Hypertrophic scars and keloids: a review and current treatment modalities

Vandana Soni,Rajesh Mondal,Sanjeev Tripathi,Poornima Agrawal,Kumud Soni,Vishal Gour

doi:10.1186/s41702-020-00063-8

Abstract

Hypertrophic scars (HTS) are raised, red, rigid, inflexible cell-like, and cosmetic problems precipitated due to multiple underlying dermal injuries such as burn, surgery, and trauma during which aberrant wound healing with more pathological deposition of the extracellular matrix than degradation leads to their spawning. Till date, well established and specific treatments for HTS have not been reported; hence, the need of recent developments is thrusted with novel drug delivery vision. This review will try to encompass all the agogs to HTS, definition, pathophysiology, mechanism of hypertrophic scar formation, the role of growth factors in hypertrophic scarring, and their difference with keloids. Further, it will illuminate the available medicaments and recent advances in novel topical drug delivery systems such as ethosomes, transethosomes, liposomes, solid lipid nanoparticles, and microsponges for treatment of HTS.

Highlights

Scar is a cutaneous development in the skin, culminated by biological wound healing processes
Actual cause behind disposing of this phenomenon lies in certain critical paradigms of wound healing where the transformation of a wound clot into a granulation tissue hinges on the delicate balance of extracellular matrix proteins deposition and degradation rhythmically, and when this process is disrupted, abnormalities in natural scarring appear, resulting in either keloid or hypertrophic scar formation (Gauglitz et al 2011a, 2011b)
Our aim in this review is to present the modern available therapies and their mechanism of action for keloids and Hypertrophic scars (HTS) mitigation

Summary

Introduction

Scar is a cutaneous development in the skin, culminated by biological wound healing processes. In HTS and keloids, fibroblasts have upregulation of CTGF transcription and an exaggerated capacity for CTGF transcription in response to TGF-β stimulation, which suggested the blockage of CTGF activity, and further reduction of pathologic scar formation.

Results

Conclusion