IMMUNOPATHOGENETIC MECHANISMS OF LIGAMENTUM FLAVUM FIBROTIC REMODELING AND POSTOPERATIVE EPIDURAL FIBROSIS IN DEGENERATIVE LUMBAR SPINAL STENOSIS (LITERATURE REVIEW)

Resume. Degenerative lumbar spinal stenosis is not limited to mechanical narrowing of the spinal canal. Hypertrophy of the ligamentum flavum represents an active fibrotic process characterized by loss and fragmentation of elastic fibers, collagen accumulation, fibroblast-to-myofibroblast transition, macrophage involvement, and activation of multiple inflammatory and profibrotic signaling pathways. Clinical observations demonstrate the importance of the ligamentous component: ligamentum flavum hypertrophy has been reported in 42.7% of patients with lumbar stenosis, with frequency increasing markedly with age. Molecular studies identify TGF-β1/Smad signaling as one of the central pathways of remodeling, while single-cell studies demonstrate fibroblast heterogeneity, SPP1-positive macrophages, and complex cell-to-cell interactions. Mechanical stress, hypoxia, oxidative stress, lipid metabolism, autophagy, and epigenetic regulation further modify the fibrotic response. Postoperative epidural fibrosis develops through related inflammatory and matrix-remodeling mechanisms, although the resected ligamentum flavum itself should not be regarded as the direct anatomical source of the postoperative scar. Keywords: lumbar spinal stenosis, ligamentum flavum, hypertrophy, fibrosis, TGF-β1, SPP1, macrophages, myofibroblasts, epidural fibrosis, immunopathogenesis.

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