Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “WOUND HEALING”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

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↗
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

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↗
PubMed2001

Wound healing.

Wounds and wound healing have been studied in the medical arena for centuries, however, in recent decades new advances have emerged in this extensive field. Currently, the wound healing process is studied at the molecular level giving new insights to the physiological process of wound closure and the lack thereof. With development of new treatment modalities the potential for earlier wound closure and ultimately increased quality of life for chronic wound patients is emerging. As understanding of the delicate balance of molecules within the wound increases, options for treating patients will also increase. Again, an understanding of the wound healing process is vital not only when employing these new treatment options, but also for proper patient care.

Chronic Disease↗
PubMed2002

Curcumin differentially regulates TGF-beta1, its receptors and nitric oxide synthase during impaired wound healing.

Wound healing is a highly ordered process, requiring complex and coordinated interactions involving peptide growth factors of which transforming growth factor-beta (TGF-beta) is one of the most important. Nitric oxide is also an important factor in healing and its production is regulated by inducible nitric oxide synthase (iNOS). We have earlier shown that curcumin (diferuloylmethane), a natural product obtained from the plant Curcuma longa, enhances cutaneous wound healing in normal and diabetic rats. In this study, we have investigated the effect of curcumin treatment by topical application in dexamethasone-impaired cutaneous healing in a full thickness punch wound model in rats. We assessed healing in terms of histology, morphometry, and collagenization on the fourth and seventh days post-wounding and analyzed the regulation of TGF-beta1, its receptors type I (tIrc) and type II (tIIrc) and iNOS. Curcumin significantly accelerated healing of wounds with or without dexamethasone treatment as revealed by a reduction in the wound width and gap length compared to controls. Curcumin treatment resulted in the enhanced expression of TGF-beta1 and TGF-beta tIIrc in both normal and impaired healing wounds as revealed by immunohistochemistry. Macrophages in the wound bed showed an enhanced expression of TGF-beta1 mRNA in curcumin treated wounds as evidenced by in situ hybridization. However, enhanced expression of TGF-beta tIrc by curcumin treatment observed only in dexamethasone-impaired wounds at the 7th day post-wounding. iNOS levels were increased following curcumin treatment in unimpaired wounds, but not so in the dexamethasone-impaired wounds. The study indicates an enhancement in dexamethasone impaired wound repair by topical curcumin and its differential regulatory effect on TGF-beta1, it's receptors and iNOS in this cutaneous wound-healing model.

Activin Receptors, Type I↗
PubMed1997

General principles of wound healing.

Wound healing is a complex process involving different biologic and immunologic systems. Despite improvements in diagnostics and therapy, wound failures remain a clinical problem. The approach to a nonhealed wound is an interdisciplinary challenge that should not be underestimated. Better understanding of the complex wound-healing cascade helps our approach to wound healing and its possible failure. Manipulations of the involved immunologic features offer future therapeutic strategies.

Cell Division↗