Understanding and Fixing Perioral Dermatitis

 We are nearing the 60th anniversary of the term “Perioral dermatitis,” first appearing in a 1964 publication by Mihan and Ayers. Unfortunately, it swept together all the previous banal versions of eczematous facial disorders and mixed them with the new virulent steroid-induced rosacea-like facial dermatitis before we understood the difference. There have been at least two epidemics of steroid-induced perioral dermatitis after mid-potency corticosteroids were marketed for treating facial dermatitis. These truly were a lower face dermatitis “on steroids.”  

A Brief History of Perioral Dermatitis

The first epidemic was 1962-1972, and dermatologists were at first mystified and confused by a new type of “rosacea-like” lower face dermatitis that was quite resistant to treatment. This epidemic began slowly with heavy reliance on the new 1% hydrocortisone creams, but dermatologists were able to manage it somewhat. In retrospect, Dermatology literature from these times suggests that approximately 10% of people using 1% hydrocortisone on the face were developing an early version of TSW, topical steroid withdrawal. Most of these susceptible people very likely were prone to Rosacea-related conditions. 

The epidemic became severe after 1964, with the invention and introduction of hydrocortisone valerate and fluorinated topical steroids like triamcinolone. But at the time, it made no sense to physicians that corticosteroids would cause inflammation, and most dermatologists did not believe the steroids caused the first epidemic.

The second epidemic was in the early 1990s when 0.1% mometasone furoate was promoted as “effective for facial seborrheic dermatitis.” Unfortunately, physicians understood very little about the first epidemic and then trusted the marketing that mometasone was safely used on the face for a chronic condition. These two large-scale events contributed to many dermatologists developing an aversion to treating facial problems like seborrheic dermatitis and atopic dermatitis with even low potency topical steroids. As a result, some teaching institutions were teaching: “Never use steroids on the face.” Some of this, we would learn, was related to “mixed fears from mixed discussions” about perioral dermatitis and topical corticosteroids.

By the late 1970s, physicians at Mayo Clinic thoroughly understood how to prevent, treat, and avoid TSW and continued to use low potency topical steroids on the face for chronic recurring dermatitis. Thoroughly understanding the complex subject of Perioral dermatitis turned out to be one of the great detective stories in Dermatology.

Dermatologists Agree On Perioral Dermatitis Cause

Most dermatologists don’t remember that the etiology, the cause of the virulent new version of perioral dermatitis, was a raging controversy during the 1960s and 1970s. During the 1960s, most dermatologists did not believe the steroids caused it. They were consistently misled by patients who insisted their facial rash problems were present “before” they used the topical steroid. Often times the patient and the physician would blame a recently used new product for the worsening of their condition. It was not until the late 1970s that all dermatologists agreed that hydrocortisone valerate and potent fluorinated steroids had triggered the epidemic of virulent perioral dermatitis. 

Reviewing the dermatologic literature from 1964-to 1979 is extremely helpful in understanding the original confusion and mixed messages among Dermatologists about Perioral dermatitis. It’s also important to understand that the earliest versions were milder. By using old skills, the dermatologists of the late 1950s were able to mitigate and treat many cases that occurred during the early years of using plain hydrocortisone. They used combinations of gentle compresses and compounds of sulfur or ichthyol in bland creams. Patients also did well when the topical steroid was less than 1% hydrocortisone from 1958-to 1962. However, after introducing hydrocortisone valerate and fluorinated steroids, the resulting perioral dermatitis was more virulent and very resistant to these treatments. While dermatologists were confused by patients who swore their facial problems pre-dated using the topical steroids, it was the dramatic and sudden worsening of Rosacea patients using fluorinated steroids that became a crucial clue.

British Dermatological Advances In Perioral Dermatitis

A leading British dermatologist Daryl S. Wilkinson, in a 1979 review of Perioral dermatitis appearing in the British Journal of Dermatology, pointed out that:

“the usual prior treatments for perioral and para-nasal eczematous and papulopustular eruptions (sulfur, ichthyol, and bland creams) failed dramatically in the treatment of the new version of perioral dermatitis. In fact, this new type of perioral dermatitis was extremely intolerant to these previous therapies.” 

He confirmed that before introducing topical hydrocortisone in the late 1950s, dermatologists successfully treated facial eczematous rashes with gentle compresses and bland creams containing ichthyol or sulfur (ancient Egyptian treatments). 

Dermatologists were so good at treating banal facial eczematous eruptions that the term Perioral dermatitis did not appear in our literature until 1964, when Mihan and Ayers gave the disease its present name. Unfortunately, dermatologists in their discussions of the 1960s did not take care to continue to distinguish between banal non-steroid induced versions of perioral dermatitis and steroid-induced perioral dermatitis. Many discussions on the topic failed to include that there had always been versions of perioral dermatitis that were spontaneous and unrelated to topical steroids. These conditions often re-emerged after the TSW had run its course after weeks or months off the steroids. This led to much confusion that persists to this day.  

German dermatologist Gerhard Weber first began to publish in 1972 that it was the steroids causing the condition that was eventually called TSW. Back then, it was called things like steroid rosacea, steroid addiction, steroid acne, and rebound phenomenon.

Fortunately, the antibiotic Tetracycline became available to dermatologists by the 1960s. It was not long before they discovered Tetracycline was helpful for both Rosacea patients and for patients with severe perioral dermatitis. We now understand that antibiotics like Tetracycline can reduce inflammation and correct immune dysregulation at the heart of these problems.

Dr. Wilkinson made several trips to visit his friends in the Mayo Department of Dermatology. Since this observation from Dr. Wilkinson in 1979, he made it clear it was beneficial to lump together all spontaneous versions and assert there are two kinds of Perioral dermatitis. One type is caused by prolonged use of topical steroids on the face, and the other type occurs spontaneously in children, teens, and adults and has existed since the ancient Egyptians began treating skin problems. The latter type has always been around, and it often was the reason the topical steroids were used and subsequently caused the steroid-induced version of perioral dermatitis. 

The spontaneous type was often mild eczematous inflammation associated with early onset of teenage acne, barrier problems, atopic dermatitis, seborrheic dermatitis, irritant dermatitis from saliva or kinds of toothpaste, early Rosacea, lower face acne in adult women, irritation from physical touching (hand, telephone, chin strap), and other versions of contact dermatitis. Wilkinson described many of these as paranasal dermatitis and perioral eczematous eruptions in women. When hydrocortisone became available, treating these spontaneous conditions was much easier than the compounding needed for the older bland creams, ichthyol, and sulfur. With the new invention, topical steroids, physicians attempted to treat all of these spontaneous eczematous versions of facial rash.

The Poor Understanding of Perioral Dermatitis

Throughout the 1960s and 70s, mixing these two historically distinct types of perioral dermatitis in a discussion contributed to poor understanding both then and now. Most patients insisted they had the perioral problem ‘before’ the topical steroid was initiated. Back then, there was no mechanism to explain how a topical steroid causes inflammation, acneiform lesions, and rebound phenomenon. Experiencing the rebound phenomenon, patients would often blame whatever product had been recently added as the cause of their problems.

By 1972 dermatologist Gerhard Weber declared in a publication that it was the topical steroids causing the epidemic of perioral dermatitis in Germany. But it was not until the late 1970s that most dermatologists agreed that topical steroids were the primary cause. The epidemic began to subside when most physicians understood that the fluorinated steroid must be withdrawn, and the patient treated with oral Tetracycline (circa 1969-1972.)

Steroid Rebound Phenomenon and Perioral Dermatitis

Author Ian Sneddon presciently commented in 1976, “this does not seem to be purely an anti-microbial effect.” Several authors recommended either topical 1% hydrocortisone or 0.1% hydrocortisone butyrate used with oral Tetracycline immediately after discontinuing the potent fluorinated steroid. This was done to mitigate the severity of the rebound phenomenon. The mild steroid was tapered off after a few weeks and the Tetracycline continued for six to eight weeks minimum. It was also reported that many patients improved by simply switching them from fluorinated steroids to either 1% hydrocortisone or to 0.1% hydrocortisone butyrate (Locoid® cream). 

Some patients were able to clear the vicious cycle and get back into immunologic balance without the use of oral Tetracycline. From 1979 forward, many dermatologists used nonmonograph (less than 2%) sulfur with hydrocortisone acetate to successfully treat chronic facial conditions like Rosacea and seborrheic dermatitis without inducing perioral dermatitis or worsening Rosacea. There were also products with 2%-5% sulfur that could be added for Rosacea patients. When oral antibiotics were employed, these could significantly reduce the resolution time of both types of perioral dermatitis (spontaneous type and steroid-induced type).

Dermatologists also used these topical strategies to treat the spontaneous banal forms of perioral dermatitis. When irritant dermatitis occurred from acne medications like retinoids, these strategies were beneficial and safely avoided the TSW syndrome. 

When acne first develops in children, teens, and adult females, there can be a mildly eczematous, inflammatory component. Often these “sensitive” new acne patients have barrier problems or a background of seborrhea, atopy, or Rosacea. These patients are at high risk of irritations from acne medications and perioral dermatitis from steroids. They must not be treated with fluorinated steroids, or they will very quickly evolve from banal spontaneous perioral dermatitis to perioral steroid dermatitis. Mixing the two types of perioral dermatitis in discussions has long contributed to confusion regarding treating these conditions.

Perioral Dermatitis: Modern-Day Solutions

Multi-factorial spontaneous perioral dermatitis and steroid perioral dermatitis is frequently seen in the same patient, but they should always be separated in discussions. Most dermatologists understand this and have the tools to sort out the pre-existing spontaneous conditions. A proper diagnosis and regular follow-up supervision are essential. Patients can develop new sensitivities and triggers for contact dermatitis with aging. Discussions with a more precise separation of these two historically distinct clinical entities serve to place fears about steroids in perspective and better help our patients.

Long-Term Perioral Dermatitis Management

SmartLotion, our eczema cream, when used as directed, can be used daily for years to manage perioral dermatitis. So if you’re worried about topical steroid withdrawal (TSW) or the 0.75% hydrocortisone effect on your perioral dermatitis, this PubMed long-term safety study should lay your fears to rest.

Steven Harlan MD

Board Certified Dermatologist

Inventor of SmartLotion®

Further Reading On Perioral Dermatitis

Note from the editor

Our blog is full of helpful advice regarding eczema and how to best deal with flare-ups. You can also check out our skincare guide for further skincare information.

Dr. Harlan curated the below reading list (references). It’s an excellent place to start if you want to dig deeper into perioral dermatitis.

Harlan, S.L. (2008) Steroid Acne and Rebound Phenomenon. J Drugs Dermatol. June, Vol. 7, Issue 6, 547-550.

Wilkinson, D.S. et al. (1979) Perioral dermatitis: a 12-year review. Br. J. Derm. 101, 245-257.

Mihan, R. and Ayres, S.Jr. (1964) Perioral Dermatitis. Arch Derm., 89,803.

Weber, G. (1976) Perioral Dermatitis, an Important Side-Effect of Corticosteroids. Dermatologica 152 (Suppl. 1) 161-172.

Weber, G. (1972) Rosacea-like Dermatitis: Contraindications or Intolerance Reaction to Strong Steroids. Br. J. Derm., 86,253.

Gupta AK, Nicol K. (2004) The use of sulfur in dermatology. J Drugs Dermatol. JulAug; 3(4):427-31.

Lin AN, Reimer RJ, Carter DM. Sulfur revisited.(1988) J Am Acad Dermatol 18(3): 553-8.

Ellis,C.N., Stawiski,M.A. (1982) The Treatment of Perioral Dermatitis, Acne Rosacea, and Seborrheic Dermatitis. Med Clin of N America July 68(4): 819-30.

Macdonald, A., Feiwel, M. (1972) Perioral Dermatitis: Aetiology and Treatment With Tetracycline. Br. J. Derm. 87,315-319.

Sneddon, I.B. (1976) The Treatment of Steroid-Induced Rosacea and Perioral Dermatitis. Dermatologica 152(Suppl. 1) 231-237.

Guin, J. (1981) Complications of topical hydrocortisone. J Amer Acad Dermatol 4(4),417-422.

Brogden, R.N., Pinder,R.M. (1976) Hydrocortisone 17- Butyrate: A New Topical Corticosteroid Preliminary Report. Drugs 12, 249-257