Keloid : Pathogenesis
Image Description
Pathogenesis: The pathogenesis of keloid is multifactorial and is influenced by genetic predisposition as well as local tissue tension. About 50% of patients (especially those with multiple lesions) have a positive family history. With whole genome sequencing, a susceptibility gene ASAHI has been mapped to 8q23.3-p21.3 region.
There is dysregulation of collagen remodeling during the scar healing process, resulting in increased synthesis of collagen I and III, under the influence of TGF-β. Keloid fibroblasts show reduced apoptosis. Wnt/β-catenin pathway, which plays a role in normal wound healing and fibrosis, is strongly up-regulated. In addition, epigenetic changes have been observed in multiple pathways promoting fibrosis. An association of keloid has been noted with palmar, plantar and penile fibromatoses as well as connective tissue disease, including scleroderma, Ehlers-Danlos syndrome, and Rubinstein-Taybi syndrome.
The image shows keloid along the side of neck and upper chest in an adult female.
There is dysregulation of collagen remodeling during the scar healing process, resulting in increased synthesis of collagen I and III, under the influence of TGF-β. Keloid fibroblasts show reduced apoptosis. Wnt/β-catenin pathway, which plays a role in normal wound healing and fibrosis, is strongly up-regulated. In addition, epigenetic changes have been observed in multiple pathways promoting fibrosis. An association of keloid has been noted with palmar, plantar and penile fibromatoses as well as connective tissue disease, including scleroderma, Ehlers-Danlos syndrome, and Rubinstein-Taybi syndrome.
The image shows keloid along the side of neck and upper chest in an adult female.