Fibroplasia complicates a broad spectrum of diseases affecting many organ systems. Examples include cirrhosis, pulmonary fibrosis, as well as abnormal scar formation seen in bowel adhesions, joint contractures, keloid formation, and burn wounds. Fetal dermal wound repair is characterized by scarless repair with a lack of fibroplasia, restoration of normal dermal architecture, and is accomplished with minimal inflammation. In contrast, adult wounds heal with varying degrees of scar formation and have an exuberant inflammatory response. Factors released in the hemostatic wound plug, such as platelet-derived growth factor, promote inflammation, in part, through stimulation of pro- inflammatory cytokine production growth factor, promote inflammation, in part, through stimulation of pro-inflammatory cytokine production. Pro- inflammatory cytokines, such as interleukin-6 and interleukin-8, then recruit inflammatory cells such as polymorphonuclear cells, monocytes, and macrophages into the wound. Once in the wound, these cells become activated and amplify the inflammatory cytokine cascade resulting in more inflammation and cytokine production. In addition, these inflammatory cells produce growth factors that stimulate fibroblast proliferation and collagen production resulting in scar formation. We hypothesize that production of the anti-inflammatory cytokine interleukin-10 (IL-10) is up-regulated during fetal wound repair preventing amplification of the inflammatory process creating a permissive environment for scarless wound repair.
