Wound healing Cell proliferation

Attracts CLA+ T cells and directs them into the skin Attracts lymphocyte subsets during inflammation facilitates certain immune response Stimulates proliferation of epidermal and epithelial cells inhibits gastric secretion involves in wound healing Induces proliferation and migration fenestration in capillary endothelial cells Inhibits endothelial cell proliferation, vasculogenesis, neovessel formation inhibits angiogenesis of vascular beds suppresses tumor growth induces apoptosis and myeloperoxidase activity from neutrophils... 

Contact inhibition is observed in the process of wound healing and describes the ability of a tissue to stop cell proliferation again after cellular multiplication has filled up the defect caused by a wound. 

Fibrosis is a dynamic progression of dysregulated wound healing that results from chronic inflammation. It is a common pathology regardless of the tissue involved, and therefore, the mechanisms that progress to fibrosis can be widely applied. The recruitment, activation, and proliferation of inflammatory cells and their cooperation with resident cells appears to rely on the action of chemokines and the differential expression of the chemokine receptors by these cells. Thus, chemokine receptors make particularly attractive therapeutic targets. 

Recently, the activities of host defense peptides related to the resolution of infection have been suggested to result in part from nondirect antimicrobial activities. It has been postulated that immunomodulation may represent the primary action of these peptides in vivo as the immunomodulatory activities are retained under physiological conditions in contrast to the direct antimicrobial activities of most natural mammalian host defense peptides. These immunomodulatory activities include, but are not limited to, direct chemotactic activity, induction of chemokines and other immune mediators, stimulation of leukocyte degranulation and other microbicidal activities, effects on leukocyte and epithelial cell survival and apoptosis, stimulation of epithelial and endothelial cell proliferation, promotion of wound healing and angiogenesis, antiendotoxic and anti-inflammatory activities, and adjuvant fiinctions. These will be described in detail in the following sections and a summary is found in Table 1. 

In vitro, chlorhexidine can adversely affect gingival fibroblast attachment to root surfaces. Furthermore, protein production in human gingival fibroblasts is reduced at chlorhexidine concentrations that would not affect cell proliferation. Such findings corroborate earlier studies showing delayed wound healing in standardized mucosal wounds after rinsing with 0.5% chlorhexidine solution. 

The technology of Low Level Laser Therapy (LLLT) was introduced into clinical medicine more than three decades ago. This form of treatment has great appeal due to its novelty, ease in use, relatively cost-efficient and low morbidity profile [5], LLLT has been shown to improve remarkably the process of wound healing in humans [5-8] and animal models [9-11], In vitro studies demonstrated that LLLT has a stimulating effect on cell mitosis [12] and proliferation and migration of fibroblasts [13], keratinocytes [14, 15] and endothelial cells [16], LLLT enhances NO secretion [17] and cytokine production [18, 19] and may lead to increased dermal angiogenesis [20],... 

Fibrosis resulting in the loss of normal organ structures is the hallmark of chronic rejection. The fibrosis may be due to wound healing, which is then followed by the cellular necrosis of acute rejection. However, it must be pointed out that chronic rejection develops many times in the absence of acute rejection. Fibrosis may be a result of several diverse factors such as equation of chronic rejection with chronic delayed-type hypersensitivity reaction, injury to blood vessels and resulting response to chronic ischemia, the proliferation of smooth muscle cells in the intima of arterial walls producing vascular occlusion, or persistent viral infections that will induce cellular immune response. 

EGF — Angiogenesis, wound healing, proliferation/ differentiation of basal epithelial cells — Epithelial cells... 

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