Atopic cheilitis is a variant of atopic dermatitis. As in atopic dermatitis elsewhere on the body, atopic cheilitis occurs in association with a personal or family history of atopy. It is exacerbated by frequent wet/dry cycles, lip licking and lip biting, and exposure to allergens or irritants, lip cosmetics, as well as some systemic medications, such as isotretinoin (commonly known as Accutane), that cause dryness.

Angular cheilitis (AC), also known as perlèche (from the French “to lick”), is an inflammatory condition that occurs at the corners of the mouth. It is most often seen in elderly people who have diabetes.

AC appears in seniors, when atrophy of the perioral muscles of facial expression causes a pocketing at the corners of the mouth, resulting in an overhang of the upper lip over the lower lip, resulting in a moist deep furrow at the angles of the mouth. Other contributing factors, such as poor-fitting dentures, malocclusion, lack of teeth, and bone resorption, may lead to drooling or vertical shortening of the face, thus accentuating the melolabial crease.

Coexistent atopic cheilitis, lip licking in children, mouth breathing, and the presence of orthodontic devices are also risk factors. Vitamin and iron deficiency are often blamed, but rarely proven as a cause of AC.

Perioral dermatitis also known as periorificial dermatitis is a rosacea-like eruption seen primarily in young women between the ages of 15 and 40 and in young children (see also Eyelids and Periorbital Area and Nose and Paranasal Area). As with rosacea, the etiology of perioral dermatitis is unknown.

Tooth whiteners and fluoridated toothpaste have occasionally been implicated, but without any consistent evidence. It is accepted, however, that the frequent application of high-potency, and less commonly, low-potency topical corticosteroids, or inhaled corticosteroids can cause a topical steroid-induced rosacea/periorificial dermatitis-like eruption in some individuals.

Herpes simplex virus infection of the lips and perioral area is caused most often by herpes simplex virus-1 (HSV-1). HSV-1 is mainly associated with oral-facial infections (“cold sores” or “fever blisters”); less often, HSV-2 may be the cause. Neonatal herpes simplex occurs when newborns are exposed to HSV-2 via the birth canal of an actively infected mother who has an HSV-1 or, more commonly, HSV-2 infection, during a vaginal delivery.

Primary HSV infections (see also Oral Cavity) are acquired in infancy and early childhood (Fig. 8-6) and most are subclinical; however, when HSV is symptomatic, the most common clinical presentation in infants and children occurs in the oropharyngeal epithelium where it can be quite severe (see Fig. 9-5).

The virus is highly contagious and is spread by direct contact with the skin or mucous membranes. It invades and replicates in neurons as well as in epidermal and dermal cells. Virions travel from the initial site of infection on the skin or mucosa to the sensory dorsal root ganglion where the virus becomes incorporated into the genetic material of the cells and remains latent until it becomes reactivated.