Which of the following is FALSE regarding polymorphonuclear neutrophils (PMNs) and their role in wound healing?
Polymorphonuclear neutrophils (PMNs) are the first infiltrating cells to enter the wound site, peaking at 24 to 48 hours. Increased vascular permeability, local prostaglandin release, and the presence of chemotactic substances such as complement factors, interleukin-1 (IL-l), tumor necrosis factor-α (TNF-α), transforming growth factor-β (TGF-β), platelet factor 4, or bacterial products all stimulate neutrophil migration. The postulated primary role of neutrophils is phagocytosis of bacteria and tissue debris. PMNs are also a major source of cytokines early during inflammation, especially TNF-α, which may have a significant influence on subsequent angiogenesis and collagen synthesis. PMNs also release proteases such as collagenases, which participate in matrix and ground substance degradation in the early phase of wound healing. Other than their role in limiting infections, these cells do not appear to play a role in collagen deposition or acquisition of mechanical wound strength. On the contrary, neutrophil factors have been implicated in delaying the epithelial closure of wounds.
The proliferative phase of wound healing occurs how long after the injury?
Normal wound healing follows a predictable pattern that can be divided into overlapping phases defined by the cellular populations and biochemical activities: (1) hemostasis and inflammation, (2) proliferation, and (3) maturation and remodeling. The proliferative phase is the second phase of wound healing and roughly spans days 4 through 12. It is during this phase that tissue continuity is reestablished. Fibroblasts and endothelial cells are the last cell populations to infiltrate the healing wound, and the strongest chemotactic factor for fibroblasts is platelet-derived growth factor (PDGF). Upon entering the wound environment, recruited fibroblasts first need to proliferate, and then become activated, to carry out their primary function of matrix synthesis remodeling. This activation is mediated mainly by the cytokines and growth factors released from wound macrophages.
Which of the following is true regarding the fibroblastic phase of wound healing?
The maturation and remodeling of the scar begins during the fibroblastic phase, and is characterized by a reorganization of previously synthesized collagen. Collagen is broken down by matrix metalloproteinases (MMPs), and the net wound collagen content is the result of a balance between collagenolysis and collagen synthesis. There is a net shift toward collagen synthesis and eventually the reestablishment of extracellular matrix composed of a relatively acellular collagen- rich scar. Wound strength and mechanical integrity in the fresh wound are determined by both the quantity and quality of the newly deposited collagen. The deposition of matrix at the wound site follows a characteristic pattern: fibronectin and collagen type III constitute the early matrix scaffolding; glycosaminoglycans and proteoglycans represent the next significant matrix components; and collagen type I is the final matrix. By several weeks postinjury the amount of collagen in the wound reaches a plateau, but the tensile strength continues to increase for several more months. Fibril formation and fibril cross-linking result in decreased collagen solubility, increased strength, and increased resistance to enzymatic degradation of the collagen matrix. Fibrillin, a glycoprotein secreted by fibroblasts, is essential for the formation of elastic fibers found in connective tissue. Scar remodeling continues for many (6- 12) months postinjury, gradually resulting in a mature, avascular, and acellular scar. The mechanical strength of the scar never achieves that of the uninjured tissue.
Which of the following is commonly seen in Ehlers-Danlos syndrome (EDS)?
Ehlers-Danlos syndrome (EDS) is a group of 10 disorders that present as a defect in collagen formation. Over half of the affected patients manifest genetic defects encoding alpha chains of collagen type V, causing it to be either quantitatively or structurally defective. These changes lead to "classic" EDS with phenotypic findings that include thin, friable skin with prominent veins, easy bruising, poor wound healing, atrophic scar formation, recurrent hernias, and hyperextensible joints. Gastrointestinal (GI) problems include bleeding, hiatal hernia, intestinal diverticula, and rectal prolapse. Small blood vessels are fragile, making suturing difficult during surgery. Large vessels may develop aneurysms, varicosities, arteriovenous fistulas, or may spontaneously rupture.
Patients with Marfan syndrome are associated with what genetic decect?
Patients with Marfan's syndrome have tall stature, arachnodactyly, lax ligaments, myopia, scoliosis, pectus excavatum, and aneurysm of the ascending aorta. Patients who suffer from this syndrome are also prone to hernias. Surgical repair of a dissecting aneurysm is difficult, as the soft connective tissue fails to hold sutures. Skin may be hyperextensible, but shows no delay in wound healing. The genetic defect associated with Marfan's syndrome is a mutation in the FBN-1 gene which encodes for fibrillin. Previously, it was thought that structural alteration of the microfibrillar system was responsible for the phenotypic changes seen with the disease. However, recent research indicates an intricate relationship that FBN-1 gene products play in TGF-β signaling.
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