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Male‐pattern hair loss, also termed androgenetic alopecia (AGA), is a highly prevalent age‐related condition that is characterized by a distinct pattern of hair loss from the frontotemporal and vertex regions of the scalp. The phenotype is highly heritable and hormone dependent, with androgens being the recognized critical hormonal factor. Numerous molecular genetic studies have focused on genetic variation in and around the gene that encodes the androgen receptor. More recently, however, the availability of high‐throughput molecular genetic methods, novel methods of data analysis and sufficiently large sample sizes have rendered possible the systematic investigation of the contribution of other components of the androgen receptor pathway or hormonal pathways beyond the androgen receptor signalling pathways. Over the past decade, genome‐wide association studies of increasingly large cohorts have enabled the genome‐wide identification of genetic risk factors for AGA, and yielded unprecedented insights into the underlying pathobiology. The present review discusses some of the most intriguing genetic findings on the relevance of (sex)hormonal signalling in AGA. [ABSTRACT FROM AUTHOR]

Introduction: Temporal recession in male-pattern baldness is common. The method of marking of temporal point practiced worldwide, described by Walter P. Unger, does not help in marking temporal triangle border in Indian population. We have found aesthetically superior way of marking temporal point and easy method of construction of lower border of temporal triangle. Case Series: The new marking was applied over 126 young male patients from March 2014 to December 2017; they were regularly followed up and results were observed. Conclusion: With the new method of marking, we found that the lower border of temporal triangle can be easily constructed and temporal point can be more aesthetically placed in Indian population. [ABSTRACT FROM AUTHOR]

Androgenetic alopecia ( AGA) is a highly heritable condition, and the most common form of hair loss in men. The phenotype is characterized by an androgen-dependent, progressive loss of hair from the scalp, which may commence during puberty. Up to 80% of European men experience some degree of androgen-dependent hair loss during their lifetime. Current treatment options for AGA have limited efficacy, and improved understanding of the underlying biological causes is required to facilitate novel therapeutic approaches. To date, molecular genetic studies have implicated 12 genomic regions in AGA and identified a number of candidate genes. The latter include those encoding the androgen receptor ( AR), the histone deacetylases ( HDAC) 4 and 9, and the WNT molecule WNT10 A. However, the majority of contributing genetic risk factors still await identification. This review describes the current status of AGA genetic research. We discuss the strength of the genetic approach and anticipated developments in the field, and how these will facilitate the systematic unravelling of AGA pathobiology, a process which may lead to the identification of new therapeutic targets. [ABSTRACT FROM AUTHOR]

A recent meta-analysis of 7 genome-wide association studies on early balding (alopecia) revealed single nucleotide polymorphism variants in the region of the amyotrophic lateral sclerosis (ALS) gene TAR DNA-binding protein 43 (TARDBP/TDP-43). We therefore explored the association of early-onset alopecia and ALS in the Health Professionals Follow-up Study, a large cohort of 51,529 US men. In 1992, the participants (then aged 46–81 years) were asked to report their hair line pattern at age 45 years. During the follow-up period (1992–2008), 42 men were diagnosed with ALS. Of those, 13 had reported no alopecia, 18 had reported moderate alopecia, and 11 had reported extensive alopecia at age 45 years. Those who reported extensive alopecia had an almost 3-fold increased risk of ALS compared with those who reported no alopecia (relative risk = 2.74, 95% confidence interval: 1.23, 6.13). Furthermore, we observed a linear trend of increased risk of ALS with increasing level of balding at age 45 years (Ptrend = 0.02). In conclusion, men with early-onset alopecia seem to have a higher risk of ALS. The mechanisms underlying this association deserve further investigation. [ABSTRACT FROM PUBLISHER]

Objective To restore hair, making the scalp look natural, by using follicular unit transplantation technique. Patients and methods Hair transplantation surgeries were performed on consecutive 250 patients between the ages of 24-69 years by 'follicular unit transplantation (FUT)' method from January, 2006. Patterns were classified according to the age group. All the procedures were done under local anesthesia as an outpatient procedure. A small strip of scalp containing hair with dimensions of 15-20cm x 1.5-2.1cm was excised from the occipital regions with the patient in prone position. The donor area was closed primarily using a non-absorbable 3-0 material with lower edge trichophytic closure technique. The hair-bearing strip was dissected into units containing clusters of one, two, three, and four follicles, under magnification. The anterior hairline was drawn preoperatively on each patient. Implantation of the follicular units was initiated immediately after the slits formation. A minimum of 1500 and maximum of 3235 follicular units were placed in one session. Transplanted areas were left open without any dressing. The donor area was covered with a small dressing which was removed the next morning. The first washing was started after 48 hours. The donor area stitches were removed after 10-12 days. Results The mean age of the patients was 36.6 years. Majority of the patients (65.2%) were in 21-35 years age group. 28% of the patients belonged to type V of Norwood classification. The transplanted hair entered into the 'telogen' phase and were lost within 2-4 weeks. The regrowth started in the third month, but it varied from patient to patient. The results were achieved in 8-9 months. No hematoma, infection or necrosis was observed in the early postoperative period. Mild periorbital edema was observed in 9 patients only, however, it disappeared in the first week. Two patients displayed the inclusion cysts which were managed by drainage and, topical and oral antibiotics. Conclusion Good planning, carefully prepared follicular units, and careful placement provide results that was satisfying for both the surgeon and the patient. [ABSTRACT FROM AUTHOR]

Androgens are assumed to play a central role in the pathophysiology of both prostate cancer (PC) and androgenic alopecia (AA). A correlation between the two phenotypes may be relevant for identification of men at high risk of PC. We evaluated the association between AA at different ages and PC in a large case-control study. Methods: The case group comprised 938 PC patients recruited from a population-based cancer registry. The controls (n =2160) were a random sample of the male general population. All subjects completed a questionnaire on risk factors for cancer, including questions on hair pattern at different ages using an adapted version of the Hamilton-Norwood scale, race and family history of PC. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using multivariable logistic regression. Results: Baldness at early age appeared to be associated with a lower risk of PC (baldness at age 20: OR=0.86; 95% CI 0.69–1.07 and baldness at age 40: OR=0.81; 95% CI 0.70–0.96). Baldness at completion of the questionnaire was not associated with PC: OR=1.10; 95% CI 0.89–1.34. An isolated ‘frontal baldness’ or ‘vertex baldness’ pattern was not significantly associated with PC at any age. Presence of a combined ‘frontal and vertex’ baldness pattern at age 40 was associated with a decreased risk of PC (OR=0.62; 95% CI 0.45–0.86). There were no significant associations between AA and aggressive PC. Conclusions: We did not find consistent positive associations between AA at different ages and PC. Surprisingly, if anything, baldness at early age is inversely related to PC in this study. Androgenic alopecia is not useful as an indicator of men at high risk of PC. [Copyright &y& Elsevier]

A letter to the editor is presented regarding the study that demonstrates fine mapping of androgen receptor (AR) and ectodysplasin A2 receptor (EDA2R) locus among patients with androgenetic alopecia (AGA).

Background Finasteride, a competitive inhibitor of the enzyme 5α-reductase II, is widely used as a medical treatment for patients with male-pattern baldness (MPB), which is affected by the distribution of androgenic steroids. It is also notable that the androgenic effect in MPB is different for each region of the head. Objectives To study the effect of the drug finasteride, we quantified androgenic steroids in the vertex and occipital scalp hair and in the plasma of patients with MPB. Methods The patients with MPB, aged 23–52 years, were treated with finasteride 1 mg daily for 5 months. The hair and plasma samples were hydrolysed, extracted with n-pentane, and derivatized with MSTFA : NH4I : DTE (1000 : 4 : 5, v/w/w). We analysed the concentrations of dihydrotestosterone (DHT) and testosterone (T) in the hair and plasma using gas chromatography–mass spectrometry (GC-MS). Results In the hair, the ratio of DHT/T was decreased in the vertex scalp hair after the individual received finasteride ( P < 0·005). However, we found no significant difference in the ratio of DHT/T in the occipital scalp hair before and after individuals received finasteride. Like the results in the vertex scalp hair, the ratio of DHT/T in the plasma was remarkably decreased after finasteride administration ( P < 0·001). Conclusions This study supports the effect of finasteride in patients with MPB by examining the decreased level of DHT/T in scalp hair and in plasma. Thus, in view of the androgenic effect in the different hair regions, the vertex scalp hair plays a more important role for patients with MPB treated with finasteride than does the occipital hair. [ABSTRACT FROM AUTHOR]

Summary: Many studies link the development of androgen‐related disorders to the overexpression of two proteins, 5α‐reductase and androgen receptor (AR). In this commentary, we use microcompetition to explain how common latent viruses can cause transcription factor deficiency, overexpression of 5α‐reductase and AR, and male‐pattern baldness. [ABSTRACT FROM AUTHOR]