MYCOSES OF THE ORAL CAVITY
INTRODUCTION
Oral mycoses are very varied lesions which can be white, black, brown or even sometimes orange.
The most common oral mycoses are candidiasis, usually due to the proliferation of Candida albicans, a saprophytic germ that becomes opportunistic when local conditions become favorable to its growth.
DEFINITION
These are mouth conditions caused by fungi of endogenous origin, mainly represented by Candida albicans.
Oral candidiasis includes several clinical forms: thrush, black hairy tongue, etc. It is common for the oral location to be not isolated and instead participate in a real disease with multiple locations: vulvovaginal, groin, breasts, various folds (fingers, etc.), digestive tract, respiratory tract, etc.
ETIOPATHOGENESIS:
- Intrinsic factors
• Physiological: age (newborn,
infant before 1 year, old person); pregnancy.
• Premises: hyposialia or xerostomia, lack of hygiene, etc.
• Endocrine terrain: diabetes, hypoparathyroidism, thyroid insufficiency.
• Nutritional deficiencies: iron deficiency.
• Immunosuppression: AIDS.
• Intercurrent infectious or malignant disease: cancer, blood diseases, bone marrow aplasia, etc.
- Extrinsic factors
They are essentially iatrogenic:
• Medications: Iterative, massive antibiotic therapies, interrupted too early and poorly conducted, corticosteroids, immunosuppressants, contraceptives, cervico-facial radiotherapy and chemotherapy
• Surgery: digestive, cardiac, organ transplants, prostheses.
poor oral hygiene and smoking,
ORAL MYCOSES:
A classification of the main species responsible for oral mycoses can be proposed, distinguishing yeasts, filamentous fungi, and exotic fungi.
- Yeasts:
Candida:
Candida albicans is the most common etiological agent. It is a yeast that lives in a saprophytic state in the human digestive tract.
Its dissemination occurs from the digestive tract:
• by contiguity; genital, respiratory and skin.
• by hematogenous route; the kidneys and the eye.
• by sexual intercourse.
Other species of Candida are occasionally pathogenic for the oral cavity: C tropicalis, C pseudotropicalis, C glabrata, C krusei, C parapsilosis…
Filamentous fungi:
Extrapulmonary Aspergillus: Fungi common in the environment (soil, plants, seeds, etc.), they live off decomposing organic matter. Human contamination occurs through inhalation of spores.
- Exotic mycoses:
Histoplasmosis: The two organisms responsible for human infection are Histoplasma capsulatum and Histoplasma duboisii.
CLINICAL FORMS OF ORAL CANDIDIASIS
- Acute forms
Pseudomembranous form or “thrush”
It affects young children, especially infants, and even cachectic, immunocompromised adults.
It is located on the free buccal mucosa, respecting the gum, begins with red macules that merge and gives a diffuse erythematous stomatitis. Efflorescences in gains of pearly white semolina more or less thick are individualized; these are easily detached with the tongue depressor without bleeding.
The functional signs are discreet: simple burning sensation and absence of adenopathies.
This form generally responds well to treatment, but with a risk of becoming chronic and extending. It can be fatal.
- Acute atrophic (erythematous) form:
This is a diffuse depapillating glossitis that begins at the median sulcus and then spreads to the entire tongue. This form is often due to taking broad-spectrum antibiotics or the combination of several antibiotics.
The clinical signs are more marked, because there are numerous erosions on an intense inflammation.
- Chronic forms
A-Hyperplastic (or moniliatic granuloma)
It presents a pseudo-tumoral appearance, a raised, adherent white lesion, with or without erythema, single homogeneous or multiple nodules. It is often located on the inner side of the cheeks in the retro-commissural area and less found on the dorsal side of the tongue or the palate.
B-Angular cheilitis (perlèche)
Localized preferentially at the commissure but also on the vermilion, angular cheilitis has an erythematous appearance, sometimes ulcerated in the form of a fissure. It extends backwards to the level of the retrocommissural mucosa and the inner face of the cheeks. Often bilateral and recurrent, there are unilateral localizations. Angular cheilitis is generally associated with a picture of hypovitaminosis, hyposialia and decreased DVO.
C-Median rhomboid glossitis
Generally asymptomatic, it is located in front of the lingual V, a flat, depapillated median zone, more or less indurated on the surface. A uranitis characterized by a palatal erythematous area in a “mirror” shape is often observed.
D-Prosthetics
It has a bright red mucous appearance with a velvety surface that is rarely cardboard-like. Small confluent vesicles and erosions appear in severe cases. This form should be distinguished from a simple subprosthetic erythema due to an iatrogenic prosthesis.
E-The black hairy tongue
Wrongly associated with candidiasis, it is an oxidation of the filiform papillae of the dorsal surface of the tongue, with hyperkeratinization. Candidal lesions are rarely found there.
Differential diagnoses must be made: tobacco keratoses, lichen planus, etc. Erythematous forms must be differentiated from burns, erosive lichen, anemia, etc.
DEEP MYCOSES OF THE ORAL CAVITY
1-Nasosinusal aspergillosis:
Most often located in the maxillary sinus, it is mainly of dental etiology: apical granuloma, following dental extraction, buccosinusal communication and especially apical protrusion of the paste. The zinc oxide used in the filling pastes would promote the growth of the fungus: Aspergillus fumigatus.
2-Histoplasmosis:
It is a systemic granulomatous and suppurative mycosis caused by Histoplasma capsulatum, a fungus widespread in the eastern and central United States and in tropical regions. It manifests clinically at the level of the oral mucosa by persistent nonspecific ulcerations accompanied by satellite adenopathies.
3-Systemic candidiasis:
Candida albicans is the main species responsible for deep fungal infection. Hematogenous dissemination is favored by immunodepression, in the context of nosocomial infections often from an intravascular catheter (major burns, prolonged bone marrow failure, etc.). The picture is that of a septic syndrome, with a high mortality rate.
Mycological examination
The sample is taken by swabbing in order to detect Candida by direct examination and culture.
Direct examination under a microscope, without fixation, with Gram or MGG (May Grunwald Giemsa) staining reveals yeasts, small cells of 2 to 4 microns, oval or budding, accompanied or not by mycelial filaments.
Culture in a specific medium allows us to count the colonies which must be greater than 30 to confirm the diagnosis.
The performance of an antifungal test remains exceptional. This examination is indicated for atypical, chronic forms, recurrent lesions or those resistant to first-line antifungal treatments.
ADDITIONAL EXAMINATIONS
Histological examination
Histological examination is not systematically indicated. The presence of these mycelial filaments is highlighted by staining such as PAS (Periodic Acid Schiff).
TREATMENT
The primary objective is to eliminate or modulate the risk factor:
General: antibiotic treatment, corticosteroid therapy, nutrition, unbalanced diabetes, etc.
Local: hyposialia, asialia, poor oral hygiene, prosthetic inadequacy…to which we add a local or systemic antifungal prescription.
Local prescription:
in the form of gel, oral suspension or lozenge
There are two main families:
Polyenes (derived from actinomycetes) Polyenes act on the plasma membrane of Candida by reducing the membrane permeability of these cells. Their spectrum of action is broad. Resistance is rare but can occur during prolonged treatment in immunocompromised patients.
Azoles (synthetic) Azoles act on the synthesis of the Candida membrane. Their spectrum of action is very broad, in local application, their concentration is very high and they have an action on Gram + cocci bacteria. Resistance is very exceptional and rare.
If the diagnosis is confirmed, one of the following molecules is prescribed:
Amphotericin B: (Fungizone)
From the polyene family, its antifungal spectrum is broad.
Routes of administration: administered orally, non-toxic, it does not cross the oral and digestive mucosa.
Dosage: oral suspension (100 mg/ml) 10%: 3 to 4 teaspoons as a mouthwash for 15 to 20 days.
Miconazole: (Daktarin®)
Miconazole has a local action on candidiasis, but several drug interactions must be taken into account: AVKs, hypoglycemics (sulfamides), pregnant and breastfeeding women.
It exists in the form of oral gel: Daktarin® 2% to keep in the mouth to increase its effectiveness; or 125 mg capsules for digestive candidiasis, 1 to 2 g per day in 3 to 4 doses.
Systemic prescription
In cases of extensive mucosal lesions, inaccessible to local treatment, which occur in a context of genetic or acquired immune deficiency, the use of systemic antifungal treatments is indicated.
CONCLUSION :
Oral candidiasis is a very common infection that requires special attention from the general practitioner . The diagnosis is often clinical, guided by the elements of the medical questionnaire and the clinical examination. It sometimes requires a mycological or even histological examination for atypical and recurrent forms. The treatment of these lesions is often local, in some cases of significant immunodepression, systemic treatment is associated.
MYCOSES OF THE ORAL CAVITY
Cracked teeth can be healed with modern techniques.
Gum disease can be prevented with proper brushing.
Dental implants integrate with the bone for a long-lasting solution.
Yellowed teeth can be brightened with professional whitening.
Dental X-rays reveal problems that are invisible to the naked eye.
Sensitive teeth benefit from specific toothpastes.
A diet low in sugar protects against cavities.