Abstract
The mechanisms regulating hypertrophic scar (HTS) formation are multifactorial and complex. Early inflammation following dermal injury is believed to be a critical and essential event in the progression of normal wound healing and repair. It is generally accepted that acute inflammatory responses are necessary for normal wound repair, while chronic or excessive inflammation may lead to pathological scarring and fibrosis. A new study published in Experimental Dermatology revisited this topic and demonstrated that reduced and/or delayed early immunological responses were actually associated with HTS formation (1).
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