Acta Dermatovenerol Croat

2008;16(2):96-100

REVIEW

Perioral Dermatitis
Suzana Ljubojevi1, Jasna Lipozeni1, Petra Turi2
University Department of Dermatology and Venereology, Zagreb University Hospital
Center and School of Medicine; 2Faculty of Pharmacy and Biochemistry, University of
Zagreb, Zagreb, Croatia
1

Corresponding author:
Suzana Ljubojevi, MD, PhD
University Department of Dermatology
and Venereology
Zagreb University Hospital Center and
School of Medicine
alata 4

Summary Perioral dermatitis is an inflammatory facial skin disorder

that predominantly affects women. It is rarely diagnosed in children. The
etiology of perioral dermatitis is unknown; however, uncritical use of topical corticosteroids often precedes skin lesions. There is a written diagnostic work-up, differential diagnosis and treatment.
Key words: rosacea-like dermatitis, steroid facial dermatitis, papulopustular facial dermatitis

HR-10000 Zagreb
Croatia
[email protected]
Received: November 9, 2007
Accepted: March 14, 2008

Introduction
Perioral dermatitis (PD), rosacea-like dermatitis, periorificial dermatitis, light-sensitive seborrheic, chronic papulopustular facial dermatitis,
papulopustular facial dermatitis, granulomatous
perioral dermatitis, lupus-like perioral dermatitis,
stewardess disease are synonyms for a chronic
papulopustular facial dermatitis. It mostly occurs in
young women. The clinical and histologic features
of the lesions resemble those of rosacea. Patients
require systemic and/or topical treatment, evaluation of the underlying factors, and reassurance. In
1957, Frumess and Lewis described cyclic dermatitis affecting the skin of the perioral region, principally among young females, by the term light
sensitive seborrhoeid (1).

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Epidemiology
PD predominantly affects women, who account for an estimated 90% of cases. The number of male patients is assumed to be increasing
because of changes in their cosmetic habits. PD
may occur but is rarely diagnosed in children (2,
3). The vast majority of patients are women aged
20-45 years (2).
Pathogenesis
There may be more than one cause of PD
(Table 1). The etiology of PD remains unknown;
however, the uncritical use of topical steroids for
minor skin alterations of the face often precedes
the manifestation of the disease (5). The underlying cause cannot be detected in all patients. Once

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PD has developed, corticosteroid creams seem to

help, but the disorder reappears when the treatment is discontinued. In fact, PD usually comes
back even worse than it was before the use of steroid creams. The use of inhaled prescription steroid sprays applied into the nose and mouth can
also induce PD. Fluorinated toothpaste, overuse
of heavy face creams and moisturizers, especially
those with a petrolatum or paraffin base, and the
vehicle isopropyl myristate are another common
cause. Physical factors such as UV light, heat and
wind worsen PD. Many investigators have considered that infections may cause PD. Microbiologic
factors such as fusiform spirilla bacteria, Candida
species, Demodex folliculorum and other fungi
have been cultured from lesions. Their presence
has no clear clinical relevance. Hormonal factors
are suspected because of the premenstrual deterioration observed. Oral contraceptives may also
be a causative factor. Gastrointestinal disturbances such as malabsorption have been considered
as well (5).

Clinical Features
The disease 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 (Figs
1 and 2). The papules and pustules have mainly
perioral locations. The predominant locations of
PD lesions are the perioral area, nasolabial fold
and lateral portions of lower eyelids. In an extreme variant of the disease called lupus-like PD,
granulomatous infiltrates have a yellowish aspect
at diascopy. A frequently seen feature of PD is a
border of normal skin separating lesional skin from
the lips (Fig. 1). In the perioral type, discrete to
moderate erythematous papules and pustules are
found circularly, with a clear zone of 3-5 mm under
the lower lip (Fig. 1).

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2008;16(2):96-100

Figure 1. A patient with perioral type of steroid

dermatitis

Complications
Although PD is limited to the skin and is not
a life-threatening condition, emotional problems
may occur because of the disfiguring character of
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
identified. 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
yellowish discoloration after diascopy. This entity
is called lupus-like PD. Scarring may be a problem
with the lupoid form of PD.

Table 1. Etiology of perioral dermatitis

Drugs
Cosmetics
Physical factors
Microbiologic factors
Miscellaneous factors

Topical steroids
Inhaled prescription steroid sprays
Fluorinated toothpaste
Skin care ointments and creams
UV light
Heat
Wind
Fusiform spirilla bacteria
Candida species
Hormonal factors (oral contraceptives)
Gastrointestinal disturbances (malabsorption)
Emotional stress

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Figure 2. Perioral dermatitis. Diffuse erythematous papule, papulopustules which appear on eczematous skin
Histopathology
Histopathologic appearances of the biopsies
are similar to those of rosacea (4). Changes in
the follicular epidermis are marked by most of the
authors (6). They suggest that the disorder might
be provoked by some external irritant (6). Biopsies
should be taken from the chin or nasolabial groove
and should include at least 1 papule. It must be admitted that the changes are not diagnostic. Usually
the clinical picture and history of the disease determine the diagnosis (5). Histopathologic examination of early papular lesions shows eczematous
changes consisting of mild acanthosis, epidermal
edema and parakeratosis. There are mainly ectatic venules and lymphocytes, mild edema and
sparse lymphatic perivascular infiltration. Usually, small peripheral areas of the hair follicles are

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2008;16(2):96-100

edematous and are invaded by inflammatory cells.

Sometimes follicular abscesses can be seen. The
abscess cavity contains many polymorphonuclear
leukocytes. Elastic fibers confirm the presence of
elastic degeneration. Demodex mite can sometimes be demonstrated as an incidental finding.
Examination of late papular lesions reveals diffuse
hypertrophy of the connective tissue, accompanied by hyperplasia of sebaceous follicles. In the
dermis, occasionally there is discrete epithelioid
cell granuloma of the noncaseating type with perifollicular predominance and scanty Langerhans
giant cells. Caseating granulomata are characteristic features of granulomatous PD (5).

Diagnosis
Clinical diagnosis
The diagnosis is made clinically. Usually good
history of the disease, which reveals prolonged
use of local corticosteroids or contact with other
potential cause factors (Table 1) is enough. Clinical picture is also characteristic. Predominantly
there are erythematous papules and papulopustules, usually localized in the perioral region. In
more than 98% of cases, rebound phenomenon
occurs (5). There is gradual disappearance of all
symptoms, and relapses are rare unless corticosteroids are repeatedly administered.
Laboratory diagnosis
No laboratory abnormalities can be expected
(4, 5). Prick tests and specific IgE testing against
a mixture of aeroallergens have been used to test
for skin barrier dysfunction. In a German study, PD

Table 2. Differential diagnosis of face rashes resembling perioral dermatitis

Rosacea
Seborrheic dermatitis
Acne vulgaris
Facial demodicosis
Lupus miliaris disseminatus faciei
Polymorphous light eruption
Contact dermatitis
Haber syndrome (familial rosacea-like
dermatosis)
Granulomatous periorificial dermatitis

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usually centrofacial disease

no comedones
usually rhinophyma is present
predominantly retroauricular, nasolabial region, eyebrow
and scalp are affected
main symptom is scaling
comedones, papules, pustules, nodule, cysts
affects younger population
mycology isolation of Demodex folliculorum)
little scars are present
spontaneous regression
itchy red papules, vesicles or plaques
after sun exposure
border of the rash immerging into normal skin
begins in childhood, intraepidermal epitheliomas,
keratotic plaques and scars
in prepubertal children; yellow-brown papules limited to
the perioral, perinasal and periocular regions

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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 (7).
Differential diagnosis
PD is usually a straightforward clinical diagnosis (5). However, on differential diagnosis few
facial skin diseases should be excluded (Table 2).
Facial demodicosis (infestation with Demodexfolliculorum) clinically resembles PD and should be
excluded, especially when anti-inflammatory therapies fail. Patients who are prone to acne or rosacea may experience worsening while undergoing topical immunomodulating therapy (e.g., with
tacrolimus ointment). Haber syndrome, or familial
rosacea-like dermatosis with intraepidermal epitheliomas, keratotic plaques and scars, is a rare
genodermatosis that begins in childhood. Granulomatous periorificial dermatitis manifests most
commonly in prepubertal children as yellow-brown
papules limited to the perioral, perinasal and periocular regions. The condition is self-limiting and is
not associated with systemic involvement.

Treatment
The first step in therapeutic management
should be discontinuation of all suspected topicals
which, however, usually leads to relapse of skin
lesion. One should insist on abandonment of all
cosmetics, soaps, detergents, moisturizers, abrasives, adstrigents, day or night creams, skin conditioners, etc. Washing with mild water only, using
fingers is suggested by some authors. However,
this null (zero) therapy is hard for many patients,
so local neutral treatment such as neutral local
creams and compresses (chamomile tea, physiologic solution, etc.) have to be used. The duration
of treatment is shorter with men because they give
up the idea of ever being cured sooner than the
women do. Sometimes the physician must provide
a great deal of psychological support during office
visits. Some of the patients develop corticosteroid
dependence and therefore need medical help including psychological support to break the habit
(8).
The patients have to be told that exacerbation
is to be expected and that it may take many weeks
to purify, and that the disease slowly regresses
when exogenous factors are eliminated. Some
investigators treat rebound phenomenon patients
with hydrocortisone, because hydrocortisone cuts
down the violence of the rebound reaction, while

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2008;16(2):96-100

allowing the atrophic collagen to recover (9). Others taper the dose of topical corticosteroids by reducing the frequency of administration (10).
The second factor in treatment is suppression
of bacterial infection in hair follicles with systemic
antibiotics. The population of Propionibacterium
acnes within follicles is markedly elevated in patients who apply local corticosteroids. Propionibacterium acnes inflame follicles directly by producing
agents chemotactic for polymorphonuclear leukocytes. Fusobacteria are often found in PD induced
by fluorinated corticosteroids. Besides these two
bacteria, in facial dermatoses induced by local
corticosteroids one can find gram-negative bacteria, staphylococci or sometimes even streptococci. Preference is given to lipophilic tetracyclines
like oxytetracycline, monocycline or doxycycline,
100-250 mg per day for 3-4 months, rarely longer.
To prevent poststeroid flare, oral tetracyclines are
contraindicated in children younger than 11 years.
Acceptable treatment for children includes oral as
well as topical erythromycin and topical metronidazole. If there is no response to full dose of tetracyclines, one may have to resort to isotretinoin.
Quite low doses are effective; usually 5 mg as a
simple daily dose for about 3 months; even 2-3
mg/day may be helpful. Precautions must be taken in women of childbearing potential. In less severe cases only, a neutral local therapy combined
with anti-inflammatory agents can be used, mostly
local erythromycin and metronidazole, neomycin,
clindamycin and oxytetracycline administered in a
nongreasy base (e.g., gel, lotion or cream). They
have both moisturizing and antibiotic effects. The
response of PD to metronidazole is the result of
the drugs anti-inflammatory and immunosuppressive effects rather than the direct antimicrobial
action (12). Topical antiacne medications such as
adapalene and azelaic acid have been used (13)
in open studies. Ointments should be avoided.
In severe cases of PD, local immunomodulatory
creams such as tacrolimus and pimecrolimus can
be used (14,15).
Topical antipruritics containing no corticosteroids, such as liquid pramoxine hydrochloride, offer excellent symptomatic relief. The response to
local treatment with sulfur, resorcin and ichthyol
was very unsatisfactory.
Conclusion
PD has become a quite common facial dermatitis nowadays because of the inappropriate use of
topical steroids on the face. Various environmental sensitivities have been reported. The link to

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rosacea is not certain but the two disorders occur

in the same population and both respond to the
same drugs.

References
1. Frumess GM, Lewis HM. Light-sensitive seborrheid. Arch Dermatol 1957;75:245-8.
2. Monders SM, Lucky AW. Perioral dermatitis in
childhood. J Am Acad Dermatol 1992; 27:68892.
3. Sneddon I. Perioral dermatitis. Br J Derm
1972;87:430.
4. Kammler H. Perioral dermatitis. E medicine.
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5. Ljubojevi S, Basta-Juzbai A, Lipozeni J.
Steroid dermatitis resembling rosacea-etiopathogenesis and treatment. JEADV 2002;
16:121-6.
6. Ackerman AB: Histologic Diagnosis of Inflammatory Skin Diseases. Philadelphia:
Lea&Febiger;1978. pp.803-5
7. Dirschka T, Tronnier H, Flster-Holst R. Epithelial barrier function and atopic diathesis in
rosacea and perioral dermatitis. Br J Dermatol
2004;150:1136-41.

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8. Wells K, Brodell RT. Topical corticosteroid addiction: a cause of perioral dermatitis. Postgrad Med 1993;93:225-30.
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dermatitis. J Am Acad Dermatol 1991; 87:42529.
13. Webster GF. Rosacea and Related Disorders.
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Dermatology. Edinburg:Mosby;2003. pp. 54552.
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inflammatory dermatoses with tacrolimus ointment. Arch Dermatol 2004;140:457-60.
15. Goldman D. Tacrolimus ointment for the treatment of steroid induced rosacea: a preliminary
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