Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (687 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
The paired bands of yellow elastic tissue that connect adjoining laminae of the vertebrae. With the laminae, it forms the posterior wall of the spinal canal and helps hold the body erect.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Flaval Ligament; Flaval Ligaments; Ligament, Flaval; Ligaments, Flaval; Ligamenta Flava.
Where it fits in the MeSH classification
- Broader topics
- Ligaments, Articular
Research landscape
PubMed indexes 1,062 records tagged with the MeSH heading “Ligamentum Flavum” (counts retrieved 2026-10-31). 350 of them (33.0%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 384 records.
Reviews account for 92 records (8.7%) and meta-analyses for 6. Randomized controlled trials number 7 (0.7%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 95 |
| 2000-2009 | 233 |
| 2010-2019 | 384 |
| 2020 onward | 350 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 92 | 8.7% |
| Meta-analyses | 6 | 0.6% |
| Randomized controlled trials | 7 | 0.7% |
Method: PubMed query "Ligamentum Flavum"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in anatomy and physiology
Anatomy describes how body structures are built and physiology describes how they normally work, so most findings here are descriptive or mechanistic rather than evidence about treatment. Much of what is known comes from dissection, imaging, tissue studies and experiments in animals, and measurements in healthy volunteers can differ from those in people with disease or at different ages. Normal ranges vary between individuals and populations. Check whether a result was measured in people or in another species, the age and health of the participants, and the method used.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
Leptin-induced inflammation by activating IL-6 expression contributes to the fibrosis and hypertrophy of ligamentum flavum in lumbar spinal canal stenosis [1]
Abstract reading summary — source excerpts
- Opening excerpt
- 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).
- Closing excerpt
- 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.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (231 words)
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 (PPin 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.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 29436483 · DOI · PMC5874260
MiR-132-3p Regulates the Osteogenic Differentiation of Thoracic Ligamentum Flavum Cells by Inhibiting Multiple Osteogenesis-Related Genes [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Ossification of the ligamentum flavum (OLF) is a disorder of heterotopic ossification of spinal ligaments and is the main cause of thoracic spinal canal stenosis.
- Closing excerpt
- Overall, these results suggest that miR-132-3p inhibits the osteogenic differentiation of LF cells by targeting FOXO1, GDF5 and SOX6.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (179 words)
Ossification of the ligamentum flavum (OLF) is a disorder of heterotopic ossification of spinal ligaments and is the main cause of thoracic spinal canal stenosis. Previous studies suggested that miR-132-3p negatively regulates osteoblast differentiation. However, whether miR-132-3p is involved in the process of OLF has not been investigated. In this study, we investigated the effect of miR-132-3p and its target genes forkhead box O1 (FOXO1), growth differentiation factor 5 (GDF5) and SRY-box 6 (SOX6) on the osteogenic differentiation of ligamentum flavum (LF) cells. We demonstrated that miR-132-3p was down-regulated during the osteogenic differentiation of LF cells and negatively regulated the osteoblast differentiation. Further, miR-132-3p targeted FOXO1, GDF5 and SOX6 and down-regulated the protein expression of these genes. Meanwhile, FOXO1, GDF5 and SOX6 were up-regulated after osteogenic differentiation and the down-regulation of endogenous FOXO1, GDF5 or SOX6 suppressed the osteogenic differentiation of LF cells. In addition, we also found FOXO1, GDF5 and SOX6 expression in the ossification front of OLF samples. Overall, these results suggest that miR-132-3p inhibits the osteogenic differentiation of LF cells by targeting FOXO1, GDF5 and SOX6.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 27556448 · DOI · PMC5000765
Mechanical stress induces elastic fibre disruption and cartilage matrix increase in ligamentum flavum [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Lumbar spinal stenosis (LSS) is one of the most frequent causes of low back pain and gait disturbance in the elderly.
- Closing excerpt
- The findings also suggest that fusion surgery, which eliminates intervertebral instability, may change the property of the LF and lead to the relief of patients' symptoms.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (155 words)
Lumbar spinal stenosis (LSS) is one of the most frequent causes of low back pain and gait disturbance in the elderly. Ligamentum flavum (LF) hypertrophy is the main pathomechanism of LSS, but the reason for its occurrence is not clearly elucidated. In this study, we established a novel animal model of intervertebral mechanical stress concentration and investigated the biological property of the LF. The LF with mechanical stress concentration showed degeneration with elastic fibres disruption and cartilage matrix increase, which are similar to the findings in hypertrophied LF from patients with LSS. By contrast, decreased Col2a1 expression was found in the LF at fixed levels, in which mechanical stress was strongly reduced. These findings indicate that mechanical stress plays a crucial role in LF hypertrophy through cartilage matrix increase. The findings also suggest that fusion surgery, which eliminates intervertebral instability, may change the property of the LF and lead to the relief of patients' symptoms.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 29026131 · DOI · PMC5638934
Cartilage intermediate layer protein inhibits ligamentum flavum hypertrophy mediated by TGF-β1/SMAD3/SERPINE2 signaling pathway [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Lumbar Spinal Stenosis (LSS), a degenerative disorder, greatly impacts the elderly, often leads to discomfort, neurological problems, and a diminished quality of life.
- Closing excerpt
- This research explores the function of CILP in LFH through the use of sophisticated bioinformatics, human samples, and experimental models, identifying its regulatory influence via the TGF-β1/SMAD3/SERPINE2 pathway.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (122 words)
Lumbar Spinal Stenosis (LSS), a degenerative disorder, greatly impacts the elderly, often leads to discomfort, neurological problems, and a diminished quality of life. Ligamentum flavum hypertrophy (LFH), a marked influencor in LSS, is characterized by fibrosis resulting from excessive extracellular matrix deposition, largely driven by the differentiation of fibroblasts and inflammatory processes. Transforming growth factor β1 (TGF-β1) is pivotal in the LFH advancement by promoting fibrosis, highlighting its potential as a target for therapeutic strategies. Cartilage intermediate layer protein (CILP), known to regulate TGF-β1 activity in other tissues, may have potential in mitigating LFH. This research explores the function of CILP in LFH through the use of sophisticated bioinformatics, human samples, and experimental models, identifying its regulatory influence via the TGF-β1/SMAD3/SERPINE2 pathway.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41663775 · DOI · PMC12909686
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Ligamentum flavum fibrosis and hypertrophy: Molecular pathways, cellular mechanisms, and future directions [5]
- Research article Assessment of injury to the thoracolumbar posterior ligamentous complex in the setting of normal-appearing plain radiography [6]
- Research article Pathology of ossification of the posterior longitudinal ligament and ligamentum flavum [7]
- Research article The prevalence and clinical characteristics of thoracic spinal stenosis: a systematic review [8]
- Research article Outcomes and Complications Following Laminectomy Alone for Thoracic Myelopathy due to Ossified Ligamentum Flavum: A Systematic Review and Meta-Analysis [9]
- Research article Cyst of the ligamentum flavum [10]
References
- Sun C, Wang Z, Tian JW, Wang YH. Leptin-induced inflammation by activating IL-6 expression contributes to the fibrosis and hypertrophy of ligamentum flavum in lumbar spinal canal stenosis. . 2018. PMID 29436483 · DOI · PMC5874260
- Qu X, Chen Z, Fan D, Sun C, Zeng Y. MiR-132-3p Regulates the Osteogenic Differentiation of Thoracic Ligamentum Flavum Cells by Inhibiting Multiple Osteogenesis-Related Genes. . 2016. PMID 27556448 · DOI · PMC5000765
- Hayashi K, Suzuki A, Abdullah Ahmadi S, Terai H, Yamada K, Hoshino M, et al.. Mechanical stress induces elastic fibre disruption and cartilage matrix increase in ligamentum flavum. . 2017. PMID 29026131 · DOI · PMC5638934
- Dong J, Li P, Wu L, Meng S, Liu G, Chen X, et al.. Cartilage intermediate layer protein inhibits ligamentum flavum hypertrophy mediated by TGF-β1/SMAD3/SERPINE2 signaling pathway. . 2026. PMID 41663775 · DOI · PMC12909686
- Sun C, Zhang H, Wang X, Liu X. Ligamentum flavum fibrosis and hypertrophy: Molecular pathways, cellular mechanisms, and future directions. FASEB J. 2020. PMID 32608536 · DOI
- Lee JY, Vaccaro AR, Schweitzer KM, Lim MR, Baron EM, Rampersaud R, et al.. Assessment of injury to the thoracolumbar posterior ligamentous complex in the setting of normal-appearing plain radiography. Spine J. 2007. PMID 17630140 · DOI
- Ono K, Yonenobu K, Miyamoto S, Okada K. Pathology of ossification of the posterior longitudinal ligament and ligamentum flavum. Clin Orthop Relat Res. 1999. PMID 10078125 · DOI
- Chen G, Fan T, Yang X, Sun C, Fan D, Chen Z. The prevalence and clinical characteristics of thoracic spinal stenosis: a systematic review. Eur Spine J. 2020. PMID 32671614 · DOI
- Osman NS, Cheung ZB, Hussain AK, Phan K, Arvind V, Vig KS, et al.. Outcomes and Complications Following Laminectomy Alone for Thoracic Myelopathy due to Ossified Ligamentum Flavum: A Systematic Review and Meta-Analysis. Spine (Phila Pa 1976). 2018. PMID 29940604 · DOI · PMC6252088
- Baker JK, Hanson GW. Cyst of the ligamentum flavum. Spine (Phila Pa 1976). 1994. PMID 8029749 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.