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Purpose <p>Adult spinal deformity (ASD) is prevalent in aging populations and often managed with multi-level spinal fusion surgery. A major postoperative complication is proximal junctional failure (PJF), a condition at the upper end of spinal constructs linked to poor muscle quality. While risk factors such as age, alignment, body mass index, and bone density are known, the molecular basis—particularly in paraspinal muscles—remains unclear. This study examines morphological and genetic characteristics of paraspinal muscles in ASD patients to identify predictors of PJF.</p> Methods <p>Thirty-four ASD patients undergoing posterior spinal fusion (≥ 4 levels to the pelvis) were prospectively enrolled. Paraspinal muscle biopsies were collected intraoperatively from two levels below the upper instrumented vertebra. Patients were followed for at least 30 months, with PJF defined as requiring revision due to junctional pathology. Gene expression of 42 target genes, and histological analysis of muscle, fat, and connective tissue were performed. Differences between 16 PJF and 18 non-PJF patients were statistically analyzed.</p> Results <p>Patients were in their 6th decade with a mean follow-up of 43 months. In the PJF group, the myogenic gene ASB15 was 2.18 fold change (FC) downregulated (<i>p</i> = 0.00804), and the fatty metabolism gene FABP4 was significantly upregulated (FC = 1.42, <i>p</i> = 0.0401) versus non-PJF patients. FABP4 expression correlated with multifidus functional cross sectional area on MRI (<i>r</i> = 0.673; <i>p</i> = 0.008). No significant differences in histologic muscle morphology or fiber size were found.</p> Conclusion <p>This study identifies significant differences in paraspinal muscle gene expression associated with the development of PJF following ASD surgery. Downregulation of the myogenic gene ASB15 and upregulation of the fatty metabolism gene FABP4 in patients who developed PJF highlight potential molecular mechanisms contributing to compromised paraspinal muscle quality and junctional integrity.</p>

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Altered myogenic and lipid metabolism gene expression in paraspinal muscles of patients with adult spinal deformity who develop proximal junctional failure

  • 期刊论文

  • 发表日期：

    2026年5月23日

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  • Pearce B. Haldeman,
  • Gregory M. Mundis,
  • Camille Nosewicz,
  • Anica Tillu,
  • Robert K. Eastlack,
  • Bahar Shahidi

摘要

Purpose

Adult spinal deformity (ASD) is prevalent in aging populations and often managed with multi-level spinal fusion surgery. A major postoperative complication is proximal junctional failure (PJF), a condition at the upper end of spinal constructs linked to poor muscle quality. While risk factors such as age, alignment, body mass index, and bone density are known, the molecular basis—particularly in paraspinal muscles—remains unclear. This study examines morphological and genetic characteristics of paraspinal muscles in ASD patients to identify predictors of PJF.

Methods

Thirty-four ASD patients undergoing posterior spinal fusion (≥ 4 levels to the pelvis) were prospectively enrolled. Paraspinal muscle biopsies were collected intraoperatively from two levels below the upper instrumented vertebra. Patients were followed for at least 30 months, with PJF defined as requiring revision due to junctional pathology. Gene expression of 42 target genes, and histological analysis of muscle, fat, and connective tissue were performed. Differences between 16 PJF and 18 non-PJF patients were statistically analyzed.

Results

Patients were in their 6th decade with a mean follow-up of 43 months. In the PJF group, the myogenic gene ASB15 was 2.18 fold change (FC) downregulated (p = 0.00804), and the fatty metabolism gene FABP4 was significantly upregulated (FC = 1.42, p = 0.0401) versus non-PJF patients. FABP4 expression correlated with multifidus functional cross sectional area on MRI (r = 0.673; p = 0.008). No significant differences in histologic muscle morphology or fiber size were found.

Conclusion

This study identifies significant differences in paraspinal muscle gene expression associated with the development of PJF following ASD surgery. Downregulation of the myogenic gene ASB15 and upregulation of the fatty metabolism gene FABP4 in patients who developed PJF highlight potential molecular mechanisms contributing to compromised paraspinal muscle quality and junctional integrity.