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<p>Keloids and refractory hypertrophic scars are severe fibroproliferative disorders that disproportionately affect darker skin phototypes, particularly Asian and African populations. Due to high recurrence rates with monotherapy, we conducted a narrative review (2019–2026) evaluating postoperative radiotherapy, integrating advances in single-cell transcriptomics, mechanobiology, and epigenetics. Radiotherapy acts beyond canonical DNA damage, exerting potent anti-angiogenic, anti-inflammatory, and epigenetic effects. Based on the oxygen enhancement ratio (OER), a short delay (24–48&#xa0;h) for electron beam irradiation may exploit reperfusion-associated reoxygenation; however, most current evidence supports early postoperative radiotherapy. It also counteracts mechanotransduction-driven YAP/TAZ signaling and targets mesenchymal fibroblast reservoirs responsible for recurrence. Clinically, hypofractionated regimens aiming for a BED₁₀ &gt; 30&#xa0;Gy are recommended (with awareness of α/β ratio uncertainty and variations by anatomical site, skin phototype, and modality). Multimodal management integrating surgery, radiotherapy, “chemical offloading” (corticosteroids or botulinum toxin), and mechanical tension reduction is advocated. Use in pediatric or pregnant patients requires strict ethical justification; application in hypertrophic scars should be reserved for rare refractory or keloid-like cases after failure of conservative therapy. Outcome evaluation should combine patient-reported measures (POSAS, SCAR-Q) with objective tools such as high-frequency ultrasound, with surveillance exceeding 5&#xa0;years for pigmentary changes. Future priorities include multicenter RCTs to standardize BED thresholds, exploration of proton/heavy-ion therapies, radiosensitizers, and prospective keloid radiotherapy registries in high-incidence regions like East Asia to enable genetically and biomechanically stratified precision therapy.</p><p>Level of Evidence: not gradable.</p>

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Postoperative radiotherapy for keloids and refractory hypertrophic scars: from biological mechanisms to clinical practice

  • 期刊论文

  • 发表日期：

    2026年5月30日

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  • Saiqian Wang,
  • Mengying Xu,
  • Zijing Zhang,
  • Jinsheng Li

摘要

Keloids and refractory hypertrophic scars are severe fibroproliferative disorders that disproportionately affect darker skin phototypes, particularly Asian and African populations. Due to high recurrence rates with monotherapy, we conducted a narrative review (2019–2026) evaluating postoperative radiotherapy, integrating advances in single-cell transcriptomics, mechanobiology, and epigenetics. Radiotherapy acts beyond canonical DNA damage, exerting potent anti-angiogenic, anti-inflammatory, and epigenetic effects. Based on the oxygen enhancement ratio (OER), a short delay (24–48 h) for electron beam irradiation may exploit reperfusion-associated reoxygenation; however, most current evidence supports early postoperative radiotherapy. It also counteracts mechanotransduction-driven YAP/TAZ signaling and targets mesenchymal fibroblast reservoirs responsible for recurrence. Clinically, hypofractionated regimens aiming for a BED₁₀ > 30 Gy are recommended (with awareness of α/β ratio uncertainty and variations by anatomical site, skin phototype, and modality). Multimodal management integrating surgery, radiotherapy, “chemical offloading” (corticosteroids or botulinum toxin), and mechanical tension reduction is advocated. Use in pediatric or pregnant patients requires strict ethical justification; application in hypertrophic scars should be reserved for rare refractory or keloid-like cases after failure of conservative therapy. Outcome evaluation should combine patient-reported measures (POSAS, SCAR-Q) with objective tools such as high-frequency ultrasound, with surveillance exceeding 5 years for pigmentary changes. Future priorities include multicenter RCTs to standardize BED thresholds, exploration of proton/heavy-ion therapies, radiosensitizers, and prospective keloid radiotherapy registries in high-incidence regions like East Asia to enable genetically and biomechanically stratified precision therapy.

Level of Evidence: not gradable.