Keloids and hypertrophic scars are caused by cutaneous injury and irritation, including trauma, insect bite, burn, surgery, vaccination, skin piercing, acne, folliculitis, chicken pox, and herpes zoster infection. Notably, superficial injuries that do not reach the reticular dermis never cause keloidal and hypertrophic scarring. This suggests that these pathological scars are due to injury to this skin layer and the subsequent aberrant wound healing therein. The latter is characterized by continuous and histologically localized inflammation. As a result, the reticular layer of keloids and hypertrophic scars contains inflammatory cells, increased numbers of fibroblasts, newly formed blood vessels, and collagen deposits. Moreover, proinflammatory factors, such as interleukin (IL)-1α, IL-1β, IL-6, and tumor necrosis factor-α are upregulated in keloid tissues, which suggests that, in patients with keloids, proinflammatory genes in the skin are sensitive to trauma. This may promote chronic inflammation, which in turn may cause the invasive growth of keloids. In addition, the upregulation of proinflammatory factors in pathological scars suggests that, rather than being skin tumors, keloids and hypertrophic scars are inflammatory disorders of skin, specifically inflammatory disorders of the reticular dermis. Various external and internal post-wounding stimuli may promote reticular inflammation. The nature of these stimuli most likely shapes the characteristics, quantity, and course of keloids and hypertrophic scars. Specifically, it is likely that the intensity, frequency, and duration of these stimuli determine how quickly the scars appear, the direction and speed of growth, and the intensity of symptoms. These proinflammatory stimuli include a variety of local, systemic, and genetic factors. These observations together suggest that the clinical differences between keloids and hypertrophic scars merely reflect differences in the intensity, frequency, and duration of the inflammation of the reticular dermis. At present, physicians cannot (or at least find it very difficult to) control systemic and genetic risk factors of keloids and hypertrophic scars. However, they can use a number of treatment modalities that all, interestingly, act by reducing inflammation. They include corticosteroid injection/tape/ointment, radiotherapy, cryotherapy, compression therapy, stabilization therapy, 5-fluorouracil (5-FU) therapy, and surgical methods that reduce skin tension.

The increase in the number of randomized controlled trials over the past decade has greatly improved scar management, although these studies suffer from various limitations. The hypertrophic scar/keloid treatment algorithms that are currently available are likely to be significantly improved by future high-quality clinical trials.

Keloids tend to occur on highly mobile sites with high tension. This study was designed to determine whether body surface areas exposed to large strain during normal activities correlate with areas that show high rates of keloid generation after wounding. Eight adult Japanese volunteers were enrolled to study the skin stretching/contraction rates of nine different body sites. Skin stretching/contraction was measured by marking eight points on each region and measuring the change in location of the marked points after typical movements. The distribution of 1,500 keloids on 483 Japanese patients was mapped. The parietal region and anterior lower leg were associated with the least stretching/contraction, while the suprapubic region had the highest stretching/contraction rate. With regard to keloid distribution, there were 733 on the anterior chest region (48.9%) and 403 on the scapular regions (26.9%). No keloids were reported on the scalp or anterior lower leg. Because these sites are rarely subjected to skin stretching/contraction, it appears that mechanical force is an important trigger that drives keloid generation even in patients who are genetically predisposed to keloids. Thus, mechanotransduction studies are useful for developing clinical approaches that reduce the skin tension around wounds or scars for the prevention and treatment of not only keloids but also hypertrophic scars.

The propeller flap is a useful reconstructive tool that can achieve good cosmetic and functional results. A flap should be called a propeller flap only if it fulfils the definition above. The type of nourishing pedicle, the source vessel (when known), and the degree of skin island rotation should be specified for each flap.

Summary Background Data Mechanical forces play an important role in tissue neovascularisation and are a constituent part of modern wound therapies. The mechanisms by which Vacuum Assisted Closure (VAC) modulates wound angiogenesis are still largely unknown. Objective To investigate how VAC treatment affects wound hypoxia and related profiles of angiogenic factors as well as to identify the anatomical characteristics of the resultant, newly formed vessels. Methods Wound neovascularization was evaluated by morphometric analysis of CD31- stained wound cross sections as well as by corrosion casting analysis. Wound hypoxia and mRNA expression of HIF-1α and associated angiogenic factors were evaluated by pimonidazole hydrochloride staining and quantitative RT-PCR, respectively. VEGF protein levels were determined by western blot analysis. Results VAC-treated wounds were characterized by the formation of elongated vessels aligned in parallel and consistent with physiologically function, compared to occlusive dressing control wounds that showed formation of tortuous, disoriented vessels. Moreover, VAC-treated wounds displayed a well-oxygenated wound bed, with hypoxia limited to the direct proximity of the VAC-foam interface, where higher VEGF levels were found. By contrast, occlusive dressing control wounds showed generalized hypoxia, with associated accumulation of HIF-1α and related angiogenic factors. Conclusions The combination of established gradients of hypoxia and VEGF expression along with mechanical forces exerted by VAC therapy was associated with the formation of more physiological blood vessels compared to occlusive dressing control wounds. These morphological changes are likely a necessary condition for better wound healing.

Adipose-derived stem cells together with VEGF transduction can enhance the survival and quality of transplanted fat tissues.

There has been a long-standing need for guidelines on the diagnosis and treatment of keloids and hypertrophic scars that are based on an understanding of the pathomechanisms that underlie these skin fibrotic diseases. This is particularly true for clinicians who deal with Asian and African patients because these ethnicities are highly prone to these diseases. By contrast, Caucasians are less likely to develop keloids and hypertrophic scars, and if they do, the scars tend not to be severe. This ethnic disparity also means that countries vary in terms of their differential diagnostic algorithms. The lack of clear treatment guidelines also means that primary care physicians are currently applying a hotchpotch of treatments, with uneven outcomes. To overcome these issues, the Japan Scar Workshop (JSW) has created a tool that allows clinicians to objectively diagnose and distinguish between keloids, hypertrophic scars, and mature scars. This tool is called the JSW Scar Scale (JSS) and it involves scoring the risk factors of the individual patients and the affected areas. The tool is simple and easy to use. As a result, even physicians who are not accustomed to keloids and hypertrophic scars can easily diagnose them and judge their severity. The JSW has also established a committee that, in cooperation with outside experts in various fields, has prepared a Consensus Document on keloid and hypertrophic scar treatment guidelines. These guidelines are simple and will allow even inexperienced clinicians to choose the most appropriate treatment strategy. The Consensus Document is provided in this article. It describes (1) the diagnostic algorithm for pathological scars and how to differentiate them from clinically similar benign and malignant tumors, (2) the general treatment algorithms for keloids and hypertrophic scars at different medical facilities, (3) the rationale behind each treatment for keloids and hypertrophic scars, and (4) the body site-specific treatment protocols for these scars. We believe that this Consensus Document will be helpful for physicians from all over the world who treat keloids and hypertrophic scars.

A number of surgical techniques have been developed to promote periodontal tissue regeneration. Bone marrow-derived stem cells have also been shown to promote periodontal tissue regeneration. In this study, we sought to determine whether adipose-derived stem cells (ASCs) can promote periodontal tissue regeneration as well. ASCs were isolated from a Wistar rat, passaged twice, mixed with platelet-rich plasma (PRP) obtained from inbred rats, and implanted into the periodontal tissue defect that had been generated in the test rats. Tissue specimens were harvested after 2, 4, and 8 weeks for histological analysis. Rats that received PRP only or were not implanted served as controls. A small amount of alveolar bone regeneration was observed 2 and 4 weeks after ASC/PRP implantation. Moreover, 8 weeks after implantation, a periodontal ligament-like structure was observed along with alveolar bone. These observations suggest that ASCs can promote periodontal tissue regeneration in vivo. Because large amounts of human lipoaspirates are readily available, and their procurement induces only low morbidity, ASCs may be useful in future clinical cell-based therapy for periodontal disease.