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Wound Healing, Ulcers, and Scars
Published in Ayşe Serap Karadağ, Lawrence Charles Parish, Jordan V. Wang, Roxburgh's Common Skin Diseases, 2022
Saloni Shah, Christian Albornoz, Sherry Yang
Clinical findings: Keloids will specifically grow beyond the border of the initial wound and will typically present with similar pigmentation of the patient’s skin (Figure 17.10). In contrast, hypertrophic scars are always confined to the region of the presenting wound and will typically present as erythematous lesions with variable pigmentation.
Common rhinology and facial plastics viva topics
Published in Joseph Manjaly, Peter Kullar, Advanced ENT Training, 2019
Keloids are caused by a proliferation of atypical fibroblasts at the site of skin injury. This leads to excessive deposition of initially type-3 collagen, which is then replaced by type-1 collagen. The risk of keloid formation is related to skin pigmentation, with the highest risk in Afro-Caribbeans, and is most common in young adults. They are most common when a wound is not aligned with relaxed skin tension lines (RSTLs). A keloid extends beyond the margin of the original injury or scar, whereas a hypertrophic scar does not.
Retinoids and Concomitant Surgery
Published in Ayse Serap Karadag, Berna Aksoy, Lawrence Charles Parish, Retinoids in Dermatology, 2019
In a study performed in 1986, keloid development was observed in six patients who underwent dermabrasion while they were on systemic isotretinoin therapy or after they had recently completed such therapy. All patients in this study developed keloids in atypical locations. The authors concluded that dermabrasion should be delayed in those patients who are taking or recently have been on isotretinoin therapy. Dermabrasion might have been performed on deeper layers of dermis in this case series study and it is accepted that this practice can increase the risk of proliferative scar formation, but this issue is not clear in the study. It is known that retinoids display modulatory effects on the metabolism of connective tissue, including suppression of collagenase. Authors have suggested that this effect may enhance keloid formation secondary to mechanical dermabrasion (22).
Molecular response of keloids to ionizing radiation: targeting FOXO1 radiosensitizes keloids
Published in International Journal of Radiation Biology, 2023
Min Hong, Xiaoqian Li, Yulan Liu, Wei Mo, Bin Shi, Shigao Chen, Tao Yan, Yuhong Shi, Daojiang Yu, Shuyu Zhang
In susceptible individuals, keloids may occur during the process of wound healing of cutaneous injury, which generally means abnormal proliferation of fibroblasts and extracellular matrix (ECM) deposition (Lyu et al. 2019). They are not just a matter of appearance because of wound hyperhealing. They can be pruritic and painful, causing both physical and psychological stress to the patient (Davis et al. 2013; Li et al. 2014; Glass 2017). Compared with normal skin, keloids have a higher ratio of type I/III collagen and lower expression of fibrillin-1 and decorin (Jumper et al. 2015). The clinical treatment for keloids includes intralesional corticosteroids, 5-fluorouracil, silicone-based products, laser therapy, pressure therapy, surgical resection, cryotherapy and radiotherapy (Gold et al. 2014). However, there is currently no universally effective treatment, and most therapies are successful for only a subset of patients and have limited long-term success, with high recurrence rates (Andrews et al. 2016). For instance, a 45% to 100% recurrence rate may occur when using surgical excision alone (Arno et al. 2014), while the effective rate of surgical resection combined with radiotherapy is 67% to 98% (Al-Attar et al. 2006). Although radiotherapy is an effective tool, the low tolerance of normal tissue and resistance of abnormal tissues still lead to the risk of alternative treatment after radiotherapy (Long et al. 2016). Therefore, it is imperative to develop novel means to increase the sensitivity of keloids to radiation, which would then reduce secondary insults.
A comparison expression analysis of CXCR4, CXCL9 and Caspase-9 in dermal vascular endothelial cells between keloids and normal skin on chemotaxis and apoptosis
Published in Journal of Plastic Surgery and Hand Surgery, 2022
Xinhang Dong, Mingzi Zhang, Yuanjing Chen, Chengcheng Li, Youbin Wang, Xiaolei Jin
To some extent, keloids are an inflammatory disease involving the reticular dermis layer, and injuries of the reticular dermis and abnormal wound healing are major causes of the disease. Studies have shown that pro-inflammatory cytokines such as TNF-α (tumor necrosis factor-α), IL-1α (interleukin-1α), IL-1β (interleukin-1β) and IL-6 (interleukin-6) in keloid tissue are highly expressed, which could promote chronic inflammation and cause invasive growth of keloids [17]. As it is shown in the KEGG pathway analysis from Enrichr, inflammatory mediator regulation of TRP channels is significantly enriched in the KEGG pathway, including up-regulated DEGs of PRKCG, PRKCE, TRPV4, TRPV2, CALML4, ADCY1 and PRKACB. In this process, a large number of blood vessels are formed, while the functions are not complete. Moreover, due to the increase of blood vessel permeability and the induction of chemokines, a great number of inflammatory factors accumulate in the extracellular matrix, which is consistent with the high inflammation status shown by the HE staining results.
Targeting of keloid with TRAIL and TRAIL-R2/DR5
Published in Journal of Dermatological Treatment, 2021
Pengfei Sun, Zhensheng Hu, Bo Pan, Xiaosheng Lu
Keloid is formed by skin trauma or pathological overgrowth of skin fibroblasts (1). Its characteristics include continuous growth in the range of proliferation, appearance higher than the normal skin surface, causing pain and itching feeling, and so on (2). Keloid is a common and frequently-occurring disease in plastic surgery. And it is also a refractory disease with extremely difficult clinical treatment. Like tumor diseases, it has the characteristics of treatment resistance and high recurrence rate after treatment (3–7). At present, clinicians regard keloid as a benign skin tumor limited to the skin surface (8–10). However, the pathogenesis of keloid and tumor is similar, including p53, Fas gene mutation or oncogene activation (11–14). The clinical treatment of keloid, such as drug injection treatment, surgical resection, cryotherapy, laser treatment and other therapeutic effects are poor (15–17). In recent years, it has been found that the formation of keloid is related to the imbalance of apoptosis of fibroblasts in scar and TRAIL can mediated apoptosis of fibroblasts (18,19). Therefore, the use of TRAIL and its receptors in the treatment of keloid has become a hot research topic.