Wound healing remodeling

The dermis provides a base for the epidermis and contains fibroblasts that elaborate proteins, such as collagens and elastin, which are crucial for the skin s structural integrity. In addition, mast cells, enriched in a variety of proinflammatory substances, play an important role in tissue remodeling, wound healing, and fibrosis. 

It is concluded that chronic leg ulcer patients probably lack the mechanisms that normalise their levels of antioxidant enzymes, which normally decrease at early stages of wound healing in order to allow blood granulocytes and tissue macrophages to perform their function in cleansing the wounded area. Consequently re-epitheUalisation and matrix remodeling processes are delayed. LLLT stimulates... 

Invasive or surgical placement of a biomedical device produces tissue trauma, resulting in the formation of a wound site. Normal wounds heal and remodel over time to restore tissue homeostasis in the absence of implanted materials. Interestingly, sites of long-term implants do not heal properly the ensuing FBR prompted by the... 

The influence of mechanical forces on skin structure and remodeling has been studied extensively in an attempt to do the following to understand wound healing and reduce hypertrophic scarring, to increase the skin surface area using balloon expanders, to study the reorganization and... 

The most important reaction requiring ascorbate as a cofactor is the hydroxylation of proline residues in collagen. Vitamin C is, therefore, required for the maintenance of normal connective tissue as well as for wound healing since synthesis of connective tissue is the first event in wound tissue remodeling. 

Taken together, the identification of mast cell hyperplasia and mediator release at sites of tissue fibrosis and wound healing, observations in animal models, and study of the actions of mast cell products, has provided much circumstantial evidence that mast cells are involved in tissue remodelling, healing and fibrosis. It is unlikely that mast cells are essential in these responses, but more likely that they augment them. Complex interactions between different connective tissue components, mast cells and other inflammatory cells are likely to operate, and are unlikely to be fully delineated in humans in vivo. It seems reasonable to hypothesize however that initial mast cell mediator release has the potential to activate fibroblasts, which may then promote the recruitment at d proliferation of further mast cells, explaining the mast cell hyperplasia often witnessed at sites of chronic inflammation. 

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