Pathophysiology of Angular Cheilitis
Angular cheilitis develops through a multifactorial process involving moisture-induced maceration of the perioral skin at the mouth corners, creating an ideal environment for opportunistic fungal and bacterial overgrowth, with Candida albicans being the predominant pathogen in immunocompromised and older populations. 1, 2
Primary Infectious Mechanism
The fundamental pathophysiologic process begins with moisture accumulation and maceration at the labial commissures, which disrupts the normal skin barrier and creates favorable conditions for microbial colonization 3, 4. This is particularly pronounced in older adults and immunocompromised individuals due to several converging factors:
- Candida albicans represents the most common fungal pathogen, with 84% of long-term care facility residents colonized with yeast 1
- Staphylococcus aureus frequently co-exists, cultured from lesions in approximately 62% of cases alongside Candida in 70% 4
- The infection represents overgrowth of endogenous resident fungi rather than new pathogen acquisition, particularly associated with antimicrobial and corticosteroid use 1
Predisposing Anatomic and Mechanical Factors
Several mechanical factors create the moisture-rich environment necessary for pathogen proliferation:
- Loss of vertical dimension in edentulous patients or those with ill-fitting dentures causes deepening of the labial commissures, trapping saliva 3, 5
- Chronic drooling or lip-licking behavior maintains persistent moisture 3
- Age-related loss of skin elasticity and facial volume creates deeper folds at mouth corners 5
Nutritional Deficiency Pathways
Nutritional deficiencies compromise epithelial integrity and immune function, creating vulnerability to infection:
- Riboflavin (B2) deficiency is the primary nutritional cause, classically presenting with angular cheilitis, glossitis, photophobia, and corneal vascularization 1
- Iron deficiency impairs epithelial cell turnover and immune function, representing an overlooked predisposing factor particularly relevant in older adults 1
- Pyridoxine (B6) deficiency causes angular stomatitis with seborrheic dermatitis, cheilosis, and glossitis 1
- Folate deficiency produces angular stomatitis, oral ulcers, and glossitis 1
These deficiencies weaken the mucosal barrier, making tissues more susceptible to the infectious component.
Immunologic Vulnerability in Target Populations
In older adults and immunocompromised individuals, several immunologic factors amplify susceptibility:
- Immune senescence impairs both antibody and cellular responses in elderly patients 6
- Depressed antibody production against common pathogens occurs even in early immune dysfunction 6
- Lymphopenia and neutropenia reduce phagocytic capacity and intracellular killing 6
- Systemic conditions such as diabetes mellitus, HIV/AIDS, and hematologic malignancies further compromise local and systemic immunity 7, 5
Clinical Manifestation Pathway
The pathophysiologic cascade produces characteristic clinical features:
- Erythema, fissuring, and crusting develop at the lip corners as the initial inflammatory response 7
- Moist maceration and ulceration progress as moisture persists and infection deepens 3
- Chronic inflammation perpetuates the cycle, as damaged tissue continues to trap moisture and support microbial growth 4
Key Pathophysiologic Distinction
Angular cheilitis differs from other forms of oral candidiasis in that ulceration can be a primary feature due to the mechanical stress and fissuring at the commissures, whereas oral candidiasis typically presents as white plaques or erythematous patches without primary ulceration 2. The angular location subjects tissue to constant movement and tension, promoting fissure formation.