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PubMed1991

TGF-beta and wound healing.

Wound healing comprises an ordered sequence of events including cell migration and proliferation, synthesis of extracellular matrix, angiogenesis and remodelling. TGF-beta regulates many of these processes. Animal models are used to study healing of simple linear incision wounds and deeper dermal wounds under normal and impaired conditions. TGF-beta increases the rate of healing and the breaking strength of the repaired tissue. It also enhances angiogenesis and consequent blood flow to dermal wounds, partly by stimulating the local release of other growth factors. TGF-beta reverses the adverse affects of glucocorticoids on wound healing and thus may be useful in the treatment of chronic ulcers or wounds in patients whose normal responses have been impaired by therapy with steroids, radiation or other drugs.

Animals↗
PubMed1982

[Morphology and biochemistry of wound healing].

Wound healing was investigated by morphological and biochemical methods. The results show that wounds cause disturbances in the equilibrium between the physiological anabolic and catabolic processes of cells, ground substance, and fibers (with increased turnover rates). The primary increase of catabolism is responsible for the secondary compensatory enhanced anabolism, especially of proteoglycans and collagen. Kind, size, and localization of wounds determine the course of wound healing and therefore the extent of adaptation of structure, function, and biomechanical capacities on the surrounding uninjured tissue.

Animals↗
PubMed1993

Nutrition and wound healing.

Wound healing is a complex process following injury that ideally will end in complete restoration of the damaged tissue and function. Nutrition is one of the most important determinants in successful wound healing. Proper identification of nutritional deficiencies and rapid intervention will increase the chances of successful wound closure.

Humans↗
PubMed2006

Targeting matrix metalloproteases to improve cutaneous wound healing.

Wound repair is a physiological event in which tissue injury initiates a repair process leading to restoration of structure and function of the tissue. Cutaneous wound repair can be divided into a series of overlapping phases including formation of fibrin clot, inflammatory response, granulation tissue formation incorporating re-epithelialisation and angiogenesis and finally, matrix formation and remodelling. Matrix metalloproteases (MMPs) are a family of neutral proteases that play a vital role throughout the entire wound healing process. They regulate inflammation, degrade the extracellular matrix (ECM) to facilitate the migration of cells and remodel the new ECM. However, excessive MMP activity contributes to the development of chronic wounds. Selective control of MMP activity may prove to be a valuable therapeutic approach to promote healing of chronic ulcers. Recent evidence indicates that the anticoagulant, activated protein C may be useful in the treatment of non-healing wounds by preventing excessive protease activity through inhibition of inflammation and selectively increasing MMP-2 activity to enhance angiogenesis and re-epithelialisation.

Animals↗
PubMed1987

[Significance of epidermal cytokines within the scope of wound healing].

Wound healing involves inflammation as well as repair of injured tissue. A variety of soluble mediators is involved in the regulation of the different phases of wound healing. Recently it has been shown that in addition to inflammatory cells, keratinocytes are able to produce distinct immunomodulating cytokines. Injurious stimuli significantly enhance mediator production and enable keratinocytes to activate various inflammatory cells such as granulocytes, lymphocytes, monocytes, natural killer cells and fibroblasts. Thus, cytokines released by keratinocytes may play an important regulatory role in inflammation, as well as within the framework of repair of damaged tissue.

Collagen↗
PubMed1992

Wound healing and wound contraction after palatal surgery and implantation of poly-(L-lactic) acid membranes in beagle dogs.

The effect of implantation of poly-(L-lactic) acid membranes on wound healing and wound contraction after palatal surgery was investigated macroscopically in beagle dogs. Thirty beagle dogs were randomly assigned to two experimental groups (group L and LM; both n = 12) and a control group (group C; n = 6). At 12 weeks of age, a soft-tissue defect was created in the median region of the palate by excising a standardized elliptical mucoperiosteal flap. This defect was closed according to the Von Langenbeck technique, leaving two areas of denuded bone. Immediately after surgery, poly-(L-lactic) acid membranes were implanted on the denuded bony areas in the animals of the LM group. In the L group, no poly-(L-lactic) acid membrane was used. Tattoo points were placed in the mucoperiosteum on opposite wound margins in all groups to quantify wound contraction. Standardized intraoral photographs were taken at regular intervals. Wound surface areas and weekly increments of the distance between the tattoo points were calculated. Clinical wound healing was significantly retarded in animals of the LM group. Wound contraction was comparable in both experimental groups and was restricted to the first 2 weeks after surgery. Corresponding lateral migration of the tattoo points in the median region of the palate in these groups occurred in the first week after surgery, followed by wound contraction in the second week. Implantation of poly-(L-lactic) acid membranes following palatal wounding in beagle dogs had no beneficial short-term effects on wound healing and contraction.

Analysis of Variance↗
PubMed2002

Wet wound healing.

Wound treatment in a flexible transparent chamber attached to the perimeter of the wound and containing a liquid has been extensively tested in preclinical experiments in pigs and found to offer several advantages. It protects the wound; the liquid medium or saline in the chamber provides in vivo tissue culture-like conditions; and antibiotics, analgesics, and various molecules can be delivered to the wound through the chamber. The wound chamber causes no injury to the wound itself or to the surrounding intact skin. Topical delivery of, for instance, antibiotics can provide very high concentrations at the wound site and with a favorable direction of the concentration gradient. A series of 28 wounds in 20 patients were treated with a wound chamber containing saline and antibiotics. Most patients had significant comorbidity and had not responded to conservative or surgical management with débridement and delayed primary closure or skin grafts. Six wounds had foreign bodies present; four of these were joint prostheses. Seven patients were on corticosteroids for rheumatoid arthritis, lupus, or chronic obstructive pulmonary disease, and four patients had diabetes. Most patients were treated with the wound chamber in preparation for a delayed skin graft or flap procedure, but one was treated with a wound chamber until the wound healed. Twenty-five of the wounds (89 percent) healed, and five wounds (18 percent) required additional conservative management after the initial chamber treatment and grafting procedure. Of the three wounds that did not heal, one healed after additional chamber treatment, one had a skin graft that did not take, and one required reamputation at a higher level. Antibiotic delivery was less than one intravenous dose daily, which avoided the potential for systemic absorption to toxic levels. Antibiotics such as vancomycin and gentamicin could be used in concentrations of up to 10,000 times the minimal inhibitory concentration. Forty-eight hours after application, 20 percent or more of the original antibiotic concentration was present in the wound chamber fluid. In conclusion, the wound chamber provides a safe, powerful tool in the treatment of difficult infected wounds.

Adolescent↗
PubMed1999

[Immune regulation of wound healing].

Wound healing is a complex cascade of biochemical and cellular events designed to achieve restoration of tissue integrity following injury. Immune cells are critical for the outcome of healing. Much has been learned about the individual events that are involved in this process. Knowledge is scant, however, about the spatial and temporal interweaving of these events and how one step sets the stage for subsequent observed phenomena. Imbalance of stimulating and inhibiting factors causes failure of healing. Immunosuppressive states interfere with a normal immune response and impair wound repair. Clinically, new therapeutic approaches to modulate impaired healing are based on a knowledge of immune regulation of wound healing.

Animals↗
PubMed1989

Fibronectin is overproduced by keloid fibroblasts during abnormal wound healing.

Wound healing in certain individuals leads to the development of keloid tumors which exhibit abnormal collagen metabolism and an increased abundance of extracellular matrix components. Comparison of fibronectin levels in fibroblasts derived from keloids and normal dermis revealed a relative increase in intracellular and extracellular fibronectin in the keloid-derived cells. While fibronectin was similarly processed, compartmentalized, and degraded by both cell types, fibronectin biosynthesis was found to be accelerated as much as fourfold in keloid fibroblasts due to a corresponding increase in the amount of accumulated fibronectin mRNA. These changes account for the elevated steady-state level of the molecule in keloid fibroblasts and suggest that increased fibronectin in keloid lesions is due to overproduction by the wound-healing fibroblasts. Glucocorticoid treatment stimulated fibronectin biosynthesis in both normal and keloid fibroblasts. However, the amount of stimulation was less for the keloid-derived cells, indicating a limitation on maximal rates of fibronectin biosynthesis. These observations suggest that separate mechanisms act to control basal and maximal rates of fibronectin production. Biosynthesis of the 140-kilodalton fibronectin receptor was also found to be increased in keloid fibroblasts, suggesting some level of coordinate regulation for fibronectin and fibronectin receptor expression.

Adult↗
PubMed1999

Role of phenytoin in wound healing--a wound pharmacology perspective.

Topical agents used for the enhancement of wound healing are designed to act locally and, therefore, do not undergo classic systemic metabolic modification. This commentary reviews the potential role of a vulnerary agent, phenytoin, (PHT), from a wound pharmacology perspective. This agent may have the potential to alter the dynamics of wound healing, suggesting a therapeutic use for the stimulation of chronic wounds. Oral PHT therapy is used widely for the treatment of convulsive disorders, and about half the patients treated develop gingival overgrowth as a side-effect. This apparent stimulatory effect has prompted its assessment in wound healing. Investigations into the mechanisms of gingival overgrowth also provide clues to its action in wound healing, and important similarities and differences are discussed. It appears also that both gingiva and skin are important extrahepatic sites for xenobiotic metabolism, and analysis of the biochemical mechanisms should lead to the design of safer analogues for wound healing. On the other hand, differences between the pharmacokinetics of topical PHT in these tissue situations indicate that different formulations are required for gingival and cutaneous wound healing and during the changing course of wound healing itself.

Administration, Topical↗
PubMed2001

[Surgical biology of wound healing].

Wound healing is a dynamic, interactive process involving soluble mediators, blood cells, extracellular matrix, and parenchymal cells. It has three phases-inflammation, tissue formation, and tissue remodelling-that overlap in time. Tissue remodelling of an acute wound is closely controlled by regulatory mechanisms which maintain a delicate balance between synthesis and degradation, leading to normal healing. In chronic wounds (diabetic foot, venous ulcer, pressure sore), the healing process is disturbed by various factors which prolong the inflammatory phase, creating a cascade of tissue responses which perpetuate a "non-healing" state. Among those factors we recognize tissue necrosis, infection, tissue hypoxia, exsudates with excess of inflammatory cytokines. The local treatment of chronic wounds with modern dressings, although efficacious, is too slow and too conservative. By transforming a chronic wound into an acute, the surgeon not only remove those disturbing factors but re-establishes the dynamic process of a normal wound healing.

Acute Disease↗
PubMedDate not supplied

Nutritional support in wound healing.

Wounds place increased metabolic and hence nutritional demands on patients, which may not always be met, especially in older patients in the community. Patients may be deficient in carbohydrates, protein and amino acids, fatty acids and certain micronutrients. Nutritional support may be needed to promote wound healing. Nurses should be able to assess the risk of poor nutrition in patients with wounds and have a role in ensuring adequate nutrition through the normal diet or supplementation where necessary.

Energy Intake↗
PubMed1998

The role of apoptosis in wound healing.

Wound healing involves a series of rapid increases in specific cell populations that prepare the wound for repair, deposit new matrices and finally, mature the wound. Upon completing their tasks, these specific cell types must be eliminated from the wound prior to the progression to the next phase of healing. The most logical method of cellular down-regulation is through apoptosis. Apoptosis allows for the eliminations of entire populations without tissue damage or an inflammatory response. This review discusses which cells dominate the various phases of tissue repair and how the cellular pattern may vary after differing types of injury. The potential mechanisms involved in the down-regulation of inflammation and fibrosis are also covered. The studies that support the hypothesis that apoptosis is involved in the regulation of wound healing are discussed. The evidence supporting potential cell signals involved in the induction of apoptosis in tissue repair are examined. Finally, the review ends with a presentation of how dysregulation of apoptosis can lead to pathologic forms of healing such as excessive scarring and fibrosis. By understanding the mechanisms controlling apoptosis and tissue repair, one may eventually develop therapeutic modalities to minimize scarring, a final pathway for many disease processes.

Animals↗
PubMed2001

IL-1 plays a critical role in oral, but not dermal, wound healing.

Wound healing is a well-orchestrated complex process leading to the repair of injured tissues. After injury, proinflammatory cytokines act as important modulators of the inflammatory process. IL-1 expression has been regarded as necessary for healing; however, its effects have also been implicated in delayed wound repair. Currently, there is no consensus or direct evidence that IL-1 activity plays a central role in the healing process. The present investigation was undertaken to define the role of IL-1R signaling in the healing outcome of an excisional wound in the palate or scalp of mice that had targeted deletions of the IL-1R type 1 (IL-1R1(-/-)) compared with matched wild-type mice. Histomorphometric analysis was undertaken to assess the degree of healing and the recruitment of polymorphonuclear and mononuclear phagocytes. After 14 days, wild-type mice exhibited complete closure of intraoral wounds, while IL-1R1(-/-) animals had only partial closure (50%). In the IL-1R1(-/-) mice, healing tissues exhibited a persistent inflammatory cell infiltrate, which did not occur in wild-type animals. Treatment with antibiotics significantly diminished the persistent inflammatory infiltrate and improved healing in the experimental animals. In contrast to oral wounds, the rate of healing and recruitment of polymorphonuclear cells in scalp wounds was similar in IL-1R1(-/-) and wild-type mice. The present data underscore the importance of IL-1 in wound healing in a challenging environment and identify its principal role in facilitating the healing process by protecting an open wound from bacterial insult. In a less challenging environment, the production of new connective tissue and its coverage by migrating epithelium are minimally affected by the absence of IL-1 activity.

Animals↗
PubMed2002

A novel sustained-release matrix based on biodegradable poly(ester amide)s and impregnated with bacteriophages and an antibiotic shows promise in management of infected venous stasis ulcers and other poorly healing wounds.

Healing of poorly vascularized and venous stasis ulcers is often refractory to therapy, particularly when they are infected. Systemic antibiotic therapy may be of little benefit in this setting because of poor penetration of the antibiotic into the wound and the frequent associated emergence of bacterial strains resistant to common antimicrobial agents. Given the clinical significance of these problems, there is a need to explore alternative management approaches for these difficult-to-treat wounds. PhagoBioDerm is a novel wound-healing preparation consisting of a biodegradable polymer impregnated with an antibiotic and lytic bacteriophages, which was recently licensed for sale in the Republic of Georgia (one of the former Soviet Union republics). In 1999-2000, in Tbilisi, Georgia, 107 patients who had ulcers that had failed to respond to conventional therapy were treated with PhagoBioDerm alone or in combination with other interventions. The wounds/ulcers healed completely in 67 (70%) of 96 patients for whom follow-up data were available. In 22 cases in which microbiologic data were available, healing was associated with the concomitant elimination of, or a reduction in, specific pathogenic bacteria in the ulcers. Our findings suggest that this slow-release biopolymer is safe and of possible benefit in the management of refractory wounds, and they support the apparent utility of bacteriophages in this setting. Further studies, including carefully designed clinical trials, will be required to rigorously evaluate the efficacy of this novel wound dressing preparation.

Adult↗
PubMed2006

A study on mRNA expressions of fibronectin in dermal and cerebral wound healing for wound age estimation.

We investigated mRNA expressions of fibronectin for wound age estimation during dermal and cerebral wound healing. Fibronectin mRNA expressions in the injured skin peaked at 8h post-injury. The expressions were detected in endothelial cells before and after injury, whereas they were detectable in the epidermal cells at 1-240 h, in fibroblasts at 1-72 h, in neutrophils and macrophages at 8-72 h, respectively. However, the expressions in epidermal cells became relatively weak in the subacute phase. Fibronectin mRNA expressions of the injured cerebrum increased after the intervention and peaked at 48 h, whereas there was a slight decrease during 24h post-injury. Although fibronectin mRNA was seen exclusively in the endothelial cells of the intact cerebrum, it was also detected in astrocytes during wound healing. From these findings, it was considered that fibronectin played an important role in dermal and cerebral wound healing. Expression of fibronectin mRNA was considered to indicate the acute phase of dermal wound healing, and the subacute phase of cerebral wound healing.

Animals↗
PubMed1989

Principles of wound healing.

Wound healing can be divided into immediate (zero to 1 hour), early (1 to 24 hours), intermediate (1 to 7 days), and late (greater than 7 days) stages. Many physical and physiologic events occur simultaneously and sequentially during these stages to produce the final wound scar. The processes of skin retraction, scab formation, would debridement, wound contraction, epithelial migration and proliferation, fibroplasia, and collagen maturation all must occur for healing to be successful. Many factors affect the size and shape of the resulting scar, including anatomic location and skin tension forces, systemic condition of the patient, blood supply to the wound, nutritional factors, environmental temperature, the presence of systemic drugs, wound infection, motion, wound oxygen gradient, wound moisture, and bandaging. Ideally, each of the factors would occur at a level compatible with optimal healing, but, in many clinical cases, one or more factors compromise normal, rapid healing. When we intervene with therapy, we probably adversely affect another factor in healing, while trying to correct the factor that is out of balance. In these decisions, the effects of our treatment on wound healing should be considered. The trade-off should be weighed and the treatment pursued only as long as necessary to allow healing to progress; then it should be discontinued or changed. With these considerations, it is hoped that we can attain healing at the most rapid physiologic rate.

Animals↗
PubMed2005

Animal models for adult dermal wound healing.

Wound healing in adult mammals proceeds by a series of overlapping highly coordinated events. Dermal wound repair commences with the arrest of hemorrhage followed by an inflammatory response, re-epithelialization of the wound, and formation of granulation tissue within the wound space, culminating in the production of a scar. In order to study the processes involved in the repair of wounded tissue, we have developed a rodent model utilizing full thickness incisional and excisional dermal wounds, which allow for macroscopic observations and also provide tissue for the histological and immunocytochemical analysis of acute wounds and scarring.

Animals↗