Collagen deposition

Upon resolntion of the pathogen, the second phase of wonnd healing occurs where re-epithelialization and neovascularization are essential for wound closure. Formation of new blood vessels (angiogenesis) (Barcelos et al. 2005 Roy et al. 2008), fibrin matrices (Midwood et al. 2006), and collagen deposits (Seppinen et al. 2008) are all events that promote the wound closure process. 

Fig. 14.1. The Thl/Th2 balance is central to the regulation of normal wound repair. Tissue injury results in the initiation of an inflammatory response, mediated by a variety of cells and their by-products. Immune cells are recruited and cross-regulate the Thl/ Th2 balance that occurs in response to the cytokine environment. This balance is in turn cross-regulated by the chemokine/chemokine-receptor expression profile, which functions to amplify the inflammatory process. Cells residing in the injured tissue release profibrotic mediators, which promote fibroblast activation, proliferation, and differentiation to the myofibroblast phenotype. Myofibroblasts produce collagen to repair damaged tissue, which is an event that is favored by the inhibition of MMP activity. The Thl/Th2 balance is central to whether a normal or aberrant wound-repair process is established A Thl environment promotes normal tissue resolution (fibrinolysis), whereas a Th2 environment maintains the progression of fibrotic disease (excessive collagen deposition).

These results should be contrasted with the situation with sensors that were implanted over 30 days. The lag in these devices rose to 15-30 min. There was also a decline in sensitivity of the sensors to glucose, sensor accuracy, and the degree of closed-loop glycemic control.4 Based on the known effects and time course of collagen deposition that occurs as part of the foreign body reaction,12 13 it is very likely that this decline in sensor function was a direct result of this process. The effect of the foreign body reaction on the function of biosensors has been comprehensively reviewed by Wisniewski and colleagues.14 15... 

Our belief is that vascularizing compounds can increase vessel growth within the encapsulation tissue surrounding a foreign body and probably improve sensor function modestly. Nonetheless, they have not been found to overcome the relentless process of collagen deposition and capsule formation caused by the foreign body reaction, which eventually blocks sensor function. In addition, they could have several major side effects. 

Williams EJ, Benyon RC, Trim N, Hadwin R, Grove BH, Arthur MJP, Unemori EN, Iredale JP. Relaxin inhibits effective collagen deposition by cultured hepatic stellate cells and decreases rat liver fibrosis in vivo. Gut 2001, 49, 577-583. 

The major factors impacting sensor performance, whatever the physiological basis, are the degree of local vascularity and the loss of functional microvessels, together with the eventual presence and thickness of a fibrous capsule. Continued inflammation and collagen deposition eventually reach an equilibrium state, and the thickness of the fibrous capsule has been proposed as an index of biocompatibility.32 The thickness and vascularity of the capsule depend on the size, surface texture, and porosity of the implant.33-35... 

For any implanted device that is intended for long-term use, collagen encapsulation of the device will occur due to the immune response to the device.60 Collagen deposition typically begins at roughly 5-7 days postimplantation and takes up to a month to reach completion. In terms of calibration of the microdialysis probe, this layer of material will provide additional mass transport resistance and could be denoted as a trauma layer. 

The acute inflammatory process is associated initially with increased HA levels, the result of the cytokines released by the polymorphonuclear leukocytes, the predominant cells of the acute inflammatory process. The erythema, swelling, and warmth of the acute process are followed later by the characteristic dry appearance and the formation of wrinkles. The precise mechanisms are unknown, but may relate to the differences between acute and chronic inflammatory cells and the attendant chemical mediators released by such cells. Alternatively, initiation of a wound healing response, with collagen deposition, may be a mechanism invoked for the premature aged appearance of the skin in chronic inflammation. 

Longaker, M.T. et al., Studies in fetal wound healing, VI. Second and early third trimester fetal wounds demonstrate rapid collagen deposition without scar formation. J. Ped. Surg., 25, 63, 1990. 

Cirrhosis Liver disease characterized by loss of the normal microscopic lobular structure with fibrosis (collagen deposition). Usually the result of chronic exposure to a noxious agent such as ethanol. 

The hydroxyproline values agreed very well with the results of the morphometric fibrosis measurement. Without simultaneous administration of selected experimental agents, porcine serum treatment resulted in a pronounced accumulation of collagen in the liver. The formation of these collagen deposits was reduced in a dose-dependent manner using selected experimental agents. 

Hepatic cirrhosis is typically the end stage of liver disease. Cirrhosis describes an irreversible change (Treinen-Moslen, 2001) characterized by accumulation of excessive collagen deposition in the form of bridging fibrosis which disrupts the hepatic architecture. Cirrhosis may be micronodular or macronodular depending on the amount of fibrosis and tissue regeneration. Liver transplantation is the only solution to restore adequate liver fimction in human medicine. 

Evidence indicates that steroids affect other cells and substances that modulate inflammation. Exposure of human basophils to steroid in culture inhibits histamine release induced by an IgE-dependent stimulus. Steroids inhibit phospholipase A2, which prevents biosynthesis of arachidonic acid and subsequent formation of prostacyclin, thromboxane A, prostaglandins, and leukotrienes. Steroids also decrease capillary permeability and fibroblast proliferation and the quantity of collagen deposition, thereby influencing tissue regeneration and repair. 

Corsini E, Luster MI, Mahler J, et al. 1994. A protective role for T lymphocytes in asbestos-induced pulmonary inflammation and collagen deposition. Am J Respir Cell Mol Biol 11 531-539. 

Cirrhosis occurs most frequently in the setting of alcoholic liver disease and represents the final common pathway of a number of chronic liver diseases. The development of cirrhosis is characterized by the appearance of fibroblasts and collagen deposition. This is accompanied by a reduction in liver size and the formation of nodules of regenerated hepatocytes. As a result, total liver content of cytochrome P450 is reduced in these patients. Initially, fibroblasts deposit collagen fibrils in the sinusoidal space, including the... 

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