PD is a common, chronic inflammatory, papulopustular/vesicular dermatitis with morphological and histological similarities to rosacea. It was first described in 1957 as a cyclical, light-sensitive seborrhoeid affecting the perioral area in young women (19). The term perioral dermatitis was later introduced by Mihan and Ayres in 1964 after describing the condition in 21 patients (20). PD is associated with symptoms of skin sensitivity including burning and stinging and has a significant impact on patient quality of life (21). Like many patients with skin sensitivity, affected individuals also describe intolerance of sunlight, heat, and wind in addition to various cosmetics that tend to exacerbate their symptoms (22).
It has a spectrum of clinical manifestations lending itself to many synonyms including periorofacial dermatitis, rosacea-like dermatitis, chronic papulopustular facial dermatitis, facial Afro-Caribbean childhood eruption, lupus-like PD, and granulomatous perioral/periorofacial dermatitis.
PD predominantly affects young to middle-aged women who account for approximately 90% of cases (23). It is now however becoming increasingly common in men and can also occur in children and adolescents. In childhood and infancy, it has a slight female predominance and can present as early as 6 months with a peak incidence in those younger than 5 years of age (24).
The morphological features of PD consist of small (1–2 mm) grouped, superficial, erythematous papules, papulovesicles, or papulopustules in a predominantly perioral distribution. This distinctive pattern in the perioral area and nasolabial folds helps distinguish PD from rosacea, which is mainly centrofacial in presentation. The lesions of PD can also affect the periorbital area and lateral portion on the lower eyelids. Papules may be superimposed on thin confluent erythematous plaques resembling a nonspecific dermatitis, and the sparing of vermillion border is a characteristic clinical finding in many patients.
Although the pathogenesis and etiology of PD is still unclear, several factors and causes have been postulated. The overuse of emollients on affected skin areas is thought to be a relevant contributing factor, while topical steroids, although initially improving symptoms, can result in significant rebound after cessation of use. Indeed, systemic and inhaled corticosteroids can also lead to the development of PD (25,26). Infective agents are also thought to play a role in the pathogenesis of PD. Fusiform spirilla bacteria, demodex folliculorum, and candida, for example, have all been cultured from lesions of patients with PD. Whether their presence is causative or consequential of the environment is yet to be established. A hormonal link has also suggested given its temporal association with menses, pregnancy, and the oral contraceptive pill (27).
Histopathologically, the papules of PD have a granulomatous component similar to that of rosacea. Early papules demonstrate an eczematous picture, while later, more chronic lesions reveal diffused hypertrophy of connective tissue and hyperplasia of sebaceous follicles.
Although there is no accepted, standard treatment regime for PD at the time of writing, initial measures should include appropriate skin care advice. As a first step, discontinuation of potential causative and exacerbating agents such as cosmetics, emollients, and topical corticosteroids is advised. Patients are advised to wash their face with warm water only and to use liquid or gel sunscreens if required. Although some authors suggest a watch-and-wait approach, this can be unacceptable for many patients. Topical treatments include antibiotics such as metronidazole, erythromycin, or clindamycin, which have been found to be moderately effective in the treatment of PD (28). Topical calcineurin inhibitors (pimecrolimus, tacrolimus) have also demonstrated efficacy, particularly in the setting of steroid-induced PD. However, caution is advised given the occasional reports of granulomatous eruptions after using these preparations (29,30). More recently, Praziquantel 3% ointment was shown to improve symptoms of PD and quality of life in adult patients treated daily for 4 weeks (31). Systemic treatment includes the use of oral antibiotics for a period of 4–6 weeks. Commonly used agents include oxytetracycline, doxycycline, and erythromycin (particularly in the pediatric population where tetracycline-induced teeth staining is a concern). The option of oral isotretinoin is reserved for patients failing to respond to oral antibiotics. It is prescribed at doses between 0.05 and 0.1 mg/kg, lower than that used in acne vulgaris (31).
Although sharing many clinical features with rosacea including symptoms of skin sensitivity, the natural history of PD thankfully bears less resemblance. Following appropriate treatment and clearance, subsequent relapses are uncommon.
SD is a common, chronic, and recurrent inflammatory skin disease characterized by the presence of thin erythematous scaly plaques and patches with ill-defined borders. It mainly affects sebum-rich areas of the body such as the scalp, face, upper chest, and back and may be associated with symptoms of sensitive skin such as pruritus (32). SD is common, affecting approximately 11% of the general population and up to 70% of infants in the first 3 months of life (33). Among adults, the peak incidence is in the third and fourth decades of life and is often associated with a substantially negative impact on quality of life (34). The severity of SD is highly variable and occurs more frequently in certain medical conditions including Parkinson’s disease, familial amyloidosis, and trisomy 21. Abrupt onset and severe recalcitrant SD may also be the result of underlying human immunodeficiency virus infection where it is the most common dermatoses (occurring in 31% of patients including those on antiretrovirals). It can occur in the setting of immunosuppressant medication (renal transplant patients) and with certain psychotropic medications. Patients also report emotional stress and fatigue as exacerbating factors (35).
The diagnosis of SD is a clinical one characterized by the presence of itchy erythematous patches with greasy scales. Commonly affected sites include the scalp, anterior hairline, eyebrows, glabella region of the forehead, nasolabial folds, ears, central chest (petaloid appearance), and genital region. Scalp involvement typically results in fine scale/dandruff that may be associated with signs of inflammation such as erythema, or indeed, local or generalized scaling may appear in isolation.
Although the exact pathogenesis of SD is not completely understood, it is thought to be dependent upon three factors: sebum, microbial metabolism (specifically, Malassezia yeasts), and individual susceptibility (36–39). There appears to be a strong association with yeast colonization particularly of the genus Malassezia spp (40). This is evidenced by the clinical improvement observed in patients treated with antifungal medication and a reduction in Malassezia spp. seen. Sebum lipid degradation and subsequent production of modified unsaturated short-chain fatty acids by Malassezia spp. means they are more capable of penetrating skin and inducing inflammation. Applications of genetic and proteomic techniques have also resulted in a greater understanding of the mechanisms involved in SD and dandruff. It now appears likely that yeast genes are switched on to produce different irritants or metabolites on both dandruff and SD-affected skin. The Malassezia species, M. globosa and M. restricta, are most commonly associated with these conditions. The production of oleic acid and other inflammatory molecules by these species can induce scaling and immunostimulation as oleic acid is a ligand for aryl hydrocarbon receptors involved in contact sensitization (39).
Several treatment options exist for the management of SD. These include topical antifungals and anti-inflammatories, keratolytics, and tar products.
Topical antifungals, particularly the azoles (ketoconazole), are established and effective treatment for SD (41