Review ArticleClinical Review

Common white lesions of the oral cavity

Review of clinical presentations and management

Philippe Harris, Caroline Bissonnette, Paul Tabet and René Wittmer
Canadian Family Physician January 2025; 71 (1) 19-25; DOI: https://doi.org/10.46747/cfp.710119

Abstract

Objective To provide primary care physicians with a review of common oral white lesions and a practical management algorithm.

Sources of information Between January and April 2024 relevant literature and clinical guidelines were searched for using the PubMed MEDLINE database with no date limitation.

Main message A broad differential diagnosis exists for white lesions of the oral cavity. Fungal infections; human papillomavirus–related proliferations; reactive lesions secondary to physical, thermal, or chemical injuries; and premalignant or malignant clinical entities can all present as white lesions. Prompt recognition and proper management are therefore important. In certain instances, short-term follow-up of nonsuspicious lesions may be considered to assess for regression, persistence, or progression. Other lesions require timely investigations and treatment. Furthermore, providing patients with adequate counselling for lifestyle risk factors, including tobacco and alcohol use, is of utmost importance.

Conclusion White lesions of the oral cavity are prevalent and may be encountered routinely in primary care settings. Recognizing the most common conditions and becoming proficient in their clinical management enhances patient care. Primary care physicians can play a crucial role in early detection of oral pathology. Proper triage of suspicious lesions can subsequently help decrease the wait time to see a specialist and avoid unnecessary medical visits for patients.

White lesions of the oral cavity are common and include a range of conditions of differing causes. Among these, oral leukoplakias (OLs) are noteworthy, as they are associated with a potential risk of malignant transformation. Oral leukoplakia as defined by the World Health Organization refers to a white plaque of questionable risk on the oral mucosa1,2 and does not constitute a definitive diagnosis in itself. In recent years the epidemiology of head and neck cancers has shifted. An increase in incidence of human papillomavirus−positive oropharyngeal squamous cell carcinoma has been observed alongside a decrease in human papillomavirus−negative oropharyngeal squamous cell carcinoma cases.3 However, in the case of OL and oral squamous cell carcinoma (OSCC), tobacco smoking and alcohol consumption remain the most important risk factors.4-8

The purpose of this review is to present the most common oral white lesions and offer a clinical management algorithm that can be used in primary care settings.

Case description

A 76-year-old man presented to the primary care clinic for routine care. The patient reported he had recently noticed an ulceration on his tongue. He reported mild discomfort but was able to eat and drink normally. His medical history was noncontributory. The patient was a non-smoker and drank alcohol on occasion. Upon examination, a large ulcerated erythroleukoplakia (red and white plaque) of the left lateral border of the tongue was identified (Figure 1). The lesion was heterogeneous overall but had a large area presenting as a thin homogeneous leukoplakia. Sharply demarcated borders were obvious in the inferior and anterior portions of the lesion. The erythroleukoplakia was non-indurated on palpation. There was no palpable head and neck lymphadenopathy.

Figure 1.
Figure 1.

Left lateral border of the tongue showing thin homogeneous white plaque (black arrows) with ulceration (white arrow)

Sources of information

A literature search was performed between January and April 2024 in the PubMed MEDLINE database with no date limitations. The MeSH terms oral leukoplakia and practice guidelines were independently used as well as free-word searches for leukoplakia, candidiasis, frictional keratosis, oral lichen planus, oral cancer, and proliferative verrucous leukoplakia.

Main message

A thorough assessment of patients presenting with a white lesion in the oral cavity, including medical history, social history, and a complete head and neck examination, can provide useful diagnostic information for further management.

Candidiasis. Oral candidiasis, commonly known as thrush, is a fungal infection caused by Candida species. The most common form of candidiasis is chronic erythematous candidiasis.9 It presents as widespread oral erythema typically affecting the dorsal tongue and hard palate. Denture-related stomatitis is associated with denture wear and presents as erythema involving the surfaces underlying the dentures, which typically have positive culture results for Candida species.9 Pseudomembranous candidiasis is characterized by white pseudomembranes (Figure 2A) that can be scraped off to expose an erythematous base.9 Primary care providers should differentiate between a coated tongue characterized by keratin accumulation on the dorsal surface and oral candidiasis (Figure 2B). Risk factors for oral candidiasis include immunosuppression, such as uncontrolled diabetes, hematolymphoid malignancies, and HIV-AIDS; oral dryness or hyposalivation due to medication or age; and prior use of either inhaled or topical antibiotics or corticosteroids.9 Patients with asthma who take inhaled corticosteroids are at higher risk of candidiasis, typically involving the soft and posterior hard palate. Treatment usually consists of a topical or systemic antifungal medication for 7 to 14 days and follow-up within 2 weeks of the antifungal therapy.9 Certain patients may require an extended course of antifungal medication for up to 4 weeks. While the 2016 Infectious Diseases Society of America guideline on candidiasis does not recommend routinely screening for HIV in adults with candidiasis, clinicians should consider screening in patients with immunodeficiency risk factors or in those with an unexplained pattern of relapse.9 Patients wearing dentures or other oral appliances should be counselled to remove and soak their dentures or appliances in an antifungal solution, as not doing so may result in unsuccessful treatment.

Figure 2.
Figure 2.

Candidiasis vs keratin accumulation: A) Candidiasis of the soft and posterior hard palate presenting as white pseudomembranes. B) Coated tongue not associated with oral candidiasis.

Frictional keratosis. Chronic irritation results in thickening of the stratum corneum (hyperkeratosis), which manifests as white plaques with irregular and generally blended borders. Traumatic oral lesions are associated with opposing teeth and therefore often affect the retromolar trigone and cheeks. Patients with a habit of cheek chewing (morsicatio buccarum) present with shaggy hyperkeratosis with occasional small fragments of epithelium detaching from the mucosa (Figure 3A). Patients with edentulous areas on the alveolar ridge may also develop irregular white plaques due to chronic friction (Figure 3B), especially from chewing food.10 Frictional keratosis is a benign condition and treatment is limited to avoidance of chronic frictional trauma.

Figure 3.
Figure 3.

Frictional keratosis: A) Morsicatio buccarum on the left buccal mucosa. B) Benign alveolar ridge keratosis of the inferior right retromolar trigone.

Leukoedema. Leukoedema presents as a grey-white surface change on the buccal mucosa (inner cheek). Its cause involves intracellular edema without evidence of malignancy.11 As such, leukoedema is not considered a pathologic entity but rather a variant of normal anatomy. It is more prevalent among patients of African descent, those who chew betel quid, and smokers.11,12 The diagnosis of leukoedema can be confirmed by stretching the affected mucosa, which results in attenuation or complete disappearance of the white colour.11

Oral hairy leukoplakia (OHL). Oral hairy leukoplakia is a benign condition presenting as white, streaky parallel patches, usually on the lateral borders of the tongue.13 Other sites of involvement include the dorsal and ventral surfaces of the tongue and in rare cases the buccal mucosa. Presentation may be unilateral or bilateral. It is suspected to be caused by the reactivation of Epstein-Barr virus and reinfection of epithelial cells.14 Most cases have been reported in immunocompromised patients, including patients with HIV infection particularly in the setting of AIDS, but have also occurred in immunocompetent patients.15,16 However, there are numerous reports of OHL in immunocompetent patients and patients with local immunosuppression (eg, from topical corticosteroids). As such, OHL should be considered regardless of the patient’s immune competency.17 This condition carries no risk of malignant transformation to OSCC.14 However, biopsy is required to rule out dysplastic change or OSCC. Since OHL is a benign condition, treatment is only indicated for aesthetic reasons or rare cases of discomfort. Antiviral therapy targeting Epstein-Barr virus has been shown to reduce OHL in immunocompetent patients. However, this therapy is not curative, as lesions usually recur following discontinuation.18 Similarly, antiretroviral therapy was associated with a reduction in OHL prevalence among patients with HIV participating in clinical trial units in the United States and Haiti, but it is not a cure.19 Expected outcomes of treatment versus possible side effects should be discussed with the patient before initiating treatment.

Oral lichen planus (OLP). Oral lichen planus is an immune-mediated condition that classically presents as reticular white striations (Wickham striae) on an erythematous base (Figure 4). Common intraoral sites of lesions include the buccal mucosa bilaterally, tongue, and gingiva.20 An ulcerated surface can develop in erosive lichen planus and pain ensues, especially with exposure to spicy, acidic, or hot foods. Alternatively, OLP may present as linear, annular, or papular white lesions. White plaques with blended borders may be identified on the dorsal surface of the tongue. Lichen planus may also affect the skin, genital mucosa, and in rare cases the esophageal mucosa. Numerous medications, including antihypertensive drugs and statins, have been reported to produce lichenoid reactions, which may have acute or delayed onset. An isolated lichenoid lesion in contact with a dental restoration, particularly one made of amalgam, may point to a lichenoid reaction to the dental material.21 The potential for malignant transformation of OLP and lichenoid lesions of the oral mucosa is still a subject of controversy.22 Current estimates of the transformation rate range from 1.4% to 4.9%, with tongue lesions and erosive and atrophic lesion subtypes being associated with higher rates of malignant transformation.23-26 Since OLP is a chronic disease, treatment is warranted for symptomatic lesions, as courses can last months to years. First-line treatment of OLP is topical corticosteroids such as 0.05% fluocinonide (gel, ointment, or cream), 0.05% clobetasol (gel, ointment, or cream), and 0.5 mg/5 mL of dexamethasone elixir.27 Louisy et al offer a detailed and comprehensive clinical algorithm for treatment of OLP.27 If there is an isolated lichenoid lesion, if the presentation is atypical, or if lesions do not improve with corticosteroids, a biopsy is warranted to support the clinical diagnosis of OLP and exclude epithelial dysplasia. Long-term clinical followup is also recommended.

Figure 4.
Figure 4.

Oral lichen planus: Reticular white striae along with regions of erythema on the right buccal mucosa.

Differential diagnoses. The number of differential diagnoses for white lesions is vast. Other common white lesions include thermal and chemical burns, which present as whitish pseudomembranes that can be scraped off, leaving an exposed eroded base. Toothpaste and mouthwash may cause contact reactions leading to superficial mucosal sloughing (Figure 5A). Management is based on selecting gentle oral hygiene products and follow-up of symptoms after 2 weeks, although some irritative lesions can take up to 1 or 2 months to resolve.28,29 Similar presentations of erythematous mucosa can be caused by contact reactions with products such as mint and cinnamon.30 Human papillomavirus can cause papillary or verrucose benign epithelial proliferations (eg, squamous cell papilloma, verruca vulgaris), which are commonly experienced by people of all ages31 (Figure 5B). Of note, other infectious diseases can present as oral white lesions. Syphilis should be considered in the differential diagnosis for leukoplakia in the context of the current upsurge in incidence in Canada.32 Secondary syphilis can present as white to pinkish plaques (mucous patches) on the lateral border of the tongue and labial and buccal mucosa.33,34

Figure 5.
Figure 5.

Differential diagnosis: A) Superficial mucosal sloughing. B) Squamous papilloma on the left dorsolateral tongue.

Malignant and premalignant lesions. Oral leukoplakia is a clinical diagnosis defined by the World Health Organization as a white plaque of questionable risk after having excluded other known conditions (Figure 1 [black arrows] and Figure 6A).1,2 It usually has sharply demarcated borders visible on clinical examination. The prevalence of OL ranges from 2.6% to 4.0%.35,36 This condition is of importance since malignant transformation occurs in 7.2% to 9.8% of cases.8,37 Persistent lesions in non-smokers tend to have a higher malignancy transformation rate and worse outcomes than similar lesions in smokers. Oral leukoplakia without epithelial dysplasia on biopsy findings still carries a risk of malignant transformation, although lower, and requires clinical follow-up. Erythroleukoplakias (Figure 6B) and proliferative leukoplakia (also known as proliferative verrucose leukoplakia) have been associated with a higher risk of malignant transformation than OL. The latter has an estimated malignant transformation rate of approximately 50% to 70% over time.26,38

Figure 6.
Figure 6.

Malignant and premalignant oral leukoplakia and erythroleukoplakia: A) Thin, homogeneous leukoplakia of the right lateroventral tongue. B) Erythroleukoplakia of the left lateral aspect of the tongue.

Proliferative leukoplakia (PL) first presents as thin, homogeneous white plaques and slowly progresses to a multifocal presentation (Figures 7A and 7B). The white plaques may develop a verrucose structure, although this may not be present or prominent. It is more common in postmenopausal women, with a 2.72:1 female-to-male ratio.39 Diagnosis warrants a biopsy to evaluate the presence of dysplasia. Unfortunately, PL is difficult to treat and has a high rate of recurrence. Common treatment strategies include surgical excision, laser ablation,40 and cryotherapy.39 However, none of these treatments have been shown to reduce the risk of malignant transformation substantially over time. Close clinical follow-up of the lesions every 3 to 4 months is essential, regardless of surgical or pharmacologic interventions being performed. There have been a few experimental randomized controlled trials showing some promising results with imiquinod and nivolumab immunotherapy.41-43 However, more research is required to evaluate the long-term risks of recurrence and malignant transformation.

Figure 7.
Figure 7.

Proliferative leukoplakia shown as multifocal homogeneous white plaques involving (A) the lower anterior gingiva and lower labial mucosa and (B) the upper anterior gingiva and upper labial mucosa

General investigations and management. This review of oral white lesions has selected common clinical presentations, but numerous other clinical entities exist. This section describes a general approach for investigating and managing oral lesions, with a special focus on malignant and premalignant lesions in primary care contexts.

The patient’s medical history, including associated risk factors, should be reviewed. This includes active or past tobacco use and alcohol consumption. The lesion should be clinically assessed, with visual and tactile examination of the area. Box 1 presents clinical parameters associated with an increased risk of malignancy.35-37,44-46 These parameters include the anatomic site of the lesion, with the tongue being highest risk and the hard palatal mucosa being lowest risk. The presence of red components (erythroplakia or erythroleukoplakia) and induration should heighten the level of suspicion. A nonhomogeneous site with a verrucose or speckled appearance should increase the suspicion of malignancy. Well-defined margins and a surface area exceeding 200 mm2 are also concerning features. However, absence of these clinical features does not mean oral premalignant and malignant entities are not present, as all precancers and cancers can occur anywhere and without risk factors.

Box 1.

Risk factors for malignancy, high-risk lesion sites, and clinical features that may indicate malignancy

Risk factors

  • Older age (ie, men aged 50 to 70 y and women aged 60 to 80 y)

  • Tobacco smoking

  • Consumption of alcohol

  • Consumption of betel quid, pan masala, or gutkha

  • Immunosuppression (certain primary immunodeficiency syndromes, HIV infection, iatrogenic disorders)

  • History of head and neck cancer

  • Pre-existing potentially malignant oral disorder

High-risk lesion sites

  • Tongue (highest risk)

  • Floor of mouth

  • Soft palate

  • Gingiva

  • Buccal mucosa

  • Labial mucosa

  • Hard palate (lowest risk)

Clinical features of concern

  • Nonhomogeneous appearance (verrucose, speckled, etc)

  • Red component (erythroplakia or erythroleukoplakia)

  • Lesion surface area >200 mm2

  • Chronic nonhealing ulceration

  • Induration

  • Head and neck lymphadenopathy

  • Other signs and symptoms: paresthesia, tongue hypomobility, pain, dysphagia, odynophagia

Data from Mortazavi et al,35 Mello et al,36 Guan et al,37 Speight et al,44 Warnakulasuriya and Ariyawardana,45 and Mashberg and Samit.46

If a reactive lesion is suspected, elimination of potential causal factors and irritants, such as tobacco smoking or sharp tooth edges, may be the first step. Short-term follow-up of nonsuspicious lesions is necessary to assess regression, persistence, or progression.47 Persistence or progression at follow-up warrants a referral for biopsy.

A 2016 practice guideline by Shaw and Beasley reports a lack of high-level evidence supporting the management of OL but provides consensus-based recommendations for biopsy and further histopathologic assessment.48 Biopsy remains the criterion standard test for malignancy, as a definitive histopathologic diagnosis will inform subsequent steps for the patient and their medical team.20 Table 1 presents indications for referral to a specialist, which should be considered if first-line treatment does not yield satisfactory results or if the diagnosis remains unclear.

View this table:
Table 1.

Suggested timing of referral in the context of primary care

In cases where no cause is determined, or in the presence of a persistent nonhealing ulceration of the oral mucosa, an incisional biopsy should promptly be performed to exclude or confirm dysplasia or OSCC (Figure 8).49 Several biopsies can be performed when a lesion is large.

Figure 8.
Figure 8.

Primary care algorithm for investigation and management of oral white lesions

Careful description of the lesion and sharing of pathologic findings with other oral health professionals involved in the patient’s care are important to ensure proper tracking of the lesion’s evolution. Description should include anatomic site, colour, texture, appearance, margins, and size. Clinical images should be taken when possible to facilitate follow-up and monitor evolution. More importantly, providing the patient with adequate counselling for lifestyle risk factors, including tobacco and alcohol cessation, is of utmost importance. For most primary care physicians, oral biopsies are not part of training. Therefore, proper management may involve referral to an otolaryngologist–head and neck surgeon, oral pathologist, oral medicine specialist, oral surgeon, or appropriately trained general dentist.

Case resolution

The patient underwent mapping biopsies near the ulceration and in the more homogeneous area (anterior and inferior regions). The biopsy findings of the ulcerated region revealed moderate to severe epithelial dysplasia (high-grade dysplasia) where as the biopsy findings from the homogeneous area exhibited mild epithelial dysplasia (low-grade dysplasia). There was no evidence of invasive carcinoma. Complete ablation of the lesion was performed, and the patient was scheduled for follow-up every 3 to 4 months to ensure absence of recurrence.

Conclusion

Oral white lesions may present in different forms and range from benign to malignant. Recognition of oral white lesions, proper follow-up, and prompt referral if required are essential for appropriate management. Primary care physicians play a central role in early detection of these oral pathologies and their treatment when possible. Proper triage of suspicious lesions can subsequently help decrease wait times for specialists and avoid unnecessary visits for patients.

Acknowledgment

The clinical images in Figures 1 to 7 were provided by Dr Caroline Bissonnette with the permission of the patients.

Notes

Editor’s key points

  • ▸ This review describes a general approach for investigating and managing oral white lesions, with a focus on malignant and premalignant lesions in the primary care context.

  • ▸ The patient’s medical history, including associated risk factors, should be reviewed thoroughly, including active or past tobacco and alcohol use. Clinical assessment of the suspected lesion with visual and tactile examination of the area should be performed.

  • ▸ Clinical parameters associated with an increased risk of malignancy include the anatomic site of the lesion, with the tongue being at highest risk and the hard palatal mucosa at lowest risk. The presence of red components (erythroplakia or erythroleukoplakia), induration, or a nonhomogeneous site with a verrucose or speckled appearance should heighten the level of suspicion. Well-defined margins and a surface area exceeding 200 mm2 are also features of concern.

  • ▸ If a reactive lesion is suspected, elimination of potential causal factors and irritants, such as tobacco smoking or sharp tooth edges, may be the first step. Short-term follow-up of nonsuspicious lesions is necessary to assess regression, persistence, or progression. Persistence or progression at follow-up warrants referral for biopsy.

Footnotes

  • Contributors

    All authors contributed to conducting the literature review and to preparing the manuscript for submission.

  • Competing interests

    None declared

  • This article is eligible for Mainpro+ certified Self-Learning credits. To earn credits, go to https://www.cfp.ca and click on the Mainpro+ link.

  • This article has been peer reviewed.

  • La traduction en français de cet article se trouve à https://www.cfp.ca dans la table des matières du numéro de janvier 2025 à la page e7.

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Common white lesions of the oral cavity
Philippe Harris, Caroline Bissonnette, Paul Tabet, René Wittmer
Canadian Family Physician Jan 2025, 71 (1) 19-25; DOI: 10.46747/cfp.710119
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