HEMATOLOGICAL DISORDERS AND IMPAIRED WOUND HEALING: MECHANISMS, CLINICAL CHALLENGES, AND MANAGEMENT STRATEGIES

Abstract

Wound healing is a complex, highly programmed biological cascade that includes four overlapping stages: hemostasis, inflammation, proliferation, and remodeling. It is based on the structural and functional integrity of blood components that include erythrocytes, leukocytes, platelets, and plasma proteins as the key elements that supply the important molecular machinery of tissue repair. This review will address how these molecular and cellular pathways are interrupted in the case of particular hematological conditions like anemias, coagulopathies, and the leukemic process, and highlight the therapeutic issues of these high-risk groups. Localized hypoxia observed in red blood cell disorders such as sickle cell disease and anemia prevents the production of collagen and angiogenesis. Infection becomes chronic, with a long-term period of inflammation, which is caused by dysfunctions of the immune system, including leukemia. Moreover, platelet and clotting diseases, such as thrombocytopenia and hemophilia, impair primary hemostasis and decrease the supply of essential growth factors, including PDGF and TGF-beta; thus, preventing the substitution of the healing phase with the proliferative one. In addition to cellular deficiencies, they frequently amplify oxidative stress and cytokine signaling dysregulation, which provides a highly hostile microenvironment and destroys the extracellular matrix. This multi-systemic interference implies the need to monitor blood viscosity and microcirculation specifically and provide high-quality clinical care that is based on the treatment of hematological pathology and the application of modern therapeutic techniques like platelet-rich plasma (PRP), recombinant growth factors, and stem cell therapy. Such disruptions can be important to understand to achieve better patient outcomes and prevent life-threatening complications.