Chapters authored
Diabetic Foot Ulcer: A Historical Overview
This chapter reviews the historical discoveries and the evolution of medical practices in the management of diabetic foot ulcers (DFUs). The knowledge acquired by ancient civilizations such as Babylon, China, Egypt, and India was further developed by the Greeks and Romans, who made significant improvements in foot amputations. The Arabs preserved and expanded these records, making them accessible to scientists during the European Renaissance. It was not until the early twentieth century that a better understanding of the complex etiological factors of DFUs began to emerge. A turning moment in the history of DFUs occurred in 1921 with the discovery of insulin, which effectively divided the timeline into two distinct periods: pre-insulin and post-insulin. While the role of revascularization in treating ischemic DFUs was established in the 1950s and 1960s, the importance of offloading was recognized in the 1970s and 1980s. Recently, the focus of DFU management has shifted to prevention, and multidisciplinary care involving podiatrists, nurses, endocrinologists, surgeons, and infectious disease specialists. Through the utilization of advanced technology and innovative therapies, we are now closer than ever to a future where DFUs will no longer pose a threat to patients’ health.
Part of the book: Diabetic Foot Ulcers
Diabetic Foot Ulcer Wound Healing and Tissue Regeneration: Signaling Pathways and Mechanisms
This chapter digs into the complexities of diabetic foot ulcer (DFU) wound healing, encompassing cellular responses from fibroblasts, keratinocytes, and macrophages, as well as humoral responses involving the release of growth factors and cytokines. The normal wound healing process is hindered in diabetics by factors like infections, venous insufficiency, impaired oxygenation, age-related changes, immune dysfunction, and a dry environment, contributing to delayed and challenging wound healing. The discussion then focuses on the intricate interplay of signaling cascades, including PI3K/Akt, MAPK/ERK, and Wnt/β-catenin, in the pathology of DFUs. Diabetes induces disruptions in the PI3K/Akt pathway, impeding cell migration and angiogenesis due to compromised insulin signaling and increased oxidative stress. Abnormalities in the MAPK pathway, essential for inflammation and tissue remodeling, further impact wound closure in DFUs. Additionally, downregulation of the Wnt/β-catenin pathway, crucial for tissue regeneration, contributes to immune dysfunction, delaying healing in diabetic wounds. Finally, the chapter explores multifaceted factors contributing to the pathogenesis of DFUs, including epigenetic modifications, oxidative stress, advanced glycation end products (AGEs), the polyol pathway, diacylglycerol-protein kinase C (DAG-PKC) activation, and the nitric oxide (NO) pathway. Persistent hyperglycemia in diabetes hinders wound healing, causing chronic ulcers and complications. Addressing these mechanisms is crucial for revolutionizing management.
Part of the book: Diabetic Foot Ulcers