Follicles Wound Healing

Protein is obviously what everyone’s body part is made up of protein and so the fibrous tissue which is result to healing if low protein this tissue is not synthesized and high protein can increase it rates. Carbohydrates, as they are provide the main structural materials required for growth, repair, and maintenance of tissue. A&P 9th ed. Pg.50

Hair: composed of columns of dead, keratinized cells bound together by extracellular proteins. Hair has two main sections: The shaft- superficial portion that extends out of the skin and the root- portion that penetrates into the dermis. Surrounding the root of the hair is the hair follicle. At the base of the hair follicle is an onion-shaped structure called the bulb Papilla of the hair and the matrix within the bulb

Stechmiller, J. K. (2010). Understanding the Role of Nutrition and Wound Healing. Nutrition in Clinical Practice, 25(1), 61-68. doi:10.1177/0884533609358997

Skin repair is an important physiological process which is essential for homeostasis, restoring barrier function and preventing infection (Martin, 2009; Boateng and Catanzano, 2015). Wound healing is defined as a complex, dynamic and the specific biological process associated with the phenomena of tissue regeneration and growth (Mazumder et al., 2016). Regeneration can be defined as a tissue that significantly damaged either completely or partially removed and tissue's original function and cell types must be functional and structurally restored (Mazumder et al., 2016). The process of healing comprises a cytokine, blood cells, extracellular matrix and growth factor (Joao De Masi et al., 2016). The growth factor is a protein that activates and

The main outcome measures were the percent area of the wound compared to baseline area of the wound. As the wound decreased in size it is theoretically assumed that the wound is healing. The central concepts of the study were based on ultraviolet-C positive effects on wound healing in vitro. In vitro studies effects include; modification of growth factors, fibronectin release from fibroblast, epidermal cell proliferation, killing of pathogens, accelerated DNA synthesis, and antibiotic-resistant organisms.

Integra is a synthetic wound dressing frequently used to treat burn wounds (Figure 5). It is a bilayer composed of bovine tendon collagen glycosaminoglycan (chondroitin-6-sulphate) cross-linked to it, onto which a silicone (synthetic polysiloxane polymer) membrane is sealed to the upper surface to act as a protective temporary epidermis. The silicone layer is applied as a liquid monomer; curing occurs on the surface of the collagen at room temperature. It serves to control moisture loss from the wound. Water flux across this silicone membrane is the same as that across normal epidermis. The collagen-GAG matrix contains pores ranging from 70 to 200 µm that are invaded by host fibroblasts upon application to an excised wound bed. The pore size was carefully designed by adjusting the collagen-GAG mixture. In GAG-free collagen, the resulting structure was more closed than in collagen-GAG matrices. Smaller pores can delay, or even prevent, biointegration, whereas larger pores would provide an insufficient attachment area for invading host cells. Freeze-drying procedures followed by slow sublimation are used to control pore size too. The degradation rate of 30 days of the collagen-GAG sponge is controlled by glutaraldehyde-induced cross-links. The polypeptide collagen is used for its low levels of antigenicity (it has minimal rejection potential) and because it exerts a hemostatic effect on vascular wounds. Collagen is already found in skin. It is degraded by collagenase deposited

Patients at Long Term Care Facilities are generally debilitated and elderly people who have incontinence problems. Incontinence makes treating pressure ulcers very difficult because it alters tissue tolerance and reapplying products becomes very costly. Usually negative pressure wound therapy (NPWT) is used to treat pressure ulcers but it is also very costly and does not match with some wound locations. Collagen plays a vital role in the wound healing process by creating a framework for the adhesion, movement, and production of new cells. This study determined the effects and uses of Type 1 formulated collagen on granulation tissue formation and reepithreelialization in chronic pressure ulcers.

This paper will be a research critique on the article “Frequent Application of the New Gelatin-Collagen Nonwoven Accelerates Wound Healing”, by Schiefer, J.L. and Rath, R, and each section will be examined using our textbook “Understanding Evidence-Based Practice”. The article’s main focus was on determining the effect of healing when using multiple collagen nonwoven applications to chronic wounds. Twelve mini-pigs where used to test this technique and the findings indicated that this method was promising, because the wounds had a faster healing rate when multiple application of gelatin-collagen nonwoven was used as treatment. Analyzing the articles components, we can see that although it does contain preliminary

The main outcome measures were the percent area of the wound compared to baseline area of the wound. As the wound decreased in size it is theoretically assumed that the wound is healing. The central concepts of the study were based on ultraviolet-C positive effects on wound healing in vitro. In vitro studies effects include; modification of growth factors, fibronectin release from fibroblast, epidermal cell proliferation, killing of pathogens, accelerated DNA synthesis, and antibiotic-resistant organisms.

At 6 hours, the wound closure in the control (Fig. 1a), diabetic (Fig. 1c) and diabetic groups supplemented with whey protein (Fig. 1e) was not visible. In contrast, wound closure in the diabetic rats supplemented with whey protein at 4 days after the injury (Fig. 1f) was greater than the diabetic rats (Fig. 1d) and nearly similar to the control rats (Fig. 1f).

Wound closure was determined as a decline in the wound area over study time period and also efficiently examined under in vivo conditions via quantitative measurement of skin wound area at specified time intervals in acute and streptozotocin (STZ) induced diabetic mice models (Sharpe et al., 2013). Experimental data set indicating original wound morphology and how the wound size reduced over time in NCs treated swiss albino mice as compared to their respective controls at day 3, 8 and 14 post-wounding (acute) and at day 3, 10, and 18 post-wounding (diabetic) has been presented in Fig. 6.13

“The process by which tissue repair takes place is termed wound healing and is comprised of a continuous sequence of inflammation and repair, in which epithelial, endothelial, inflammatory cells, platelets and fibroblasts briefly come together outside their normal domains, interact to restore a semblance of their usual discipline and having done so resume their normal function”. ("The Cellular Biology of Wound Healing" 2016)

Stem cells are multipotent which give rise to multiple cell types and are known for their self-renewing and tissue differentiation abilities. Research has shown SCs to have successful results in the field of skin regeneration (Duscher, 2016). SCs of interest for wound healing include adult mesenchymal stem cells (MSC’s), embryonic stem cells (ESC’s), and induced pluripotent stem cells (IPSC’s). MSCs are isolated mainly from the bone marrow and other tissues such as adipose and nerve tissues and are administered locally as well as systemically with little to no immunoreactivity (Tartarini, 2016). MSCs regenerative benefits in wound injury is not seen in its structural capabilities rather it’s seen in its escape of trophic mediators (Duscher, 2016). Bone marrow MSCs injected in wound sites produce high amounts of collagen and growth factors leading to faster healing, epithelialization, angiogenesis, and cellularity (Duscher, 2016). Studies also show that bone marrow derived MSCs injected in injury sites had decreased wound size, increased vascularity and dermal thickness (Duscher, 2016). Although MSCs for wound therapy has been proven effective and well tolerated in patients, there still seems to be limitations such as invasiveness of their harvest, cost of resources, and hazards that deal with growing cell cultures to attain healing

Many studies on wound healing stages have found abnormal changes in remolding stage, and the main change in this stage was the imbalance in collagen production and degradation. This imbalance in collagen production and degradation was hypothesized to be the cause of keloid scars formation. Although many studies have been conducted on keloid in order to understand its pathophysiology, the full picture of keloid pathophysiology still unclear yet. For the sake of keloid treatment, many treatment regimens were invented to overcome formation of keloid scar as a complication after wound healing. Although there have been many scholars work on finding a treatment for keloid, there are many obstacles to reach the complete cure and avoid recurrence. Keloid treatments were categorized into three categories. These categories are noninvasive medical therapies, surgical and other invasive therapies, and therapies under investigation. In Noninvasive medical therapies category, the majority of treatments in this category exert their effects mainly throughout repression of the fibroblast proliferation rate, ECM synthesis, collagen synthesis, inflammation, enhancing of MMP expression in order to reduce the keloid scar formation. Surgical and other invasive therapies category, although this type of treatment is very popular, it has a high rate of recurrence when it is used alone. Many studies on keloid have shown that the combination therapy is the best therapy, and it has been shown that it reduces the rate of recurrence. For instance, combination of cryotherapy therapy or the surgical management with corticosteroid or 5-Flourouracil therapy was found to give clinical outcomes better than use of either therapy alone. Therapeutic under investigation category, it is including all new therapies

Li et al.,(109) investigated whether human MSCs contribute to the repair of skin appendages after injury. They co-cultured BrdU-labeled MSCs with heat-shocked confluent sweat gland cells SGCs, in vitro. They found that a subset of adult MSCs differentiated into SGCs. The percentage of differentiation was found to be enhanced by EGF and the injured microenvironment. In vivo, when they intravenously injected Labelled MSCs into full- thickness skin wounds in rats, Labelled cells were noted in hair follicles, sebaceous glands, blood vessels and dermis in full-thickness wounds and the incorporated cells in hair follicles and sebaceous glands were positive for pan-cytokeratin. After wound healing, some labelled MSCs returned to the bone marrow,