Systemic Impact of Breast Reconstruction

Normal wound repair generates a physiological angiogenic response to deliver nutrients and inflammatory cells to injured tissue. The angiogenic response enables the removal of debris with a central role in the development of a granulation tissue framework for wound closure. The mediators of wound angiogenesis include soluble factors such as VEGF, tumor necrosis factor (TNF), TGF-b, bFGF, and platelet-derived growth factor (PDGF). Angiogenic activators (e.g., VEGF) and inhibitors (e.g., thrombospondin-1) participation has been described at various stages of wound repair, suggesting that the neo-angiogenic process is regulated through a balance of vessel growth and regression. It has been suggested that the inflammatory cells and flogosis mediators found in tumors contribute to tumor growth, progression, and immunomodulation. Patients undergoing major oncological resections, intended as a tissue-damaging process, might develop cytokine dysregulation and subsequent postsurgical immunosuppression, especially when the operation is of long duration, recapitulating a wound repair-like environment. The balance between pro- and anti-angiogenic factors should be investigated in order to better understand the relation between stroma—tumor interaction with a possible systemic expression that may increase the risk of a local as well as a distant tumor spreading.