Keloid scars are formed by polyclonal fibroblasts.

We hypothesized that keloids are composed of polyclonal fibroblasts and are not tumors derived from a single abnormal cell. That is, they are not monoclonal fibroblast neoplasms but rather are formed by intrinsically normal polyclonal fibroblasts that are responding to an abnormal extracellular signal. This hypothesis was tested using a polymerase chain reaction-based assay to examine X-chromosome inactivation and thereby determine clonality of keloid tissue. Six of 12 keloid samples analyzed were polyclonal. Three were genetically noninformative, and 3 were monoclonal. The presence of polyclonal specimens is consistent with our hypothesis and predicts that keloids result from intrinsically normal fibroblasts that are responding to an abnormal extracellular signal. This result can guide future genetic and molecular studies to identify this proposed abnormal regulatory signal, which we expect to be an important regulator of normal and diseased scarring.