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.     

Wound healing and T-lymphocytes

T-cell depletion leads to impaired wound healing. We studied the effect of combined T-helper and T-suppressor lymphocyte depletion on wound healing and compared it with the effect of all T-cell depletion. Groups of 10 male balb/c mice, 8 weeks old, underwent a 2.5-cm skin incision and subcutaneous implantation of polyvinyl alcohol sponges. Twenty-four hours prior to wounding one group was treated with 3OH12, a rat anti-mouse monoclonal antibody against the Thy-1.2 antigen present on all T-cells (1 mg); another group received 1 mg each of GK1.5 (anti-L3T4, CD4; anti-helper/effector subset) and 2.43 (anti-Lyt 2.1, CD8; anti-suppressor/cytotoxic subset). All monoclonal antibodies are cytotoxic in vivo. Controls received 1 mg of nonspecific rat IgG. Treatments were repeated weekly. Animals were sacrificed at 2 and 4 weeks postwounding. Equal depletion of all T- and Th- and Ts-subsets in peripheral blood and spleens was noted in the two experimental groups at sacrifice. Depleting Thy-1.2 cells (all T-cells) impaired wound healing as assessed by wound breaking strength and collagen synthesis. Combined anti-T-helper/effector and T-suppressor/cytotoxic depletion resulted in improved wound-healing parameters. This suggests that there is a Thy-1.2+, L3T4-, Lyt2- subpopulation of T lymphocytes which normally stimulates wound healing.     

Wound healing agents

This report presented a review of the process of wound healing as well as influencing factors in the process such as wound healing agents. A greater understanding of the alterations in diabetes mellitus allows selection of the optimal wound healing agents to provide a more optimistic approach to wound closure for this large population of diabetics. We have reviewed some of the most common products use adjuncts to the healing process. With newer innovation such as the use of negative pressure dressings and HBO therapy, the treatment of diabetic wound continues to improve. With the increased number of healing agents, it is important to consider the kind of wound and the conditions present when selecting one healing agent over another.     

Wound healing primer

Surgeons often care for patients with conditions of abnormal wound healing, which include conditions of excessive wound healing, such as fibrosis, adhesions, and contractures, as well as conditions of inadequate wound healing, such as chronic nonhealing ulcers, recurrent hernias, and wound dehiscences. Despite many recent advances in the field, which have highlighted the importance of adjunct therapies in maximizing the healing potential, conditions of abnormal wound healing continue to cause significant cost, morbidity, and mortality. To understand how conditions of abnormal wound healing can be corrected, it is important to first understand the basic principles of wound healing.     

Wound healing and diabetes mellitus

Diabetes mellitus is one of the major contributors to chronic wound healing problems. When diabetic patients develop an ulcer, they become at high risk for major complications, including infection and amputation. The pathophysiologic relationship between diabetes and impaired healing is complex. Vascular, neuropathic, immune function, and biochemical abnormalities each contribute to the altered tissue repair. Despite treatment of these chronic wounds, which involves tight glucose control and meticulous wound care, the prognosis for their healing is quite poor. Newer modalities that deliver natural or engineered growth factors show a great deal of promise. All of the studies clearly show the continued need for well-controlled clinical trials.     

Wound healing in nerve

The scope of this article is to provide a framework for the surgical approach to wound healing in nerve for the twenty-first century. The last decade has contributed information on the ultra-microscopic structure and function of nerve, the molecular events relating to neural regeneration, and the capabilities of nerve as a cell and nerve as tissue to respond to injury.     

Wound healing following mastectomy

Local complications following mastectomy are of considerable importance if peri-operative chemotherapy is to be used. A retrospective survey of 100 patients following Patey mastectomy was therefore undertaken to investigate problems associated with wound healing in the absence of such therapy. The survey showed that 18% of patients developed postoperative wound infection, this being severe in 50% of cases. Varying degrees of total wound breakdown occurred in 9% of patients while delayed healing occurred in a further 5%. The incidence of seroma was 25%, and the majority of these patients required further drainage. There was a significant association between seroma formation and wound infection (P less than 0.05). The mean length of hospital stay in patients without wound infection was 11.7 days, but was increased to 27.3 days when infection occurred (P less than 0.001).     

Intravenous anaesthesia: new drugs,new concepts,and clinical applications

Canadian Journal of Anesthesia/Journal canadien d'anesthésie - The availability of short-acting, potentiv anaesthetic drugs, and improvements in drug delivery systems specifically designed...     

Wound healing in Mac‐1 deficient mice

Mac‐1 (CD11b/CD18) is a macrophage receptor that plays several critical roles in macrophage recruitment and activation. Because macrophages are essential for proper wound healing, the impact of Mac‐1 deficiency on wound healing is of significant interest. Prior studies have shown that Mac‐1^?/? mice exhibit deficits in healing, including delayed wound closure in scalp and ear wounds. This study examined whether Mac‐1 deficiency influences wound healing in small excisional and incisional skin wounds. Three millimeter diameter full thickness excisional wounds and incisional wounds were prepared on the dorsal skin of Mac‐1 deficient (Mac‐1^?/?) and wild type (WT) mice, and wound healing outcomes were examined. Mac‐1 deficient mice exhibited a normal rate of wound closure, generally normal levels of total collagen, and nearly normal synthesis and distribution of collagens I and III. In incisional wounds, wound breaking strength was similar for Mac‐1^?/? and WT mice. Wounds of Mac‐1 deficient mice displayed normal total macrophage content, although macrophage phenotype markers were skewed as compared to WT. Interestingly, amounts of TGF‐β1 and its downstream signaling molecules, SMAD2 and SMAD3, were significantly decreased in the wounds of Mac‐1 deficient mice compared to WT. The results suggest that Mac‐1 deficiency has little impact on the healing of small excisional and incisional wounds. Moreover, the findings demonstrate that the effect of single genetic deficiencies on wound healing may markedly differ among wound models. These conclusions have implications for the interpretation of the many prior studies that utilize a single model system to examine wound healing outcomes in genetically deficient mice.