Peer Reviewed

Photo Essay

An Atlas of Lingual Lesions, Part 2

Alexander K. C. Leung, MD
Clinical Professor of Pediatrics, University of Calgary; Pediatric Consultant, Alberta Children’s Hospital, Calgary, Alberta, Canada

Benjamin Barankin, MD
Dermatologist, Medical Director, and Founder, Toronto Dermatology Centre, Toronto, Ontario, Canada

Kin Fon Leong, MD
Pediatric Dermatologist, Pediatric Institute, Kuala Lumpur General Hospital, Kuala Lumpur, Malaysia

Helen Tam-Tham, PhD
Medical Student, University of Calgary, Calgary, Alberta, Canada

Leung AKC, Barankin B, Leong KF, Tam-Tham H. An atlas of lingual lesions, part 2. Consultant. 2019;59(6):180-183.

EDITOR’S NOTE: This article is part 2 of a 5-part series of Photo Essays describing and differentiating conditions affecting the tongue and related structures in the oral cavity. Part 1 was published in the May 2019 issue (access it at Parts 3 through 5 will be published in upcoming issues of Consultant.


Oral Candidiasis

Oral candidiasis is most commonly caused by Candida albicans and occasionally by Candida glabrata, Candida guilliermondii, Candida tropicalis, Candida pseudotropicalis, Candida lusitaniae, Candida krusei, Candida parapsilosis, and Candida dubliniensis.1,2 It is the most common fungal infection in the oral cavity of infants and among predisposed individuals at any age.1 

In the pediatric age group, oral candidiasis affects 2% to 5% of otherwise healthy newborn infants.1 Premature and very-low-birth-weight infants are at the highest risk.1 The sex ratio is approximately equal.1 

Predisposing factors include the use of broad-spectrum antibiotics, the use of inhaled or systemic corticosteroids, diabetes mellitus, xerostomia, chemotherapy, radiation therapy to the head and neck area, cellular immunodeficiency states such as HIV, and older adults who wear dentures.3-5

The classic (most common) presentation of oral candidiasis is pseudomembranous candidiasis (commonly known as oral thrush), which is characterized by white, curd-like, discrete coating or plaques on the tongue, buccal mucosa, soft palate, hard palate, and oral pharynx (Figures 1 and 2).6 The adherent pseudomembrane is composed of desquamated epithelial cells, keratin, leukocytes, necrotic tissue, and food particles. Removal of the plaques by wiping with gauze may reveal raw, erythematous, and sometimes bleeding mucosa underneath.6 Oropharyngeal candidiasis, if severe, can impair speech, feeding, and quality of life.1 Occasionally, the infection can spread to the esophagus, resulting in esophageal candidiasis.1


candidiasis 1
Figure 1

Candidiasis 2
Figure 2

Erythematous oral candidiasis, also known as atrophic candidiasis, is characterized by smooth erythematous patches occurring most often on the palate, gum, and dorsum of the tongue, with no evidence of pseudomembranous overgrowth.2 The color intensity may vary from fiery red to a hardly discernable pink spot.1 Characteristically, chronic atrophic candidiasis, a subset of erythematous oral candidiasis, occurs in patients wearing dentures, and the lesion is typically limited to the gingival mucosa in contact with the denture.

Oral candidiasis is usually asymptomatic.4,5 Some children may experience fussiness, decreased feeding, and/or refusal to feed. Older children and adults may experience a metallic, bitter, or sour taste, a burning sensation in the mouth, dysphagia, and halitosis.4,5 There is a tendency for easy bleeding of the affected areas.5

The diagnosis is often clinical, especially if the lesion has a classical presentation. If necessary, the diagnosis can be confirmed by potassium hydroxide wet-mount examination of swabs taken from the affected area or by culture of the fungus.

For treatment, oral candidiasis usually responds well to oral nystatin, fluconazole, itraconazole, or clotrimazole.1 The duration of treatment usually is 2 weeks, but the medication should be continued 2 to 3 days beyond resolution of the lesion.


  1. Leung AKC. Oral candidiasis. In: Leung AKC, ed. Common Problems in Ambulatory Pediatrics: Specific Clinical Problems. Vol 2. New York, NY: Nova Science Publishers; 2011:143-147.
  2. Hellstein JW, Marek CL. Candidiasis: red and white manifestations in the oral cavity. Head Neck Pathol. 2019;13(1):25-32.
  3. Dekhuijzen PNR, Batsiou M, Bjermer L, et al. Incidence of oral thrush in patients with COPD prescribed inhaled corticosteroids: effect of drug, dose, and device. Respir Med. 2016;120:54-63.
  4. Meira HC, De Oliveira BM, Pereira IF, Naves MD, Mesquita RA, Santos VR. Oral candidiasis: a retrospective study of 276 Brazilian patients. J Oral Maxillofac Pathol. 2017;21(3):351-355.
  5. Mushi MF, Bader O, Taverne-Ghadwal L, Bii C, Groß U, Mshana SE. Oral candidiasis among African human immunodeficiency virus-infected individuals: 10 years of systematic review and meta-analysis from sub-Saharan Africa. J Oral Microbiol. 2017;9(1):1317579.
  6. Millsop JW, Fazel N. Oral candidiasis. Clin Dermatol. 2016;34(4):487-494.

NEXT: Herpetic Gingivostomatitis

Herpetic Gingivostomatitis

Herpetic gingivostomatitis is the most common specific clinical manifestation of primary herpes simplex virus (HSV) infection in children.1 More than 90% of cases are caused by HSV type 1 (HSV-1).1-4 Herpetic gingivostomatitis can occur in adolescents and adults but most commonly affects children aged 6 months to 5 years, with a peak incidence between age 1 and 3 years.1-4 HSV-1 is primarily transmitted via direct contact with infected oral secretions or active lesions of other patients.5 On the other hand, HSV type 2 is spread mainly through genital sexual contact.

Herpetic gingivostomatitis has a mean incubation period of 4 days (ranging from 2 to 12 days).1 The prodrome consists of a sensation of burning or paresthesia at the inoculation site, fever, malaise, irritability, anorexia, loss of appetite, sleeplessness, and headache.2,6 

Oral lesions typically appear 1 to 2 days later and are usually accompanied by severe pain in the mouth, fever, hypersalivation, halitosis, and refusal to eat or drink.1,4 These oral lesions consist of clusters of vesicles throughout the mouth; they subsequently break down rapidly to form 1- to 5-mm shallow ulcers with a yellow-gray base and an erythematous halo.4-6 Adjacent lesions may coalesce to form irregular ulcerations.4 

Lesions may develop throughout the oral cavity, in particular on and around the lips, along the gingivae, on the anterior of the tongue (as shown in the Figure), and the hard palate.1,5 The ulcers are extremely painful and have a tendency to bleed but eventually heal without scarring.4 Typically, the gingiva is inflamed, swollen, fiery red, friable, and bleed easily when touched.5 The cervical, submandibular, and submental lymph nodes are usually swollen and tender.1,2,6 The disease process typically resolves in 10 to 14 days.1

herpetic gingivostomatitis

The major complication is dehydration that may result from poor fluid intake, compounded by fever and hypersalivation.4 The infection may spread to other parts of the body by autoinoculation, resulting in, for example, perioral lesions, herpetic esophagitis, herpetic whitlow, herpetic keratitis, and eczema herpeticum.2,4 Reactivation of the virus in the trigeminal sensory ganglion may result in herpes labialis.2 Other complications can include secondary bacterial infection, secondary bacteremia, viremia, Bell palsy, and meningoencephalitis.1,4

The diagnosis is mainly clinical, based on the typical appearance and location of the lesions.4 On occasion, viral culture, Tzanck smear, direct fluorescent antibody testing, and amplification of viral DNA using polymerase chain reaction may be performed to establish a definitive diagnosis.4,5 The gold standard for laboratory diagnosis is the viral culture.5

Treatment is mainly symptomatic with antipyretic analgesics such as ibuprofen and acetaminophen, and adequate hydration.3,7 Chlorhexidine gluconate mouthwash has been used to decrease mucosal pain and to prevent secondary infection of the ulcers.5 Systemic acyclovir may be considered for severe herpetic gingivostomatitis and, in order to be maximally effective, should be initiated within 3 days of the onset of symptoms.3



  1. Leung AKC. Herpetic gingivostomatitis. In: Leung AKC, ed. Common Problems in Ambulatory Pediatrics: Specific Clinical Problems. Vol 1. New York, NY: Nova Science Publishers; 2011:313-316.
  2. Aslanova M. Herpetic gingivostomatitis. StatPearls. Updated October 27, 2018. Accessed May 14, 2019.
  3. Goldman RD. Acyclovir for herpetic gingivostomatitis in children. Can Fam Physician. 2016;62(5):403-404.
  4. Keels MA, Clements DA. Herpetic gingivostomatitis in young children. UpToDate.​-in-young-children. Updated June 2, 2018. Accessed May 14, 2019.
  5. Mohan RP, Verma S, Singh U, Agarwal N. Acute primary herpetic gingivostomatitis [published online July 8, 2013]. BMJ Case Rep. doi:10.1136/bcr-2013-200074.
  6. Mangold AR, Torgerson RR, Rogers RS III. Diseases of the tongue. Clin Dermatol. 2016;34(4):458-469.
  7. de Suremain N, Guedj R, Fratta A, et al. Acute gingivostomatitis in children: epidemiology in the emergency department, pain, and use of codeine before its restriction. Arch Pediatr. 2019;26(2):80-85.

NEXT: Morphea (Localized Scleroderma)

Morphea (Localized Scleroderma)

Morphea, also known as localized scleroderma, is a distinctive chronic inflammatory disease that primarily affects the skin and underlying tissues, and ultimately leads to hardening and thickening of the skin due to excessive collagen deposition.1,2 The incidence of morphea is estimated to be approximately 0.4 to 2.7 cases per 100,000 population per year.3 The condition is more prevalent in white females.1,4 It has a bimodal peak age of onset, between 2 and 14 years and again between 40 and 50 years.3,4

Circumscribed or plaque morphea accounts for approximately 60% of cases in adults and 25% of cases in children.5 The condition typically presents as fewer than 3 oval or round, discrete, indurated plaques, confined to one anatomic area.5 The lesions occur most frequently on the trunk or proximal extremities (Figure 1).5 The face is one of the most common sites for the linear type of morphea.6 Uncommonly, morphea may occur on the tongue (Figure 2).6,7 The patient shown in Figure 2 had morphea affecting the left side of the chin, lower lip, and dorsal aspect of the tongue.

Morphea 1
Figure 1

Morphea 2
Figure 2

The lesion typically begins as an erythematous or violaceous macule with a smooth surface and a yellowish white center. Over time, the lesion develops central sclerosis, which is ivory-white with surrounding erythema or violaceous hue and induration.2 Eventually, the sclerotic area becomes softened and atrophic with varying degrees of postinflammatory hypopigmentation/hyperpigmentation.8 The area is often hairless and anhidrotic.

The disease may cause functional and cosmetic impairment and may impair quality of life.2 Depression and anxiety may develop.3 If the lesion crosses a joint, it may lead to restriction of joint movement and joint contractures.5

The diagnosis is mainly clinical. The use of dermoscopy facilitates visualization of pigment network-like structures and fibrotic beams; the latter indicate sclerotic dermis.9 Those dermoscopic features are characteristic of morphea.9 A skin biopsy should be considered if the diagnosis is in doubt.

In general, lesions tend to run a waxing and waning course. Most lesions regress spontaneously over 3 to 5 years, usually with residual pigmentary and atrophic changes.3 Affected patients may develop new morphea lesions over their lifetime.2

Treatment should be individualized. For some patients with uncomplicated limited circumscribed morphea, treatment might not be necessary apart from reassurance.2 Other patients with circumscribed morphea with limited and superficial involvement may benefit from treatments with topical tacrolimus, topical corticosteroids, intralesional corticosteroids, topical imiquimod, and/or topical calcipotriene.2,8 Physiotherapy should be considered if the lesion involves a joint or if there is limitation of movement and/or joint contracture.1,3 Systemic therapies should be considered for patients with subcutaneous involvement, rapidly progressive disease, or involvement of large body surface area or functionally/cosmetically sensitive areas.2 Therapeutic options include systemic methotrexate, a systemic corticosteroid, and phototherapy, alone or in combination.2,8



  1. Bielsa Marsol I. Update on the classification and treatment of localized scleroderma. Actas Dermosifiliogr. 2013;104(8):654-666.
  2. Leung AKC, Barankin B. An adolescent whose “bruises” don’t fade: what is this patchy discoloration? Morphea (localized scleroderma). Consultant Pediatricians. 2015;14(9):402-406.
  3. Browning JC. Pediatric morphea. Dermatol Clin. 2013;31(2):229-237.
  4. Pope E, Laxer RM. Diagnosis and management of morphea and lichen sclerosus and atrophicus in children. Pediatr Clin North Am. 2014;61(2):309-319.
  5. Torok KS. Pediatric scleroderma: systemic or localized forms. Pediatr Clin North Am. 2012;59(2):381-405.
  6. Dixit S, Kalkur C, Sattur AP, Bornstein MM, Melton F. Scleroderma and dentistry: two case reports. J Med Case Rep. 2016;10(1):297.
  7. Tan E, Kürkçüoğlu N, Atalağ M, Gököz A, Zileli T. Progressive hemifacial atrophy with localized scleroderma. Eur Neurol. 1989;29(1):15-17.
  8. Jacobe H, Ahn C, Arnett FC, Reveille JD. Major histocompatibility complex class I and class II alleles may confer susceptibility to or protection against morphea: findings from the Morphea in Adults and Children cohort. Arthritis Rheumatol. 2014;66(11):3170-3177.
  9. Shim W-H, Jwa S-W, Song M, et al. Diagnostic usefulness of dermoscopy in differentiating lichen sclerosis et atrophicus from morphea. J Am Acad Dermatol. 2012;66(4):690-691.