Background: Wound healing contributes to restoring skin integrity. However, scars affect soft tissue in all its layers, including the superficial and deep fascia; moreover, it has been demonstrated that the fibroblasts leading the scarring process develop from progenitors located in the superficial fascia. In the past, research into scar etiology has focused primarily on the dermal and epidermal layers, leaving the role of the fasciae largely overlooked. Many patients presenting with surgical or traumatic scars complain of the increased stiffness and thickness of the scar, reduced extensibility of the area surrounding it, and chronic pain persisting even after the healing process has been completed. The purpose of this systematic review is to investigate the non-invasive tools and methods employed for the objective evaluation of scars that involve fascial layers. Methods: A systematic literature search was conducted on PubMed and WOS. Registration DOI: 10.17605/OSF.IO/SDR3Q. Results: A total of 11 articles were selected; the etiologies of scars were surgical, traumatic, and other (keloids). The investigations were conducted using ultrasound, magnetic resonance imaging, strain elastography, and shear wave elastography on the visceral fasciae, superficial fascia, hypodermis, and musculoskeletal fasciae. Sliding of fasciae was assessed by ultrasound; thickness of fasciae was assessed by ultrasound and magnetic resonance imaging; stiffness was assessed by shear wave elastography and strain elastography; and the qualitative assessment was performed via ultrasound. Conclusions: Our literature review showed that ultrasound, magnetic resonance imaging, strain elastography, and shear wave elastography are currently adopted for investigating the sliding, thickness, stiffness, and qualitative features of scars involving fascial layers. Moreover, our research showed the existence of a gap in the scientific literature on this topic.

Background and Objectives: The thoracolumbar fascia (TLF) has been implicated in low back pain, but imaging-based characterization in specific degenerative lumbar pathologies—particularly in surgical cohorts—remains limited. To evaluate TLF thickness on Magnetic resonance imaging (MRI) and Ultrasound (US) across common lumbar pathologies, examine associations with age, body mass index, disability, and assess MRI–US agreement for TLF thickness. Materials and Methods: In this prospective single-centre cohort, adults scheduled for elective lumbar surgery underwent preoperative US (short- and long-axis at L3) and review of routine lumbar MRI (axial and sagittal T1-weighted measurements at L3) using standardized protocols. Disability was assessed using the Oswestry Disability Index (ODI). Group comparisons, correlation analyses, and intraclass correlation coefficients were used to evaluate between-diagnosis differences, patient-factor associations, and MRI–US agreement. Results: Thirty-seven patients were eligible (15 lumbar spinal stenosis, 5 discs herniations, 4 spondylolisthesis, 2 scoliosis, 9 revision surgeries, 2 trauma comparators). Median TLF thickness was 0.86 mm (0.16–1.40) on axial MRI, 1.12 mm (0.47–2.33) on sagittal MRI, 2.38 mm (1.01–5.91) on US short-axis, and 2.87 mm (1.12–5.74) on US long-axis. Axial MRI thickness differed across groups (p=0.010), driven by thinner measurements in trauma versus disc herniation (p=0.031); no significant group effects were observed on sagittal MRI or US. Age correlated positively with axial MRI thickness (p=0.021). No significant correlations were detected between ODI and TLF thickness on MRI or US. MRI–US agreement was poor, indicating the modalities are not interchangeable for TLF thickness measurement. Conclusions: TLF thickness measured on MRI and US did not consistently differentiate diagnostic groups and was not associated with disability. Thickness estimates differed substantially by modality, with poor MRI–US agreement. Larger studies with standardized acquisition and reliability testing are needed to clarify the clinical and mechanistic relevance of TLF imaging in degenerative lumbar disease and to determine whether it can support phenotype-based stratification within degenerative spine disease.

Background and Objectives: The thoracolumbar fascia (TLF) has been implicated in low back pain, but imaging-based characterization in degenerative lumbar disorders, particularly in surgical cohorts, remains limited. To describe MRI-derived and US-derived TLF thickness estimates in a heterogeneous degenerative lumbar surgical cohort and explore preliminary imaging patterns and associations with selected clinical variables. Materials and Methods: In this prospective single-center cohort, adults scheduled for elective lumbar surgery underwent preoperative US (short- and long-axis at L3) and review of routine lumbar MRI (axial and sagittal T1-weighted measurements at L3) using standardized protocols. Twenty-six patients were included (15 with lumbar spinal stenosis, five with lumbar disc herniation, four with spondylolisthesis, and two with scoliosis). Disability was assessed using the Oswestry Disability Index (ODI). Exploratory subgroup comparisons, correlation analyses, and Bland–Altman agreement analysis were used to examine subgroup patterns, patient–factor associations, and MRI–US agreement. Results: Interpretable data were available for 19 axial MRI, 18 sagittal MRI, 19 short-axis US, 15 long-axis US, and 19 ODI assessments; paired MRI–US measurements were available in 11 cases for sagittal/long-axis analysis and 12 for axial/short-axis analysis. Mean TLF thickness was 0.89 ± 0.33 mm on axial MRI, 1.16 ± 0.48 mm on sagittal MRI, 2.53 ± 1.44 mm on short-axis US, and 2.49 ± 1.14 mm on long-axis US. Exploratory subgroup analyses showed a between-diagnosis difference only for axial-MRI-derived TLF thickness (p = 0.007), with lower thickness in disc herniation than in stenosis (p = 0.008), while sagittal MRI and US thickness measures did not differ between groups (p ≥ 0.301). ODI was not consistently associated with TLF thickness on MRI or US. Conclusions: In this exploratory surgical cohort, US-derived TLF thickness values were higher than those previously reported in the literature, suggesting possible fascial alteration in degenerative lumbar disease. However, TLF thickness was not consistently associated with disability, and MRI- and US-derived measurements should be interpreted as modality-specific estimates rather than interchangeable values. Given the small heterogeneous cohort and measurement constraints, these findings are descriptive and preliminary, but they provide an imaging framework to guide future standardized studies.

Lumbar spinal stenosis (LSS) is a major cause of pain and disability, yet its pathophysiology remains incompletely understood. Although spinal decompression is the standard surgical treatment for LSS with disabling pain or with progressive neurological symptoms, clinical outcomes are often suboptimal, with reoperation required in 5–23% of cases. While degenerative changes in the vertebral canal have been extensively investigated, the potential contribution of the thoracolumbar fascia (TLF) has never been explored at the molecular level. We hypothesized that TLF undergoes extracellular matrix remodeling and inflammatory changes in LSS. Thoracolumbar fascia biopsies were collected from 14 patients undergoing spinal surgery (seven with LSS and seven controls with traumatic vertebral fractures). Total collagen content was quantified by hydroxyproline assay; collagen subtypes (I, III, VI and XII) by Western blotting; and inflammatory activity and extracellular matrix remodeling by ELISA quantification of TNF-α and MMP-2. LSS patients showed significantly higher hydroxyproline content (p = 0.026), indicating increased collagen deposition and fibrotic fascial remodeling, together with elevated MMP-2 levels (p = 0.038), consistent with active chronic extracellular matrix remodeling. TNF-α levels did not differ significantly between groups, although marked inter-individual variability was observed. Collagen subtype expression showed distinct trends but no significant differences. These findings provide the first molecular evidence of fibrotic remodeling and altered extracellular matrix turnover in TLF of LSS patients, supporting its role as an active contributor to disease pathophysiology and a potential diagnostic biomarker and therapeutic target.

Lumbar spinal stenosis (LSS) is a major cause of pain and disability, yet its pathophysiology remains incompletely understood. Although spinal decompression is the standard surgical treatment for LSS with disabling pain or with progressive neurological symptoms, clinical outcomes are often suboptimal, with reoperation required in 5-23% of cases. While degenerative changes of the vertebral canal have been extensively investigated, the potential contribution of the thoracolumbar fascia (TLF) has never been explored at the molecular level. We hypothesized that the TLF undergoes extracellular matrix remodeling and inflammatory changes in LSS. Thoracolumbar fascia biopsies were collected from 14 patients undergoing spinal surgery (7 with LSS and 7 controls with traumatic vertebral fractures). Total collagen content was quantified by hydroxyproline assay, collagen subtypes (I, III, VI and XII) by Western blotting, and inflammatory remodeling by ELISA quantification of TNF-α and MMP-2. LSS patients showed significantly higher hydroxyproline content (p = 0.026), indicating increased collagen deposition and fascial fibrosis, together with elevated MMP-2 levels (p = 0.038), supporting the presence of active chronic extracellular matrix remodeling. TNF-α levels did not differ significantly between groups, although marked inter-individual variability was observed. Collagen subtype expression showed distinct trends but no significant differences. These findings provide the first molecular evidence of fibrotic remodeling and altered extracellular matrix turnover in the TLF of LSS patients, supporting its role as an active contributor to disease pathophysiology and a potential diagnostic biomarker and therapeutic target.