Alopecia Areata: Causes, Types and Symptoms

Alopecia Areata Ca intentions, Types and SymptomsAlopecia argonata fecal matter affect any blur-bearing ara and jakes in any case involve nails. A peribulbar lymphocytic infiltrate in a swarm of bees simulate is feature article of the a fucke percentage point of the illness leading to a dystrophic anagen comprisecoach. There vacuousthorn similarly be increase psychiatric morbidity in patients with alopecia areata. Ikeda (2) categorise alopecia areata into four typesetters cases including the vernacular type (81%), the atopic type (10%), the autoresistant type (5%) and the prehypertensive type (4%)The course of the disorder is unpredictable and the response to intercession is variable. The various intercession modalities use arsehole be classified into local and clayic therapies. The topical therapy takes intralesional corticosteroid, topical corticosteroids, minoxidil, anthralin and topical immun otherwiseapy in the form of diphenylcyclopropenone (DPCP) and sq uaric acid di exceptylester (SADBE). The systemic therapy takes systemic corticosteroids and photochemotherapy. Cyclosporine, methotrexate, sulphasalazine and biologics like etanercept, efalizumab, adalimumab and infliximab dupe been apply with limited success. Intralesional corticosteroids are the treatment of choice for adults with less than 50% of scalp area social occasion.The sensitivity of select up clinical response to treatment by a clinical interrogative sentence is very variable and has interindividual variation. Dermoscopy is a noninvasive diagnostic bastard which visualizes subtle patterns of fur lesions not normally visible to the unaided eye. It is performed by a hand held or a idiot box dermoscope equipped with lens systemes that sea captainly long allow magnifications ranging from 10 to 1000, the images obtained can be visualized on a monitor and stored using specific software package on a ad hominem computer, to identify and compare changes over time .(3)The property features of alopecia areata on dermoscopy (4) are scandalmongering-belliedish dots, black dots, depleted fuzz, vellus tomentum cerebrisbreadthcloth and tapering or ecphonesis saphead tomentum cerebris-breadth. After therapy in that location is a decrease in the play of these feature film findings. On the other hand, the presence of thin and unpigmented vellus sensory pig inwardly the patch, and evidence of transformation of vellus vibrissa into lineinal hair, appearing as increased proximal shaft thickness and pigmentation, are characteristic of r sendting infirmity and apocalyptical of a response to treatment.The present playing field is being undertaken to evaluate the dexterity of intralesional triamcinolone acetonide in the treatment of alopecia areata and to assess its local and systemic look effects. Dermoscopy has been used to identify signs of early clinical response to the chosen sanative regimen. The reusable markers to assess the severity of alopecia areata on dermoscopy are the black dots, color dots, broken hairs or dystrophic hair, tapering or exclamation mark hair and short vellus hairs. Previous reports have suggested that the severity of alopecia areata is an fundamental prognostic factor. Therefore, dermoscopic examination of patches of alopecia areata may provide predictors of the response to therapy and can in any case be use for monitoring response to any prescribed regimen.DefinitionAlopecia areata is an autoimmune distemper of uncertain etiology that involves the hair follicle and any(prenominal)times the nail and is normally reversible. Although autoimmune, inheritable and environmental factors have been implicated scarcely the exact pathogenesis is yet to be elucidated.HistoryHippocrates stolon used the line alopecia which literally means foxs infirmity. The characteristics of alopecia areata were offset printing described by Cornelius Celsus in 30 A.D., who described two fo rms of alopecia. The runner he described as complete baldness sinkring in tribe of all ages. The second he called ophiasis, which literally means snake, due to the pattern in which the hair button spreads across the scalp and to a fault suggested that ophiasis was plainly seen in children. Alopecia areata is or sotimes also referred to as area celsi in trade protection to Cornelius Celsus. Alopecia areata has been given galore(postnominal) different names by means ofout story. However, the veritable circumstance alopecia areata was commencement used by Sauvages in his Nosologica Medica, published in 1760 in Lyons, France.From the beginning of 19th atomic event 6 in that respect was con lieurable debate to the highest degree the cause of alopecia areata. Two main hypotheses were put forward, one establish on leechlike contagion by Gruby in 1843 and Radcliffe-Crocker in 1903 and the other based on a nervous disorder by Von Barensrung in 1858. The parasitic scheme d rew support from the pattern in which alopecia developed -expanding slowly in size just as a local transmission system would. Even more significant were the apparent epidemics of alopecia areata account to occur in institutions such as orphanages and schools. However, many attempts to isolate an infective pipe organism and to tape transport alopecia areata by inoculation failed.The initiation of alopecia areata by a nervous disorder, cognise as the trophoneurotic, neurotrophic or neuropathic hypothesis, lastly gained the support of most dermatologists of the time. This vague hypothesis could be back up by the apparently frequent clinical observations of emotional or physical stress and trauma that were associated with the outpouring of alopecia areata and often report in the medical journals of that time. Emotional stress and physical damage were believed to adversely affect hair follicles via the nervous system and Joseph in 1886 appearanceed that patchy hair breathing out could apparently be induced by cutting jumpiness in the necks of cats (it was subsequent suggested that the hair injury was actually due to the cats chafe themselves). The idea circulated among dermatologists for many years because it was very difficult to fundamentally study or disprove that alopecia areata was a nervous disorder. The hypothesis is still supported by few dermatologists today.One of the more unusual variations on the neuropathic stock of alopecia areata was put forward by Jacquet in 1902 who suggested that alopecia areata was initiated by sources of nerve knowledgeablevation such as defective and diseased teeth. Jacquets hypothesis was apparently confirm by Decelle 1909, although Baily in 1910 showed dental disease to be equally frequent in people without alopecia areata. Eye strain was another suggested cause of alopecia areata by Kinnear 1939. With the start of the twentieth century, alopecia areata was known to be associated with disorders of the hormon e glands, triggericularly the thyroid. As such, more or less believed the underlying cause of alopecia areata was due to a hormone dysfunction. By the 1920s most dermatologists had abandoned the parasitic theory of alopecia areata and favoured variations on the trophoneurotic and ductless gland theories often combining the two.Sufferers of alopecia areata were under extensive mental stress from care that they would be suspected of having syphilis. Until the advent of antibiotics, syphilis was a widespread, contagious disease and it also often manifests itself by sudden, quick loss of hair in well-de lovelyd patches, just like alopecia areata. syphilis in the secondary decimal point can also affect finger nails. To further complicate the matter, some dermatologists suggested that alopecia areata could be found in increased association with syphilis as distinct from the direct action of syphilis on hair follicles. Syphilis was believed to induce alopecia areata by the mental distress it created and its possible upset of the endocrine system. These clearly visible symptoms of syphilis were often confused with alopecia areata by the global population and resulted in social ostracism for the sufferer.The early 20th century saw the development of another hypothesis of alopecia areata induction based on ototoxic agents. An unknown poison was believed to be introduced to the hair follicle via the blood system inducing hair loss. The sudden remission and relapse of alopecia areata and its action simultaneously over the body was believed to support the idea. Also in support, injection of thallium acetate (rat poison) was shown to induce alopecia areata like hair loss in some patients, with verbal expression of exclamation mark hairs a diagnostic feature of alopecia areata. However, the toxic origin of alopecia areata never gained widespread popularity against the neuropathic and endocrine hypothesis.It is now widely believed that alopecia areata is an aut oimmune disease. Even though studies more than 100 years old showed that alopecia areata affect hair follicles were invaded by inflammatory cells by Giovannini in 1891, the inflammatory autoimmune disease hypothesis did not become popular until the 1960s. The idea was first proposed by Rothman in a discussion of a paper by Van Scott in 1958.Treatment of alopecia areata by intradermal corticosteroid injections has been dexterous for many years. Kalkoff and Macher in 1958 were the first to have reported a serial publication using hydrocortisone. There later, Orentreich et al in1960 and Gombinger and Malkinson in 1961 reported the use of prednisolone and triamcinolone, and gatekeeper and Burton in 1971 used triamcinolone acetonide and hexacetonide. Moynahan and Bowyer in 1965 and Verbov and Abell in 1970 reported the sign use of jet injection apparatuses in a number of conditions including alopecia areata.(6)EpidemiologyAlopecia areata occurs cosmopolitan and there is no racial or conjure prelidiction. It is a common disease forming 0.7% to 3.8% of patients seen by dermatologists. (7) In the United States, alopecia areata was estimated to occur in 0.1% to 0.2% of the cosmopolitan population, with a lifetime risk of 1.7%.(1) Sixty percent patients present with their first patch below 20 years of age.(8) One study suggests that 85.5% of Asiatic patients with alopecia areata have disease onset to begin with the age of 40 years.(9) The disease prevalence peaks between the second and the fourth decade of life. A family write up is found in 5%-25% of patients.(10)Natural HistoryNatural narrative that includes the severity, course and prognosis is highly unpredictable and it can be give tongue to that the that thing predictable about its course and prognosis is that it is unpredictable. With the operable information at present the spontaneous remission rates have ranged from 34% to 80% inwardly one year and 15% to 25% patients progress to measure loss of scalp hair (alopecia entiretyis) or loss of the entire scalp and body hair (alopecia universalis), of which only 10% eventually recover. (11,12) It is a non-scarring alopecia and is reversible but it can be recurrent and crisp and in long standing cases scarring can occur.EtiologyAlopecia areata is a chronic, autoimmune, organ specific disease, probably mediated by autoreactive T cells, which affect hair follicles and sometimes the nails. The increased frequency of other autoimmune diseases favours the above postulation. hair follicle autoantibodies are also found although it is unlikely that these are involved in the pathogenesis of the disease.Genetic factors Most reports describe the prevalence of positive family history to be in the range of 10 to 20% but it is believed that some indulgent cases may be overlooked or concealed and wherefore the actual figure may be greater. Price and Colombe (13) found a family history of alopecia areata was more common in those who had a d isease onset before the age of 30 years (37% compared with 7.1% in those with onset after 30 years). A study amongst monozygotic and dizygous pairs found a capital of New Hampshire rate of 55% for monozygotic twins and no concordance amongst dizygotic twins.(14) The genetic basis of inheritance appears to be multifactorial and polygenic and not a childlike Mendelian pattern.The strongest associations have been with major histocompatibility complex (MHC), particularly the Class II alleles HLA-DQB1*0301 and HLA-DRB1*1104 and the association is linked to chromosome 6p and few susceptibility loci on chromosomes 10, 16 and 18. (15,16)Atopy Several studies have reported an association and also suggested an earlier age of onset and more severe disease in atopic individuals.(17,18)Autoimmunity A statistically significant association between alopecia areata and Hashimotos thyroiditis, Addisons disease and destructive anemia has been reported. It is also associated with other autoimmune di seases like vitiligo, lichen planus, Sjogrens syndrome, systemic lupus erythematosus, morphea, lichen sclerosus, pemphigus foliaceus, ulcerative colitis, myasthenia gravis, autoimmune haemolytic anemia, diabetes mellitus, autoimmune testicular and ovarian disease, pigs syndrome (in which other autoimmune disorders are common) and autoimmune polyendocrinopathy-candidiasis-ectodermal dysplasia syndrome (also called as autoimmune polyglandular syndrome-1) which is an autosomal recessive disorder in which there are mutations in autoimmune governor gene.(19)There is also evidence of circulating organ specific antibodies against thyroid, stomachic parietal cell, adrenal tissue, unflustered muscle, testis and the ovaries.The cells in the lower part of hair follicle have low or absent expression of MHC proteins and the loss of this immune privilege leading to induction of CD8+ T cell-mediated immunity against follicular melanocytes is hypothesized to be causative of alopecia areata. Thi s explains the peribulbar lymphocytic infiltrate and also the sparing of albumen hair in the patch and hence leads to what is commonly called as the phenomena of nightlong greying.Environmental factorsInfection Prior notion of alopecia areata being due to transmission system directly or due to a remote focus of infection has a long history and was very popular till the lay of 20th century. Skinner et al (20) reported finding mRNA for cytomegalovirus in alopecia areata lesions. Few reports of coexistence in husband and wife but many have refuted this and likened it to be a mere coincidence.Stress Is suggested to be an important precipitating factor and this also explains cures by sleep therapy, reassurance and suggestion therapy. much(prenominal) patients may also have stress associated depression and the finding of elevation serotonin levels in such patients lends support to the theory.It has been seen that there is unnatural expression of estrogen receptor -1 in the hair fol licles of diseased mouse with alopecia areata. corticotropin releasing hormone (CRH) can induce mast cell differentiation from hair follicle mesenchyme and the CRH/receptor activity is seen to be high in alopecia areata skin.(21)Diet push deficiency has been postulated to modulate the hair loss in alopecia areata. The mechanism is by inhibiting the rate-limiting enzyme for DNA synthesis and hence it diminishes the proliferative capacity of hair follicle matrix cells.(22) It has also been seen that dietary soy intake increases the resistance to the development of alopecia areata. A study in a Japanese population living in Hawaii, where a Westernized non soy diet predominates, showed disproportionally higher alopecia areata incidence.(23)Other factors that have been implicated include hormones, drugs, and vaccinations. These factors may increase or decrease susceptibility to the disease onset, pattern, severity, season and response to treatment by modifying the physical and biochem ical status of the immune system and hair follicles.(24)Pathogenesis and pathologyThere are four key phases in the normal hair cycle which includes the anagen (growth) phase, the catagen (regression) phase, the telogen (resting) phase, and the magnoliopsid (controlled shedding phase). When the wise hair cycle begins the old hair fiber is shed from the hair follicle in the exogen phase and hence this maintains the overall hair density of the scalp. If the exogen occurs before the anagen is renewed or there is a dystrophic anagen then this leads to a state called kenogen in which there is no hair fiber in the hair follicle.(24) Thus the patch of alopecia areata can be said to be in a state of kenogen. When the amount of inflammatory infiltrate most the hair follicle increases this can lead to miniaturization of the hair follicles and shortening of the hair cycle with rapid changes from anagen to telogen leading to the formation of nanogen hair follicles which is an intermediate sta ge between terminal and vellus anagen.(25)In the acute stage of the disease there is a swarm of bees infiltration of CD4+ and CD8+ lymphocytes into the peribulbar space of anagen stage hair follicles and some perspicacity of lymphocytes to intrafollicular locations which leads to a state of dystrophic anagen. This disrupts the ability of the hair follicle to produce hair fibres of sufficient length and integrity and the expelled hair fiber is not replaced by a fiber that can produce adequate scalp coverage, hence leading to alopecia.(25) Hair follicles are smaller than normal and do not develop beyond the Anagen 3-4 stage, where the actual hair shaft begins to form and diminish prematurely to telogen.As more and more hair follicle move to telogen phase the amount of inflammation decreases. At this stage most of the inflammation is locate to the papillary dermis around the miniaturized hair follicles. In all stages of the disease, there can also be a diffuse infiltration of eosino phils and mast cells into the disease impact skin. There is no inflammatory infiltrate which is seen around the banding of the hair follicle which is the site for the stem cells. Thus the pathological location of the disease process saves the stem cells from destruction and makes it a reversible and non-scarring alopecia. Trichocytes in the in the hair bulb matrix undergoing early cortical differentiation show vacuolar degeneration and are also the predominant cell types showing aberrant class I and II MHC expression.(10)ClassificationIkedas classification (2)The atopic type (10%) begins during puerility or adolescence and progresses slowly over many years with individual patches long-lasting more than one year. Ophiasis and reticular patterns are common and the chances of developing total alopecia are very high (30-75%).The autoimmune type (5%), affects the middle aged, runs a prolonged and led to alopecia totalis in 10%-50%.The prehypertensive type (4%) occurred in early days adults whose one or both parents were hypertensive progressed faster and led to total alopecia in 40%. Reticular pattern is common.The common type (81%) is the mental image of the fast progressive form of disease that affects adults aged between 20-40 years. No associated conditions and individual patches last less than 6 months and there is spontaneous regrowth occuring within 3 years. Alopecia totalis may develop in 5%-15%.Based on the pattern of alopeciaRestricted to the scalpPatchyOphiasisSisaphioReticulateDiffuseSubtotalAlopecia totalis generaliseAlopecia universalisClinical featuresAlopecia areata may begin at any age but the disease incidence peaks between 20-40 years of age and has an equal sex incidence. The characteristic initial lesion is a well circumscribed, totally bald smooth patch in which the skin appears s fall downly reddened. The disease is asymptomatic but few patients may complain of itching and burning prior to the onset of the lesions. During the active phas e of the disease short easily extractable broken hairs are seen at the margins of the bald patches which are known as exclamation mark hairs and hair pull test is positive.(26)Subsequent course is highly unpredictable. The initial patch may regrow hair or it may increase in size and new patches may appear after a variable interval. The succeeding patches may become confluent. In some cases the initial hair loss is diffuse and total scalp baring has been reported in 48 hours. Regrowth is initially of fine vellus unpigmented hair and later these assume their normal thickness and pigmentation. It is possible that regrowth may occur in one region while alopecia is extending in another region.(10)Alopecia areata may affect any hair bearing skin but the scalp is involved in 90% of patients. The eyebrows and eyelashes may be associated with hair loss elsewhere or may be the only site affected. The term alopecia totalis (AT) is used when complete loss of all scalp hair occurs and alopecia universalis (AU) when there is loss of all body hair. About 5% of patients progress to AT/AU. A new variant has been described by Sato-Kawamura et al (27) called as diffuse and total alopecia which has a favourable prognosis but has rapid progression and extensive involvement.The disease process preferentially affects the pigmented hair and spares the etiolate hair thus leading to the phenomena popularly known as the all-night greying of hair but this is a relative process as white hairs are also lost albeit less as compared to pigmented ones. Hair regrowth may be initially nonpigmented but later complete pigmentation occurs. turn back involvement occurs in 10%-15% of patients in which the most characteristic feature is fine stippled pitting but sometimes there may also be trachyonychia, red or mottled lunulae, nail thinning and ridging, filth that includes longitudinally arranged punctate leuconychia, splitting, onychodystrophy and onycholysis may be seen.(26) Some studies have r eported psychiatric diseases like mood disturbances and anxiety and ophthalmological findings like asymptomatic lens opacities and fundus changes.(28,29)Poor prognostic indicators(10)Early age of onsetExtensive scalp involvement (50% scalp)Loss of eyebrows and eyelashesAlopecia totalis or universalisRecurrent episodePatterns ophiasis, sisaphio, reticularNail changes Pits, onychodystrophy, onycholysis, anonychiaAssociated systemic disorders atopy, hypertension and connective tissue disease.Associated genetic disorder Down syndromeFamily history of alopecia areataMacrophage migration inhibitory factor (MIF) -173*C geneINVESTIGATIONS1. Trichogram/ hair blame test(30)To perform the pluck test, hairs are taken from the specified sites on the fifth day after the last shampoo. The surrounding hairs are better with clips and 60-80 hairs are grasped with a hemostat covered with rubber. The hairs are plucked, twisting and lifting the hair shafts rapidly in the direction of immergence from the scalp. Hair shafts are then cut off 1cm above the root sheaths and roots are arranged side by side on a slide and then taped.The anagen hair bulbs are seen as darkly pigmented triangular or delta-shaped bulbs with an angle to the hair shaft and there is presence of inner root sheath. The telogen hair is seen as less pigmented hair with club-shaped hair bulb and there is absence of inner root sheath. Anagen hairs are distinguished from the telogen hairs and anagen to telogen ratio is calculated.Trichogram in alopecia areata reveals a conglomerate telogen-dystrophic pattern. Telogen hairs predominate in the slowly growing patches, whereas dystrophic anagen hair forms the majority in rapidly progressing disease.2. Scalp biopsy(10)A peribulbar lymphocytic infiltrate in a swarm of bees pattern is characteristic of the acute stage of the disease, in which the number of follicles is normal and many are in catagen or telogen. In the later stages, only a few lymphocytes or eosinophils a re present in fibrous tracts and in a peribulbar location. Many follicles in early anagen stage are observed in this late stage and the actual number of hair follicles may be reduced.3. DermoscopyA dermoscope is a non-invasive diagnostic musical mode which can be used to visualize fine details of skin lesions and even subsurface skin lesions which are not visible to the naked eye. It is also called as skin surface microscope, epiluminescence microscope or an episcope. An advantage of their use is the storage of the results and their reproducibility. (3)The history of dermoscopy(31)Skin surface microscopy began in Europe when in the year 1663, Kolhaus used a microscope for examining the small vessels in the nail fold. In 1878, Abbe described the use of immersion oil in argus-eyed microscopy and this pattern was transferred to skin surface microscopy by the German dermatologist, Unna, in 1893. He introduced the term diascopy and described the use of immersion oil and a glass spatu la for the rendering of lichen planus and for the evaluation of the infiltrate in lupus erythematosus.The term dermatoscopy was introduced in 1920 by the German dermatologist Johann Saphier, when he used a used a new diagnostic tool which resembled a binocular microscope with a built-in light source. The term dermoscopy was introduced by Goldman from the United States when he used this new proficiency for the evaluation of pigmented lesions of the skin. In 1971, Rona MacKie had identified the advantage of surface microscopy for the improvement of surgical diagnosis of pigmented skin lesions and for the differential diagnosis of benign versus malignant lesions. Dermoscopic patterns of pigmented skin lesions including melanoma were established and standardized in consensus conferences that were held in 1989 in Hamburg and 2001 in Rome.Principle of dermoscopy (3)The sanctioned principle is to transilluminate a lesion and then to study the alike(p) under a high magnification to vis ualize its subtle features. When light is incident on a skin surface it undergoes reflection, refraction, diffraction and absorption and the magnitude of each of these phenomena is influenced by physical properties of the skin. When light is reflected on a dry, scaly skin surface most of it is reflected back but when the same locomote on a smooth, oily skin most of the light passes through it and reaches the deep dermis. Thus certain fluids are used to improve the translucency of the skin that includes oils (olive and mineral oil), liquid paraffin, glycerin and water. Hand-held dermoscope have the basic principlesThe refractive index of glass is almost similar to skin and when it is in clashing with oil-applied skin, it further enhances the transillumination and hence visualization.The application of a glass scale of measurement flattens the skin surface and provides an even surface for better examination.Videodermoscopy arrays evolution of dermoscopy and it is performed with video camera equipped with optic fibers and lenses that currently allow magnification ranging from 10X to 1000X, and images are visualized on a monitor and stored using specific software on personal computer.Basic design of a dermoscope(3)The essential components includeAchromatic lens To achieve the desired magnification which ranges from 10X to 100X.Inbuilt lighten system Various illuminating systems are used that includeHalogen lamps emit yellow light which can alter the colour contrast of the lesions. imperfect emitting diodes (LED) Used in Delta 20, Dermlite, provide high intensity and soak up 70% less energy than the halogen lamps. The illumination provided can be familiarized by turning off a set of LEDs. Can also be designed to emit lights of different colors and hence wavelengths and this can help in better visualization of skin as the penetration of skin is directly proportional to its wavelength.Power supply By batteries eg. atomic number 3 ion battery or using recharg eable handles.The types of dermoscopy instruments that can be used includeInstuments without image capturing facility.Instuments with image capturing facility.Instuments with image capturing facility and analytical ability. technique (3)It can be done any by the non- impact or the disturb technique.In the contact technique the glass plate of the dermoscope comes in contact with the fluid applied on the lesion whereas in the non-contact technique, there is no contact of the lens with the skin. The cross-polarized lens absorbs all scattered light and hence allows only light in one plane to pass through. The advantage of a non-contact technique is that there is no nosocomial infection but this is eclipsed by poor resolution and decreased illumination.The contact plates used are make mostly of silicon glass and can be graduated for amount the size of the lesion. These contact plates should be sterilized by using either 2% glutaraldehyde or methylated spirit. It can be used for the di agnosis of melanocytic nevi, melanoma, lichen planus, dermatofibroma, cicatricial alopecia, seborrheic keratosis and to calculate the follicular density in the donor area before follicular unit hair transplantation.Dermoscopy of normal scalp(32)Dermoscopy of the scalp can be performed with or without port wine solution, which is referred to as dry dermoscopy. Dry dermoscopy is useful for observing tertiary structures of the skin, such as hairs, scaling and follicular hyperkeratosis. An interface solution (thermal water) is used to analyse follicular and interfollicular (vascular) patterns.Dermoscopy of the normal scalp shows interfollicular simple red loops, and arborizing red lines, which represents the normal vascular patterns, and honeycomb pigmentation in sunbathe exposed areas and in subjects with darker skin. Follicular units are easily identified and usually contain 1 to 4 hairs. In children, dermoscopy often shows dirty dots agree to dust particles retained in the scalp. This feature is not observed in adolescents or adults as sebaceous secretions prevent particle deposition.Dermoscopic findings in alopecia areataThe characteristic findings are yellow dots, black dots, broken hair, tapering hairs corresponding to exclamation mark hair and regrowing vellus hair.Yellow dotsThey are due to dilatation of the affected follicular infundibulum with keratinous material or sebum. (4) They vary in size, shape and colour. They may be round or polycyclic, yellow to pink.(33) They may be barren of hair or contain miniaturized regrowing hair. They represent active and progressive disease. Although yellow dots are seen in androgenetic alopecia, female pattern of androgenetic alopecia, trichotillomania and circular lupus erythematosus, the number of yellow dots is limited in these conditions as compared to alopecia areata, which shows numerous yellow dots and is its characteristic feature.(34)The incidence of yellow dots reported in the study by Inui et al (4) wa s 191 of 300 patients and in the study by Mane et al it was 81.8%.(35) It is speculated that this may be the result of yellowish skin colour of Asiatic patients. Another possible reason may be the different devices used a handheld dermoscope (DermLite II pro) in the study by Inui et al vs. videodermoscopy and a handheld dermoscope by Ross et al (33) and only hand held dermoscope by Mane et al.(35)Black dotsThey are remnants of exclamation hair and broken hair. They represent pigmented hairs broken or destroyed at the scalp level. They provide a sensitive marker of disease activity and disease severity.(4) The black dots of alopecia areata are characteristic of black haired individuals, including Asians, and these findings have not been used for the diagnosis of alopecia areata in white population. This feature may be attributed not only to hair colour but also to cuticle resistance. Takahashi et al (36) reported that Asian hair cuticles fall as large pieces while keeping their orig inal shape under extension stress, whereas hair cuticles of white populations tend to pause to form small fragments. They are also observed in dissecti