31.2 Oral Candidiasis

Oral Candidiasis

Oral candidiasis is an opportunistic fungal infection primarily caused by the dimorphic yeast Candida albicans, an endogenous commensal organism present in the oral microbiota of 40–60% of healthy individuals. Transformation from benign budding blastospore (yeast) to invasive, tissue-penetrating pseudo-hyphae and true hyphae occurs when host local or systemic immune surveillance is disrupted.

Predisposing Local and Systemic Factors

Candida is an opportunistic pathogen; successful management mandates identifying and eliminating underlying predisposing factors:

• Local Factors:
  • Removable prostheses: Continuous night-time denture wear, poor acrylic hygiene, fitting-surface microporosity, low pH and anaerobic microenvironment beneath maxillary dentures.
  • Inhaled Corticosteroids: Fluticasone or beclometasone inhalers used for asthma/COPD without a spacer device or failing to rinse the mouth with water following inhalation.
  • Salivary gland hypofunction (Xerostomia): Loss of antimicrobial histatins, calprotectin, and secretory IgA due to Sjögren's syndrome, therapeutic head and neck radiotherapy, or polypharmacy (anticholinergics, tricyclic antidepressants, diuretics).
  • Tobacco smoking: High carbohydrate/hydrocarbon load enhances candidal adhesion.
  • Topical antimicrobial agents: Broad-spectrum antiseptic mouthwashes disrupting bacterial antagonism.
• Systemic Factors:
  • Systemic broad-spectrum antibiotic therapy: Eradication of normal competing oral flora allows unrestrained candidal overgrowth.
  • Immunosuppressive states: HIV infection (CD4+ T-cell depletion <200/μL is strongly heralded by pseudomembranous candidiasis), cytotoxic chemotherapy, organ transplantation, primary immunodeficiencies.
  • Endocrine disorders: Poorly controlled Diabetes Mellitus (hyperglycaemic saliva provides a substrate for candidal growth and impairs neutrophil chemotaxis/phagocytosis), Addison's disease, hypoparathyroidism (autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy / APECED).
  • Nutritional deficiencies: Severe iron deficiency anaemia, vitamin B12 or folate deficiency.
  • Extremes of life: Neonates (immature immune system and lack of competing oral microflora) and frail elderly individuals.

Clinical Subtypes of Oral Candidiasis

                                    Oral Candidiasis
                                           │
         ┌────────────────────────┬────────┴────────┬────────────────────────┐
         ▼                        ▼                 ▼                        ▼
  Pseudomembranous           Erythematous      Hyperplastic          Angular Cheilitis
  • Creamy white plaques   • Fiery red mucosa • Firm white plaques  • Commissural crusting
  • WIPES OFF              • Painful burning  • NON-WIPEABLE        • C. albicans + S. aureus
  • Raw erythematous base  • Denture-related  • Retromolar / cheek  • Reduced vertical
  • Infants, HIV, steroids • Newton types I-III• Dysplasia risk (5-10%)  dimension (VDO)

1. Pseudomembranous Candidiasis ("Thrush"):

   • Clinical Picture: Superficial, soft, creamy-white or pale-yellow curdy plaques resembling milk curds or cottage cheese, distributed across the buccal mucosa, soft palate, dorsum of the tongue, and labial sulci.
   • Diagnostic Hallmark: The plaques can be easily scraped or wiped off with a dry gauze swab or tongue depressor, revealing an underlying erythematous, raw, bleeding, or painful base.
   • Microscopy: Gram stain or PAS (Periodic acid–Schiff) stain reveals desquamated epithelial cells, polymorphonuclear leukocytes, and abundant branching candidal pseudo-hyphae and blastospores.
   • Setting: Common in infants, elderly denture wearers, patients on high-dose inhaled or systemic steroids, and immunosuppressed individuals (classic opportunistic hallmark of undiagnosed HIV/AIDS).

2. Erythematous (Atrophic) Candidiasis:

   • Characterized by bright red, depapillated, inflamed mucosal surfaces without white pseudomembranes. Two primary presentations exist:
     • Acute Erythematous Candidiasis (Acute Antibiotic Stomatitis): Follows a course of broad-spectrum antibiotics (e.g., amoxicillin, cephalosporins). Presents as generalised, painful, fiery red mucosal erythema with marked depapillation and loss of filiform papillae on the dorsum of the tongue, creating a smooth, glazed, burning ("raw beef") tongue.
     • Chronic Erythematous Candidiasis (Denture-Related Stomatitis): The most common form of oral candidiasis in general dental practice. Confined strictly to the mucosal area covered by the fitting surface of an upper complete or partial acrylic denture. Characteristically asymptomatic or producing mild burning.

Newton's Classification of Denture Stomatitis

$\text{Newton Class: } \mathbf{Type\ I\ (Pinpoint)} \longrightarrow \mathbf{Type\ II\ (Diffuse\ Erythema)} \longrightarrow \mathbf{Type\ III\ (Papillary\ Hyperplasia)}$

1. Chronic Hyperplastic Candidiasis (Candidal Leukoplakia):

   • Clinical Picture: Dense, firm, rough, translucent to opaque white plaques located predominantly on the retrocommissural buccal mucosa (bilaterally) and occasionally the lateral margins of the tongue.
   • Diagnostic Hallmark: Unlike pseudomembranous thrush, hyperplastic candidiasis CANNOT be wiped or scraped off.
   • Malignant Transformation Potential: This is an established Oral Potentially Malignant Disorder (OPMD). It carries an estimated 5% to 10% risk of malignant transformation to oral squamous cell carcinoma. Histopathology reveals candidal hyphae invading perpendicular to the superficial parakeratinised layer, parakeratosis, microabscesses of polymorphonuclear leukocytes in the upper spinous layer (Munro microabscesses), and variable degrees of epithelial dysplasia.
   • Management: Requires definitive incisional biopsy to evaluate dysplasia, followed by prolonged systemic antifungal therapy (e.g., fluconazole for 2–4 weeks) and surgical excision if dysplasia persists.

2. Angular Cheilitis (Perlèche):

   • Clinical Picture: Symmetrical or unilateral erythematous fissuring, maceration, crusting, and ulceration at the labial commissures (angles of the mouth).
   • Microbiology: A mixed polymicrobial infection involving Candida albicans (~60%), Staphylococcus aureus (~35%), and occasionally beta-haemolytic streptococci.
   • Aetiological Drivers:
     • Reduced Vertical Dimension of Occlusion (VDO): Overclosure due to severe tooth wear or worn, ill-fitting dentures creates deep, folded cutaneous creases at the corners of the mouth, continuously macerated by pooled saliva.
     • Incompetent lip seal and drooling in elderly patients.
     • Underlying reservoir: Almost always co-exists with an intraoral candidal reservoir (e.g., untreated Newton Type II denture stomatitis).
     • Haematinic deficiency: Iron deficiency anaemia, riboflavin (B2), and B12 deficiencies.

Antifungal Pharmacology & Critical Clinical Interactions

Successful management requires treating both the oral mucosa and the prosthetic appliance:

1. Denture Hygiene Protocol:

   • The denture must be removed at night (at least 6–8 hours daily).
   • Mechanical cleansing with a soft brush and neutral soap.
   • Chemical disinfection: Soak all-acrylic dentures in 0.1% sodium hypochlorite (Milton solution) for 15–30 minutes daily (kills fungal spores). Contraindication: Sodium hypochlorite must NEVER be used on dentures with metal components (cobalt-chromium clasps/frameworks) because it causes severe oxidation, pitting, and corrosion. For metal-containing dentures, soak in 0.2% chlorhexidine gluconate or alkaline peroxide solutions.

2. Topical Antifungal Agents:

   • Nystatin Oral Suspension (100,000 units/mL): Polyene antifungal that binds to fungal cell membrane ergosterol, creating pores that leak potassium and cellular contents. Dosage: 1 mL rinse and hold in the mouth for several minutes before swallowing, 4 times daily (qds) after meals for 7–14 days. Safe in pregnancy and lactation as it has negligible systemic absorption.
   • Miconazole Oromucosal Gel (20 mg/g): Imidazole antifungal inhibiting 14-α-demethylase, impairing ergosterol synthesis. Dosage: 2.5 mL applied to the oral mucosa (and fitting surface of the clean denture) 4 times daily after food for 7–14 days (continue for 48 hours after lesions resolve).

[!CAUTION] Life-Threatening Clinical Trap — Miconazole and Warfarin Interaction: Miconazole is a potent, irreversible inhibitor of the hepatic cytochrome P450 enzyme CYP2C9. CYP2C9 is the primary enzyme responsible for metabolising the active S-enantiomer of warfarin. Even topical or oromucosal administration of miconazole gel undergoes sufficient systemic absorption to severely inhibit warfarin breakdown. This causes a precipitous, catastrophic spike in the patient's International Normalized Ratio (INR), frequently driving the INR >10.0 and precipitating fatal intracerebral, gastrointestinal, or retroperitoneal haemorrhage. Miconazole (oral gel or cream) is ABSOLUTELY CONTRAINDICATED in any patient taking warfarin. In patients taking warfarin, use Nystatin as the first-line agent, as nystatin is not absorbed and exhibits zero CYP interactions.

1. Systemic Antifungal Agents:
   • Fluconazole Capsules (50 mg / 100 mg): Triazole antifungal. Reserved for immunocompromised patients, widespread refractory candidiasis, chronic hyperplastic candidiasis, or chronic mucocutaneous candidiasis. Standard dosage: 50 mg daily orally for 7 to 14 days (100 mg daily for 2–3 weeks in hyperplastic candidiasis). Monitor liver function tests in prolonged therapy; note that fluconazole also inhibits CYP enzymes and interacts with warfarin, phenytoin, and sulfonylureas.