Keloids: Review of Pathogenesis and Evidence-Based Treatment Modalities

Abstract

Keloids are fibroproliferative growths resulting from dysregulated healing following tissue injury with the subsequent deposition of excessive and disorganized collagen (Figure 1). Prolonged chronic inflammation in the reticular dermis in particular during healing, is thought to precede the development of keloids. Experimental studies have demonstrated an increased release of growth factors, cytokines, and multiple immune cells. The inflammatory cells secrete factors implicated in chronic inflammation, fibrosis and itch, among many others. 

Keloids demonstrate an autosomal dominant transmission with an incomplete penetrance, beginning most commonly in the 2nd and 3rd decades of life. Keloids can be seen in all patients, but most frequently in those of skin of colour, particularly individuals from North Africa, South America, the Middle East, India, and China. Areas of skin where keloids have the highest propensity to develop are related to other risk factors, including sites on the skin where an injury occurs due to dermatologic disease or external processes, high skin tension, and dense pilosebaceous content. Hypertension and obesity also appear to be associated with the development of keloids at a systemic level. Keloids may present as a single lesion or a few lesions, or they can be widespread, developing without any known preceding trigger. 

In addition to distress from the physical appearance, keloids cause additional morbidity from pain (i.e. allodynia, burning, and stinging) and pruritus. The Th2 cytokines, which are both profibrotic and pruritogenic, play a role and C-nerve fiber neuropathy ensues, producing pain and itch.