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Perioral dermatitis
Perioral dermatitis
Perioral dermatitis
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Perioral dermatitis
Other namesPeriorificial dermatitis
Papules around mouth and nostrils with some background redness and sparing of vermillion border
SpecialtyDermatology
SymptomsPapules, pustules, red skin
ComplicationsSkin infection
CausesUnknown[1]
Risk factorsTopical steroids, cosmetics, moisturiser
Diagnostic methodBased on symptom and appearance
Differential diagnosisRosacea, acne
TreatmentNone, tetracycline

Perioral dermatitis, also known as periorificial dermatitis, is a common type of inflammatory skin rash.[2] Symptoms include multiple small (1–2 mm) bumps and blisters sometimes with background redness and scale, localized to the skin around the mouth and nostrils. Less commonly, the eyes and genitalia may be involved.[3] It can be persistent or recurring, and resembles particularly rosacea and to some extent acne and allergic dermatitis. The term "dermatitis" is a misnomer because this is not an eczematous process.[4]

The cause is unclear.[1] Topical steroids are associated with the condition and moisturizers and cosmetics may contribute.[4] The underlying mechanism may involve blockage of the skin surface followed by subsequent excessive growth of skin flora. Fluoridated toothpaste and some micro-organisms, including Candida may also worsen the condition, but their roles in this condition are unclear.[5] It is considered a disease of the hair follicle with biopsy samples showing microscopic changes around the hair follicle. Diagnosis is based on symptoms.[5]

Treatment is typically by stopping topical steroids, changing cosmetics, and in more severe cases, taking tetracyclines by mouth.[1][6] Stopping steroids may initially worsen the rash. The condition is estimated to affect 0.5-1% of people each year in the developed world. Up to 90% of those affected are women between the ages of 16 and 45 years, though it also affects children and the elderly, and has an increasing incidence in men.[7][8]

History

[edit]

The disorder appears to have made a sudden appearance with a case of 'light sensitive seborrhoeid' in 1957, which is said to be the first nearest description of the condition. By 1964, the condition in adults became popularly known as perioral dermatitis, but without clear clinical criteria.[3] In 1970, the condition was recognized in children. Whether all rashes around the mouth are perioral dermatitis has been frequently debated.[9] That this condition should be renamed periorificial dermatitis has been proposed.[3] Darrell Wilkinson was a British dermatologist who gave one of the earliest 'definitive' descriptions of 'perioral dermatitis' and noted that the condition was not always associated with the use of fluoridated steroid creams.[8][10][11]

Signs and symptoms

[edit]
Periorificial dermatitis

A stinging and burning sensation with rash is often felt and noticed, but itching is less common.[7] Often, the rash is steroid responsive, initially improving with application of topical steroid.[1] The redness caused by perioral dermatitis has been associated with variable levels of depression and anxiety.[10]

Initially, there may be small pinpoint papules on either side of the nostrils. Multiple small (1-2mm) papules and pustules then occur around the mouth, nose and sometimes cheeks. The area of skin directly adjacent to the lips, also called the vermillion border, is spared and looks normal. There may be some mild background redness and occasional scale.[12] These areas of skin are felt to be drier and therefore there is a tendency to moisturize them more frequently. Hence, they do not tolerate drying agents well, and they often worsen the rash.[8]

Perioral dermatitis is also known by other names, including rosacea-like dermatoses, periorofacial dermatitis and periorificial dermatitis. Unlike rosacea, which involves mainly the nose and cheeks, there is no telangiectasia in perioral dermatitis. Rosacea also has a tendency to be present in older people. Acne can be distinguished by the presence of comedones and by its wider distribution on the face and chest.[10] There are no comedones in perioral dermatitis.[4]

A variant of perioral dermatitis called granulomatous perioral dermatitis (GPD) is often seen in prepubertal children or in darker skin phenotypes. GPD lesions may appear yellow on a diascopy. Patients report irritation but are usually asymptomatic.[13] For children with GPD, a skin biopsy showing granulomatous infiltrate is needed to confirm diagnosis in an atypical patient. If the GPD is mild, treatment is not mandatory.[14]

Causes

[edit]

The exact cause of perioral dermatitis is unclear; however, some associations are suspected. There have been clinical trials to look at the link between perioral dermatitis and steroids, infections, and typical facial products.[15] These factors may play a role in the development of perioral dermatitis.[1][3] Although light exposure has been discounted as a causal factor, some reports of perioral dermatitis have been made by some patients receiving Psoralen and ultraviolet A therapy.[12] It is important to note that an underlying cause can not always be known for patients as the exact mechanism of action to develop perioral dermatitis is not known.[16]

Corticosteroids

[edit]

Perioral dermatitis can occur with corticosteroids. Corticosteroids are anti-inflammatory medications used to reduce swelling and redness caused by the body. There are different forms of steroids, many of which can contribute to the development of perioral dermatitis.[15] Some of these are topical corticosteroids, oral corticosteroids, and inhaled corticosteroids. There have been clinical trials that show a correlation between these corticosteroids; however, a direct cause has not been confirmed. The highest link seems to be with topical corticosteroids in comparison to the others, and there seems to be a higher chance of the development of perioral dermatitis with stronger steroids.[15][12] It has also been seen that chronic use of steroids shows a higher rate of developing perioral dermatitis. Discontinuing the steroids often initially worsens the dermatitis, which leads to some conflicting beliefs, as some people believe the steroids were initially controlling the condition.[4] Perioral dermatitis tends to occur on the drier parts of the face and can be aggravated by drying agents, including topical benzoyl peroxide, tretinoin, and lotions with an alcohol base.[8]Reports of perioral dermatitis in renal transplant recipients treated with oral corticosteroids and azathioprine have been documented.[5]

Infections

[edit]

Topical corticosteroids may lead to an increase in microorganism density in the hair follicle.[12] Microorganisms are small living things that a person is not able to see without a microscope. Normally, people have microorganisms all over their bodies, but corticosteroids can change the type and amount. This may lead to an infection. The role of infectious agents such as Candida species, Demodex folliculorum, and fusobacteria has not been confirmed, but could be potential causes for development as well.[17][15][18] There are different types of the infections such as bacterial, yeast, and parasitic. From different clinical trials, it seems that a bacterial infection is more likely to lead to perioral dermatitis than the other types.[15]

Cosmetics

[edit]

Cosmetics play an important role as potential causal factors for perioral dermatitis.[5] Cosmetics in this case include a variety of products that are applied to the face such as moisturizer, foundation, and sunscreen.[15] It is especially seen when these products contain petroleum, paraffin, or isopropyl myristate.[16] Applying large quantities of a moisturizing creams regularly causes persistent hydration of the layer which may cause impairment and occlusion of the barrier function, irritation of the hair follicle, and proliferation of skin flora. Occlusion is the sealing of the moisture. Proliferation is when cells continue to divide to create new healthy cells. This is a process that cells of all kinds normally and often do. For some people, this act of moisturizing excessively can affect the typical proliferation of skin flora. Skin flora are the typical bacteria and cells that sit on a person's face. Transepidermal water loss is also seen as associated with perioral dermatitis.[15] Transepidermal water loss is water that is lost from the inside of the body by going through the skin to the outside world. There are associations that water loss is greater in older adults, but perioral dermatitis can still occur in younger people.[19] Barrier dysfunction is seen as a large cosmetic association to perioral dermatitis.[2] Combining this with night cream and foundation significantly increases risk of perioral dermatitis 13-fold.[8][10] In a similar fashion, foundation and sunscreen also create extra occlusive layers that may affect the skin. Physical sunscreens also have been seen to have an associations[20] These are potential associations to perioral dermatitis and thoughts of how it may cause perioral dermatitis; however, the exact pathology is still unknown.[15] This also does not mean that those that use these products will be sure to develop perioral dermatitis.

Other Potential Causes

[edit]

Various other potential factors are suspected to cause or worsen perioral dermatitis; however, sufficient research has not been conducted to demonstrate a link as strong as that with corticosteroids. Hormonal changes may be linked to causing perioral dermatitis.[16] Oral contraceptives (birth control pills) may also have a link as they significantly impact the hormonal balance of the people taking them.[16] Hormones are natural chemicals in the body that act as messengers by relaying information to different parts of the body. These levels are normally regulated by the body; however, they can be changed by other factors such as oral contraceptives. Gastrointestinal (GI) changes may also be linked with perioral dermatitis.[16] The GI system includes all the organs for food to be broken down, absorbed, and excreted out of the body. The condition may be potentially worsened by fluoridated toothpaste, excessive wind, or heat.[1][3][16] The possibility of an association with wearing a veil has been documented as well.[5] Some other miscellaneous factors include emotional stress, malabsorption, and latex gloves.[13]

Perioral dermatitis can also be caused by other factors, such as stress, oily secretions, and fluid intake, all of which were impacted as COVID cases increased, which further increased the rates of wearing masks. This, in turn, resulted in an increased level of stress and oil secretions along the face and decreased intake of water.[21]

Pathophysiology

[edit]

The pathophysiology of perioral dermatitis is related to disease of the hair follicle, as is now included in the ICD-11, due to be finalized in 2018.[22] Lip licker's dermatitis or perioral irritant contact dermatitis due to lip-licking is considered a separate disease categorized under irritant contact dermatitis due to saliva.[23]

Perioral dermatitis is frequently histologically similar to rosacea, with the two conditions overlapping considerably. There is a lymphohistiocytic infiltrate with perifollicular localization and marked granulomatous inflammation. Occasionally, perifollicular abscesses may be present when pustules and papules are the dominant clinical findings.[7]

There is a possible discovery of new information that perioral dermatitis develops due to damage to the skin barrier in the facial area, which may lead to the patient's skin becoming exposed to both internal and external factors that contribute to the development of perioral dermatitis.[24]

Diagnosis

[edit]

A diagnosis of perioral dermatitis is typically made based on the characteristics of the rash. A skin biopsy is usually not required to make the diagnosis, but can be helpful to rule out other skin diseases that may resemble perioral dermatitis. Extended patch testing may also be useful to rule out allergic contact causes.[5] If the skin biopsy shows signs of other components such as bacteria, the healthcare workers can do further lab testing, such as culture or other tests like a diascopy.[25]

Other skin diseases that may resemble perioral dermatitis include:

Treatment

[edit]

Multiple treatment regimes are available, and treatment algorithms have been proposed.[1]

Treatment regimens are advised to treat perioral dermatitis using the lowest possible dose for antibiotics and other therapies.[26]

Most treatment plans were developed through trial and error. Treatment plans usually consist of a systemic treatment such as an oral antibiotic or a topical treatment like metronidazole.[27]

However, many factors can contribute to the development of perioral dermatitis in patients, as well as their severity of the disease. This can cause to develop many treatment plans that would cater the best towards the patient.[28]

Perioral dermatitis usually resolves within a few months without medication by limiting the use of irritants, including products with fragrance, cosmetics, benzoyl peroxide, occlusive sunscreens, and various acne products. This is called zero treatment. Topical corticosteroids should be stopped entirely if possible.[6][29] Abrupt discontinuation of a topical corticosteroid may lead to rebound flares that can be worse than the primary dermatitis.[13][27] If the flare proves intolerable, temporary use of a less potent topical corticosteroid can often be helpful.[17] Slowly reducing the use of topical corticosteroids over time can help prevent rebound flares.[27]

Topical retinoids and benzoyl peroxide are potentially irritating products that can cause inflammation of the skin and should be avoided.[30]

Medication

[edit]

Several medications, either applied directly to the skin or taken by mouth, may speed recovery. These include tetracycline, doxycycline, and erythromycin.[31] Tetracycline is given at a daily dosage of 250 to 500 mg twice a day for 4 to 8 weeks.[27] Gastrointestinal issues, diarrhea, and photosensitivity are possible short term side effects when taking tetracycline.[27] Sarecycline, a narrow-spectrum tetracycline antibiotic, has a lower potential of causing bacterial resistance and gastrointestinal issues compared to other tetracycline medications. Possible side effects of Sarecycline include nausea and sunburn, which are very rare.[32] Pregnant women and pediatric patients can not take tetracycline due to possible harm to the fetus and severe staining of developing teeth.[27] Erythromycin is often given as an alternative for those who cannot take tetracycline, given at a daily dosage of 250 to 500 mg. Erythromycin may be used as a cream.[6] Doxycycline is a second-generation tetracycline with improved absorption and a broader antibacterial spectrum.[27] Doxycycline is most often the first antibiotic drug choice, given at a daily dosage of 100 mg for up to a month before considering tapering off or stopping. Sometimes, a longer duration of low doses of doxycycline is required.[8] Possible side effects of doxycycline include gastrointestinal issues and irritation in the esophagus.[27]

Metronidazole is less effective, but it is available in a gel and can be applied twice daily. For pediatric patients, metronidazole can be used as an alternative to tetracycline. Metronidazole comes in various concentrations ranging from 0.75% to 2%. Higher concentrated metronidazole did not equate to shorter time to cure times.[27] If the perioral dermatitis was triggered by a topical steroid, then pimecrolimus cream has been suggested as effective in improving symptoms.[8] However, this has also been documented to cause the condition.[4] Topical pimecrolimus is often used in treating corticosteroid-induced perioral dermatitis due to it being a non-steroid-based cream. Pimecrolimus is generally well tolerated, with a rare side effect of a burning sensation at the application site.[27]

Topical adapalene has been reported to resolve a case of perioral dermatitis in 4 weeks without any side effects. The dose used was 1% adapalene gel once a day at night. The patient did not have a recurrence during the 8-month follow-up period.[27][33]

The most common medications to treat perioral dermatitis are oral tetracycline, pimecrolimus cream, and azelaic gel. However, some of these medications can't be used for prolonged periods, otherwise they will no longer be effective against the disease. For example, the use of pimecrolimus cream for more than four weeks will be ineffective, while the use of azelaic acid gel for more than six weeks will be ineffective. While these two medications previously mentioned decrease in effectiveness after a certain period, oral tetracycline, on the other hand, have been shown to have decreased effectiveness if used prior to twenty days of disease diagnosis.[34]

While there may be other topical medications that can be effective against perioral dermatitis, such as erythromycin emulsion or metronidazole cream, studies have shown that their effectiveness varied among different randomized controlled trials. As a result, these two topical medications, amongst others, may not be the ideal solution for perioral dermatitis.[35]

For more rare cases, cefcapene pivoxil hydrochloride, a beta-lactam antibiotic, has been used in treating perioral dermatitis presumably caused by Fusobacteria. Improvement was visible in 1 to 2 weeks and cured in 2 to 5 weeks.[27] Isotretinoin was used in treating granulomatous perioral dermatitis at a dose of 0.7 mg/kg/day isotretinoin for 20 weeks. However, the patient was also taking a series of combination therapies. Isotretinoin also requires long-term monitoring for potential side effects.[27]

More studies lately show other possible solutions to use for the treatment, one such study shows the use of the TRPV1 inhibitor 4-t butylcyclohexanol. The TPRV receptor activates as a defense against possible pain, like inflammatory reactions, which could lead to the possible development of perioral dermatitis. The study presents that the symptoms of perioral dermatitis in patients take it shows improvement within 8 weeks.[36]

When giving patients their medication, healthcare workers must be aware of the possibility of the perioral dermatitis returning to the patient again, as well as exacerbation. If the perioral dermatitis comes back again, the medication that they took prior may not work the second time around, so the healthcare workers may need to create a secondary treatment plan around the return of the disease.[37]

Prognosis

[edit]

Perioral dermatitis is likely to fully resolve with short courses of antibiotics, but if left untreated, it can persist for years and take on a chronic form.[12]

In some cases, it can be resolved for the patient to stop taking external factors that may contribute to the development of perioral dermatitis.[25]

Improvement with tetracyclines is usually seen after 4 days and significantly so after 2 weeks.[4] In severe cases, longer periods of treatment may be required to achieve cosmetic satisfaction.[7]

Epidemiology

[edit]

Most commonly in females between the ages of 16 and 45 years, perioral dermatitis also occurs equally in all racial and ethnic backgrounds, and includes children as young as three months, and is increasingly reported in males.[18] In children, females are more likely to be affected. It has an incidence of up to 1% in developed countries.[7] While perioral dermatitis is more prevalent amongst young females compared to male, the reason behind why is unclear.[38]

In adults, women are more likely to be affected than men. The most affected age group is those in their twenties or thirties. However, in children, the most affected populations are those before puberty, and boys are more affected than girls.[39]

Amongst the few adult men who find themselves diagnosed with perioral dermatitis, it has been shown in multiple studies that the reason behind it is due to their taking volatile alkyl nitrates, an inhaled product used to relax muscles.[40]

Impacts

[edit]

Many individuals who have perioral dermatitis, amongst other skin issues, have an increased risk of experiencing mental health issues, such as depression, anxiety, and stress.[41] This is particularly more prevalent in adolescents, compared to adults, due to the presence of more social stigmas during one's teen years as opposed to one's adulthood.[42]

Individuals who use topical steroids long past standard treatment plans or chronically may increase the risk of developing other severe diseases, such as severe dermatitis.[43]

See also

[edit]
Wikimedia Commons has media related to Perioral dermatitis.

References

[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Perioral dermatitis

View on Grokipedia
from Grokipedia
Perioral dermatitis was first described in by Frumess and Lewis as "light-sensitive seborrheid," a cyclic affecting the perioral primarily in young women; the condition became known as perioral dermatitis by the 1960s. Perioral dermatitis is a benign, inflammatory characterized by clusters of small red papules, pustules, and occasionally scaly plaques that primarily affect the around the mouth, with possible extension to the nasolabial folds, chin, and periorbital regions. It often resembles acne vulgaris or in appearance but lacks comedones and typically spares the of the lips. The condition is most common in young to middle-aged women, though it can occur in children, adolescents, and men as well. The etiology of perioral dermatitis remains incompletely understood, but it is frequently linked to the prolonged use of topical corticosteroids, particularly fluorinated varieties, which may disrupt the skin barrier and promote microbial overgrowth. Other contributing factors include certain , skincare products containing heavy emollients or preservatives, fluoridated toothpaste, and hormonal influences such as those related to oral contraceptives. In some cases, it manifests as a variant known as periorificial dermatitis when involving areas around the eyes, , or anogenital region, or granulomatous periorificial dermatitis in pediatric populations. Clinically, perioral dermatitis presents with asymptomatic to mildly pruritic or burning lesions, often accompanied by dryness, scaling, or , and it tends to follow a chronic, relapsing course if triggers persist. is primarily clinical, based on history and examination, with rarely needed to rule out differentials like seborrheic dermatitis or . Management focuses on identifying and eliminating provocateurs, followed by treatment with topical agents such as , erythromycin, or , and oral tetracyclines (e.g., or ) for moderate to severe cases, leading to resolution in weeks to months. is generally favorable with adherence to therapy, though recurrences are common without preventive measures like using fragrance-free, non-comedogenic skincare.

Introduction and History

Definition and Classification

Perioral dermatitis is a chronic papulopustular facial eruption primarily affecting the perioral area, characterized by small inflammatory papules, pustules, and scaly erythematous patches. It represents a benign inflammatory that most commonly manifests in young adult females, though it can occur in children and males as well. The eruption typically forms a ring-like pattern around the mouth without involving the lips themselves. Perioral dermatitis is classified as a subtype of rosacea-like dermatoses, and many dermatologists regard it as a variant of given the overlap in clinical presentation and response to therapies such as topical or oral antibiotics. The nomenclature "perioral" specifically denotes involvement around the , whereas "periorificial dermatitis" is used when the condition extends to other facial orifices, such as the nose or eyes. Historical synonyms include light-sensitive seborrheid and rosacea-like , reflecting earlier understandings of its photosensitive and acneiform features. Clinical criteria for identifying perioral dermatitis emphasize the presence of discrete papules and pustules without comedones, along with characteristic sparing of the and . This distinguishes it from acne vulgaris, which features comedones, and from seborrheic dermatitis, which involves greasy scales in seborrheic distribution areas. Although primarily perioral, the condition may briefly extend to perinasal or periocular regions in broader periorificial presentations.

Historical Background

Perioral dermatitis was first described in 1957 by Frumess and Lewis as a "light-sensitive seborrheid," characterized by a cyclic eruption primarily affecting young women in the perioral region. This initial report marked the recognition of the condition as a distinct entity, though it was initially linked to seborrheic dermatitis variants influenced by light exposure. In 1964, Mihan and Ayres coined the term "perioral dermatitis" to more accurately describe the papulopustular eruption around the , emphasizing its independence from seborrhea or . During the , the condition gained prominence due to its frequent association with the widespread use of potent topical corticosteroids on the face, leading to its classification as a variant of steroid-induced or rosacea-like eruption. Incidence peaked in the and as topical steroid prescriptions increased, with reports noting resolution upon discontinuation of these agents. A key milestone in the was the identification of fluoridated toothpaste as a potential trigger, based on case series where switching to non-fluoride formulations led to improvement in affected patients. In the and , research evolved to explore multifactorial etiologies beyond steroids, including microbial involvement such as fusobacteria, demonstrated through histopathological and microbiological analyses of lesional . Studies during this period also began highlighting epidermal barrier dysfunction as a contributing factor, with observations of and impaired integrity in patients. By the , understanding shifted toward a complex interplay of factors, incorporating ; recent metagenomic analyses have revealed distinct bacterial compositions in perioral lesions, such as the prevalence of an uncultured Neisseriales bacterium, compared to healthy . Treatment history in the 2020s has incorporated topical calcineurin inhibitors, such as and , as steroid-sparing alternatives, particularly effective in pediatric cases and showing clearance rates of up to two-thirds with twice-daily application. These developments reflect a broader recognition of the condition's inflammatory and immune-mediated components.

Clinical Features

Signs and Symptoms

Perioral dermatitis typically manifests with primary symptoms including a burning or stinging sensation around the , often accompanied by mild itching. These sensations arise due to in the affected skin and may be exacerbated by common triggers such as topical corticosteroids or fluorinated toothpastes. Secondary symptoms frequently include dryness and flaking of the skin in the perioral area, contributing to discomfort and a rough texture. The characteristic signs consist of clusters of small, 1-2 mm papules and pustules situated on an inflamed base, often with associated scaling. A key feature is the typical sparing of the skin immediately adjacent to the , known as the , which helps distinguish this condition from similar eruptions. In the acute phase, pustules predominate, while the chronic phase may show persistent redness and the development of , leading to a more fixed . Associated features can include occasional involvement of the periocular region, resulting in mild or .

Variants and Locations

Perioral dermatitis classically manifests in the perioral region, involving the nasolabial folds, , and upper area, with a characteristic sparing of the of the lips. The rash may extend to adjacent facial areas, including the , periorbital regions, and nose, though it typically avoids the cheeks. In these classic presentations, small erythematous papules and pustules cluster in these locations, often accompanied by scaling or . Several variants of perioral dermatitis exhibit distinct anatomical distributions or morphological features. The glucocorticoid-induced variant, also known as , arises from prolonged topical use and primarily affects the central face, including perioral and periorbital areas, with rebound flares upon discontinuation. Infantile perioral dermatitis, occurring in children under 2 years, predominantly involves the perioral and perinasal regions but can extend to the periocular area, presenting as a red, bumpy, often itchy rash consisting of small, flesh-colored or erythematous papules and rarely pustules. Common triggers include topical corticosteroids, fluorinated toothpaste, or other irritants; no food or drink is known to cause or worsen perioral dermatitis, including foods such as sweet potatoes. It should be distinguished from a related but distinct condition, perioral contact dermatitis (irritant contact dermatitis), which causes a temporary rash around the mouth from skin contact with acidic foods (e.g., tomatoes, oranges, strawberries). Sweet potato allergies are rare and may cause general hives, itching, or rashes, but not specifically perioral dermatitis or localized food irritation mimicking it. The granulomatous variant features deeper, monomorphic nodules or persistent yellowish-brown papules, most commonly around the , eyes, and , and is frequently observed in prepubertal children of African descent. The periorificial variant broadens the distribution beyond the perioral zone, encompassing periocular dermatitis around the eyes and, less commonly, anogenital involvement in both children and adults, often triggered by distinct local factors such as fluoridated or . Special considerations include the ocular variant, which may present with or alongside periorbital papules, and rare extensions to vulvar or genital areas in adults, manifesting as erythematous papules in periorificial skin folds.

Etiology and Pathophysiology

Etiological Factors

Perioral dermatitis arises from a complex interplay of etiological factors, predominantly involving preventable exogenous triggers that disrupt the delicate perioral skin barrier. The most significant contributor is the prolonged use of topical s on the face, particularly potent fluorinated varieties such as betamethasone valerate, which are implicated in the majority of adult cases. These agents initially suppress inflammation but often lead to a upon withdrawal, exacerbating the eruption with papules and . A strong association exists between prior topical corticosteroid application and disease onset, with discontinuation frequently precipitating initial worsening before improvement. Certain skincare products further promote the condition by irritating the skin or altering its . Heavy emollients, greasy sunscreens, and fluoridated toothpastes are common culprits, as they may occlude pores or introduce irritants directly to the perioral area. Preservatives in , such as those found in anti-aging formulations, can similarly compromise the epidermal barrier, fostering an environment conducive to . Occupational exposure among users heightens risk due to frequent application of such products. Microbial overgrowth plays a contributory role in some instances, though true infections are uncommon. Proliferation of mites in facial follicles has been observed in affected individuals, potentially triggering inflammatory responses in susceptible skin. Similarly, Fusobacterium species from the oral have been detected in a substantial proportion of cases, with studies identifying them in up to 81% of perioral dermatitis lesions via specialized staining techniques. Rare opportunistic infections, such as , may also mimic or exacerbate the condition but are not primary drivers. Additional triggers include hormonal fluctuations, such as those occurring during , and the use of oral contraceptives, which may alter sebum production or immune responses in the skin. Environmental allergens can provoke flares in sensitized individuals, though specific culprits vary. These factors collectively underscore the importance of identifying and eliminating exogenous irritants to prevent onset or recurrence. Importantly, no foods or drinks are known to cause or exacerbate perioral dermatitis, including sweet potatoes or other dietary items. This distinguishes the condition from irritant contact dermatitis (also referred to as perioral contact dermatitis), a separate entity that can be triggered by direct skin contact with acidic or irritating foods such as tomatoes, oranges, or strawberries, particularly in children. Sweet potato allergies are rare and may cause generalized allergic reactions, such as hives or widespread itching, but are not associated with the specific presentation of perioral dermatitis.

Pathophysiological Mechanisms

The pathophysiological mechanisms of perioral dermatitis involve a multifactorial interplay of barrier disruption, dysregulated , microbial imbalances, and vascular alterations, leading to the characteristic papulopustular eruption. A primary driver is barrier dysfunction, particularly in the , often precipitated by topical use, which impairs lipid organization and tight junctions, resulting in elevated (TEWL) and enhanced penetration of irritants and allergens. This barrier impairment renders the hyper-reactive, promoting a cycle of irritation and in the perioral region. The inflammatory response in perioral dermatitis involves activation of the , leading to recruitment of inflammatory cells and of barrier defects. Microbial contributes to chronic inflammation by altering the cutaneous , with studies—as of 2025—showing distinct bacterial compositions in affected skin compared to healthy controls, including overgrowth of potentially pathogenic species like fusobacteria and reduced diversity that favors inflammatory cascades. Fungal elements, such as Candida species, may also play a role in sustaining local irritation, though no overt infection is typically present. Vascular changes manifest as dilation of superficial dermal vessels, contributing to the observed in perioral dermatitis, potentially amplified by neurogenic involving release from sensory nerves, which heightens perioral sensitivity and perpetuates the inflammatory milieu. These mechanisms collectively explain the localized, relapsing nature of the condition, often triggered by external factors like topical agents.

Diagnosis

Clinical Evaluation

The clinical evaluation of perioral dermatitis begins with a detailed history taking to identify potential triggers and the temporal course of the condition. Patients are routinely questioned about prior use of topical corticosteroids on the face, as this is a frequent precipitating factor, often leading to rebound worsening upon discontinuation. Inquiries also cover skincare routines, including the application of heavy , moisturizers, or fluoridated dental products, which may contribute to irritation. The onset of symptoms is typically subacute, with patients reporting initial mild redness progressing to papules and pustules. Physical examination focuses on visual inspection of the affected areas, revealing the hallmark distribution of small erythematous papules and pustules clustered around the mouth, often sparing the of the , with possible extension to the nasolabial folds or eyes. assesses for associated tenderness or burning sensation in the lesions, which may be present in active cases. Adjunctive tests are not routine in typical presentations. Diagnosis relies on the combination of these clinical features—erythematous papulopustules in a perioral distribution without comedones—without the need for laboratory tests in typical presentations. is reserved for atypical or refractory cases, where may demonstrate , follicular , and a perivascular lymphocytic infiltrate, supporting the but showing nonspecific changes. To monitor progression, especially during the initial zero-therapy phase involving discontinuation of all topical agents, serial clinical photography is recommended to document evolution and guide reassurance, as temporary worsening may occur before improvement.

Differential Diagnosis

Perioral dermatitis (POD) must be differentiated from other facial dermatoses that present with papulopustular or erythematous eruptions, as misdiagnosis can lead to inappropriate treatments. Acne vulgaris features open and closed comedones (blackheads and whiteheads) alongside inflammatory papules, pustules, and nodules, whereas POD lacks comedones and typically involves smaller, clustered papulopustules without deeper cystic lesions. is characterized by persistent facial , flushing, telangiectasias, and sometimes phymatous changes or ocular involvement, contrasting with POD's more discrete papulopustular clusters confined to the perioral area without prominent vascular features or episodic flushing. Seborrheic dermatitis manifests with greasy, yellow scales in seborrheic distribution areas such as the nasolabial folds, eyebrows, and , and it often responds to agents, unlike POD which presents with fine, non-greasy papules and mild scaling but does not respond to antifungals. Contact dermatitis, either allergic or irritant, is suggested by a history of exposure to specific allergens or irritants like or topical agents, featuring vesicular, eczematous, or edematous changes rather than the uniform papulopustular morphology of POD. Irritant contact dermatitis can cause temporary perioral rashes from contact with acidic or irritating foods (e.g., tomatoes, citrus fruits, strawberries), particularly in children—this condition is known as perioral irritant contact dermatitis or food-related contact dermatitis and is distinct from perioral dermatitis proper, which is not triggered or exacerbated by any foods or drinks and is primarily associated with topical corticosteroids and other factors such as fluorinated toothpaste. Patch testing can confirm allergen-specific reactions absent in POD. Other conditions to consider include allergic reactions to cosmetics, which may mimic POD through perioral erythema and scaling but are identified via temporal association with product use and resolution upon discontinuation, differing from POD's steroid-exacerbated course. Impetigo presents with honey-crusted erosions from bacterial superinfection, often with regional lymphadenopathy, unlike the sterile papulopustules of POD. Sarcoidosis may appear as granulomatous papules in a periorificial distribution but involves systemic symptoms, biopsy-proven non-caseating granulomas, and lacks the pustular elements seen in POD.

Treatment

Pharmacological Approaches

The primary pharmacological approach for perioral dermatitis involves oral , which exert effects rather than direct antibacterial action, making them first-line for moderate to severe cases. , administered at 40-100 mg daily for 4-12 weeks, is commonly recommended due to its efficacy in reducing papules, pustules, and , with subantimicrobial doses (e.g., 40 mg) minimizing side effects while targeting inflammation. (250-500 mg twice daily) or (50-100 mg daily) serve as alternatives, showing similar response rates in . , taken orally at 200-500 mg daily, is a suitable alternative for patients intolerant to tetracyclines, particularly in milder presentations or during . Topical therapies are preferred for mild or as adjuncts to systemic treatment, applied once or twice daily for 4-12 weeks. 0.75-1% gel or cream effectively reduces inflammatory lesions with fewer systemic risks, supported by randomized trials demonstrating comparable outcomes to oral antibiotics in select cases. Clindamycin lotion or gel and are additional options for mild cases. Erythromycin 2% solution or gel targets similar inflammatory pathways, offering a safe option for children and pregnant individuals. 1% cream, a inhibitor, is used off-label to modulate immune responses, though evidence is limited to smaller studies showing remission in steroid-induced cases; initial use of topical corticosteroids should be strictly avoided to prevent . For cases involving mites or refractory inflammation, adjunctive topical 1% cream addresses potential mite-related triggers, with case reports documenting clearance in persistent perioral dermatitis unresponsive to standard antibiotics. In rare granulomatous variants (affecting less than 5% of patients), low-dose oral (0.3-0.5 mg/kg daily) may be considered under specialist supervision to regulate sebaceous activity and keratinization, though its use is reserved for non-responders due to potential side effects. Recent case reports as of 2024 also support off-label use of topical 1.5% cream for granulomatous perioral dermatitis. Treatment duration typically spans 4-12 weeks, followed by gradual tapering—such as reducing to every other day or switching to topical maintenance—to prevent , as abrupt cessation can lead to rebound flares. Recent updates from the 2020s highlight 15% gel as an alternative for mild cases, leveraging its and properties in open-label studies showing symptom improvement without antibiotics. Efficacy of these agents is enhanced when combined with avoidance of known triggers.

Non-Pharmacological Management

Non-pharmacological management of perioral dermatitis centers on minimizing irritation and supporting skin barrier recovery through lifestyle modifications and simplified skincare practices. A cornerstone approach is zero-therapy, which entails the complete cessation of all topical corticosteroids, , heavy emollients, and other facial products to halt and allow natural resolution of mild cases. This discontinuation often leads to an initial rebound flare, typically resolving within 2-4 weeks as the skin barrier stabilizes without external interference. Following the zero-therapy phase, a minimalist skincare regimen is recommended to maintain hydration without provocation. Gentle, non-foaming cleansers free of fragrances, exfoliants, and preservatives should be used for washing, paired with lightweight, non-comedogenic moisturizers to prevent dryness. Avoidance of fluoridated is advised, as exposure has been linked to around the in susceptible individuals; switching to a fluoride-free alternative can reduce symptom persistence. For barrier repair, emollients containing ceramides may be introduced cautiously if tolerated, promoting skin integrity without additives. Lifestyle adjustments further aid management by addressing potential exacerbators. Patients are encouraged to limit intake of spicy foods, alcohol, and hot beverages, which can induce facial flushing and indirectly worsen in some cases. Incorporating techniques, such as or relaxation exercises, supports overall skin health by mitigating stress-induced flares. Patient education is integral to long-term success, emphasizing recognition and avoidance of personal triggers like specific or environmental factors. Patch testing for contact allergens is recommended if an allergic component is suspected, helping tailor avoidance strategies. Regular follow-up ensures adherence to these measures, significantly reducing recurrence rates through sustained compliance. In severe cases, these non-pharmacological strategies complement pharmacological interventions as outlined in dedicated treatment protocols.

Prognosis and Complications

Disease Course and Recovery

Without intervention, perioral dermatitis typically follows a chronic or relapsing course spanning weeks to years, with persistent or relapsing papules and around the perioral area. With appropriate treatment, such as topical or oral antibiotics, approximately 90% of cases achieve significant resolution within 4 to 8 weeks, though full clearance may take up to 12 weeks in some instances. Relapse is common upon re-exposure to triggers like topical corticosteroids or certain , highlighting the importance of ongoing avoidance measures. Key factors influencing recovery include early diagnosis and intervention, strict adherence to zero-therapy (abstaining from all skincare products and cosmetics for several weeks), and complete avoidance of fluorinated corticosteroids, which can accelerate healing and reduce recurrence risk. Treatment modalities like pharmacological approaches can further expedite recovery, as detailed elsewhere. In the long term, most patients attain full remission without scarring, though post-inflammatory may occur, particularly in darker tones, and typically fades over several months. In some cases, the condition may progress to .

Potential Complications

Prolonged use of topical corticosteroids, often a precipitating factor in perioral dermatitis, can lead to cutaneous , characterized by thinning and fragility of the perioral , increasing susceptibility to further irritation and damage. In severe or untreated cases, particularly the granulomatous variant, scarring may develop, resulting in permanent textural changes around the mouth. Secondary bacterial or fungal infections can also arise in pustular lesions due to disrupted , potentially exacerbating and delaying resolution. In periocular variants of periorificial dermatitis, the condition may extend to the eyelids, leading to chronic or , which can cause persistent ocular discomfort and necessitate specialist . Although rare, untreated extension to adjacent areas heightens the of these inflammatory eye complications. Treatment with oral tetracyclines, a common approach, carries risks of gastrointestinal upset, including and , particularly in prolonged courses. Overuse of these antibiotics may contribute to bacterial resistance, complicating future management of skin infections. Misdiagnosis, such as with acne vulgaris, can delay appropriate care and contribute to emotional distress associated with visible facial lesions. Prompt recognition and treatment typically mitigate these risks, supporting uncomplicated recovery.

Epidemiology and Impacts

Prevalence and Demographics

Perioral dermatitis exhibits an annual incidence of approximately 0.5% to 1% in the general population of industrialized countries, according to older estimates. This rate appears lower in less industrialized regions, likely due to differences in access to and use of topical corticosteroids and . A 2025 population-level study using healthcare data from 2017-2023 reported an overall of 0.336% and annual incidence of 0.158%, with both metrics increasing over the study period. The condition shows a strong association with prior use of topical steroids on the face, which predisposes affected individuals and contributes to higher occurrence in populations with frequent cosmetic applications. Demographically, perioral dermatitis predominantly impacts young women aged 20 to 45 years, representing 80% to 90% of cases. The gender disparity is pronounced in adults, with a female-to-male of about 9:1. In pediatric populations, the infantile or periorificial form is increasingly recognized, with the highest annual incidence observed in children aged 0 to 9 years at approximately 0.145%. distribution in infants is approximately equal. Geographically, the condition is more prevalent in developed countries where cosmetic and use is widespread. There is no strong racial or ethnic predilection, as it occurs across all backgrounds worldwide.

Societal and Psychological Impacts

Perioral dermatitis, characterized by a visible facial rash around the , often leads to significant psychological distress due to its location on a highly exposed area. Patients frequently experience and , which can result in social withdrawal and avoidance of interpersonal interactions. In a study of 543 patients with facial dermatoses including perioral dermatitis, anxiety was reported by 37.6% of participants compared to 14.9% in controls, while depression affected 21.7% versus 6.8% in the control group; these rates were particularly elevated among younger individuals and those in professions emphasizing appearance, such as modeling or public-facing roles. The condition also imposes a societal burden through increased healthcare utilization. Visible symptoms prompt multiple consultations with dermatologists, contributing to the overall workload in dermatology practices, where facial inflammatory conditions like perioral dermatitis account for a notable portion of outpatient visits. The visible nature of the may lead to and , potentially resulting in . This can deter individuals, particularly men who comprise a smaller proportion of diagnosed cases, from seeking timely medical help due to reluctance or . On a positive note, awareness of perioral dermatitis has grown since 2020 through public discussions by media figures and news outlets, which have helped normalize the condition and encouraged access to online support resources for affected individuals.

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