1. Activated LF cells exposed to macrophages can impact the stimulus of angiogenesis-related factors.…”

Section: Discussionmentioning

confidence: 99%

Analysis of the Relationship between Ligamentum Flavum Thickening and Lumbar Segmental Instability, Disc Degeneration, and Facet Joint Osteoarthritis in Lumbar Spinal Stenosis

et al. 2016

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Study DesignCross-sectional study.PurposeTo investigate the relationship between ligamentum flavum (LF) thickening and lumbar segmental instability and disc degeneration and facet joint osteoarthritis.Overview of LiteraturePosterior spinal structures, including LF thickness, play a major role in lumbar spinal canal stenosis pathogenesis. The cause of LF thickening is multifactorial and includes activity level, age, and mechanical stress. LF thickening pathogenesis is unknown.MethodsWe examined 419 patients who underwent computed tomography (CT) myelography and magnetic resonance imaging after complaints of clinical symptoms. To investigate LF hypertrophy, 57 patients whose lumbar vertebra had normal disc heights at L4–5 were selected to exclude LF buckling as a hypertrophy component. LF thickness, disc space widening angulation in flexion, segmental angulation, presence of a vacuum phenomenon, and lumbar lordosis at T12–S1 were investigated. Disc and facet degeneration were also evaluated. Facet joint orientation was measured via an axial CT scan.ResultsThe mean LF thickness in all patients was 4.4±1.0 mm at L4–5. There was a significant correlation between LF thickness and disc degeneration; LF thickness significantly increased with severe disc degeneration and facet joint osteoarthritis. There was a tendency toward increased LF thickness in more sagittalized facet joints than in coronalized facet joints. Logistic regression analysis showed that LF thickening was influenced by segmental angulation and facet joint osteoarthritis. Patient age was associated with LF thickening.ConclusionsLF hypertrophy development was associated with segmental instability and severe disc degeneration, severe facet joint osteoarthritis, and a sagittalized facet joint orientation.

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Section: Discussionmentioning

confidence: 99%

Analysis of the Relationship between Ligamentum Flavum Thickening and Lumbar Segmental Instability, Disc Degeneration, and Facet Joint Osteoarthritis in Lumbar Spinal Stenosis

et al. 2016

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“…Multiple studies supported that LF hypertrophy is a major pathogenic factor of central LSS4,12,22), and that LF hypertrophy has close relationship with mechanical stress2,7,9,10,16). Furthermore, repetitive (longer duration) wide motion (wide segmental angulation) in maximal stenotic level could be considered as high mechanical stress that may lead to development of LF hypertrophy7). Together, the results suggest that even though there are several factors that may be related to the development of central LSS, LF hypertrophy could be the major anatomical causes of RNRs formation in central LSS patients.…”

Section: Discussionmentioning

confidence: 99%

Radiological Significance of Ligamentum Flavum Hypertrophy in the Occurrence of Redundant Nerve Roots of Central Lumbar Spinal Stenosis

Hur

Kwon

et al. 2012

J Korean Neurosurg Soc

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ObjectiveThere were previous reports of redundant nerve roots (RNRs) focused on their clinical significance and pathogenesis. In this study, we investigated the significant radiologic findings that correlate with RNRs occurrence. These relations would provide an advanced clue for clinical significance and pathogenesis of RNRs.MethodsRetrospective research was performed with data from 126 patients who underwent surgery for central lumbar spinal stenosis (LSS). Finally, 106 patients with common denominators (inter-observer accuracy : 84%) were included on this study. We divided the patients into two groups by MRI, patients with RNRs and those with no RNRs (NRNRs). Comparative analyses were performed with clinical and radiologic parameters.ResultsRNRs were found in 45 patients (42%) with central LSS. There were no statistically significant differences between the two groups in severity of symptoms. On the other hand, we found statistically significant differences in duration of symptom and number of level included (p<0.05). In the maximal stenotic level, ligamentum flavum (LF) thickness, LF cross-sectional area (CSA), dural sac CSA, and segmental angulation are significantly different in RNRs group compared to NRNRs group (p<0.05).ConclusionRNRs patients showed clinically longer duration of symptoms and multiple levels included. We also confirmed that wide segmental angulation and LF hypertrophy play a major role of the development of RNRs in central LSS. Together, our results suggest that wide motion in long period contribute to LF hypertrophy, and it might be the key factor of RNRs formation in central LSS.

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“…The major causes of LSCS are aberrant osteophyte formation within the facet joints, disc protrusion, and hypertrophy of the ligamentum flavum (LF) [1]–[3]. The LF covers most of the posterior and lateral part of the spinal canal; therefore, LF hypertrophy contributes directly to mechanical compression of the nerve root or cauda equina, or indirectly to vascular insufficiency, which leads to inadequate blood flow and oxygenation [2], [4], [5]. Several studies have investigated the mechanism underlying LF hypertrophy, but the mechanism has not been fully elucidated.…”

Section: Introductionmentioning

confidence: 99%

“…Several growth factors and inflammatory cytokines, such as transforming growth factor (TGF)-β1, participate in the pathological processes [2], [4], [5], [7]–[10]. TGF-β1 is a key factor in tissue fibrosis [11]–[15] and is abundantly expressed in hypertrophied degenerative LF tissues from LSCS patients [4].…”

Section: Introductionmentioning

confidence: 99%

“…These previous reports suggested that TGF-β1 plays important roles in LF hypertrophy through induction of fibrosis in LF tissues in the pathogenesis of LSCS. Previously, several studies suggested that mechanical stress causes accelerated LF degeneration and hypertrophy [1], [2], [5], [10], [16], [17]. Sairyo et al reported that mechanical stress causes micro-injury in LF tissues and that repeated micro-injury induces chronic inflammation and subsequent tissue fibrosis [2].…”

Section: Introductionmentioning

confidence: 99%

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Angiopoietin-Like Protein 2 Induced by Mechanical Stress Accelerates Degeneration and Hypertrophy of the Ligamentum Flavum in Lumbar Spinal Canal Stenosis

et al. 2014

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Chronic inflammation and subsequent fibrosis induced by mechanical stress play an important role in ligamentum flavum (LF) hypertrophy and degeneration in patients with lumbar spinal canal stenosis (LSCS). Angiopoietin-like protein 2 (Angptl2) is a chronic inflammatory mediator induced under various pathological conditions and increases the expression of TGF-β1, which is a well-characterized mediator in LF hypertrophy. We investigated whether Angptl2 is induced by mechanical stress, and whether it contributes to LF hypertrophy and degeneration by activating the TGF-β1 signaling cascade. In this study, we investigated human LF tissue and LF fibroblasts isolated from patients who underwent lumbar surgery. We found that Angptl2 was abundantly expressed in fibroblasts of hypertrophied LF tissues at both the mRNA and protein levels. This expression was not only positively correlated with LF thickness and degeneration but also positively correlated with lumbar segmental motion. Our in vitro experiments with fibroblasts from hypertrophied LF tissue revealed that mechanical stretching stress increases the expression and secretion of Angptl2 via activation of calcineurin/NFAT pathways. In hypertrophied LF tissue, expression of TGF-β1 mRNA was also increased and TGF-β1/Smad signaling was activated. Angptl2 expression in LF tissue was positively correlated with the expression of TGF-β1 mRNA, suggesting cooperation between Angptl2 and TGF-β1 in the pathogenesis of LF hypertrophy. In vitro experiments revealed that Angptl2 increased levels of TGF-β1 and its receptors, and also activated TGF-β1/Smad signaling. Mechanical stretching stress increased TGF-β1 mRNA expression, which was partially attenuated by treatment with a calcineurin/NFAT inhibitor or Angptl2 siRNA, indicating that induction of TGF-β1 expression by mechanical stretching stress is partially mediated by Angptl2. We conclude that expression of Angptl2 induced by mechanical stress in LF fibroblasts promotes LF tissue degeneration by activation of TGF-β1/Smad signaling, which results in LF hypertrophy in patients with LSCS.

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The Angiogenic Capacity From Ligamentum Flavum Subsequent to Inflammation

Cited by 32 publications

References 43 publications

Analysis of the Relationship between Ligamentum Flavum Thickening and Lumbar Segmental Instability, Disc Degeneration, and Facet Joint Osteoarthritis in Lumbar Spinal Stenosis

Analysis of the Relationship between Ligamentum Flavum Thickening and Lumbar Segmental Instability, Disc Degeneration, and Facet Joint Osteoarthritis in Lumbar Spinal Stenosis

Radiological Significance of Ligamentum Flavum Hypertrophy in the Occurrence of Redundant Nerve Roots of Central Lumbar Spinal Stenosis

Angiopoietin-Like Protein 2 Induced by Mechanical Stress Accelerates Degeneration and Hypertrophy of the Ligamentum Flavum in Lumbar Spinal Canal Stenosis

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