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Background <p>Chronic Achilles tendon rupture (CATR) results from delayed diagnosis or treatment, leading to retracted tendon ends filled with biomechanically inferior scar tissue. Limited scar resection (LSR) offers a less invasive surgical option by preserving and repairing scar tissue between tendon stumps, but the quality of healing remains suboptimal. Polydeoxyribonucleotide (PDRN) has demonstrated pro-healing properties in tendon disorders, yet its effects on scar remodeling after LSR are unknown.</p> Methods <p>Chronic Achilles tendon rupture was induced in male Sprague-Dawley rats by full-thickness transection without repair and 4 weeks of unrestricted activity. Animals were randomized into four groups: normal, control (conservative treatment), LSR, and LSR+PDRN. Outcomes were assessed at 3 and 6 weeks post-intervention via macroscopical scoring, biomechanical testing (maximum load, stiffness, stress), histology (modified Movin score), and immunohistochemistry (COL I/III expression).</p> Results <p>Compared to conservative treatment, LSR technique demonstrated a faster recovery of maximum load to baseline levels, regardless of whether it was combined with PDRN adjuvant therapy. With PDRN supplementation, stiffness was also restored to baseline. Biomechanical outcomes improved throughout the healing process in all experimental groups, with the LSR+PDRN group exhibiting higher maximum load, stiffness, and stress than both the control and LSR groups. At week 3, the LSR+PDRN group showed enhanced fibroblast proliferation and COL III secretion. By week 6, COL I expression was significantly better in the LSR+PDRN group compared to the control and LSR groups, although it still differed from that of normal Achilles tendon.</p> Conclusion <p>PDRN treatment enhances the biomechanical strength, histological structure, and COL I composition of the scar tissue following LSR in a rat model of CATR.</p>

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Polydeoxyribonucleotide improves scar healing following limited scar resection for chronic Achilles tendon rupture in a rat model

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月9日

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  • Haochun Zhang,
  • Wenguang Wu,
  • Yun Su,
  • Chi Xiao,
  • Hongxun Wang,
  • Fengcheng Cui,
  • Weixuan Duan,
  • Xiangjun Meng

摘要

Background

Chronic Achilles tendon rupture (CATR) results from delayed diagnosis or treatment, leading to retracted tendon ends filled with biomechanically inferior scar tissue. Limited scar resection (LSR) offers a less invasive surgical option by preserving and repairing scar tissue between tendon stumps, but the quality of healing remains suboptimal. Polydeoxyribonucleotide (PDRN) has demonstrated pro-healing properties in tendon disorders, yet its effects on scar remodeling after LSR are unknown.

Methods

Chronic Achilles tendon rupture was induced in male Sprague-Dawley rats by full-thickness transection without repair and 4 weeks of unrestricted activity. Animals were randomized into four groups: normal, control (conservative treatment), LSR, and LSR+PDRN. Outcomes were assessed at 3 and 6 weeks post-intervention via macroscopical scoring, biomechanical testing (maximum load, stiffness, stress), histology (modified Movin score), and immunohistochemistry (COL I/III expression).

Results

Compared to conservative treatment, LSR technique demonstrated a faster recovery of maximum load to baseline levels, regardless of whether it was combined with PDRN adjuvant therapy. With PDRN supplementation, stiffness was also restored to baseline. Biomechanical outcomes improved throughout the healing process in all experimental groups, with the LSR+PDRN group exhibiting higher maximum load, stiffness, and stress than both the control and LSR groups. At week 3, the LSR+PDRN group showed enhanced fibroblast proliferation and COL III secretion. By week 6, COL I expression was significantly better in the LSR+PDRN group compared to the control and LSR groups, although it still differed from that of normal Achilles tendon.

Conclusion

PDRN treatment enhances the biomechanical strength, histological structure, and COL I composition of the scar tissue following LSR in a rat model of CATR.