Collagens wound healing

A group of heritable disorders. Clinical features include hyperelastic skin, hyperextensible joints, easy bruising and poor wound healing. Collagen has decreased content of hydroxylysine. Deficient enzyme may be Lysyl oxidase (EC 1.4.3.6), Lysyl protocollagen hydroxylase (EC 1.14.11.4) or Procollagen peptidase (C-endopeptidase EC 3.4.24.19, or A-endopepti-dase EC 3.4.24.14). 

C Ascorbic acid Coenzyme in hydroxylation of proline and lysine in collagen synthesis antioxidant enhances absorption of iron Scurvy—impaired wound healing, loss of dental cement, subcutaneous hemorrhage... 

Recently, the notion that the chronicity of inflammation may not actually drive the fibrogenic process has been widely appreciated (Tables 1, 2, and 3). Some propose that it is indeed the alteration of the mesenchymal cell phenotypes that disrupts the balance between collagen synthesis and degradation in the wound-healing process, highlighted by clinical evidence that shows unsuccessful treatment of fibrosis with anti-inflammatory or immunosuppressive drugs (18,19). One scenario is that mesenchymal cells (myofibroblasts and fibroblasts) are phenotypically altered and thus do not undergo apoptosis after resolution. 

Zinc normally aids wound healing in terrestrial invertebrates. Wounding of the optic tentacle, foot tissue, and partial shell removal in Helix aspersa, a terrestrial gastropod, resulted in deposition of zinc in the wound area after 2 to 5 days. Increased zinc in Helix wound areas may be necessary to promote protein synthesis, collagen formation, and mitotic cell division (Ireland 1986). 

Fibroblasts and connective Poor wound healing and Impair fibroblast proliferation and collagen... 

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. 

The cell biology of wound healing is the subject of a comprehensive monograph [1]. The biochemistry of collagen [2], fibronectin [3], proteoglycans [4] and of other components of the ECM [5,6] have been treated in some detail. The synthesis and biological behavior of ECM analogs has been previously reviewed [7, 8]. 

When collagen-GAG matrices which can significantly delay the onset of wound contraction are seeded with a minimum density of easily separable skin cells (basal cells) from the same animal, and the cell-seeded matrices are then grafted, wound healing is affected in an even more profound way In this case,... 

The active form of vitamin C is ascorbate acid (Figure 28.8). The main function of ascorbate is as a reducing agent in several different reac lions. Vitamin C has a well-documented role as a coenzyme in hydroxy lation reactions, for example, hydroxylation of prolyl- and lysyl-residues of collagen (see p. 47). Vitamin C is, therefore, required for the mainte nance of normal connective tissue, as well as for wound healing. Vitamin C also facilitates the absorption of dietary jron from the intestine. 

A partial list of physiological functions til at have been determined to be affected by vitamin C deficiencies includes (1) absorption of iron (2) cold tolerance, maintenance of adrenal cortex (3) antioxidant (4) metabolism of tryptophan, phenylalanine, and tyrosine (5) body growth (6) wound healing (7) synthesis of polysaccharides and collagen (8) formation of cartilage, dentine, bone, and teeth and (9) maintenance of capillaries. 

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