Keloid Pathophysiology: Fibroblast or Inflammatory Disorders?

Abstract

Background: Keloids are defined as a benign dermal fibroproliferative disorder with no malignant potential. They tend to occur following trivial trauma or any form of trauma in genetically predisposed individuals. Keloids are known to grow beyond the margins of the wound and are common in certain body parts. The pathophysiology of keloid remains unclear, and fibroblasts have been presumed to be the main cells involved in keloid formation. Understanding the mechanism(s) of keloid formation could be critical in the identification of novel therapeutic regimen for the treatment of the keloids.

Objective: To review the pertinent literature and provide updated information on keloid pathophysiology.

Data source: A Medline PubMed literature search was performed for relevant publications.

Results: A total of 66 publications were retrieved, with relevant publications on the etiology and pathogenesis as well as experimental studies on keloids. All articles were critically analyzed, and all the findings were edited and summarized.

Conclusion: There is still no consensus as on what is the main driving cell to keloid formation. One may, however, hypothesize that keloid formation could be a result of an abnormal response to tissue injury, hence resulting in an exaggerated inflammatory state characterized by entry of excessive inflammatory cells into the wound, including macrophages, lymphocytes, and mast cells. These cells seem to release cytokines including transforming growth factor β1 that stimulate fibroblasts to synthesize excess collagen, which is a hallmark of keloid disease.