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Perioral dermatitis

Article  in  Acta dermatovenerologica Croatica: ADC / Hrvatsko dermatolosko drustvo · February 2008

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Acta Dermatovenerol Croat 2008;16(2):96-100 REVIEW

Perioral Dermatitis
Suzana Ljubojević1, Jasna Lipozenčić1, Petra Turčić2

1
University Department of Dermatology and Venereology, Zagreb University Hospital
Center and School of Medicine; 2Faculty of Pharmacy and Biochemistry, University of
Zagreb, Zagreb, Croatia

Corresponding author: Summary Perioral dermatitis is an inflammatory facial skin disorder

Suzana Ljubojević, MD, PhD that predominantly affects women. It is rarely diagnosed in children. The
etiology of perioral dermatitis is unknown; however, uncritical use of topi-
University Department of Dermatology
cal corticosteroids often precedes skin lesions. There is a written diag-
and Venereology nostic work-up, differential diagnosis and treatment.
Zagreb University Hospital Center and
Key words: rosacea-like dermatitis, steroid facial dermatitis, papulo-
School of Medicine
pustular facial dermatitis
Šalata 4
HR-10000 Zagreb
Croatia
suzana.ljubojevic@t-com.hr

Received: November 9, 2007

Accepted: March 14, 2008

Introduction Epidemiology
Perioral dermatitis (PD), rosacea-like derma- PD predominantly affects women, who ac-
titis, periorificial dermatitis, light-sensitive sebor- count for an estimated 90% of cases. The num-
rheic, chronic papulopustular facial dermatitis, ber of male patients is assumed to be increasing
papulopustular facial dermatitis, granulomatous because of changes in their cosmetic habits. PD
perioral dermatitis, lupus-like perioral dermatitis, may occur but is rarely diagnosed in children (2,
stewardess disease are synonyms for a chronic 3). The vast majority of patients are women aged
papulopustular facial dermatitis. It mostly occurs in 20-45 years (2).
young women. The clinical and histologic features
of the lesions resemble those of rosacea. Patients Pathogenesis
require systemic and/or topical treatment, evalua- There may be more than one cause of PD
tion of the underlying factors, and reassurance. In (Table 1). The etiology of PD remains unknown;
1957, Frumess and Lewis described cyclic derma- however, the uncritical use of topical steroids for
titis affecting the skin of the perioral region, prin- minor skin alterations of the face often precedes
cipally among young females, by the term “light the manifestation of the disease (5). The underly-
sensitive seborrhoeid” (1). ing cause cannot be detected in all patients. Once

96
Ljubojević et al. Acta Dermatovenerol Croat
Perioral dermatitis 2008;16(2):96-100

PD has developed, corticosteroid creams seem to

help, but the disorder reappears when the treat-
ment is discontinued. In fact, PD usually comes
back even worse than it was before the use of ste-
roid creams. The use of inhaled prescription ste-
roid 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 consid-
ered 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 dete-
rioration observed. Oral contraceptives may also
be a causative factor. Gastrointestinal disturbanc-
es such as malabsorption have been considered
as well (5).
Figure 1. A patient with perioral type of steroid
Clinical Features dermatitis

The disease is limited to the skin. Skin lesions

occur as grouped follicular reddish papules, papu-
Complications
lovesicles and papulopustules on an erythema- Although PD is limited to the skin and is not
tous base with a possible confluent aspect (Figs a life-threatening condition, emotional problems
1 and 2). The papules and pustules have mainly may occur because of the disfiguring character of
perioral locations. The predominant locations of facial lesions and the possibly prolonged course
PD lesions are the perioral area, nasolabial fold of the disease. An initial rebound effect frequently
and lateral portions of lower eyelids. In an ex- occurs during the weaning of the steroid. This phe-
treme variant of the disease called lupus-like PD, nomenon is rare when no underlying cause can be
granulomatous infiltrates have a yellowish aspect identified. Chronic course is not uncommon. The
at diascopy. A frequently seen feature of PD is a development of a lupoid dermal infiltrate is consid-
border of normal skin separating lesional skin from ered to be a feature of the maximal variant of the
the lips (Fig. 1). In the perioral type, discrete to disease. The diagnosis is made on the basis of
moderate erythematous papules and pustules are yellowish discoloration after diascopy. This entity
found circularly, with a clear zone of 3-5 mm under is called lupus-like PD. Scarring may be a problem
the lower lip (Fig. 1). with the lupoid form of PD.

Table 1. Etiology of perioral dermatitis

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

ACTA DERMATOVENEROLOGICA CROATICA 97

Ljubojević et al. Acta Dermatovenerol Croat
Perioral dermatitis 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 some-
times be demonstrated as an incidental finding.
Examination of late papular lesions reveals diffuse
hypertrophy of the connective tissue, accompa-
nied by hyperplasia of sebaceous follicles. In the
dermis, occasionally there is discrete epithelioid
cell granuloma of the noncaseating type with peri-
follicular predominance and scanty Langerhans
giant cells. Caseating granulomata are character-
istic features of granulomatous PD (5).
Figure 2. Perioral dermatitis. Diffuse erythema-
tous papule, papulopustules which appear on ec- Diagnosis
zematous skin
Clinical diagnosis
Histopathology The diagnosis is made clinically. Usually good
Histopathologic appearances of the biopsies history of the disease, which reveals prolonged
are similar to those of rosacea (4). Changes in use of local corticosteroids or contact with other
the follicular epidermis are marked by most of the potential cause factors (Table 1) is enough. Clini-
authors (6). They suggest that the disorder might cal picture is also characteristic. Predominantly
be provoked by some external irritant (6). Biopsies there are erythematous papules and papulopus-
should be taken from the chin or nasolabial groove tules, usually localized in the perioral region. In
and should include at least 1 papule. It must be ad- more than 98% of cases, rebound phenomenon
mitted that the changes are not diagnostic. Usually occurs (5). There is gradual disappearance of all
the clinical picture and history of the disease de- symptoms, and relapses are rare unless cortico-
termine the diagnosis (5). Histopathologic exami- steroids are repeatedly administered.
nation of early papular lesions shows eczematous
changes consisting of mild acanthosis, epidermal Laboratory diagnosis
edema and parakeratosis. There are mainly ec- No laboratory abnormalities can be expected
tatic venules and lymphocytes, mild edema and (4, 5). Prick tests and specific IgE testing against
sparse lymphatic perivascular infiltration. Usu- a mixture of aeroallergens have been used to test
ally, small peripheral areas of the hair follicles are for skin barrier dysfunction. In a German study, PD

Table 2. Differential diagnosis of face rashes resembling perioral dermatitis

• usually centrofacial disease
Rosacea • no comedones
• usually rhinophyma is present
• predominantly retroauricular, nasolabial region, eyebrow
Seborrheic dermatitis and scalp are affected
• main symptom is scaling
• comedones, papules, pustules, nodule, cysts
Acne vulgaris
• affects younger population
Facial demodicosis • mycology isolation of Demodex folliculorum)
• little scars are present
Lupus miliaris disseminatus faciei
• spontaneous regression
• itchy red papules, vesicles or plaques
Polymorphous light eruption
• after sun exposure
Contact dermatitis • border of the rash immerging into normal skin
Haber syndrome (familial rosacea-like • begins in childhood, intraepidermal epitheliomas,
dermatosis) keratotic plaques and scars
• in prepubertal children; yellow-brown papules limited to
Granulomatous periorificial dermatitis
the perioral, perinasal and periocular regions

98 ACTA DERMATOVENEROLOGICA CROATICA

Ljubojević et al. Acta Dermatovenerol Croat
Perioral dermatitis 2008;16(2):96-100

patients experienced significantly increased tran- allowing the atrophic collagen to recover (9). Oth-
sepidermal water loss compared with rosacea pa- ers taper the dose of topical corticosteroids by re-
tients and a control group, which indicated a skin ducing the frequency of administration (10).
barrier function disorder. This type of testing is not The second factor in treatment is suppression
routinely used (7). of bacterial infection in hair follicles with systemic
antibiotics. The population of Propionibacterium
Differential diagnosis
acnes within follicles is markedly elevated in pa-
PD is usually a straightforward clinical diag- tients who apply local corticosteroids. Propionibac-
nosis (5). However, on differential diagnosis few terium acnes inflame follicles directly by producing
facial skin diseases should be excluded (Table 2). agents chemotactic for polymorphonuclear leuko-
Facial demodicosis (infestation with Demodexfol- cytes. Fusobacteria are often found in PD induced
liculorum) clinically resembles PD and should be by fluorinated corticosteroids. Besides these two
excluded, especially when anti-inflammatory ther- bacteria, in facial dermatoses induced by local
apies fail. Patients who are prone to acne or ro- corticosteroids one can find gram-negative bacte-
sacea may experience worsening while undergo- ria, staphylococci or sometimes even streptococ-
ing topical immunomodulating therapy (e.g., with ci. Preference is given to lipophilic tetracyclines
tacrolimus ointment). Haber syndrome, or familial like oxytetracycline, monocycline or doxycycline,
rosacea-like dermatosis with intraepidermal epi- 100-250 mg per day for 3-4 months, rarely longer.
theliomas, keratotic plaques and scars, is a rare To prevent poststeroid flare, oral tetracyclines are
genodermatosis that begins in childhood. Granu- contraindicated in children younger than 11 years.
lomatous periorificial dermatitis manifests most Acceptable treatment for children includes oral as
commonly in prepubertal children as yellow-brown well as topical erythromycin and topical metroni-
papules limited to the perioral, perinasal and peri- dazole. If there is no response to full dose of tet-
ocular regions. The condition is self-limiting and is racyclines, one may have to resort to isotretinoin.
not associated with systemic involvement. Quite low doses are effective; usually 5 mg as a
simple daily dose for about 3 months; even 2-3
Treatment mg/day may be helpful. Precautions must be tak-
The first step in therapeutic management en in women of childbearing potential. In less se-
should be discontinuation of all suspected topicals vere cases only, a neutral local therapy combined
which, however, usually leads to relapse of skin with anti-inflammatory agents can be used, mostly
lesion. One should insist on abandonment of all local erythromycin and metronidazole, neomycin,
cosmetics, soaps, detergents, moisturizers, abra- clindamycin and oxytetracycline administered in a
sives, adstrigents, day or night creams, skin con- nongreasy base (e.g., gel, lotion or cream). They
ditioners, etc. Washing with mild water only, using have both moisturizing and antibiotic effects. The
fingers is suggested by some authors. However, response of PD to metronidazole is the result of
this “null (zero) therapy” is hard for many patients, the drug’s anti-inflammatory and immunosuppres-
so local neutral treatment such as neutral local sive effects rather than the direct antimicrobial
creams and compresses (chamomile tea, physi- action (12). Topical antiacne medications such as
ologic solution, etc.) have to be used. The duration adapalene and azelaic acid have been used (13)
of treatment is shorter with men because they give in open studies. Ointments should be avoided.
up the idea of ever being cured sooner than the In severe cases of PD, local immunomodulatory
women do. Sometimes the physician must provide creams such as tacrolimus and pimecrolimus can
a great deal of psychological support during office be used (14,15).
visits. Some of the patients develop corticosteroid Topical antipruritics containing no corticoste-
dependence and therefore need medical help in- roids, such as liquid pramoxine hydrochloride, of-
cluding psychological support to break the habit fer excellent symptomatic relief. The response to
(8). local treatment with sulfur, resorcin and ichthyol
The patients have to be told that exacerbation was very unsatisfactory.
is to be expected and that it may take many weeks
to purify, and that the disease slowly regresses Conclusion
when exogenous factors are eliminated. Some PD has become a quite common facial derma-
investigators treat rebound phenomenon patients titis nowadays because of the inappropriate use of
with hydrocortisone, because hydrocortisone cuts topical steroids on the face. Various environmen-
down the violence of the rebound reaction, while tal sensitivities have been reported. The link to

ACTA DERMATOVENEROLOGICA CROATICA 99

 Ljubojević et al. Acta Dermatovenerol Croat
Perioral dermatitis 2008;16(2):96-100

rosacea is not certain but the two disorders occur 8. Wells K, Brodell RT. Topical corticosteroid “ad-
in the same population and both respond to the diction”: a cause of perioral dermatitis. Post-
same drugs. grad Med 1993;93:225-30.
9. Sneddon IB. The treatment of steroid-induced
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