The etiologies of cheilitis are numerous and varied. Each gives a rather special clinical aspect. They also determine the prognosis and management. They will be detailed below.
The mechanism depends on the cause of cheilitis.
The cold and wind are two factors that frequently cause drying and desquamation of the lips, which is followed by cracking. Transverse fissures appear secondarily that can become chronic, especially in the midline of the lower lip. Persistent lip-licking often aggravates these lesions, and sometimes by a bacterial or fungal secondary infection.
Chronic Actinic Cheilitis
Chronic actinic cheilitis is secondary to prolonged exposure, for years, to ultraviolet (UV) rays, often related to the professional context (agriculture, marine, outdoor work, altitude). More often it affects men in their 50s with clear skin. It predominately affects the lower lip. It can be desquamative, atrophic, sometimes leucokeratotic, even crustal, fissured, or erosive. The lesions can be unifocal, multifocal, or reach the entire vermilion. The limits between the vermilion and the skin are not clear. The photo-exposed skin may also be the site of actinic elastosis or actinic keratoses. Chronic actinic cheilitis has been classified by the World Health Organizations (WHO) as a "potentially malignant condition." UV light causes damage to DNA, causing mild to moderate dysplasia, which can progress to squamous cell carcinoma. One or more biopsies are recommended for dysplasia or carcinoma, even in the absence of clinical signs of malignancy. The carcinomatous transformation is systematically evoked in cases of induration, infiltration or ulceration of chronic actinic cheilitis, and needs to be investigated with multiple biopsies.
Acute Actinic Cheilitis
It is related to intense exposure to UV radiation. It primarily affects the lower lip, which is more exposed to ultraviolet (UV) than the upper lip. It is a painful condition with erythema and edema, and possibly even vesicles and bullae followed by erosions and crusting. Skin conditions involving increased photosensitivity (photosensitivity in lupus, drug-induced photosensitivity, in particular, due to voriconazole) are predisposing factors.
Differential diagnoses are herpetic recurrence disease, photodermatosis (lupus), photosensitization induced by topical or systemic drugs.
Allergic cheilitis is secondary to contact with an allergenic substance related to a delayed hypersensitivity reaction. It can be acute or chronic. In acute cases, it produces erythema, edema, and vesicles, followed by crusting and pruritus. The lesions are poorly delineated, crossing over to the cutaneous side of the lips and sometimes further. Chronic allergic cheilitis is dry, erythematous and squamous, and there may even be fissures; there may be moderate pruritus or none at all. Allergens are multiple, that is why the diagnosis is difficult.
Anamnesis must be precise and detailed to look for any causative agent in contact with the oral mucosae; patch testing can confirm the diagnosis of delayed hypersensitivity in some cases.
There are numerous clinical manifestations of traumatic cheilitis depending on the origin.
Caustic cheilitis is an acute irritation of the lips, or even a burn, secondary to the topical application of a chemical product. Clinically, there is painful inflammatory edema which may progress to bullous or phlyctenular, then erosive and crusty lesions. Lesions are limited to the contact area. In severe cases, lesions may be necrotic and ulcerated depending on the product causing it.
Atopic patient (adult or child) may have erythematous and squamous cheilitis with fissures of both lips and commissures associated with lichenification, or even radial peri-buccal fissures. Pruritus is common. It can occur alongside a flare-up of the skin disease or separately.
Erythema multiforme (EM) and Stevens-Johnson syndrome (SJS) are mucocutaneous and systemic manifestations side effects of an immuno-allergic reaction to an infectious agent (EM) or drug (SJS). Oral involvement is very evocative. It presents as erosive and crusty cheilitis associated with diffuse erosive stomatitis.
Retinoid treatments (isotretinoin, acitretin, alitretinoin) may cause erythematous and squamous cheilitis that is dry and erosive with fissures. It correlates with a daily dose of treatment.
Viral cheilitis: It is mainly due to the herpes simplex virus, especially type 1. The primary herpes infection (herpetic gingivostomatitis) combines post-vesicular erosive and crusted cheilitis with diffuse stomatitis leading to dysphagia, perioral vesicles, fever and cervical lymphadenopathy. Recurrence of oral herpes affects the lips in most cases. It manifests as a cluster of vesicles accompanied by a burning sensation. Next, the vesicles erode to leave behind crusted erosions that resolve in a week.
Bacterial Cheilitis: The most common cause of bacterial cheilitis is infection with group A Streptococcus or Staphylococcus
Mycotic cheilitis: Cheilitis caused by candida manifests with erythema and painful edema of the lips, sometimes with fissures, and it is usually accompanied by acute (pseudo-membranous candidiasis) or chronic stomatitis, and/or angular cheilitis. The diagnosis is confirmed by taking a specimen for mycological examination.
Parasitic cheilitis: Leishmaniasis is a possible cause of cheilitis in endemic regions. It gives the appearance of a chronic plaque ulcero-crustose, lipoid and painless, occupying part or the entire lip.
It is a chronic inflammation with tumefaction and sometimes suppuration of salivary glands at the lower lip and heterotopic salivary glands at the vermilion zone. The most cases are reported in adults between 50 and 70 years of age. The etiology is unknown, but it probably involves multifactorial causes associating irritation, mechanical, climate, and genetic factors. The most common clinical form is the simple cheilitis glandularis, which manifests as a moderate thickening of the lower lip with inflammatory dilated gland duct orifices, and pressure here will elicit a droplet of saliva.
This is labial edema affecting one or both lips that is intermittent at first, then permanent. The diagnosis is made following a biopsy that will demonstrate granulomas without necrosis, and with a lymphocytic infiltrate. Cheilitis granulomatosa can be isolated, idiopathic (Miescher cheilitis granulomatosa) or associated with various systemic conditions (sarcoidosis, Crohn’s disease, tuberculosis). The complete form of Melkersson Rosenthal syndrome combines cheilitis granulomatosa, peripheral facial paralysis, and a fissured tongue.
Nutritional Deficiency Cheilitis
Several nutritional deficiencies such as avitaminosis B2, B9, B12, scurvy (vitamin C), iron deficiency, or zinc deficiency may cause exfoliative cheilitis associated with other oral manifestations (stomatitis, erythematous glossitis). In pellagra (vitamin PP deficiency), vermilion is shiny and cracked, sometimes eroded. The diagnosis is made through biological assays.
Other Inflammatory Causes of Cheilitis
Lupus: All types of lupus can entail cheilitis.
Lichen: Keratotic lichen planus of the lips produces painless leukokeratosis. Erosive lichen planus triggers painful and widespread ulceration of the buccal mucosa and the lips.
Bullous Autoimmune: Pemphigus, in particular, can entail erosive and crusted cheilitis. Biopsy and immunofluorescence confirm the diagnosis. The cheilitis will resolve with treatment of the skin disease.
The diagnosis of most cheilitis is based on clinical signs and a careful anamnesis. A biopsy is required in cheilitis granulomatosa to confirm the diagnosis. Once the diagnosis of granulomatous cheilitis is made, a thorough etiological assessment is necessary. A biopsy is also important in chronic actinic cheilitis if there is suspicion of malignant transformation. Finally, in case of allergic cheilitis, an allergy survey is required. It includes a careful history and appropriate allergy tests.
The therapeutic management of cheilitis is symptomatic and etiological:
Because of the many causes of cheilitis, the management is best done with a multidisciplinary team. The key is to make the diagnosis and the cause. For patients with chronic actinic cheilitis, referral to a plastic surgeon, dermatologist and oncologist is recommended as the treatment may vary from surgery, topical chemotherapy, laser or photodynamic therapy. Acute cheilitis can be managed by the primary care provider or nurse practitioner by offering the patient emollients. Patients with allergic cheilitis may require topical steroids and infectious causes may require antibiotics. The prognosis for patients with cheilitis depends on the cause; however, recurrence is common. In chronic cases, the quality of life is poor. (Level V)
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