Claudia Clair

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.

Fascia has traditionally been described as a passive connective tissue mainly composed of collagen types I and III. Recent research, however, has revealed its structural and functional complexity, suggesting the possible presence of additional collagen types. This study aimed to quantify the presence and distribution of collagen types I, III, VI, and XII in human superficial and deep fasciae to improve understanding of fascial extracellular matrix composition. Superficial and deep fascia samples were collected from 19 adult patients (ages 20–83 years; thigh and lumbar area). Histology, Azan Mallory staining, hydroxyproline quantification, Western blotting, and immunohistochemistry were performed. The results indicated that deep fascia contained significantly more total collagen than superficial fascia (0.55 ± 0.17 µg/mg vs. 0.36 ± 0.14 µg/mg, p < 0.01). Collagen type VI was the most abundant and widely distributed subtype in both superficial and deep fasciae (mean ratio equal to 0.24 ± 0.13 and 0.27 ± 0.10, respectively), nearly double that of collagen types I (0.12 ± 0.07 and 0.11 ± 0.08), III (0.13 ± 0.09 and 0.17 ± 0.11), and XII (0.13 ± 0.11 and 0.13 ± 0.04). Moreover, statistically significant anatomical differences were observed, despite considerable interindividual variability. Fasciae from the thigh showed higher levels of collagen types I and III (mean ratio of 0.17 and 0.27, respectively, in deep fascia; 0.14 for both types in superficial fascia), whereas fasciae of the lumbar region exhibited greater levels of collagen types VI and XII (ratio equal to 0.33 and 0.15, respectively, in deep fascia; 0.36 and 0.20 in superficial fascia). Overall, these findings highlighted the structural complexity and regional specialization of human fasciae, with potential functional implications for mechanotransduction and tissue adaptation.

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.

Fascia has traditionally been described as a passive connective tissue mainly composed of Collagen types I and III. Recent research, however, has revealed its structural and functional complexity, suggesting the possible presence of additional collagen types. This study aimed to quantify the presence and distribution of Collagen types I, III, VI, and XII in human superficial and deep fascia to improve understanding of fascial extracellular matrix composition. Superficial and deep fascia samples were collected from 19 adult patients (ages 20–83 years; thigh and lower back). Histology, Azan Mallory staining, hydroxyproline quantification, Western blotting, and immunohistochemistry were performed. Results indicated that deep fascia contained significantly more total collagen than superficial fascia (0.55 ± 0.17 µg/mg vs. 0.36 ± 0.14 µg/mg, p<0.01). Collagen type VI was the most abundant and diffusely distributed subtype in both superficial and deep fascia (mean ratio equal to 0.24 ± 0.13 and 0.27 ± 0.10, respectively), nearly double that of Collagen types I (0.12 ± 0.07 and 0.11 ± 0.08), III (0.13 ± 0.09 and 0.17 ± 0.11), and XII (0.13 ± 0.11 and 0.13 ± 0.04). Moreover, statistically significant anatomical differences were observed, although individual variability remained considerable. Fasciae from the thigh showed higher levels of Collagen types I and III (mean ratio of 0.17 and 0.27, respectively, in deep fascia; 0.14 for both types in superficial fascia), whereas fasciae of the low back region exhibited greater levels of Collagen types VI and XII (ratio equal to 0.33 and 0.15, respectively, in deep fascia; 0.36 and 0.20 in superficial fascia). Overall, these findings highlighted the structural complexity and regional specialization of human fasciae, with potential functional implications for mechanotransduction and tissue adaptation.

In recent years, the interest in the comprehension of the fasciae has significantly grown, together with the necessity of finding a consensus for a terminology of the fasciae in the research and clinical fields. Furthermore, it is becoming necessary to categorize the various types of fascia (superficial, deep, visceral, neural) since they possess different anatomical characteristics, and are implicated in different pathophysiological pathways. While in the past we have described the deep/muscular fascia, the aim of this work is to summarize and catalog the information relating to the human superficial fascia (thickness, cellular end extracellular matrix component, innervation, vascularization).

In recent years, the interest in the comprehension of the fasciae has significantly grown, together with the necessity to find a consensus for a terminology of the fasciae in the research and clinical fields. Furthermore, it is becoming necessary to categorize the various types of fascia (superficial, deep, visceral, neural) since they possess different anatomical characteristics, and are implicated in different pathophysiological pathways. While in the past we have described the deep/muscular fascia, the aim of this work is to summarize and catalogue the information relating to the superficial fascia (thickness, cellular end extracellular matrix component, innervation, vascularization).