Angular cheilitis (perleche)

Meet the patient

A 78-year-old edentulous man on warfarin for atrial fibrillation returns for the third time with cracked, sore, bleeding corners of the mouth; his dentures are ten years old and rock when he chews. The last doctor gave him a "strong steroid cream" that helped for a week, then the fissures came back deeper.^[1][2]

Three things decide his care, and the vignette hides all of them: he needs an antifungal, not a steroid; he needs the cause corrected (the dentures) or it will never settle; and — the trap that can hurt him — miconazole oral gel potentiates his warfarin and can bleed him. Hold those three and the management writes itself.^[1]

What angular cheilitis is — and why the name matters

Angular cheilitis is inflammation of the labial commissures — the corners of the mouth — where vermilion meets perioral skin. It is clinically erythema, maceration, fissuring, crusting and pain at one or (more typically) both angles, often extending a few millimetres onto both surfaces.^[1]

Perleche comes from the French pourlécher, "to lick one's lips" — a name that survives because lip-licking is still a driver, especially in children. The word cheilitis itself means inflammation of the lip, so candidates must localise it: angular cheilitis is at the commissures, distinct from actinic, contact, exfoliative, glandular and granulomatous cheilitis, each with its own aetiology and prognosis.^[1]

It is a sentinel condition, not just a sore corner. Most cases are benign and self-limited when treated, but persistent or recurrent disease demands a systematic search for an underlying systemic predisposition — iron, vitamin B12 or folate deficiency, diabetes, immunodeficiency, even haematological malignancy. Treat the corner, then investigate the patient.^[1][3]

The three-step cascade — and why mixed infection is the rule

The pathogenesis is one cascade in three steps: saliva pools, the stratum corneum macerates, then microbes colonise. Understanding the cascade tells you why a single cream often fails and why the denture matters more than the drug.^[1]

Step one — saliva pooling. Loss of teeth or a worn denture drops the vertical dimension, the mandible overcloses, and deep commissural folds form that trap saliva by gravity. Xerostomia paradoxically predisposes too, because thickened saliva loses its antimicrobial proteins; sialorrhoea in children and neurological disease does the opposite, raising the moisture burden.^[1][2]

Step two — maceration. Saliva is alkaline relative to skin (about pH 6.5 to 7.0 versus skin about 5.0) and carries digestive enzymes, so it softens and lifts the stratum corneum until it fissures with the slightest stretch. The result is a warm, moist, nutrient-rich pocket — a culture plate at the corner of the mouth.^[1][3]

Step three — colonisation. Candida albicans is the single commonest organism, present in about 70 percent of cases; it switches from yeast to invasive pseudohyphae above pH 6.5 and at 37 degrees, secreting aspartyl proteinases and phospholipases. Staphylococcus aureus follows in about 20 percent, usually seeded from the anterior nares; beta-haemolytic streptococci are less common, and mixed Candida plus Staphylococcus infection is the rule in up to half of culture-positive cases — which is exactly why miconazole, with both antifungal and weak antistaphylococcal activity, is the rational first choice.^[1][3]

The clinical picture — and the trap of the unilateral lesion

Bilateral is the rule; unilateral should make you pause. The classic lesion is an erythematous, moist, macerated plaque at the commissure with a grey-white surface and a linear fissure (a rhagade) that tears painfully on mouth opening; it evolves through crusting and, if chronic, lichenification and post-inflammatory hyperpigmentation.^[1]

Atypical presentations flag the host. In HIV it can be severe, bilateral, rapidly progressive with concurrent thrush and oral hairy leukoplakia, sometimes the first manifestation, typically below a CD4 of 200; in diabetes it recurs with vulvovaginal or balanitis candidiasis; in infants it follows lip-licking, pacifiers and drooling; and in the mask era, friction and moisture under face coverings have produced a recognisable "mask mouth" picture.^[3][4]

Differential — and the lesions you must not call perleche

The differential of a sore lip corner is wide, and the dangerous one is squamous cell carcinoma of the lip. A systematic approach by distribution, morphology and associated features separates them.^[1]

The discriminator line: angular cheilitis is bilateral and confined to the commissures; anything unilateral, indurated, non-healing or involving the whole vermilion is something else — and the unilateral non-healing lesion gets biopsied.^[1][5]

The bedside round — read the lip, then read the patient

The goal of the assessment is to find the predisposing factor, because treating the infection alone guarantees recurrence. Take a structured history — onset, denture fit and hygiene, diet, systemic symptoms (fatigue, polyuria, weight loss, dysphagia), medications (xerostomia-inducing, anticoagulants), habits (lip-licking, betel quid), HIV risk, sun exposure — and then examine the lesion, the mouth and the patient together.^[1]

Examine the dentures with and without them in: the lower face shortened, deepened nasolabial folds and "drooping angle" folds all signal lost vertical dimension; friable erythematous palatal mucosa under the denture is denture stomatitis. Look in the nose for staphylococcal vestibulitis, and on the skin and hands for the systemic clues — pallor, koilonychia, atrophic glossitis, oral thrush.^[1][2]

Investigations — clinical first, panel for the persistent case

Angular cheilitis is fundamentally a clinical diagnosis; tests are for the case that will not behave. Investigate when it is persistent (over two weeks despite topical therapy), recurrent (two or more episodes), carries clues to systemic disease, or is unilateral, indurated or non-healing — the last mandating biopsy to exclude SCC.^[1]

^{[1] [3]}

Send an oral or commissural swab for bacterial and fungal culture when first-line therapy fails, to catch non-albicans Candida (often azole-resistant) and MRSA; swab the anterior nares and decolonise if staphylococcal carriage is the source. Add an HIV test when disease is recurrent with oral candidiasis, intrinsic factor antibodies for suspected pernicious anaemia, a coeliac screen for malabsorption, and patch testing if allergic contact cheilitis is plausible. Biopsy the unilateral, indurated or non-healing lesion.^[1][3]

Management — two pillars, applied together, with one drug-interaction trap

Two pillars, applied simultaneously: treat the infection with a topical antimicrobial, and correct the predisposing factor. Treating the infection alone is the commonest reason for recurrence; the data are blunt about it — over half recur without cause correction, under 10 percent with it.^[1]

^[1]

Step 1 — topical antifungal, first-line

Topical antifungals are the first-line treatment for most clinicians, though the evidence is thin: the literature holds just two randomised trials, both decades old. The most consistent results in the main treatment review came from a combination ointment of 1 percent isoconazole nitrate with 0.1 percent diflucortolone valerate — an antifungal broad enough to cover dermatophytes and bacteria, paired with an anti-inflammatory component. Whatever agent is chosen, it only works alongside correction of the cause. ^[1]

Step 2 — add a topical antibacterial if staphylococcus is confirmed

If a swab confirms Staphylococcus aureus, or yellow crusting suggests impetiginous superinfection unresponsive to antifungal alone, add fusidic acid 2 percent cream three times daily for 7 to 10 days (UK and India) or mupirocin 2 percent three times daily (US, and the MRSA choice). If nasal carriage is the source, decolonise with mupirocin nasal ointment twice daily for 5 to 7 days plus chlorhexidine body wash. ^[1]

Step 3 — correct the cause (mandatory)

Without this step, recurrence is near-certain. For the denture: reline, rebase or remake it to restore vertical dimension, and institute a hygiene regimen — remove at night, brush daily with a non-abrasive cleaner, and soak overnight in chlorhexidine 0.2 percent, dilute hypochlorite (Milton) or alkaline peroxide; apply miconazole to the fitting surface if denture stomatitis is present. ^[1][2]

For nutrition: test for and replace documented deficiencies of iron, vitamin B12 and folate — B-vitamin supplementation is one of the measures proposed in the review — and optimise glycaemic control. Counsel against lip-licking; a plain barrier ointment helps break the cycle. ^[1]

Step 4 — systemic therapy for refractory or immunocompromised disease

If disease persists despite adequate topical therapy and cause correction, or the patient is immunocompromised, escalate to systemic antifungal treatment guided by swab results. In high-risk groups, antifungal prophylaxis reduces both the incidence and the severity of oral candidal infection, so specialist input is worth having early. ^[1][3]

Step 5 — refer when the diagnosis or the cause is beyond the clinic

Refer to dermatology or oral medicine for diagnostic uncertainty, suspected SCC, plasma cell or granulomatous cheilitis, or refractory disease; to maxillofacial or prosthodontics for denture correction and for biopsy or excision of suspected SCC; and to haematology or gastroenterology for severe nutritional deficiency, pernicious anaemia or malabsorption.^[1][5]

The pitfalls — DEFECT

^[1]

How angular cheilitis patients come to harm — the preventable list

• Bleeding from a miconazole-warfarin interaction because nobody checked the drug chart — the preventable harm.^[1]
• Recurrence ad infinitum because the denture, the iron or the diabetes was never addressed.^[1][2]
• Missing HIV or diabetes behind recurrent "just cracked lips".^[3]
• Missing squamous cell carcinoma of the lip in a unilateral non-healing lesion written off as perleche.^[1]
• Worsening Candida with a topical steroid, or masking an SCC with one.^[1]
• Subacute combined degeneration of the cord from giving folate before correcting B12 deficiency.^[1]

Prognosis and disposition

The prognosis is excellent when the cause is found and treated. With appropriate topical therapy and correction of the predisposing factor, most cases resolve within one to three weeks; recurrence runs over 50 percent without cause correction and under 10 percent with it. In the immunocompromised, prognosis tracks immune reconstitution — recurrent disease persists until the underlying deficiency is addressed.^[1]

Most patients are managed in primary care or dental practice with topical therapy and cause correction. Refer to dermatology for refractory or uncertain disease, to oral medicine for complex immunocompromised or orofacial granulomatosis, to maxillofacial or prosthodontics for denture work and biopsy, and to haematology or gastroenterology for severe deficiency or malabsorption.^[1][5]

Special populations

^{[1] [2] [3]}

Evidence, guidelines and regional differences

The evidence base is limited by the absence of large randomised trials — most guidance rests on narrative reviews, case series and expert opinion, with miconazole the most-studied and preferred topical agent precisely because of its dual antifungal and antistaphylococcal activity. The Akpan and Morgan review anchored the role of Candida albicans and topical azoles; the denture-stomatitis literature reinforces that the denture is a Candida biofilm reservoir and that overnight soaking and interdisciplinary dental collaboration matter.^[1][2][3]

A newer epidemiological note: angular cheilitis appeared in COVID-19 case series, plausibly from mask-wearing (moisture and friction), immunosuppression and steroid therapy — a reminder that barrier and moisture factors can shift with practice.^[4]

The mantra, and the mnemonic

^[1]

The mantra: treat the Candida and the cause on the same day — and check the warfarin before you reach for the miconazole.^[1]

Ward-round test — three stems, thirty seconds each

Stem 1 — the edentulous man on warfarin from the top of the topic (answer)ShowHide

A 78-year-old edentulous man on warfarin for atrial fibrillation has his third episode of cracked, bleeding commissures; his dentures are ten years old and rock when he chews. What is the diagnosis, and what is the trap? Model: Angular cheilitis from loss of vertical dimension (overclosure from worn, ill-fitting dentures) with mixed Candida and staphylococcal colonisation, and the drug-interaction trap is miconazole potentiating warfarin via CYP2C9 inhibition, risking dangerous INR elevation and bleeding. Treat the infection and the cause: use nystatin or clotrimazole (not miconazole gel) for the Candida in this anticoagulated patient, add fusidic acid or mupirocin if staph is confirmed, refer to prosthodontics to remake the dentures, and institute overnight soaking. The previous "steroid cream" helped briefly by suppressing inflammation but worsened the Candida and did nothing for the cause — which is why it recurred deeper.^[1][2]

Stem 2 — recurrent cracked corners in a tired young woman (answer)ShowHide

A 28-year-old vegetarian has had recurrent angular cheilitis for three months, with fatigue and a smooth, sore tongue. What is the likely underlying cause, and what panel do you send? Model: The smooth sore tongue (atrophic glossitis) plus fatigue plus recurrent candidal angular cheilitis points to nutritional deficiency, most likely iron or vitamin B12 deficiency (vegetarian diet raises B12 risk; folate and riboflavin are in the differential). Send the persistent-or-recurrent panel: FBC, serum ferritin, vitamin B12, red cell folate, HbA1c, and an oral swab if resistant; add HIV testing if risk factors. Treat with topical miconazole for the commissures and replace the deficient nutrient (iron or B12) — and correct B12 before folate if both are low, to avoid precipitating subacute combined degeneration of the cord. Investigate the cause of the deficiency (coeliac screen, intrinsic factor antibodies, upper GI endoscopy if Plummer-Vinson is suspected).^[1]

Stem 3 — a unilateral non-healing corner in a sun-damaged farmer (answer)ShowHide

A 68-year-old outdoor worker and betel-quid user has a unilateral, indurated, crusted lesion at the right commissure that has not healed in six weeks despite miconazole. What is the concern and the action? Model: The concern is squamous cell carcinoma of the lip — unilateral, indurated, non-healing beyond two to four weeks, in a sun-damaged, tobacco-and-betel-exposed older patient. Angular cheilitis is bilateral and confined to the commissure; this is not behaving like it. The action is urgent biopsy (and examination of regional nodes), not more antifungal. Actinic cheilitis and SCC are the premalignant-to-malignant pair to exclude whenever a lip lesion is unilateral and stubborn.^[1]

References5ShowHide

1. [1]Cabras M, Gambino A, Broccoletti R, et al. Treatment of angular cheilitis: A narrative review and authors' clinical experience Oral Dis, 2020.PMID 31464357
2. [2]McReynolds DE, Moorthy A, Moneley JO, et al. Denture stomatitis-An interdisciplinary clinical review J Prosthodont, 2023.PMID 36988151
3. [3]Akpan A, Morgan R. Oral candidiasis Postgrad Med J, 2002.PMID 12185216
4. [4]Riad A, Kassem I, Issa J, et al. Angular cheilitis of COVID-19 patients: A case-series and literature review Oral Dis, 2022.PMID 33043573
5. [5]Antonelli E, Bassotti G, Tramontana M, et al. Dermatological Manifestations in Inflammatory Bowel Diseases J Clin Med, 2021.PMID 33477990