Since its description in 1957 by Frumess and Lewis as a “light-sensitive seborrheid,” perioral dermatitis (PD) has continued to be a perplexing entity. (1) Many causes have been postulated, including sunlight sensitivity, birth control pills, emotional stress, fluorinated steroid creams, Candida albicans, and rosacea. We have gathered clinical and historical data implicating fluoride dentrifices as an important etiologic factor in this dermatosis. The following two cases support this observation.
Report of Cases: CASE 1. A 63-year-old woman developed PD in mid-1971 that persisted for 24 months. There were exacerbations and remissions even though she was initially treated for one month with 0.025% fluocinolone acetonide cream and then intermittently with a mixture of 1% hydrocortisone, coal tar, and diiodohydroxyquin (Cor-Tar-Quin) and 250 mg of tetracycline hydrochloride four times a day. In August 1973, it was ascertained that she had been using a fluoride dentrifice for as long as her PD had been present. She was instructed to substitute a nonfluorinated tooth polish and to continue using hydrocortisone-coal tar-diiodohydroxyquin cream. Within two weeks she was free of dermatitis. Three months later, whe resumed use of the fluoride dentrifice and within a few days developed a recurrence of the PD that cleared within one week resuming use of a nonfluoride dentrifice. She has remained free of lesions for 16 months without treatment except avoidance of fluoride toothpaste.
CASE 2 – A 20-year-old woman developed PD in July 1974. She was seen in October 1974, and it was noted that she had been using a fluoride dentrifice for “several years.” A nonfluoride dentrifice was substited, and she began therapy with 1% hydrocortisone acetate cream. Within one week the dermatitis cleared, and she remained free of dermatitis until April 1975, when she resumed use of a fluoride toothpaste. Within three days she developed a recurrence of the PD that again cleared in five and six days after resuming use of her nonfluoride dentrifice. She remained free of dermatitis until the present time with no other therapy.
Comment. – Dr. Saunders believes that he has found a cause-and-effect relationship between the use of fluoride dentrifices and “adult female acne” around the corners of the mouth. (2) For the past eighteen months, we have been conducting a clinical study with the assumption that in some patients, fluoride dentrifices cause or aggravate perioral dermatitis. The clinical and historical evidence gathered has been impressive in support of this hypothesis.
The application of fluorides for the prevention of dental caries began around 1942, (3) and by 1949 public health agencies offered treatment with 2% sodium fluoride to school-aged children throughout the United States. Beginning in the early 1950s, dentists routinely recommended treatment with 8% stannous fluoride. A commercial toothpaste containing 0.4% stannous fluoride was generally available in the United States around 1956 to 1957. In 1967, the German literature contained a reference to PD as a “new entity”, (4) and Hjorth et al noted this entity for several years prior to publication of their observations in Denmark in 1968. (5) We think this delayed recognition of PD in Europe may have been due to later marketing of fluoride-containing dentrifices outside the United States.
Stone and Willis (6,7) have shown that sodium fluoride and stannous fluoride in concentrations equal to those found in dentrifices are pro-inflammatory when applied in patch-test form to previously damaged skin, while patch testing over nontraumatized areas produced no inflammation. (7) Our hypothesis is that patients with PD have a receding minimal or preclinical perioral inflammation with mild dermal edema. We postulate that this inflammation is multifactorial and might include hand to mouth activity, subtle female premenstrual tissue edema, minimal acne, rosacea, seborrheic dermatitis, ultraviolet light exposure, or other mild inflammatory stimuli. In this setting, we feel fluoride dentrifices may act topically as a pro-inflammatory agent potentiating and perpetuating a chronic perioral inflammatory dermatosis.
We have initiated a double-blind, cross-over study in which we will use identical toothpastes except that one will contain stannous fluoride. In spite of the clinical impressions and other historical inferences, we think it prudent to refrain from drawing absolute conclusions until out study is complete.
MAJ J. RAMSEY MELLETTE, MC USA
LTC JOHN L. AELING, MC USA
COL DONALD D. NUSS, MC USA
The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the Department of the Army or the Department of Defense.
(1) Frumess GM, Lewis HM: Light-sensitive seborrheid. Arch Dermatol 75: 245-248, 1957.
(2) Saunders MA Jr: Fluoride toothpastes: A cause of acne-like eruptions. Arch Dermatol 111: 793, 1975.
(3) Bernier JL, Muhler JC: Fluoride Therapy: Improving Dental Practice Through Preventive Measures. St Louis, CV Mosby Co, 1970.
(4) Leeming JAL: Current news in dermatology (the school letter). Cutis 6:915, 1970.
(5) Hjorth N, Osmundsen P, Rook AJ, et al: Perioral dermatitis. Br J Dermatol 80:307-313, 1968.
(6) Stone OJ, Willis CJ: Enhancement of inflammation by fluoride. Texas Rep Biol Med 25:601-606, 1967.
(7) Stone OJ, Willis CJ: The effect of stannous fluoride and stannous chloride on inflammation. Toxicol Appl Pharmacol 13:322-338, 1968.