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Year : 2012  |  Volume : 23  |  Issue : 5  |  Page : 665-669
Alopecia areata of dental origin in a child

1 Department of Pedodontics, Saveetha University, Chennai, Tamil Nadu, India
2 Department of Pedodontics, Sri Ramachandra Dental College, Chennai, Tamil Nadu, India
3 Department of Pedodontics, Tagore Dental College, Chennai, Tamil Nadu, India

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Date of Submission06-Aug-2011
Date of Decision02-Feb-2012
Date of Acceptance12-Mar-2012
Date of Web Publication19-Feb-2013


Alopecia areata (AA) is a chronic inflammatory disease that involves the hair follicle. Current evidence indicates that hair follicle inflammation in AA is caused by a T-cell-mediated autoimmune mechanism occurring in genetically predisposed individuals. AA has a reported incidence of 0.1%-0.2%, with a lifetime risk of 1.7%. It has also been found that AA accounts for roughly 2% of new dermatology outpatient cases in the US and the UK, 3.8% of cases in China and 6.7% of cases in Kuwait. Pediatric AA constitutes approximately 20% of all AA cases. AA affects males and females equally. The most common site to be affected is the scalp (90%). The face, eyebrows, eyelashes, beard, underarm hair, and pubic hair may be affected and, sometimes, even the entire body. AA requires combined therapy, involving topical or intralesional corticosteroids, immune therapy with diphenylcyclopropenone, and even psychotherapy. In some cases, treatment consists of simply eliminating the dental infectious process. This case report describes AA of dental origin in a 9-year-old girl, which resolved after management of the dental problem.

Keywords: Alopecia, alopecia areata, dental foci

How to cite this article:
Samuel A V, Muthu M S, Gurunathan D, Sharma A. Alopecia areata of dental origin in a child. Indian J Dent Res 2012;23:665-9

How to cite this URL:
Samuel A V, Muthu M S, Gurunathan D, Sharma A. Alopecia areata of dental origin in a child. Indian J Dent Res [serial online] 2012 [cited 2022 Aug 10];23:665-9. Available from:
Alopecia areata (AA) (or localized alopecia) is a form of dermatitis, mainly of autoimmune origin, that is characterized by sudden appearance of round or oval patches of non-cicatricial hair loss. The condition is restricted to a specific area and shows spontaneous remissions and exacerbations. [1],[2],[3],[4],[5],[6] The patches can be mildly reddened or peachy in color. The disease can be classified based on the extent or pattern of hair loss. [7] Based on the extent of hair loss, AA is classified as follows: 1) patchy AA, in which there is a partial loss of scalp hair; 2) alopecia totalis (AT), in which 100% of scalp hair is lost; and 3) alopecia universalis (AU), in which there is a 100% loss of all scalp and body hair. [6],[8],[9],[10] Approximately 5% of AA cases will progress to AT/AU. [11] The pattern of hair loss observed in AA can vary considerably. Less common presentations can be observed in a minority of patients, including reticular patches of hair loss; ophiasis type, band-like hair loss in the parieto-temporo-occipital area; ophiasis inversus (sisapho), a very rare band-like hair loss in the fronto-parieto-temporal area; or a diffuse thinning over part of the scalp or the entire scalp. [3]

Our understanding of the etiology of AA has been continuously evolving since its first mention in 1760. [1] The etiology has been associated with emotional or physical stress, trauma, polygenic mode of inheritance, congenital or acquired, organ-specific autoimmune disease with genetic predisposition, and an environmental trigger. [12],[13] An association between AA and human leukocyte antigen (HLA) has been demonstrated, which suggests a role for T-cells and autoimmunity in this disease as well. [14],[15],[16]

Although few studies of incidence and prevalence have been performed, AA has a reported incidence of 0.1%-0.2%, with a lifetime risk of 1.7%. [17] It has also been found that AA accounts for roughly 2% of new dermatology outpatient cases in the US and the UK. [18] In China the incidence is 3.8%. [19] Pediatric AA constitutes approximately 20% of all AA cases. [20] In a prospective survey of pediatric dermatology patients from Kuwait, AA was observed to be the third most common dermatosis in children, accounting for 6.7% of the total number of patients (n=10000). [21] As many as 60% of patients with AA will present with their first patch before 20 years of age. However, a study conducted on Asian patients showed AA to have onset before 40 years of age. [5],[19] A younger age of onset has been reported to herald a poorer prognosis. [22],[23] AA predominantly affects the young male population. [24] Dan et al. in 2007 claimed that AA affects males and females equally, but contrasting results have been published. [1],[25] The most common site to be affected is the scalp (90%). [17],[19] The face, eyebrows, eyelashes, beard, underarm hair, and pubic hair may be affected, or even the entire body. [1],[4] AA has a strong psychological impact on the patient because it involves the face and scalp, where esthetic considerations plays an important role. [4],[5] When it affects the children it may lead to psychological trauma and low self-esteem.

Classic AA lesions are well demarcated, round or oval, completely bald, smooth-surfaced patches. Frequently, patients with AA show characteristic hairs known as 'exclamation point hairs,' which may be seen within or around the areas of alopecia. [7],[26],[27] These hairs are tapered toward the scalp end and thickened at the distal end. Hair-pull tests at the periphery of the lesion may be positively correlated (six hairs or more) with disease activity. [27] Rarely, AA and dental foci of infections are seen together, and only a few articles have been published in this regard. To the best of our knowledge, this is the first case report of AA of dental origin in a child. This article describes a case of AA in a 9-year-old girl, which resolved after dental management.

   Case Report Top

A 9-year-old girl was referred by a dermatologist to the department of pedodontics for re-establishing the oral health as a first step for treating the hair loss. History revealed that the patch of hair loss had occurred suddenly and the patient's parents had immediately sought the dermatologist's opinion. The dermatologist had advised systemic antifungal drugs for 3 months, but the alopecic zone did not heal. The dermatologist then referred the child to the dental department for treatment of the dental infection.

Medical history revealed no systemic disease or allergies. Extraoral examination revealed an oval alopecic zone in the left occipital region, measuring approximately 6 cm in length. The affected scalp region was smooth, soft, and devoid of hair. Exclamation mark hairs were seen at the border of the alopecic zone. The lesion was asymptomatic and well delimited [Figure 1].
Figure 1: Initial presentation of alopecia areata that is localized on the left occipital region

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Intraoral examination revealed normal appearance of soft tissues. The patient had mixed dentition. Roots were present in the maxillary right and mandibular left primary second molar region. The maxillary left and mandibular right primary second molars were decayed [Figure 2] and [Figure 3]. Radiographic examination demonstrated complete root resorption in the maxillary left primary second molar and extensive radiolucency in the mandibular right primary second molar, without pulpal involvement.
Figure 2: Preoperative intraoral maxillary arch

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Figure 3: Preoperative intraoral mandibular arch

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The roots of the maxillary right primary second molar and the mandibular left primary second molar were extracted under local anesthesia. The mandibular right primary second molar was restored with a stainless steel crown. Band-and-loop space maintainers were made for both the maxillary right and mandibular left primary second molar regions [Figure 4] and [Figure 5]. The patient was motivated to maintain good oral hygiene and to come for regular follow-up. After 3 months, although there was no significant hair growth, small hair follicles had started to appear in the alopecic zone [Figure 6]. After 5 months, there was significant hair growth, and the alopecic zone was difficult to locate. The AA finally resolved completely [Figure 7].
Figure 4: Postoperative intraoral maxillary arch

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Figure 5: Postoperative intraoral mandibular arch

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Figure 6: Appearance of alopecia areata 3 months after dental management

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Figure 7: Complete re-growth of hair in the alopecic zone after 5 months

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   Discussion Top

The idea that AA is an autoimmune disease was first suggested by Rothman following a paper presented by Van Scott on morphologic changes in pilosebaceous units and anagen hairs in AA. [28] AA is reported to be associated with other autoimmune diseases, such as myxedema and pernicious anemia. [29] In most published series, patients with AA have had an increased frequency of circulating organ-specific and non-organ-specific autoantibodies compared to normal subjects. A variety of nonspecific abnormalities in peripheral T-cell numbers and function have also been reported. [30] Circulating autoantibodies to hair follicle have been found in patients with AA. [31] These antibodies also occur in normal subjects, but less frequently and at lower titers. They recognize various epithelial compartments within the hair follicle and appear to be targeted against intracellular antigens. [32] Autoimmune mechanisms may be cited to explain AA of dental origin occurring at a distance from the site of infection. [33]

The pathogenesis of AA of dental origin is usually based on a trigemino-sympathetic reflex. [34] A peripheral stimulus of infectious or mechanical nature could be the origin of a centripetal duct composed of a triple-neuron system. This system is composed of a peripheral terminal trigeminal fiber, a bulbothalamic fiber, and a thalamocortical fiber. [4] The centrifugal duct may be principally composed of a perivascular plexus of sympathetic fibers surrounding external carotid terminal branches with which trigeminal branches develop numerous connections. In addition, all along the length of the bulb, the trigeminal descending root is intimately connected to the sympathetic nuclei. This centrifugal duct may induce an angiospasm of the pilosebaceous follicle, resulting in a trophic disorder and subsequent hair loss. [4] However, the pilosebaceous follicle is still functional and so re-growth is often observed after the peladogenic (arising due to alopecia) foci is eradicated. If the tegumentary structure is damaged as in scarred alopecia, the pilosebaceous follicle will show irreversible atrophy. [35]

Interaction between the external irritants and the host defense cells may in turn induce the appearance of endogenous chemical mediators, including neuropeptides, fibrinolytic peptides, kinins, complement fragments, vasoactive amines, lysosomal enzymes, cytokines, and immune response mediators. These immune responses are divided into antigen-antibody and cell-mediated immune reactions. Some studies have demonstrated the presence of systemically circulating immune complexes, especially in acute dental infections. [36] Although the presence of lymphocyte populations appears to have been conclusively demonstrated in acute and chronic infections in the tissues surrounding the teeth of animals, [37] their presence in humans remains to be fully confirmed. Thus, the presence of common immune mediators in the pathogenesis of both dental infection and AA could explain the dental origin of the latter.

AA due to dental irritations of maxillary origin are located above a line starting at the labial commissure and terminating at the occiput. Those of mandibular origin are located below this line. [4] In our patient, the alopecic lesion was found in the left occipital region, which is possibly explained by the presence of infection in the maxillary tooth region. However, there was decay present in the mandibular left primary second molar region also.

Alopecic patches of dental origin are generally located on the same side as the infectious process. In the case of upper maxillary teeth, these locations are typically found above a line traced along the lip commissures to occiput. When located below this line, the cause is usually in the mandibular teeth, as confirmed by a review of the most recent cases published in the literature. [4] Thus, Lesclous et al.[4] reported a case of AA involving the beard, which was caused by the proximity of a retained lower molar and the possible stimulation of the fibers of the inferior alveolar nerve. However, Montoya [2] reported a case in which the patient had a bald patch located on the contralateral side of the infected tooth. In the present case, the alopecic patch was on the left side of the scalp, above the commissure-occiput line, which can be explained by the presence of a decayed maxillary left primary second molar.

This occurrence of AA secondary to dental infection may be due to the presence of common immune mediators in both dental infection and AA. Infections of dental origin arise as a result of chemical, mechanical, or bacterial irritation, which causes an inflammatory reaction in the dental root canals followed by pulp tissue necrosis and the migration of germs towards the periradicular zone, external to the tooth. Depending on the stage of the infectious process, histological examination may reveal the presence of numerous inflammatory cells such as polymorphonuclear leukocytes, macrophages, lymphocytes, plasma cells, basophils, and eosinophils. [38] In this case, the infection was due to bacterial irritation which would have caused migration of germs to the periradicular zone and might have initiated the inflammatory response and its sequelae.

In many cases, the resolution of AA requires combined therapy involving topical or intralesional corticosteroids, immune therapy with diphenyl-cyclopropenone, [39] or even psychotherapy. In other cases, treatment consists of simply eliminating the dental problem(i.e., caries, chemical or mechanical damage, etc.) that may be causing infection or mechanical stimulation of nerve fibers. [34] In this patient, the AA did not resolve with systemic administration of antifungal drugs alone, but disappeared completely 5 months after the dental foci of infection was treated.

Thus, when a subject presents with AA (without the presence of any of the known common causes) dental counseling is advisable. A thorough dental examination is required, along with radiographic investigation, to explore possible infectious foci or sites of nerve fiber stimulation. Treatment of the dental problem may help resolve the hair loss by simply eliminating the cause, and unnecessary pharmacological intervention can be avoided.

   References Top

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Correspondence Address:
A Victor Samuel
Department of Pedodontics, Saveetha University, Chennai, Tamil Nadu
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0970-9290.107386

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  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7]

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