Exploring the mechanisms of keloid recurrence
Rozan Odeh Alkresheh, Wolfgang Jarolimek, Ross Hamilton, Fiona Wood, K. Swaminathan Iyer, Nicole M. Smith, Lucy W. Barrett, Andrew Stevenson, Mark W. Fear
BACKGROUND
Keloids are abnormal, expanding pathological disorder that usually develop following skin trauma including injury, surgeries and burns. They are thought to be caused by an imbalance between extracellular matrix (ECM) deposition and degradation. Keloid treatment usually involves different stages and a combination of therapies. However, no standard method to treat keloids has been established, and all the current therapeutic options are accompanied with a recurrence rate that can reach up to 100% after certain types of treatment, such as surgical excision. Keloid recurrence is a serious health problem that significantly impacts patients’ lives, leading to physical impairment and emotional and psychological consequences, increased healthcare costs, and repeated therapeutic interventions. As there is a lack of studies on the drivers of recurrence, this study aims to understand the molecular and cellular mechanisms behind keloid recurrence, which will be crucial to improve clinical management and patient outcomes.
CONCLUSION
In this study we report a conserved cellular composition of recurrent keloid samples from different body sites. Differential gene expression was observed in a few gene sets and their associated biological processes in the T cell cluster originating from shoulder body site, indicative of body- site specific differences in keloid phenotype. There were differences identified in the abundance of neutrophiles in diseased samples compared to normal skin, however further investigation and larger sample sizes are needed to confirm these trends. In addition, normal fibroblasts showed a
variable response to conditioned media from primary verses recurrent keloid fibroblasts, indicating distinct signalling effects associated with primary and recurrent keloid. Understanding the differences between primary and recurrent keloid and their underling mechanisms is crucial for developing better therapeutic choices and prevention strategies to reduce the burden of keloid recurrence.
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