Periorificial Dermatitis (Perioral Dermatitis)

Periorificial dermatitis (POD) is an inflammatory facial eruption characterized by grouped erythematous papules/pustules and background erythema around the mouth, nose, and/or eyes, often sparing the immediate vermilion border. It is frequently triggered or perpetuated by topical corticosteroids, fluorinated toothpaste, cosmetic irritants, and occlusive skincare. Management centers on eliminating triggers (“zero therapy”), gentle barrier repair, and anti-inflammatory topicals or systemic antibiotics. Prognosis is excellent with appropriate therapy, though steroid withdrawal flares are common.

Epidemiology

  • Most common in women aged 16–45; can occur in men and children (periocular in pediatrics).
  • Risk factors: topical/inhaled corticosteroids, heavy emollients/occlusives, fluorinated toothpaste, physical sunscreens in some, mask occlusion.

Pathophysiology

  • Barrier disruption and innate immune activation with possible Demodex/Malassezia contribution.
  • Topical steroid exposure leads to vasoconstriction followed by rebound vasodilation/inflammation on withdrawal.

Clinical Features

  • Clusters of 1–3 mm papules/pustules on an erythematous, sometimes scaly base around the perioral, perinasal, and periocular regions.
  • Often spares a narrow rim around the vermilion border.
  • Burning/tightness > itch; history of steroid use is common.
  • Variants: granulomatous periorificial dermatitis in children (monomorphic papules, more perinasal/periorbital), mask-induced POD.

Differential Diagnosis

  • Rosacea (more diffuse central facial erythema, telangiectasias; older patients), acne (comedones present), seborrheic dermatitis (greasy scale in folds), allergic contact dermatitis (pruritic eczematous plaques), lip licker’s dermatitis, impetigo, tinea faciei.

Diagnosis

  • Clinical; dermoscopy may show perifollicular scaling/vesicles.
  • Consider KOH if tinea suspected; culture if impetigo possible; patch testing if refractory or eczematous.

Management

  1. Zero therapy and trigger withdrawal
  • Discontinue topical steroids on the face; consider gradual taper if high-potency used to mitigate rebound.
  • Stop heavy/occlusive moisturizers, irritating cosmetics; switch to bland, fragrance-free routine.
  • Non-fluorinated toothpaste trial if suspected; avoid harsh sunscreens—use gentle mineral formulations as tolerated.
  1. Topical therapy (first-line for mild to moderate)
  • Metronidazole 0.75–1% gel/cream bid.
  • Azelaic acid 15–20% gel/foam bid (also helps PIH).
  • Ivermectin 1% cream qd.
  • Erythromycin 2% or clindamycin 1% gel/lotion bid.
  • Calcineurin inhibitors (pimecrolimus 1% cream or tacrolimus 0.03–0.1% ointment) are steroid-sparing options, especially periocular; note transient burning.
  • Avoid topical steroids; they worsen and prolong disease.
  1. Systemic therapy (moderate–severe or refractory)
  • Doxycycline 50–100 mg bid or 40 mg MR qd for 6–8 weeks, then taper.
  • Alternatives: minocycline, sarecycline; erythromycin/azithromycin in pregnancy/children.
  • Short courses are typical; continue topicals for maintenance.
  1. Special populations
  • Children: avoid tetracyclines; use erythromycin/azithromycin and topical metronidazole/erythromycin/pimecrolimus.
  • Pregnancy: safe options include topical metronidazole, azelaic acid, erythromycin; oral erythromycin if needed.
  1. Prognosis and counseling
  • Expect rebound flare after steroid withdrawal; reassure that control follows within weeks.
  • Recurrences linked to re-exposure to steroids/occlusive products.

References (recent guidelines and key reviews)

  • AAD and international reviews on POD management, 2022–2024.
  • Evidence syntheses on steroid-induced facial dermatoses and zero-therapy strategies, 2021–2024.
  • Pediatric granulomatous POD series and treatment outcomes, 2020–2024.

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