Perioral Dermatitis

Perioral dermatitis (POD) is a chronic papulopustular facial dermatitis. It mostly occurs in women and children.[1, 2] The clinical and histologic features of the perioral dermatitis lesions resemble those of rosacea. Patients require systemic and/or topical treatment and an evaluation of the underlying factors.

See the image below.

Perioral dermatitis. Courtesy of Professor Raimo Suhonen and DermNet New Zealand (http://www.dermnetnz.org/assets/Uploads/acne/s/pod6.jpg).

The etiology of perioral dermatitis (POD) is unknown; however, the long-term use of topical steroids for minor skin alterations of the face often precedes the manifestation of perioral dermatitis. Perioral dermatitis is limited to the skin.

An underlying cause of the perioral dermatitis (POD) cannot be detected in all patients. The etiology of perioral dermatitis is unknown; however, long-term use of topical steroids for minor skin alterations of the face often precedes the manifestation of the disease. Note the following:

• Drugs: Many patients abuse topical steroid preparations.[3] No clear correlation exists between the risk of perioral dermatitis and strength of the steroid or the duration of the abuse. Perioral dermatitis has also been reported after the use of nasal steroids[4] and steroid inhalers.

• Cosmetics: Fluorinated toothpaste[5, 6] ; skin care ointments and creams, especially those with a petrolatum or paraffin base, and the vehicle isopropyl myristate are suggested to be causative factors. In an Australian study, applying foundation in addition to moisturizer and night cream resulted in a 13-fold increased risk for perioral dermatitis. The combination of moisturizer and foundation was associated with a lesser but significantly increased risk for perioral dermatitis, whereas moisturizer alone was not associated with an increased risk. Physical sunscreens have been identified as a cause of perioral dermatitis in children.[7]

• Physical factors: UV light, heat, and wind worsen perioral dermatitis.

• Miscellaneous factors: Hormonal factors are suspected because of an observed premenstrual deterioration. Oral contraceptives may be a factor.

Frequency

United States

The incidence of perioral dermatitis (POD)  is estimated to be 0.5-1% in industrialized countries, independent of geographic factors.

International

The incidence of perioral dermatitis seems to be lower in less developed countries, but no statistics are available.

Sex

In adults, perioral dermatitis predominantly affects young females, who account for an estimated 90% of the cases. The number of male patients is assumed to be increasing because of changes in their cosmetic habits.

Age

In adults, the vast majority of patients are women aged 20-45 years. Perioral dermatitis also occurs commonly in children.

Perioral dermatitis (POD) is not a life-threatening disease. However, unexpectedly long period of treatment may be required to achieve a cosmetically satisfactory skin condition.

Reassurance and education about possible underlying factors and the time course of the disease are critical. These measures help the patient to cope with the character of the disease and help to minimize the risk of recurrences.

Patients have to be aware that initial deterioration may occur, especially if they previously used a topical steroid.

The use of all topical preparations, including cosmetics, should be avoided except the prescribed medication.

The patient should be advised that remission might not occur for many weeks, despite correct treatment.

Subjective symptoms of perioral dermatitis (POD) may consist of a sensation of stinging and burning. Itching is rare.

Often, long-term use of topical steroids for minor or even undiagnosed skin alterations precedes the development of perioral dermatitis.

Perioral dermatitis tends to be chronic.

Perioral dermatitis (POD) is limited to the skin.

Skin lesions occur as grouped follicular reddish papules, papulovesicles, and papulopustules on an erythematous base with a possible confluent aspect. The papules and pustules have primarily a perioral distribution. Other locations of involvement include the nasolabial fold and lateral portions of the lower eyelids.

In an extreme variant of the disease called granulomatous perioral dermatitis, granulomatous infiltrates have a yellowish aspect at diascopy. The lesions are confluent in a well-defined plaque delineated by the nasolabial folds and chin.[8]

Although perioral dermatitis (POD) is limited to the skin and not life threatening, emotional problems may occur because of the character of the facial lesions and the possibly prolonged course of the disease.

An initial rebound effect frequently occurs during the weaning of the steroid. This phenomenon is rare when no underlying cause can be evaluated.

A chronic course is not uncommon.

The development of a lupoid dermal infiltrate is considered to be a feature of the maximal variant of the disease. The diagnosis is made on the basis of the yellowish discoloration after diascopy. This entity is called lupuslike perioral dermatitis.

Scarring may be a problem with the lupoid form of perioral dermatitis.

The diagnosis is made clinically. No laboratory abnormalities can be expected.

In a German study,[13] perioral dermatitis (POD) patients experienced significantly increased transepidermal water loss compared with rosacea patients and a control group, which indicated a skin barrier function disorder. This type of testing is not routinely used.

Histologic findings are similar to those of rosacea, but the signs of actinic skin damage are generally less intense and vary according to the patient's age. Thus, a lymphohistiocytic infiltrate with perifollicular localization can be expected in all stages. A marked granulomatous inflammation and, occasionally, perifollicular abscesses may be present when pustules and papules are the dominant clinical findings.

Anti-inflammatory systemic and/or topical therapy similar to that used for rosacea is required. Photodynamic therapy (PDT) has been reported to be helpful for perioral dermatitis (POD),[14] although large studies have not yet been performed.

Topical praziquantel effectively improved symptoms of perioral dermatitis and quality of life in a small vehicle-controlled study.[15]

Treatment should be adapted to the severity and extension of the disease.

Reassurance and education about possible underlying factors and the time course of the disease are critical. These measures help the patient to cope with the disfiguring character of the disease and help to minimize the risk of recurrences.

The use of cosmetics, cleansers, and moisturizers should be avoided during treatment.

In 2014, a treatment algorithm was proposed to assist physicians in finding the appropriate therapy.[16]

Consult a dermatologist to evaluate provoking factors and to determine the individualized treatment.[17]

In general, physical activity is not restricted; however, vasodilation of dermal vessels due to strenuous physical exercise may worsen subjective symptoms.

If provoking factors can be determined, they should be avoided.

Care includes an assessment of the effectiveness of systemic therapy. Topical therapy should be adapted in accordance to the condition of the skin and the severity of the disease.

In mild cases, as well as in most children and pregnant women, individualized topical therapy is generally recommended. Antimicrobial agents (eg, metronidazole[7, 18, 19, 20] and erythromycin) are administered in a nongreasy base (eg, gel, lotion, cream). Pimecrolimus cream significantly reduced the Perioral Dermatitis Severity Index[21] (PODSI) compared with vehicle in a randomized, double-blind study in adults.[22] Pimecrolimus cream seems to be most effective in steroid-induced perioral dermatitis.[23] A retrospective medical record review from 2020 reported that topical calcineurin inhibitors are effective and well tolerated for treating periorificial dermatitis in pediatric patients.[24] Topical antiacne medications such as adapalene[25] and azelaic acid[26, 27] have been used in open studies. Ointments should be avoided.

In severe forms of perioral dermatitis, systemic treatment with antirosacea drugs is required. The drugs of choice are doxycycline (or tetracycline) and minocycline. In unresponsive and granulomatous forms, oral isotretinoin[28] may be considered. Oral erythromycin can be used in pediatric patients with more severe or refractory involvement.

Zero-therapy is based on the idea that by ceasing use of all topical medications and cosmetics, the underlying causative factor for perioral dermatitis is eliminated. This form of therapy is appropriate in very compliant patients. It may be effective predominantly in cases associated with steroid abuse or when intolerance to cosmetics is suspected.[29, 30]

In every case, an initial worsening of the symptoms may occur with treatment, especially if topical steroids are withdrawn. The patient should be made aware of this complication. In cases of preceding long-term use of topical steroids, steroid weaning with low-dose 0.1-0.5% hydrocortisone cream can be tried initially.

The use of potent topical steroids is strictly contraindicated. However, in some cases, the initial tapering use of a low-potency corticosteroid (eg, hydrocortisone cream) may be appropriate.

Class Summary

These drugs may have antibacterial and/or anti-inflammatory effects that are responsible for their effectiveness in perioral dermatitis.

Doxycycline (Oracea, Doryx, Vibramycin)

Doxycycline is the drug of choice in nonpregnant women. It inhibits protein synthesis and thus bacterial growth by binding to 30S and possibly 50S ribosomal subunits of susceptible bacteria. Alternatively, one may use tetracycline in adapted dose.

Minocycline (Dynacin, Minocin, Solodyn)

Minocycline is believed to be the most efficacious tetracycline in dermatoses of sebaceous glands. It is used to treat infections caused by susceptible gram-negative and gram-positive organisms, in addition to infections caused by susceptible Chlamydia, Rickettsia, and Mycoplasma species.

Tetracycline

Tetracycline inhibits bacterial protein synthesis by binding with 30S and possibly 50S ribosomal subunits. It has anti-inflammatory activity.

Metronidazole (Flagyl)

Metronidazole is an imidazole ring-based antibiotic active against various anaerobic bacteria and protozoa. In concentrations of 0.75-2%, it is considered to be the drug of choice for topical treatment of perioral dermatitis. Metronidazole is available in a gel, lotion, or cream.

Erythromycin (E.E.S., Erythrocin, Ery-Tab)

Topical erythromycin in concentrations of 2-4% as a gel or cream is an alternative to metronidazole for topical treatment. It inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest. It is used to treat staphylococcal and streptococcal infections.

Class Summary

These agents reduce the size of the sebaceous glands, decrease sebum secretion, and inhibit keratinization.

Isotretinoin (Amnesteem, Claravis, Sotret)

Isotretinoin is an oral agent used to treat serious dermatologic conditions. It is a synthetic 13-cis isomer of naturally occurring tretinoin (trans -retinoic acid). Both agents are structurally related to vitamin A. Isotretinoin decreases sebaceous gland size and sebum production. It may inhibit sebaceous gland differentiation and abnormal keratinization. Isotretinoin is indicated for long-standing and refractory forms of perioral dermatitis. Because of adverse effects, therapy should be prescribed only by a physician familiar with this drug (ie, dermatologist).

A US Food and Drug Administration–mandated registry is now in place for all individuals prescribing, dispensing, or taking isotretinoin. For more information on this registry, see iPLEDGE. This registry aims to further decrease the risk of pregnancy and other unwanted and potentially dangerous adverse effects during a course of isotretinoin therapy.

Class Summary

Pimecrolimus cream controls atopic dermatitis.

Pimecrolimus (Elidel)

Pimecrolimus is the first nonsteroid cream approved in the United States for mild-to-moderate atopic dermatitis. It is derived from ascomycin, a natural substance produced by the fungus Streptomyces hygroscopicus var ascomyceticus. Pimecrolimus selectively inhibits the production and release of inflammatory cytokines from activated T-cells by binding to cytosolic immunophilin receptor macrophilin-12. The resulting complex inhibits phosphatase calcineurin, thus blocking T-cell activation and cytokine release. Cutaneous atrophy is not observed in clinical trials, a potential advantage over topical corticosteroids.