Clinics in Dermatology RSS feed: Current Issue. Clinics in Dermatology brings you the most practical and comprehensive information on the treatment and care of skin disorders. Each issue features a Guest Editor and is devoted to a single timely topic relating to clinical dermatology. Clinics in Dermatology provides information that is... • Clinically oriented -- from evaluation to treatment, Clinics in Dermatology covers what is most relevant to you in your practice. • Authoritative -- world-renowned experts in the field assure the high-quality and currency of each issue by reporting on their areas of expertise. • Well-illustrated -- each issue is complete with photos, drawings and diagrams to illustrate points and demonstrate techniques. Now affiliated with the International Academy of Cosmetic Dermatology (IACD). Visit the IACD web site at: www.dermato.med.br/iacd for more information. http://www.cidjournal.com/?rss=yesElsevier Inc.en © 2012 Published by Elsevier Inc. All rights reserved. Clinics in Dermatology0738-081X303May 2012 © 2012 Published by Elsevier Inc. All rights reserved. healthpermissions@elsevier.comhttp://www.cidjournal.com/article/PIIS0738081X12000508/abstract?rss=yesEditorial Board10.1016/S0738-081X(12)00050-8Clinics in Dermatology 30, 3 (2012)2012-05-01Clinics in Dermatology2012-05-01303S0738-081X(11)X0009-3IFCIFChttp://www.cidjournal.com/article/PIIS0738081X12000533/abstract?rss=yesContents10.1016/S0738-081X(12)00053-3Clinics in Dermatology 30, 3 (2012)2012-05-01Clinics in Dermatology2012-05-01303S0738-081X(11)X0009-3iiiivhttp://www.cidjournal.com/article/PIIS0738081X11002331/abstract?rss=yesThe skin's most important function, its raison d'être, is the formation of an effective barrier between the "inside" and the "outside" worlds of the organism. An intact and well-functioning skin barrier is necessary to prevent desiccation, which permits terrestrial life on dry land. It also determines the function and appearance of the skin, ranging from tough and scaly to soft and smooth. We now know that derangements of the epidermal barrier are central to the development of all dry skin conditions, plus a myriad of diseases, including atopic dermatitis, irritant contact dermatitis, ichthyosis, and psoriasis, as well as of the development of allergies.Commentary: Epidermal barrier function: Clinical implications and therapeutic relevanceRonni Wolf, Lawrence Charles Parish10.1016/j.clindermatol.2011.08.029Clinics in Dermatology 30, 3 (2012)2012-05-01Clinics in Dermatology2012-05-01303S0738-081X(11)X0009-3255256http://www.cidjournal.com/article/PIIS0738081X11002112/abstract?rss=yesAbstract: The most important function of the skin is the formation of a barrier between the “inside” and the “outside” of the organism, which prevents invasion of pathogens and fends off chemical assaults as well as the unregulated loss of water and solutes. The physical barrier is mainly localized in the stratum corneum, which consists of protein-enriched cells and lipid-enriched intercellular domains. Any modifications in epidermal differentiation and lipid composition results in altered barrier function, a central event in various skin alterations and diseases. This contribution presents a brief description of the structure of the skin, paying attention to the most important components responsible for skin barrier function.Structure and function of the epidermis related to barrier propertiesAdone Baroni, Elisabetta Buommino, Vincenza De Gregorio, Eleonora Ruocco, Vincenzo Ruocco, Ronni Wolf10.1016/j.clindermatol.2011.08.007Clinics in Dermatology 30, 3 (2012)2012-05-01Clinics in Dermatology2012-05-01303S0738-081X(11)X0009-3257262http://www.cidjournal.com/article/PIIS0738081X11002124/abstract?rss=yesAbstract: A major function of the skin is to provide a barrier to the movement of water and electrolytes, which is required for life in a terrestrial environment. This permeability barrier is localized to the stratum corneum and is mediated by extracellular lipid-enriched lamellar membranes, which are delivered to the extracellular spaces by the secretion of lamellar bodies by stratum granulosum cells. A large number of factors have been shown to regulate the formation of this permeability barrier. Specifically, lamellar body secretion and permeability barrier formation are accelerated by decreases in the calcium content in the stratum granulosum layer of the epidermis. In addition, increased expression of cytokines and growth factors and the activation of nuclear hormone receptors (peroxisome proliferator-activated receptors, liver X receptors, vitamin D receptor) accelerate permeability barrier formation. In contrast, nitric oxide, protease-activated receptor 2 activation, glucocorticoids, and testosterone inhibit permeability barrier formation. The ability of a variety of factors to regulate permeability barrier formation allows for a more precise and nuanced regulation.Regulation of permeability barrier homeostasisKenneth R. Feingold, Mitsuhiro Denda10.1016/j.clindermatol.2011.08.008Clinics in Dermatology 30, 3 (2012)2012-05-01Clinics in Dermatology2012-05-01303S0738-081X(11)X0009-3263268http://www.cidjournal.com/article/PIIS0738081X11002173/abstract?rss=yesAbstract: The intact skin represents a barrier to the uncontrolled loss of water, proteins, and plasma components from the organism. Owing to its complex structure, the epidermal barrier with its major layer, the stratum corneum, is the rate-limiting unit for the penetration of exogenous substances through the skin. The epidermal barrier is not a static structure. The status of different functions of the epidermis can be monitored by assessing specific biophysical parameters such as transepidermal water loss, stratum corneum hydration, and skin surface pH. Variables originating from the individual as well as exogenous factors have an important influence on the epidermal barrier parameters.Influence of skin type, race, sex, and anatomic location on epidermal barrier functionRazvigor Darlenski, Joachim W. Fluhr10.1016/j.clindermatol.2011.08.013Clinics in Dermatology 30, 3 (2012)2012-05-01Clinics in Dermatology2012-05-01303S0738-081X(11)X0009-3269273http://www.cidjournal.com/article/PIIS0738081X11002288/abstract?rss=yesAbstract: Skin, together with its appendages, forms an organ with several defensive roles; among them it acts as a barrier, which is one of its very important protective functions. There has been increased interest in studying the effects of age on these functions. There are different intensities and timing involved in this process and also differences between men and women, all relating to skin structure.We review the current knowledge of the skin as a barrier in neonates and in the elderly in an attempt to explain the changes that occur with aging.Effects of age (neonates and elderly) on skin barrier functionMarcia Ramos-e-Silva, Juliana Catucci Boza, Tania Ferreira Cestari10.1016/j.clindermatol.2011.08.024Clinics in Dermatology 30, 3 (2012)2012-05-01Clinics in Dermatology2012-05-01303S0738-081X(11)X0009-3274276http://www.cidjournal.com/article/PIIS0738081X1100229X/abstract?rss=yesAbstract: The skin is a vital organ for life and, among its many functions, the role as a protective barrier is one of the most important. It is the main boundary between the body and the external environment. As defensive barrier, the epidermis protects internal organs from physical and chemical trauma, microorganism invasion, and ultraviolet radiation. It also acts in the regulation of transepidermal movement of water and electrolytes, and in preventing dehydration, all of which are essential for sustaining life. The main role is allotted to the stratum corneum and to the lipid matrix located in the intercellular space. The occurrence of dysfunction in the epidermal barrier is an important factor in the physiopathogenesis of skin diseases, particularly atopic dermatitis and psoriasis. There are few, but important, systemic changes that influence or are influenced by dysfunctions in the epidermal barrier. We review the effects of some systemic diseases on the maintenance of the skin's homeostasis.Epidermal barrier function and systemic diseasesMarcia Ramos-e-Silva, Claudio de-Moura-Castro Jacques10.1016/j.clindermatol.2011.08.025Clinics in Dermatology 30, 3 (2012)2012-05-01Clinics in Dermatology2012-05-01303S0738-081X(11)X0009-3277279http://www.cidjournal.com/article/PIIS0738081X11002185/abstract?rss=yesAbstract: The skin is the organ that acts as a barrier between the outer and inner environments of the body. It is thus exposed not only to a wide variety of physical, chemical, and thermal insults from the outside world but also to inner endogenous stimuli. Stress, once an abstract psychologic phenomenon, has taken research's center stage in recent years. The “mind–body connection” is now less of an obscure New Age term and more of an elaborate physiologic pathway by which bilateral communication occurs between body and brain. Dermatologists and dermatologic patients have long acknowledged the effect of stress on the skin and its capability to initiate, maintain, or exacerbate several skin diseases. Because disruption of epidermal barrier integrity may be important in the development of some common skin diseases, it is crucial to understand its vulnerability to psychologic stress.Psychological stress and epidermal barrier functionEdith Orion, Ronni Wolf10.1016/j.clindermatol.2011.08.014Clinics in Dermatology 30, 3 (2012)2012-05-01Clinics in Dermatology2012-05-01303S0738-081X(11)X0009-3280285http://www.cidjournal.com/article/PIIS0738081X11002197/abstract?rss=yesAbstract: A daily moisturizing routine is a vital part of the management of patients with atopic dermatitis and other dry skin conditions. The composition of the moisturizer determines whether the treatment strengthens or deteriorates the skin barrier function, which may have consequences for the outcome of the dermatitis. One might expect that a patient's impaired skin barrier function should improve in association with a reduction in the clinical signs of dryness. Despite visible relief of the dryness symptoms, however, the abnormal transepidermal water loss has been reported to remain high, or even to increase under certain regimens, whereas other moisturizers improve skin barrier function. Differing outcomes have also been reported in healthy skin: some moisturizers produce deterioration in skin barrier function and others improve the skin. Possible targets for barrier-influencing moisturizing creams include the intercellular lipid bilayers, where the fraction of lipids forming a fluid phase might be changed due to compositional or organizational changes. Other targets are the projected size of the corneocytes or the thickness of the stratum corneum. Moisturizers with barrier-improving properties may delay relapse of dermatitis in patients with atopic dermatitis. In a worst-case scenario, treatment with moisturizing creams could increase the risks of dermatitis and asthma.Effect of moisturizers on epidermal barrier functionMarie Lodén10.1016/j.clindermatol.2011.08.015Clinics in Dermatology 30, 3 (2012)2012-05-01Clinics in Dermatology2012-05-01303S0738-081X(11)X0009-3286296http://www.cidjournal.com/article/PIIS0738081X11002252/abstract?rss=yesAbstract: The past decade has witnessed an explosion of new impartial information about the complex interaction of the skin with topically applied substances, including soaps and detergents. Despite of all these new data, our knowledge on the exact pathomechanism and molecular events leading to detergent-induced barrier dysfunction remains incomplete and the answers continue to elude us.The longtime prevailing opinion which contends that the damaging effect of soaps and detergents is related to their property to extract and remove useful intercellular lipids has mostly been abandoned. Although this effect might be involved in the damaging effect, it is definitely not the sole mechanism, nor, indeed, is it even the main one. Skin proteins damage, the interaction with keratins and their denaturation, swelling of cell membranes and collagen fibers, cytotoxicity expressed with cellular lysis are other important mechanisms.One proposed mechanism is that an initial stratum corneum hyper-hydration results from a continuous disruption of the secondary and tertiary structures of keratin protein by surfactants, exposing new water-binding sites, thereby increasing the hydration of the membrane. Following evaporation of excess water, the denatured keratin possesses a decreased water-binding capacity and decreased ability to function as a barrier.Recent studies have also emphasized the effects of detergents on lipid synthesis, on lipid-metabolizing enzymes and on keratinocyte differentiation.Effect of soaps and detergents on epidermal barrier functionRonni Wolf, Lawrence Charles Parish10.1016/j.clindermatol.2011.08.021Clinics in Dermatology 30, 3 (2012)2012-05-01Clinics in Dermatology2012-05-01303S0738-081X(11)X0009-3297300http://www.cidjournal.com/article/PIIS0738081X11002203/abstract?rss=yesAbstract: New bioengineering techniques provide noninvasive opportunities to evaluate clinically the application of various products on the skin. The skin barrier function and its integrity can be studied by transepidermal water loss, stratum corneum water content, transcutaneous flux of carbon dioxide and oxygen, and transepidermal movement of ions, particularly chloride, potassium, and hydrogen ions. The benefits of noninvasive techniques are due not only to their lack of skin barrier destruction but also to their potential for early detection of any subclinical effects not detected by the naked eyes.Noninvasive test methods for epidermal barrier functionBahman Sotoodian, Howard I. Maibach10.1016/j.clindermatol.2011.08.016Clinics in Dermatology 30, 3 (2012)2012-05-01Clinics in Dermatology2012-05-01303S0738-081X(11)X0009-3301310http://www.cidjournal.com/article/PIIS0738081X11002215/abstract?rss=yesAbstract: Ichthyoses, including inherited disorders of lipid metabolism, display a permeability barrier abnormality in which the severity of the clinical phenotype parallels the prominence of the barrier defect. The pathogenesis of the cutaneous phenotype represents the consequences of the mutation for epidermal function, coupled with a “best attempt” by affected epidermis to generate a competent barrier in a terrestrial environment. A compromised barrier in normal epidermis triggers a vigorous set of metabolic responses that rapidly normalizes function, but ichthyotic epidermis, which is inherently compromised, only partially succeeds in this effort. Unraveling mechanisms that account for barrier dysfunction in the ichthyoses has identified multiple, subcellular, and biochemical processes that contribute to the clinical phenotype. Current treatment of the ichthyoses remains largely symptomatic: directed toward reducing scale or corrective gene therapy. Reducing scale is often minimally effective. Gene therapy is impeded by multiple pitfalls, including difficulties in transcutaneous drug delivery, high costs, and discomfort of injections. We have begun to use information about disease pathogenesis to identify novel, pathogenesis-based therapeutic strategies for the ichthyoses. The clinical phenotype often reflects not only a deficiency of pathway end product due to reduced-function mutations in key synthetic enzymes but often also accumulation of proximal, potentially toxic metabolites. As a result, depending upon the identified pathomechanism(s) for each disorder, the accompanying ichthyosis can be treated by topical provision of pathway product (eg, cholesterol), with or without a proximal enzyme inhibitor (eg, simvastatin), to block metabolite production. Among the disorders of distal cholesterol metabolism, the cutaneous phenotype in Congenital Hemidysplasia with Ichthyosiform Erythroderma and Limb Defects (CHILD syndrome) and X-linked ichthyosis reflect metabolite accumulation and deficiency of pathway product (ie, cholesterol). We validated this therapeutic approach in two CHILD syndrome patients who failed to improve with topical cholesterol alone, but cleared with dual treatment with cholesterol plus lovastatin. In theory, the ichthyoses in other inherited lipid metabolic disorders could be treated analogously. This pathogenesis (pathway)-driven approach possesses several inherent advantages: (1) it is mechanism-specific for each disorder; (2) it is inherently safe, because natural lipids and/or approved drugs often are utilized; and (3) it should be inexpensive, and therefore it could be used widely in the developing world.Abnormal barrier function in the pathogenesis of ichthyosis: Therapeutic implications for lipid metabolic disordersPeter M. Elias, Mary L. Williams, Kenneth R. Feingold10.1016/j.clindermatol.2011.08.017Clinics in Dermatology 30, 3 (2012)2012-05-01Clinics in Dermatology2012-05-01303S0738-081X(11)X0009-3311322http://www.cidjournal.com/article/PIIS0738081X11002264/abstract?rss=yesAbstract: Almost 2 decades ago, Williams and Elias suggested a unifying concept for the pathogenesis of disorders of cornification, according to which the integrity of the epidermal barrier and its effective function is an important factor in the regulation of epidermal DNA synthesis. Interference with the barrier integrity or function will result in epidermal hyperplasia and may be the primary event leading to hyperproliferative skin diseases, such as psoriasis.We have analyzed alterations to several structures of the epidermal barrier that might be responsible for barrier dysfunction and thus lead to hyperproliferation of the epidermis in an attempt to repair the barrier and, as a result, might be inducers of psoriasis. There are several convincing reports indicating that inhibiting of epidermal transglutaminase may lead to epidermal hyperproliferation and that this stimulus might trigger psoriasis among genetically predisposed patients.Disturbance of epidermal barrier function caused by derangement of lipid or cholesterol or ceramide synthesis leads to increased DNA synthesis and epidermal hyperplasia and as a result might be an inducer of psoriasis. We could find little evidence to show that defective defense of the epidermis or an abnormal response of it to bacteria plays a role in the pathogenesis of psoriasis.Accumulating data indicate that there is an association of psoriasis and mutations of genes within the epidermal differentiation complex, which are crucial for the development, maturation, cornification, cross-linking, and terminal differentiation of the epidermis, called psoriasis susceptibility locus 4.Abnormal epidermal barrier in the pathogenesis of psoriasisRonni Wolf, Edith Orion, Eleonora Ruocco, Vincenzo Ruocco10.1016/j.clindermatol.2011.08.022Clinics in Dermatology 30, 3 (2012)2012-05-01Clinics in Dermatology2012-05-01303S0738-081X(11)X0009-3323328http://www.cidjournal.com/article/PIIS0738081X11002276/abstract?rss=yesAbstract: Despite the acknowledged contributions of a defective epidermal permeability barrier, dryness of the skin, and the propensity to develop secondary infections to the etiology and pathophysiology of atopic dermatitis (AD), these epidermal changes have, until recently, been assumed to reflect downstream consequences that are secondary phenomena of the primary immunologic abnormality—the historical “inside-outside” view that AD is basically an intrinsic inflammatory disease.In this review, we focused on the role of the epidermal barrier function in the pathophysiology of AD. Specifically, we presented data in support of a barrier-initiated pathogenesis of AD, ie, the “outside-inside” concept. First, we reviewed the evidence on the existence of inherited barrier abnormalities in AD. Reported studies on the possible association of mutations in the filaggrin gene (FLG) and data on human tissue kallikreins (KLKs) and AD have been addressed. We then dealt with the question of the causal link between impaired epidermal barrier and inflammation. Finally, the association between innate immune defense system and the increased avidity of Staphylococcus aureus for atopic skin was examined.Despite very convincing evidence to support the barrier-initiated pathogenesis of AD, the view that AD reflects the downstream consequences of a primary immunologic abnormality cannot be dismissed out of hand. Almost every line of evidence in support of the role of the epidermal barrier as the “driver” of the disease activity can be challenged and at least partially contradicted by opposing evidence.Until more data are available and until all the dust settles around this issue, we should take advantage of what we already know and use our knowledge for practical purposes. Deployment of specific strategies to restore the barrier function in AD means the use of moisturizers as first-line therapy.Abnormal epidermal barrier in the pathogenesis of atopic dermatitisRonni Wolf, Danny Wolf10.1016/j.clindermatol.2011.08.023Clinics in Dermatology 30, 3 (2012)2012-05-01Clinics in Dermatology2012-05-01303S0738-081X(11)X0009-3329334http://www.cidjournal.com/article/PIIS0738081X11002239/abstract?rss=yesAbstract: A crucial role of the epidermal permeability barrier is obvious in contact dermatitis. An intact skin barrier prevents the penetration of harmful substances into the skin. Irritants and allergens that stay on the skin surface and come into contact with the stratum corneum only do not harm the skin. After disruption of the skin barrier, however, irritants may penetrate into the living epidermal layers, injure the keratinocyte membrane, and release cytokines, which leads to inflammation and to irritant contact dermatitis. The skin barrier is often disrupted by chronic exposure to water plus detergents, solvents, or other irritants. A disrupted barrier in irritant contact dermatitis also allows for the penetration of allergens. Allergens may come into contact with Langerhans and T cells, induce immunological reactions, and cause inflammation, which results in allergic contact dermatitis. Treatments in contact dermatitis should restore the skin barrier to prevent relapse of the disease. Topical corticosteroids, most often used in treating contact dermatitis, reduce immunological reactions and inflammation but do not lead to a complete barrier repair. Skin barrier repair is more complete after treatment with calcineurin inhibitors and bland lipid-based emollient; therefore, these preparations should be preferred for long-term treatment of contact dermatitis.Abnormal epidermal barrier in the pathogenesis of contact dermatitisEhrhardt Proksch, Jochen Brasch10.1016/j.clindermatol.2011.08.019Clinics in Dermatology 30, 3 (2012)2012-05-01Clinics in Dermatology2012-05-01303S0738-081X(11)X0009-3335344http://www.cidjournal.com/article/PIIS0738081X11002227/abstract?rss=yesAbstract: Skin health depends on an intact barrier composed of protein-rich corneocytes surrounded by the lamellar intercellular lipids. This barrier provides waterproof protection for the body, preventing infection, regulating electrolyte balance, maintaining body temperature, and providing a mechanism for sensation. Damage to the skin barrier results in skin disease that can be treated by a variety of externally applied substances, such as ceramides, hyaluronic acid, licorice extracts, dimethicone, petrolatum, and paraffin wax. These substances are found in moisturizers that are sold as cosmetics and in prescriptions as 510(k) devices. This contribution examines the formulation and effect of skin barrier creams.New treatments for restoring impaired epidermal barrier permeability: Skin barrier repair creamsZoe Diana Draelos10.1016/j.clindermatol.2011.08.018Clinics in Dermatology 30, 3 (2012)2012-05-01Clinics in Dermatology2012-05-01303S0738-081X(11)X0009-3345348http://www.cidjournal.com/article/PIIS0738081X12000454/abstract?rss=yesThe 3rd edition of Skin Disease, Diagnosis and Treatment is a synopsis of clinical dermatology that is rich in high-yield information. This valuable tool for trainees and professionals summarizes basic key concepts, differential diagnoses, and treatments of various dermatologic conditions. The book efficiently and concisely accomplishes this by highlighting pearls and presenting useful tables, pictures, and diagrams. The book cover also has an appealing color, elegant artwork, and clearer lettering than the previous edition.Adaobi I. Nwaneshiudu10.1016/j.clindermatol.2012.02.001Clinics in Dermatology 30, 3 (2012)2012-05-01Clinics in Dermatology2012-05-01303S0738-081X(11)X0009-3Book Review350350http://www.cidjournal.com/article/PIIS0738081X12000442/abstract?rss=yesAbstract: A large body of literature supports the role of psychologic stress in urticaria; however, the comorbidity between chronic idiopathic urticaria (CIU) and post-traumatic stress disorder (PTSD), a classic stress-mediated syndrome, has received little attention. The underlying etiology of urticaria is not identifiable in about 70% of patients, possibly because of difficulties with identification of a direct cause-and-effect relationship between a potential causative factor and the onset of urticaria. The core features of PTSD (Diagnostic and Statistical Manual of Mental Disorders, 4th Edition, Text Revision [DSMIV-TR]) that are important in urticaria include (1) autonomic nervous system reactivity and state of sympathetic hyperarousal that can manifest as CIU, and (2) the persistent re-experiencing of the traumatic events in PTSD, which can manifest as urticaria or angioedema, or both, affecting a previously traumatized body region (eg, urticarial wheals affecting the body region where the patient had been stabbed years earlier). The following features of PTSD make it difficult to use the cause-and-effect model for the determination of causation: (1) PTSD may first emerge years after the initial trauma and is classified as PTSD with Delayed Onset (DSMIV-TR); and (2) the traumatic triggers that precipitate the PTSD symptoms may be unique and idiosyncratic to the patient and not even qualify as stressful or traumatic by standard criteria (eg, precipitating events for the PTSD may include smell of a certain cologne that was used by the perpetrator or witnessing a scene in a movie that was reminiscent of the location where the abuse occurred). Finally, in PTSD with Delayed Onset, patients may not make a conscious association between their recurrent urticaria and their earlier traumas because they can develop classically conditioned associations between stimuli that are reminiscent of the original abuse situation and their somatic reactions such as urticaria. The clinician needs to be aware of these factors, because satisfactory resolution of the CIU may not occur without treatment of the PTSD. If the clinician suspects underlying PTSD, it is best to refer the patient to a qualified mental health professional, because detailed history taking about traumatic experiences alone can have an acute destabilizing effect and heighten PTSD symptoms in some patients.Chronic idiopathic urticaria and post-traumatic stress disorder (PTSD): An under-recognized comorbidityMadhulika A. Gupta, Aditya K. Gupta10.1016/j.clindermatol.2012.01.012Clinics in Dermatology 30, 3 (2012)2012-05-01Clinics in Dermatology2012-05-01303S0738-081X(11)X0009-3Comment and Controversy351354http://www.cidjournal.com/article/PIIS0738081X11003439/abstract?rss=yesAbstract: Lucja Frey was the first to explain the pathogenesis of the auriculotemporal syndrome, and the syndrome is recognized today as the Frey syndrome. Patients with this disease are subjected to paroxysmal paraesthesia of half of the face combined with sweating and redness. This syndrome can be found in the differential diagnosis of contemporary dermatology. Among others, it is differentiated from food allergies. The life and scientific career of Lucja Frey was brutally interrupted by the tragic times of the Holocaust.Lucja Frey (1889–1942): Life destroyed by the Holocaust—on the 70th anniversary of her deathAndrzej Grzybowski, Jarosław Sak10.1016/j.clindermatol.2011.11.017Clinics in Dermatology 30, 3 (2012)2012-05-01Clinics in Dermatology2012-05-01303S0738-081X(11)X0009-3Caretaker of the Skin355359http://www.cidjournal.com/article/PIIS0738081X11000952/abstract?rss=yesAbstract: This article suggests ways dermatologists can help solve crimes by sharing knowledge with detectives about abnormalities observed in forensic sketches of suspects.Forensic art and crime solving: a potential role for dermatologistsLois Gibson10.1016/j.clindermatol.2011.03.019Clinics in Dermatology 30, 3 (2012)2012-05-01Clinics in Dermatology2012-05-01303S0738-081X(11)X0009-3Dermatologic Disquisitions and Other Essays360363