**8. Problems with current strategies to reduce scarring**

Current strategies for non-surgical therapy for the treatment of keloids and hypertrophic scars include topical therapy and intra-lesional injections of corticosteroids. While literature has reported a success rate ranging between 50 to 100 percent; these methods have also been associated with hypopigmentation, dermal atrophy, telangiectasia, widening of the scar, and delayed wound healing [98].

#### **8.1 Prospects being explored to promote scarless-wound healing**

#### *8.1.1 Dermal stem cells*

While advances in genetic lineage-tracing technologies, cellular assays, and imaging techniques have revealed important stem and progenitor cell reservoirs in the inter- follicular epidermis, the eccrine sweat glands, and the hair follicle; given excisional wounds develop into areas lacking sweat and sebaceous glands as well as hair

follicles, further understanding of stem and progenitor cells would aide in achieving the ultimate goal of scarless wound healing following injury [99].

### *8.1.2 Interfollicular epidermis*

During wound healing of the interfollicular epidermis, a population of 'slowcycling cells' is suspected to demonstrate autocrine regulation [100, 101] until mobilised by a wound healing signal. The cell division frequency of these slow-cycling cells increases following a wound, which provides excess daughter cells that help in repairing the damage. Further, injured epithelium has been known to demonstrate behavioural plasticity with progenitors capable of reverting to multipotent states and multipotent cells differentiating to fill unipotent roles, [102, 103]. Exploring these avenues may eventually allow us to discover the hitherto undiscovered processes that would allow regenerative wound healing with negligible scarring.
