Reinnervation of Granulation Tissue

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Peripheral sensory and sympathetic postganglionic nerves also regenerate in healing wounds and play a significant role in the formation of granulation tissue

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FIGURE 2.4 Comparison of collagen organization in normal uninjured dermal architecture (a) vs collagen organization in dermal scar tissue (b). The collagen of the uninjured dermis has a reticular ("basket-weave") organization, whereas the collagen in a repaired dermis is cross-linked into thick bundles parallel to the wound surface. Reproduced with permission from Linares, 1996, From wound to scar. Burns 22:339352. Copyright 1996, Elsevier.

FIGURE 2.4 Comparison of collagen organization in normal uninjured dermal architecture (a) vs collagen organization in dermal scar tissue (b). The collagen of the uninjured dermis has a reticular ("basket-weave") organization, whereas the collagen in a repaired dermis is cross-linked into thick bundles parallel to the wound surface. Reproduced with permission from Linares, 1996, From wound to scar. Burns 22:339352. Copyright 1996, Elsevier.

because of their effects on inflammation (Gottwald et al., 1998; Kim et al., 1998). After wounding, the portion of the nerves distal to the injury degenerates within one to two days, then regenerates over the next two weeks, resulting in hyperinnervation of the granulation tissue. Subsequently, many of the nerve fibers regress. Thus reinnervation follows the same pattern of advance and recession as angiogenesis; in fact, it is possible that blood vessel and nerve regeneration are mechanistically coupled.

Denervation of wounded rat skin significantly delays wound contraction and re-epithelialization (Fukai, 2005). Injured sensory and sympathetic postganglionic nerves appear to help mediate the inflammation phase ("neurogenic inflammation") via antidromic (conduction in reversed direction) stimulation of release of neu-ropeptides such as substance P (Gottwald et al., 1998). There may be a relationship between the release of these neuropeptides and mast cell activation. There is an intimate microanatomic association of mast cells and nerves in the dermis. Nerve injury causes degranulation of mast cells, releasing histamine and cytokines that effect vasodilation, increased vascular permeability, attraction of neutrophils and macrophages, and increased fibro-blast activity. Denervation of sensory or sympathetic postganglionic fibers decreases these inflammatory effects (Gottwald et al., 1998; Kim et al., 1998; Egozi et al., 2003). However, the absence of mast cells from the skin has no effect on any aspect of dermal repair, so their effects appear to be redundant (Egozi et al., 2003).

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