ArticleSpine surgery and related research2024
Insulin Resistance as a Risk Factor for Flavum Hypertrophy in Lumbar Spinal Stenosis.
Article in Spine surgery and related research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- The MOTION randomized controlled trial for treatment of lumbar spinal stenosis using the percutaneous mild® procedure: 5-year results.Interventional pain medicine · 2026Article
- Clinical and imaging impact of diabetes mellitus on elderly patients with lumbar spinal stenosis: a retrospective propensity score-matched study with ≥5-year follow-up.Frontiers in medicine · 2026Article
- Is bilateral laminectomy and fusion superior to total laminectomy and fusion in two-level lumbar spinal stenosis?Frontiers in surgery · 2026Article
- Comparison of functional outcomes in patients with lumbar canal stenosis with and without obesity treated with lumbar decompression surgery.Frontiers in surgery · 2026Article
- Prevalence and Demographic Associations of Ligamentum Flavum Hypertrophy in Lumbar Spinal Stenosis.Orthopedic research and reviews · 2026Article
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6 authors.
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Abstract
Introduction: Ligamentum flavum (LF) hypertrophy is the main etiological factor in the development of lumbar spinal stenosis (LSS); however, its molecular pathology remains unclear. Histologically, LF hypertrophy is characterized by a reduction in elastic fibers and an increase in collagen fibers. We previously performed miRNA transcriptomic analysis on excised LF from elderly patients with LSS and identified the insulin receptor signaling along with TGFβ-mediated signaling as pathways involved in ligament hypertrophy. Therefore, this study aimed to investigate the involvement of endogenous insulin as a risk factor for LF hypertrophy in patients with LSS. Methods: A total of 1,119 patients aged ≥65 years (average: 76.1±5.9 years) treated for LSS including surgery and conservative treatment were analyzed. The flavum canal ratio (FCR) was calculated in the MRI cross-sectional image, and an FCR of 0.4275 or greater was defined as ligamentous stenosis according to Sakai's criteria. Homeostatic model assessment for insulin resistance (HOMA-IR) was calculated and values ≥2.5 were indicative of insulin resistance in Japanese people. Results: Fifty-one percent of patients with LSS exhibited LF hypertrophy, correlating with higher age, proportion of males and diabetic patients, BMI, HOMA-IR, and creatinine. Among LSS patients, 43.0% had insulin resistance, with 47.1% exhibiting LF hypertrophy and 38.6% without LF hypertrophy, with a significant difference (p<0.01). LSS patients with high insulin resistance also demonstrated significantly higher FCR (p<0.05) and a higher percentage of LF hypertrophy (p<0.01). Conditional logistic regression analysis, adjusting for age, identified HOMA-IR as a significant factor. Conclusions: The study establishes an association between LF hypertrophy and insulin resistance. Considering LF hypertrophy as an inflammation-triggered degeneration of elastic fibers, age-related changes in LF may underlie the basis of inflammatory aging.
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