Abstract
Wound healing is a highly ordered and well-coordinated process that involves several sequential phases of inflammation, haemostasis, proliferation, granular tissue formation, matrix formation and remodeling of the injured tissue. It is characterized by dynamic and reciprocal interactions among components of the extracellular matrix, growth factors, and cells. Although the proper healing of periodontal tissues is regulated by many factors like blood cells, epithelial and connective tissue cells, inflammatory cells and many soluble factors, mainly coagulation factors, growth factors and cytokines, the molecular mechanisms involved in the process of wound healing, still remain unclear. The interaction between periodontal pathogens and inflammatory process is regulated by a sequential network of cytokines which are essential for most periodontal tissue breakdown, leading to clinical signs of disease. The cytokine network takes control over inflammatory mechanisms in order to amplify or suppress tissue reactions in periodontal pathogenesis. Extracellular matrix macromolecules or some of their specific domains may play a major role in wound healing. Enhanced knowledge of these relations may suggest new therapeutic targets in wound healing process. In this review, mainly the pathophysiology of periodontal wound healing is highlighted.
Highlights
Periodontitis is one of the most common diseases in humans, characterized by progressive destruction of the tooth-supporting tissues
Reducing the Platelet-rich plasma (PRP) concentration by half stimulated the cells to secrete significantly higher hepatocyte growth factor, monocyte chemo attractant protein-1, epithelial-derived neutrophil-activating protein 78 and vascular endothelial growth factor A, as well as IL-6, which play requisite roles in granulation tissue formation, leukocyte chemotaxis, angiogenesis, re-epithelialization and tissue remodeling. These results suggest that higher PRP concentration favors inflammation, while lowering the concentration shift the healing process from inflammatory phase to proliferation and remodeling phases [39]
There is an imbalance in the expression of wound healing genes involved in the pathogenesis of periodontal lesions
Summary
Periodontitis is one of the most common diseases in humans, characterized by progressive destruction of the tooth-supporting tissues. Apart from tooth desorption, periodontitis has been linked to many systematic disorders, such as diabetes, coronary artery disease and stroke, as well as high risk of premature birth [1]. The host response to irritant follows a cascade of events involved in wound healing including vascular and cellular inflammatory events, cellular migration, proliferation and differentiation, angiogenesis and epithelialization, fibroplasia, matrix deposition and remodeling [4]. This process may be enhanced by the production of increased level of free radicals during the inflammatory phase, which leads to the inhibition of cell migration and proliferation, and damage the wound nearby tissue. This review aims to highlight the new target and recent mechanisms involved in wound healing
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