(searched for: doi:10.4103/jcrt.jcrt_20_17)
Published: 24 August 2022
Frontiers in Cell and Developmental Biology, Volume 10; https://doi.org/10.3389/fcell.2022.957363
Background: Keloid scars (KSs), which are composed of abnormal hyperplastic scar tissue, form during skin wound healing due to excessive fibroblast activation and collagen secretion. Although surgical resection and radiation therapy are used to prevent recurrence, KS recurrence rates range from 15 to 23%, and the underlying mechanism is unclear.Methods: To elucidate the mechanism of keloid recurrence, we established a PDX model and the grafts remained for over 20 weeks after transplantation on the bilateral backs of the NCG mice.Results: RNA-seq revealed that KS tissue gene expression was highly consistent before and after transplantation. Then, one side of the KS graft was irradiated with electron beam therapy (10 Gy), significant increases in vimentin and fibroblast activation protein alpha (FAP) expression were observed after irradiation and were accompanied by severe microvascular destruction. Surprisingly, 4 weeks after irradiation, significantly increased recurrence was observed with increased FAP + tissue and cell cycle regulator expression, resulting in a remarkable altered graft volume. Moreover, irradiation-induced FAP upregulation markedly facilitated radiation resistance and increased cell cycle progression, decreased senescence, and increased energy production.Conclusion: Our findings revealed that irradiation causes increased abundance of FAP + cells, which was associated with cell proliferation and delayed cellular senescence, accompanied by ATP production.
Strahlentherapie Und Onkologie, Volume 197, pp 909-915; https://doi.org/10.1007/s00066-020-01736-3
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Burns & Trauma, Volume 8; https://doi.org/10.1093/burnst/tkaa031
Keloids are a fibroproliferative disorder that can result from a cutaneous injury to the reticular dermis. Recurrence rates as high as 100% have been reported following surgical excision alone. Consequently, a variety of post-surgical techniques have been employed to prevent keloid recurrence, including the use of radiation. Although numerous studies have shown post-excisional X-rays, electron beam, lasers and brachytherapy can reduce the rate of keloid recurrence, numerous inconsistencies, including a wide range of definitions for keloid recurrence, make it difficult to compare study outcomes. The review aims to examine the various means for defining keloid recurrence in clinical trials involving the use of radiation therapy. Searches of the Cochrane Library and PubMed were performed to identify the available information for post-surgical keloid recurrence following radiation therapy. Each identified study was reviewed for patient follow-up and criteria used to define keloid recurrence. The search results included clinical studies with external beam radiation, brachytherapy and superficial radiation therapy. Many studies did not include a definition of keloid recurrence, or defined recurrence only as the return of scar tissue. Other studies defined keloid recurrence based on patient self-assessment questionnaires, symptoms and scar elevation and changes in Kyoto Scar Scale, Japan Scar Workshop Scale and Vancouver Scar Scale scores. The results of this review indicate keloidectomy followed by radiation therapy provide satisfactory recurrence rates; however, clinical studies evaluating these treatments do not describe treatment outcomes or use different definitions of keloid recurrence. Consequently, recurrence rates vary widely, making comparisons across studies difficult. Keloid recurrence should be clearly defined using both objective and subjective measures.
Burns & Trauma, Volume 8; https://doi.org/10.1093/burnst/tkz003
Once scar tissues mature, it is impossible for the surrounding tissue to regenerate normal dermal tissue. Therefore, it is essential to understand the fundamental mechanisms and establish effective strategies to inhibit aberrant scar formation. Hypertrophic scar formation is considered a result of the imbalance between extracellular matrix synthesis and degradation during wound healing. However, the underlying mechanisms of hypertrophic scar development are poorly understood. The purpose of this review was to outline the management in the early stage after wound healing to prevent hypertrophic scar formation, focusing on strategies excluding therapeutic agents of internal use. Treatment aimed at molecular targets, including cytokines, will be future options to prevent and treat hypertrophic scars. More basic studies and clinical trials, including combination therapy, are required to investigate the mechanisms and prevent hypertrophic scar formation.