Systemic Impact of Breast Reconstruction

Abstract

Normal wound repair generates an angiogenic response to deliver nutrients and inflammatory cells to injured tissue. The angiogenic response facilitates the removal of debris and is central to the development of a granulation tissue framework for wound closure. The mediators of wound angiogenesis include soluble factors such as vascular endothelial growth factor, tumor necrosis factor, transforming growth factor β, basic fibroblast growth factor, and platelet-derived growth factor, which have been identified in several wound models. Angiogenic agonists (e.g., vascular endothelial growth factor) and antagonists (e.g., thrombospondin-1) have been described at various times during repair, suggesting that the neoangiogenic stimulus may be a balance of factors changing to favor either vessel growth or vessel regression. It has been suggested that the inflammatory cells and cytokines found in tumors are more likely to contribute to tumor growth, progression, and immunosuppression than they are to mount an effective host antitumor response. Patients undergoing major oncological resections might develop cytokine production dysregulation and subsequent postsurgical immunosuppression, especially when the operation is of long duration. The balance between proangiogenic and antiangiogenic factors should be investigated.