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Keloid scarring is a fibroproliferative disorder of the skin of unknown pathophysiology, characterised by fibrotic tissue that extends beyond the boundaries of the original wound. 1 Keloids develop as a result of disturbance to skin architecture by any wound, and have a strong genetic component, appearing in ethnicities with darker skin pigmentation. 1 There are estimated to be over 11 million keloids in the developed world, with the global number unknown but expected to be higher. 2 Current dogma suggests keloid development follows a similar pathway to normal wound healing but with chronic progression, suggesting disturbance in the fine control of cellular functions that occur during wound healing. 3 Epigenetics, defined as non-base-pair sequence alterations to the DNA, is a key regulator of cell functions, and aberrant epigenetic modifications have been found to contribute to many pathologies, including keloid scars. Our knowledge of progressive fibrosis remains limited, and therapeutic options are few and commonly ineffective, with keloids commonly recurring even after surgery and adjunct treatments. There is an urgent need to gain critical knowledge that will allow us to design better therapeutic strategies and provide evidence to support clinical decisions. This review will explore the current knowledge of the contribution of epigenetic modifications such as DNA methylation, histone modification, microRNAs, long non-coding RNAs to keloid scar formation and progression, and potential treatments utilising modifiers of these processes.

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Burn injuries are traumatic experiences that can detrimentally impact an individual’s psychological and emotional wellbeing. Despite this, some survivors adapt to psychosocial challenges better than others despite similar characteristics relating to the burn. Positive adaptation is known as resilience or posttraumatic growth, depending on the trajectory and process. This review aimed to describe the constructs of resiliency and growth within the burn injury context, examine the risk factors that inhibit resilience or growth after burn (barriers), the factors that promote resilience or growth after burn (enablers), and finally to assess the impact of interventions that have been tested that may facilitate resilience or growth after burn. This review was performed according to the recently updated Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) Guidelines. An electronic search was conducted in November 2021 on the databases PubMed, Medline (1966-present), Embase (1974-present), PsycINFO for English-language peer-reviewed academic articles. There were 33 studies included in the review. Findings were mixed for most studies; however, there were factors related to demographic information (age, gender), burn-specific characteristics (TBSA, time since burn), person-specific factors (personality, coping style), psychopathology (depression, PTSD), and psychosocial factors (social support, spirituality/religion, life purpose) that were evidenced to be related to resilience and growth. One qualitative study evaluated an intervention, and this study showed that a social camp for burn patients can promote resilience. This study has presented a variety of factors that inhibit or encourage resilience and growth, such as demographic, individual, and social factors. We also present suggestions on interventions that may be used to promote growth following this adverse event, such as improving social support, coping styles and deliberate positive introspection.

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Introduction Dupuytren's disease (DD), a fibro-proliferative disorder of unknown aetiology, affects the palm and is characterised by progressive fibrosis, thickening of palmar fascia, and excess collagen deposition. Patients present with nodules, causing flexion deformity in ∼50%, resulting in loss of hand function. Excision is the standard treatment for DD, recurrence remains high. A 2015 Cochrane review concluded there is insufficient evidence to show superiority of any procedure used. Genetic and other studies have implicated WNT signalling in Dupuytren's pathology, including WNT4 dysregulation. It is not clear how WNT signalling/WNT4 plays a role in triggering DD. Methods Fibroblasts were isolated from the wrists of control healthy adult males and from a family that had inherited DD. Normal skin fibroblasts were treated with WNT4 siRNA and transcriptome of normal skin untreated, normal skin siRNA treated and DD family fibroblasts compared using RNASeq. Results Analysis of the transcriptomes from DD patient and normal fibroblasts showed significant differences including in WNT4 expression. Downregulation of WNT4 in normal fibroblasts using siRNA led to ‘DD-like’ changes in the transcriptome. Conclusion In people susceptible to DD WNT4 is downregulated even in non-fibrotic fibroblasts. Knockdown of WNT4 in normal fibroblasts led to changes making cells ‘DD-like’, suggesting downregulation of WNT4 could drive DD. Previous studies have shown that WNT4 is downregulated in DD disease in the cord cells. This study shows that WNT4 is downregulated in ‘non-disease’ cells, that downregulating WNT4 in normal skin fibroblasts leads to widespread ‘DD like’ changes in the transcriptome, suggesting WNT4 downregulation is a driver of DD disease.