[Hair transplantation-sustainably planned and performed by the physician]. / Haartransplantation ­ nachhaltige ärztliche Planung und Durchführung.

BACKGROUND AND OBJECTIVES: Microsurgical autologous hair transplantation, when performed as follicular unit transplantation, may permanently and naturally improve advanced androgenetic alopecia in men and women and also non-active scarring alopecias. MATERIALS, METHODS AND RESULTS: Sufficient donor hair and realistic patient expectations as well as an individual surgical planning of the hair distribution are crucial prerequisites for a sustainable hair restoration. They should be determined and evaluated during a personal pre-examination and consultation with the hair surgeon. Natural results can be achieved by transplanting up to several thousands of follicular units with high densities into small micro-slits. This technique also allows for increasing the hair density without injuring surrounding original pre-existing hairs. In progressive, early or advanced androgenetic alopecia, additional medical therapy is highly recommended to stabilize the condition. Otherwise, depending on supply and demand of donor hair, only a partial hair restoration can be achieved with a satisfying density. CONCLUSIONS: Since hair transplantation requires a precise sequence of surgical steps and careful handling of the tiny grafts, the skills and experience of the hair surgeon and his or her team are crucial. The medical risks of an assembly-line way of performing this surgery by non-licensed, non-physician staff, as reported from national clinics and medical tourism, should not be underestimated. The German Association of Hair Surgeons and the International Society of Hair Restoration Surgery offer patient information, as well as continuous medical education and guidelines for interested physicians to ensure the highest quality standard of care.

Alopecia areata: Clinical presentation, diagnosis, and unusual cases.

Alopecia areata (AA) is a nonscarring hair loss disorder with a 2% lifetime risk. Most patients are below 30 years old. Clinical types include patchy AA, AA reticularis, diffuse AA, AA ophiasis, AA sisiapho, and perinevoid AA. Besides scalp and body hair, the eyebrows, eyelashes, and nails can be affected. The disorder may be circumscribed, total (scalp hair loss), and universal (loss of all hairs). Atopy, autoimmune thyroid disease, and vitiligo are more commonly associated. The course of the disease is unpredictable. However, early, long-lasting, and severe cases have a less favorable prognosis. The clinical diagnosis is made by the aspect of hairless patches with a normal skin and preserved follicular ostia. Exclamations mark hairs and a positive pull test signal activity. Dermoscopy may reveal yellow dots. White hairs may be spared; initial regrowth may also be nonpigmented. The differential diagnosis includes trichotillomania, scarring alopecia, and other nonscarring hair loss disorders such as tinea capitis and syphilis.

Evidence-based (S3) guideline for the treatment of androgenetic alopecia in women and in men.

Androgenetic alopecia is the most common hair loss disorder, affecting both men and women. Initial signs of androgenetic alopecia usually develop during teenage years leading to progressive hair loss with a pattern distribution. Moreover, its frequency increases with age and affects up to 80 % Caucasian men and 42 % of women. Patients diagnosed with androgenetic alopecia may undergo significant impairment of quality of life. Despite the high prevalence and the variety of therapeutic options available, there have been no national or international evidence-based guidelines for the treatment of androgenetic alopecia in men and women so far. Therefore, the European Dermatology Forum (EDF) initiated a project to develop an evidence-based S3 guideline for the treatment of andro-genetic alopecia. Based on a systematic literature research the efficacy of the currently available therapeutic options was assessed and therapeutic recommendations were passed in a consensus conference. The purpose of the guideline is to provide dermatologists as well as general practitioners with an evidence-based tool for choosing an efficacious and safe therapy for patients with androgenetic alopecia.

Secondary cicatricial and other permanent alopecias.

Various nonfollicular scalp conditions can cause secondary scarring or permanent alopecia. Possible causes are congenital defects, trauma, inflammatory conditions, infections, and neoplasms (rarely drugs). Associated signs and symptoms and other diagnostic procedures such as histopathology may aid in the diagnosis. Detection of the underlying disorder may be difficult in end-stage lesions. Treatment is specific for active conditions. Surgery and hair transplantation are options for localized scars.

Androgenetic alopecia.

Androgenetic alopecia (AGA), or male pattern hair loss, affects approximately 50% of the male population. AGA is an androgen-related condition in genetically predisposed individuals. There is no treatment to completely reverse AGA in advanced stages, but with medical treatment (eg, finasteride, minoxidil, or a combination of both), the progression can be arrested and partly reversed in the majority of patients who have mild to moderate AGA. Combination with hair restoration surgery leads to best results in suitable candidates. Physicians who specialize in male health issues should be familiar with this common condition and all the available approved treatment options.

Alopecia areata: pathogenesis and potential for therapy.

Although the complete picture for alopecia areata (AA) pathogenesis has yet to be determined, recent research has made much progress in our understanding of the disease mechanism. Numerous circumstantial evidence supports the notion that AA is fundamentally a disease mediated by inflammatory cells and may be autoimmune in nature. Recent research has shown the hair-loss phenotype is precipitated predominantly by CD8+ lymphocytes, but the disease mechanism is driven by CD4+ lymphocytes. Although genetic susceptibility is a key contributor to disease development, disease onset and phenotypic presentation are probably modified by complex environmental interplay. On the basis of our current understanding of AA disease pathogenesis, several experimental and theoretical therapeutic approaches might be possible. However, the pathogenetic disease mechanism is particularly robust and the development of a cure for AA will be a significant challenge.

Nutrition and hair: deficiencies and supplements.

Hair follicle cells have a high turnover. A caloric deprivation or deficiency of several components, such as proteins, minerals, essential fatty acids, and vitamins, caused by inborn errors or reduced uptake, can lead to structural abnormalities, pigmentation changes, or hair loss, although exact data are often lacking. The diagnosis is established through a careful history, clinical examination of hair loss activity, and hair quality and confirmed through targeted laboratory tests. Examples of genetic hair disorders caused by reduced nutritional components are zinc deficiency in acrodermatitis enteropathica and copper deficiency in Menkes kinky hair syndrome.

What can we learn from animal models of Alopecia areata?

Alopecia areata (AA) is a hair loss disease marked by a focal inflammatory infiltrate of dystrophic anagen stage hair follicles by CD4+ and CD8+ lymphocytes. Although AA is thought to be an autoimmune disorder, definitive proof is lacking. Moreover, characterization of the primary pathogenic mechanisms by which hair loss is induced in AA is limited. In this context, animal models may provide a vital contribution to understanding AA. Recent research using animal models of AA has focused on providing evidence in support of a lymphocyte-mediated pathogenic mechanism consistent with AA as an autoimmune disease. In the future, research with both humans and animal models shall likely concentrate on identifying the primary antigenic epitopes involved in AA and the genetics of AA susceptibility. With a comprehensive understanding of the key elements in AA pathogenesis, new avenues for therapeutic research and intervention will be defined.