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Results for “WOUND HEALING”

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At least 19 recordsLinked to original sources
PubMed1975

Wound healing in man: tensile strength of healing wounds in some patient groups.

The healing of test wounds was studied in 108 patients, in whom some impairment of wound healing was suspected. A 5 cm skin wound was performed in the forearm and the strength of the wound was tested after 5 days using the technique described by Sandblom and associates with two measurements in each wound. No differences in wound strength could be registered between the two wounds in each patient, between males and females nor in patients with malignant disease compared to other patients. Patients with low serum protein or serum albumin values had significantly weaker wounds than patients with normal protein values. Patients over 80 years of age had wounds somewhat weaker than those below 70, the difference having a statistical significance of 6%. The wound strength in patients was compared to values found elsewhere for wounds in rabbits, rats, and piglets. The pigs had much higher values than others, rabbits slightly stronger than and rats about equal to humans.

Age Factors↗
PubMed1999

Differential expression of tissue inhibitors of metalloproteinases (TIMP-1, -2, -3, and -4) in normal and aberrant wound healing.

Wound healing is characterized by hemostasis, re-epithelialization, granulation tissue formation, and remodeling of the extracellular matrix. Matrix metalloproteinases and their specific inhibitors, TIMPs, contribute to these events. We investigated a total of 47 samples of normally healing wounds, chronic venous ulcers, ulcerative vasculitis, and suction blisters using immunohistochemistry and in situ hybridization, to clarify the role of TIMPs in normal and aberrant wound repair. Expression of TIMP-1 and -3 mRNAs was found in proliferating keratinocytes in 3- to 5-day-old normally healing wounds, whereas no epidermal expression was detected in chronic ulcers. However, TIMP-3 protein was found in the proliferating epidermis in 20 of 24 samples representing both full-thickness acute and chronic wounds. TIMP-1 and TIMP-3 also were abundantly expressed by spindle-shaped, fibroblast-like, and plump, macrophage-like stromal cells, as well as by endothelial cells. In normally healing wounds, TIMP-2 protein localized under the migrating epithelial tip and to the stromal tissue under the eschar more frequently than in chronic ulcers. Occasional staining for TIMP-4 protein was detected in stromal cells of chronic ulcers near blood vessels. Our results indicate that TIMP-1 and TIMP-3 may be involved both in the regeneration of the epidermis by stabilizing the basement membrane zone and in the regulation of stromal remodeling and angiogenesis of the wound bed. Lack of TIMP-2 near the migrating epithelial wound edges might contribute to uncontrolled activity of MMP-2 in chronic ulcers. We conclude also that TIMPs are temporally and spatially tightly regulated and that the imbalance between metalloproteinases and TIMPs-1, -2, and -3 may lead to delayed wound healing.

Aged↗
PubMed1999

Arnebin-1 accelerates normal and hydrocortisone-induced impaired wound healing.

Wound healing involves inflammation, cell proliferation, matrix deposition, and tissue remodeling. Interaction of different cells, extracellular matrix proteins, and their receptors are mediated by cytokines and growth factors during wound healing. In this study, we have evaluated the effect of arnebin-1, a natural product isolated from Arnebia nobilis, on normal and impaired wound healing in cutaneous punch wound model. Arnebin-1 was applied topically daily on wounds of hydrocortisone-treated or untreated animals. Arnebin-1 significantly accelerated healing of wounds with or without hydrocortisone treatment as revealed by a reduction in the wound width and gap length compared with controls. Arnebin-1 treatment promoted the cell proliferation, migration, and vessel formation to form a thick granulation tissue and re-epithelialization of the wounds. An increase in the synthesis of collagen, fibronectin and transforming growth factor-beta1 was seen in arnebin-1-treated wounds compared with the untreated control. As transforming growth factor-beta1 is known to enhance wound healing, and associated with the wound healing defect in hydrocortisone-treated wounds, the enhanced expression of transforming growth factor-beta1 at both translational and transcriptional level by arnebin-1 may be responsible for the enhancement of wound healing during normal and impaired wound repair. These studies suggest that arnebin-1 could be developed as a potent therapeutic agent for wound healing in steroid-impaired wounds.

Animals↗
PubMed1999

Neuropeptide-containing C-fibres and wound healing in rat skin. Neither capsaicin nor peripheral neurotomy affect the rate of healing.

Wound healing in rat skin was studied in standardized wounds inflicted on both hind legs after unilateral sciatic nerve sectioning and/or capsaicin-induced depletion of sensory nerve (C-fibre) neuropeptide content. Daily visual inspection, histological examination and immunohistochemistry with antibodies against substance P, calcitonin gene-related peptide (CGRP), vasoactive intestinal peptide, neuropeptide Y and a pan-neuronal marker, protein gene product 9.5 (PGP 9.5) were used to assess wound healing and determine the distribution of dermal nerve fibres. In controls, nerve fibre density in the wound tissue was low during the first few days after wound infliction, but started to increase on day 4, reaching a peak on day 7 when 25% of medial wounds and 70% of lateral wounds were healed. All wounds were healed on day 11, a scar appearing on day 14 followed by a decrease in nerve fibre density. Capsaicin treatment and/or sciatic nerve sectioning reduced the density of CGRP-immunoreactive nerve fibres by 70% and that of PGP 9.5-immunoreactive fibres by 50%. The capsaicin-induced reduction in PGP 9.5-immunoreactive nerve fibre density is attributable to partial destruction of peripheral nerve fibres. CGRP-immunoreactive and PGP 9.5-immunoreactive nerve fibre density was restored both in capsaicin-treated and denervated groups, reaching a maximum, corresponding to the original level, by days 4-10. Neither the reduction in nerve fibre density following sciatic nerve sectioning nor the impairment of sensory nerve functional capacity following capsaicin treatment affected the rate of wound healing, all wounds being closed on day 11. The study shows that it is difficult to knock out all cutaneous sensory innervation. Thirty per cent of C-fibre innervation seems enough to ensure a normal wound healing.

Animals↗
PubMed1991

Time course of wound healing.

Wound healing is a special kind of inflammation. Undisturbed wound healing is subject to a fixed time schedule of biochemical and cellular events. It is virtually impossible to deal with the time course of wound healing without describing the cellular and non-cellular events involved. The activity and mode of cell action after injury are coordinated by spatial and chronological factors, as well as by different mediators and cell-cell interacting signals. During wound healing the sequence of different signals and message substances, such as mediators of inflammation, fulfill a key function in wound repair. The report describes the time course of healing and the control of cellular events by different mediators and cell interactions. Emphasis is placed on temporal aspects, including the various signals leading to typical cellular events in wound healing.

Aging↗
PubMed1995

Wound healing.

Wound healing is a dynamic biologic process of repairing insults to the integumentary system. It is commonly divided into three phases: inflammatory, proliferative, and maturation. Each phase has unique cellular and substance constituents without which it cannot progress normally. A large variety of factors may influence any part of wound healing, including local factors such as bacteria, oxygen tension, and bleeding, and systemic factors such as the mental and physical health of the patient. There are also extrinsic factors that can be influenced by the caretakers of the wound to enhance wound healing. Areas of intervention include using antiseptic technique when one is dealing with the wound, using good surgical technique, choosing the appropriate wounding method and repair for the individual patient, and using antibiotics and special wound dressings. Modern science and technology are giving us new insights into wound healing and leading us to exciting new ways of influencing it, including the topical use of growth factors, artificial skins, cultured epithelium with and without dermal components, and electrical stimulation. The future of wound healing holds a better understanding of the complexities of the physiologic events that occur and a translation of that into a biologically active and interactive wound care.

Cell Division↗
PubMed2004

From an enhanceosome to a repressosome: molecular antagonism between glucocorticoids and EGF leads to inhibition of wound healing.

Wound healing in its complexity depends on the concerted activity of many signaling pathways. Here, we analyzed how the simultaneous presence of glucocorticoids (GC), retinoic acid (RA) and epidermal growth factor (EGF) affect wound healing at the molecular, cellular and tissue levels. We found that GC inhibit wound healing by inhibiting keratinocyte migration, whereas RA does not. Furthermore, GC block EGF-mediated migration, whereas RA does not. On the molecular level, these compounds target expression of one of the earliest markers of wound healing, cytoskeletal components, keratins K6 and K16. Both GC and RA repress their transcription, whereas EGF induces it. Interestingly, the GC inhibition is mediated by a repressosome complex consisting of four monomers of the GC receptor, beta-catenin and coactivator-associated-arginine-methyltransferase-1. GC are dominant, EGF cannot rescue GC-mediated inhibition. Pre-treatment of keratinocytes with GC shifts the balance towards the repressosome, allowing for dominant inhibition of K6 even in the presence of EGF or c-fos/c-jun. Although RA receptor gamma and glucocorticoid receptor bind to the same response element repressing transcription of keratins K6/K16, RA receptor interacts with the components of the EGF-enhanceosome (co-activators: glucocorticoid-receptor-interactive protein-1(GRIP-1)/steroid-receptors coactivator-1 (SRC-1)) without breaking it. Consequently, RA has a co-dominant effect with EGF: when present simultaneously, their effects balance each other. When keratinocytes are pre-treated with mitogen-activated protein kinase (MAPK) inhibitor, thus blocking EGF, the balance is shifted towards the RA repression. Similar to clinical findings, pre-treatment of keratinocytes with RA blocks GC-mediated inhibition. In summary, our results identify complex molecular mechanisms through which RA alleviates GC-mediated inhibition of wound healing.

Base Sequence↗
PubMedDate not supplied

Enhancement of wound healing by shikonin analogue 93/637 in normal and impaired healing.

Wound healing is a complicated biological process, which involves interactions of multiple cell types, various growth factors, their mediators and the extracellular matrix proteins. In this study, we evaluated the effects of shikonin analogue 93/637 (SA), derived from the plant Arnebia nobilis, on normal and hydrocortisone-induced impaired healing in full thickness cutaneous punch wounds in rats. SA (0.1%) was applied topically daily as an ointment in polyethylene glycol base on wounds. SA treatment significantly accelerated healing of wounds, as measured by wound contraction compared to controls in hydrocortisone-impaired animals. SA treatment promoted formation of granulation tissue including cell migration and neovascularization, collagenization and reepithelialization. The expression of basic fibroblast growth factor (bFGF) was higher as revealed by immunohistochemistry in treated wounds compared to controls. However, the expression of transforming growth factor-beta(1) was not affected by SA treatment. Since bFGF is known to accelerate wound healing, the increased expression of bFGF by SA may be partly responsible for the enhancement of wound healing. These studies suggest that SA could be further studied for clinical use to enhance wound healing.

Administration, Cutaneous↗
PubMedDate not supplied

Differential expression and localization of WNTs in an animal model of skin wound healing.

Wound healing is a dynamic process, and a variety of growth factors have a significant impact on the process. Although the WNT family has a multitude of effects on the state of various physiological pathways, the expression and role of WNT in wounded tissue have remained an enigma. The aim of this study was to assess the expression and localization of WNTs in a murine model of wound healing. RNA isolated from full-thickness cutaneous wounds from day 1 to day 21 postwounding were subjected to reverse transcription-polymerase chain reaction, and expression of WNT3, 4, 5a, and 10b were observed. Immunohistochemistry localized WNT10b to regenerating epithelial cells on day 1 and 3, and WNT4 on day 3 and 5. WNT4 also reacted with fibroblast-like cells beneath the epithelium. The cytoplasmic staining of beta-catenin, a WNT signaling molecule, in the epithelial cells indicates an activation of the WNT signaling pathway. Among target genes downstream of the pathway, matrix metalloproteinases (MMPs) degrade and remodel the extracellular matrix during wound healing. Gelatin zymography showed that MMP9 was expressed from day 1 to day 5. MMP-2 was continuously expressed, but maximally up-regulated at day 5. Activation of MMP-2 coincided with expression of membrane-type 1 MMP, suggesting an involvement of WNTs in this proteolytic cascade. Therefore, WNTs may contribute to the process of wound healing in a spatiotemporal manner.

Animals↗
PubMedDate not supplied

The biology of wound healing.

Wound healing is a complex biological process. A thorough knowledge of normal wound healing is of utmost importance for the clinicians who are involved in the care of patients with open wounds. It is imperative for every clinician who is involved in wound care to know the process which prevents, minimizes and eliminates those factors which adversely affect wound healing.

Bandages↗
PubMed1988

[Wound healing and wound dressing].

This review article intends to discuss the clinical management of wounds in respect to a pathophysiological background. Recent results of research in the field of wound healing are demonstrated. Wound healing can be seen as aseptic inflammatory response to a traumatic stimulus. The activation of the clotting cascade by the trauma induces a sequence of humoral and cellular reactions. Platelets, granulocytes and macrophages are activated stepwisely. In the first phase of wound healing the wounded tissue area will be prepared for phagocytosis by enzymatic degradation of ground substance and depolymerisation of protein macromolecules (wound edema). Following the phagocytic microdebridement mesenchymal cells proliferate and produce matrix substance. Microcirculation within the traumatized area will be restored by angiogenesis, macroscopically observed as new formed granulation tissue. This leads to the wound healing phase of scar tissue formation. In this complexity of reactions naturally many possibilities of impairment are given. The most common complication during wound healing is the infection. It can be seen as self reinforcing process. The therapy of the impairment of wound healing consists in the disruption of the specific vicious circle, in the case of an osseus infection that would be a macrodebridement (that is necrectomy) and biomechanical stabilization. The surgical management of wounds principally consists in ensuring an undisturbed sequence of the healing process. This can be done by the wound excision that supports the phagocytic microdebridement. A further possibility is to avoid overwhelming formation of edema by eliminating the traumatic stimulus, by immobilization of the injured region and by ensuring a physiological microenvironment with a primary suture if possible. There are up to the present no drugs available to enhance cell proliferation and to regulate wound healing but it seems that experimental research is successful in characterizing substances as growth factors and mediators. A second way of managing is to prevent the wound healing from troubles by using preventive measures: unbroken aseptic chain, stopping bleeding exactly and introducing sufficient drainage, avoiding of ischaemia and last not least inserting foreign substances into the tissue as few as possible.

Animals↗
PubMed2007

Topical delivery of silver nanoparticles promotes wound healing.

Wound healing is a complex process and has been the subject of intense research for a long time. The recent emergence of nanotechnology has provided a new therapeutic modality in silver nanoparticles for use in burn wounds. Nonetheless, the beneficial effects of silver nanoparticles on wound healing remain unknown. We investigated the wound-healing properties of silver nanoparticles in an animal model and found that rapid healing and improved cosmetic appearance occur in a dose-dependent manner. Furthermore, through quantitative PCR, immunohistochemistry, and proteomic studies, we showed that silver nanoparticles exert positive effects through their antimicrobial properties, reduction in wound inflammation, and modulation of fibrogenic cytokines. These results have given insight into the actions of silver and have provided a novel therapeutic direction for wound treatment in clinical practice.

Administration, Topical↗