January 1, 2004 | Robert F. Diegelmann, Melissa C. Evans
Wound healing involves a complex process with distinct phases: hemostasis, inflammation, proliferation, and remodeling. Acute wounds heal efficiently through these phases, while pathologic conditions like fibrosis and chronic ulcers disrupt this process. Normal healing begins with hemostasis, followed by inflammation where neutrophils and macrophages clear debris and release growth factors. Fibroblasts then deposit collagen during proliferation, leading to remodeling. Pathologic conditions, such as non-healing ulcers, result from chronic inflammation and excessive collagen deposition, leading to fibrosis. Fibrosis is characterized by excessive matrix deposition and reduced remodeling, often associated with increased mast cells. Chronic ulcers are marked by persistent inflammation and impaired healing. Understanding these biological processes helps in developing strategies to treat pathological conditions. Key factors include cytokines and growth factors like PDGF and TGF-β, which regulate cell signaling and tissue repair. The healing cascade involves cell signaling, matrix production, and angiogenesis. Fibroblasts produce collagen, which is crucial for tissue repair. However, excessive collagen deposition leads to fibrosis, while insufficient deposition results in weak healing. Chronic ulcers require controlled inflammation and proper wound care. This review highlights the importance of understanding normal and abnormal wound healing to improve treatment outcomes.Wound healing involves a complex process with distinct phases: hemostasis, inflammation, proliferation, and remodeling. Acute wounds heal efficiently through these phases, while pathologic conditions like fibrosis and chronic ulcers disrupt this process. Normal healing begins with hemostasis, followed by inflammation where neutrophils and macrophages clear debris and release growth factors. Fibroblasts then deposit collagen during proliferation, leading to remodeling. Pathologic conditions, such as non-healing ulcers, result from chronic inflammation and excessive collagen deposition, leading to fibrosis. Fibrosis is characterized by excessive matrix deposition and reduced remodeling, often associated with increased mast cells. Chronic ulcers are marked by persistent inflammation and impaired healing. Understanding these biological processes helps in developing strategies to treat pathological conditions. Key factors include cytokines and growth factors like PDGF and TGF-β, which regulate cell signaling and tissue repair. The healing cascade involves cell signaling, matrix production, and angiogenesis. Fibroblasts produce collagen, which is crucial for tissue repair. However, excessive collagen deposition leads to fibrosis, while insufficient deposition results in weak healing. Chronic ulcers require controlled inflammation and proper wound care. This review highlights the importance of understanding normal and abnormal wound healing to improve treatment outcomes.