The process of wound healing includes four phases: Hemostasis, inflammation, proliferation, and remodeling. Many wound dressings and technologies have been developed to enhance the body's ability to close wounds and restore the function of damaged tissues. Several advancements in wound healing technology have resulted from innovative experiments by individual scientists or physicians working independently. The interplay between the medical and scientific research fields is vital to translating new discoveries in the lab to treatments at the bedside. Tracing the history of wound dressing development reveals that there is an opportunity for deeper collaboration between multiple disciplines to accelerate the advancement of novel wound healing technologies. In this review, we explore the different types of wound dressings and biomaterials used to treat wounds, and we investigate the role of multidisciplinary collaboration in the development of various wound management technologies to illustrate the benefit of direct collaboration between physicians and scientists. K E Y W O R D Sbiomedical engineering, interdisciplinary teams, negative pressure wound therapy, wound dressings, wound healing | INTRODUCTIONA glossary of terms found in the introduction is provided in Table 1. | Overview of wound healingWound healing involves four phases: Hemostasis, inflammation, proliferation, and remodeling. 1 Wound healing begins with transient vasoconstriction of injured vessels. 2 In the initial phase, damage to the skin exposes the subendothelial collagen and tissue factor, leading to platelet aggregation. 3 In this process, Von Willebrand factor (vWF) binds to both the subendothelial collagen and the platelet receptor glycoprotein Ib/IX/V. 4 This adhesion, as well as thrombin generated by tissue factor, results in platelet activation, degranulation, and conformational change. 5 Conformational change in glycoprotein IIB/IIIA allows the binding of fibrinogen, a crucial step in platelet aggregation and formation of the platelet plug. Tissue factor and phosphatidylserine, located on the surface of platelets and endothelial cells, form a complex with circulating activated Factor VII, leading to activation of a coagulation cascade which results in the cleavage of fibrinogen to fibrin. 5 Fibrin activates Factor XIII, which acts to crosslink the fibrin monomers. The final result is a strong blood clot. 6