Oral candidiasis (or candidal stomatitis, oropharyngeal candidiasis, and moniliasis) is the specific oral mycosis caused by yeast-like fungi of the Candida genus.
More than 50% of disease cases are related to commonly spread fungi Candida albicans; other causative species for candidiasis in descending rate are C. tropicalis, C. glabrata, C. parapsilosis, or C. krusei.
C. albicans pertain to normal representatives of oral microflora, where they can be found in modest amounts. However, in some specified conditions these fungal members exert serious opportunistic infections rendering local or severe systemic disease.
C. albicans are dimorphic fungi. In the mouth, they are often present as yeast forms or blastospores with questionable virulence whereas mold-like fungal hyphal forms are capable of invading host tissues.
The transition between these two phases largely depends on changes in environmental conditions.
In addition, candidae create pseudohyphae – long filaments composed of oval fungal cells that are closely attached to their poles. It occurs due to the incomplete separation of cells after division.
Overall, all the details of the transformation of oral saprophytic candida into aggressive fungal pathogens are not yet clear completely.
It is considered that candidal strains with enhanced capacity to adhesion and colonization are generally more pathogenic. In particular, the strains with high expression of certain adhesins (e.g., hyphal wall protein 1 or extracellular mannoprotein) are referred to as more active pathogens.
Similarly, pathogenic fungi produce large amounts of hydrolytic enzymes such as proteases, phospholipase, and hyaluronidase.
Oral candidiasis is regarded as the most frequent opportunistic infection of the oral cavity that affects humans. Likewise, it is the most typical form of candidal infection and the most common form of oral mycosis.
Candidiasis affects newborns and infants, but most of all – immunocompromised persons, namely patients with HIV infection and acquired immunodeficiency syndrome (AIDS); patients with cancer under cytostatic chemotherapy; patients, treated with antibiotics of a broad spectrum of action with deep oral or intestinal dysbiosis.
Primary carriage of C. albicans predisposes to its further opportunistic infection. Candidal infection is divided into acute and chronic, primary and secondary.
Primary oral candidiasis originates from resident fungi and affects the oral cavity and perioral area. By contrast, secondary disease emerges after the spread of disseminated candidal infection that occupies the mouth and other body compartments.
Nevertheless, dissemination of oral candidiasis to other body sites (or invasive infection) is generally seldom a situation. It happens predominantly in immunocompromised patients.
There are 3 main forms of oral candidiasis:
Pseudomembranous candidiasis, or thrush, demonstrates white pseudomembranous spots upon oral mucosa that contain epithelial and fungal cells mixed with fibrin and cellular decay. The covering film is easily removed showing the red mucosal bottom. These lesions usually affect the tongue, palate, and buccal epithelium.
Chronic pseudomembranous candidiasis arises mainly in immunocompromised persons, e.g., HIV patients.
Erythematous form of the disease exposes typical smooth and reddened lesions, which are located mainly upon the tongue dorsum or palate.
The lesions are usually painful. Substantial loss of lingual papillae (or depapillation) is common here.
In most cases, this fungal infection is the result of long-term antibiotic treatment or corticosteroid therapy. That’s why it is often named “antibiotic-induced stomatitis” or “antibiotic sore mouth”.
Erythematous illness covers up to 60% of total oral candidiasis if taken with related clinical forms such as angular stomatitis and denture-related stomatitis. The latter is associated with chronic erythematous candidiasis.
Hyperplastic candidiasis is a seldom form of the disease with an incidence of about 5%.
Candida-associated lesions are the oral injuries caused by candida fungi in association with other pathogenic microorganisms. Two basic forms are known – angular cheilitis and denture-related stomatitis.
Angular cheilitis is the infection-based inflammation at mouth angles. About 20% of the disease is caused solely by candidal species, whereas 60% originate from the association of C. albicans and S. aureus.
This pathology renders angular soreness and erythematous inflammation that may result in angular fissuring. The syndrome affects elderly adults and often accompanies denture-related stomatitis
Denture related stomatitis is a low or moderate inflammatory complication that affects edentulous elderly adults wearing oral appliances (dentures).
It is generally ascertained that more than 50-60% of denture-wearing individuals exhibit denture-related stomatitis.
Dominating causative agents in this pathology are candida fungi (above 90% of the total number of cases). Thus the disease is commonly termed “Candida-associated denture-induced stomatitis” or CADIS.
The mucosal surface under dentures demonstrates the highest grades of fungal colonization in comparison with normal unaffected mucosa.
It creates acidic, moist, and relatively anaerobic surrounding that promotes further candidal growth. In addition, poor adjustment of oral prostheses causes micro-injuries of gingival mucosa.
Candidae easily attaches to the surface of damaged tissues and the polymeric surface of dentures with their multiple pits and fissures.
Microbial adherence and colonization stimulate local inflammation. This leads to continuous irritation of oral mucosa resulting in erythematous lesions.
Chronic denture-related stomatitis creates the stable reservoir for the candidal infection that in worsened conditions may expand to other areas of the oral cavity.
Diagnosis of oral candidiasis grounds
Specimens are taken from lesion sites by oral smears, swabs, or rinsing.
Microbial smears are examined by Gram stain demonstrating gram-positive candidal cells with pseudohyphae.
A fungal culture is made on the Sabouraud medium.
Oral rinse examinations help to discriminate between “normal” candidal carriage and oral candidiasis. About 7,000-7,500 colony-forming units of candidae per 1 ml of oral rinse can be found in a disease condition.
Treatment of oral candidiasis
Treatment of oral candidiasis presumes administration of topical anti-fungal drugs, such as miconazole, nystatin, levorin, or amphotericin B.
Severely immunocompromised patients, e.g., with candidiasis in AIDS, need systemic anti-fungal therapy with oral or intravenous drugs (amphotericin B, azoles, or others).
Proper oral hygiene strongly reduces candidal propagation in the oral cavity. It presumes adequate toothbrushing, smoking cessation, oral rinsing after inhalation steroid use, and regular denture disinfection with denture cleaner preparations (e.g., chlorhexidine or sodium hypochlorite).
General Characteristics of Viral Infections, Affecting Oral Cavity
Viral lesions are considered among the most common in current dental practice.
Numerous viral infections cause specific alterations within the oral cavity.
In severe influenza courses, hyperemia and cyanosis of the oral mucosa are typical. Infectious mononucleosis is followed by tonsillitis with multiple petechial rashes that covers oral mucosa.
Oropharyngeal lesions are common in parainfluenza infection, in rubella, rhinoviral and adenoviral diseases.
Manifestations in viral hemorrhagic fevers comprise severe hemorrhagic rash, cheilitis, angular stomatitis, catarrhal gingivitis. Herpes simplex virus, vesiculovirus, and herpes zoster virus, Coxsackie A viruses, the virus of vesicular stomatitis can cause infections with similar alterations in the oral cavity. The primary lesion here is a vesicle that is gradually changed into ulcerative erosion or aphtha