[libribook.com] Traumatic Scar Tissue Management 1st Edition

The diverse biological effects of NGF include the process of wound repair and
the development and survival of certain sympathetic and sensory neurons in both
the central nervous system (CNS) and PNS. NGF is secreted and synthesized by
a variety of cells, such as inflammatory and repair cells, including fibroblasts.
NGF plays a key role in the initiation and maintenance of inflammation in
various organs. Thus it has been suggested that NGF is also involved in
cutaneous wound repair. Exogenous NGF was shown to accelerate wound
healing in normal and healing-impaired diabetic mice and to promote the healing
of pressure ulcers in humans (Li et al. 1980, Lewin & Mendell 1993, Matsuda et
al. 1998, Bernabei et al. 1999, Werner & Grose 2003).
Etiological considerations thought to underlie human hypertrophic scar
formation include mechanical tension, nerve factors, inflammation, and foreignbody
reactions. Undue mechanical tension appears to be the most significant
causative factor. It is hypothesized that NGF is one of the mediators connecting
mechanical tension with pathophysiological scarring (Ramos et al. 2008, Moore
et al. 2009, Gabriel 2011, Schouten et al. 2012, Xiao 2013).
Mechanical tension stimulates mechanosensitive nociceptors and in turn,
stimulated fibers induce the hyper-release of neuropeptides and NGF, even in the
absence of mechanical tension, once the malignant cycle has begun.
Excess neuropeptides and NGF are implicated in the over-expression of repair
material, constituting pathophysiological scar formation (Xiao et al. 2013).