Oral Candidosis: Pathophysiology and Best Practice for Diagnosis, Classification, and Successful Management
Abstract
:1. Introduction
2. Interplay of Host Defenses and Candida Virulence Factors in Oral Candidosis
3. Iron Deficiency and Immunosuppression in Oral Candidosis
4. Diagnosis of Oral Candidosis
5. Classification of Oral Candidosis
6. Management for Oral Candidosis Patients
7. Conclusions and Important Suggestions for Management of Oral Candidosis
- (1)
- Maintenance of good oral and denture hygiene is crucial. It is important to remove dentures overnight, use denture cleanser, or make a new denture if an ill-fitting denture with stomatitis exists.
- (2)
- Rinsing the mouth after use of an inhaled steroid is helpful to prevent oral candidosis.
- (3)
- Glucose promotes yeast growth, and a high-carbohydrate diet enhances its adherence to oral epithelial cells. Limiting their consumption is helpful in the control of oral Candida colonization and infection.
- (4)
- Removal of heavy candidal plaques or biofilm from oral lesions by mechanical means can improve antifungal action and speed healing.
- (5)
- Nystatin tablets are significantly superior to nystatin oral suspension in treating oral candidosis. Swallowing nystatin tablets rather than sucking or dissolving them in the mouth is ineffective to treat oral candidosis.
- (6)
- The duration of antifungal treatment should be sufficient or prolonged for at least four weeks to achieve a more permanent mycological cure.
- (7)
- Early fluconazole monotherapy or fluconazole combined with nystatin is helpful to treat oropharyngeal candidosis, suppurative candodosis, or Candida-related chronic oral ulcers.
- (8)
- Attempts to increase CD4 count in patients with HIV/AIDS or thymoma are helpful to treat oral candidosis. HAART can reduce recurrent oropharyngeal candidosis.
- (9)
- Underlying predisposing factors should be identified and treated simultaneously as well as monitored regularly.
- (10)
- The final eradication of oral candidosis is by host defense system.
Funding
Institutional Review Board Statement
Informed Consent Statement
Data Availability Statement
Conflicts of Interest
References
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Systemic Host Factors | Local Host Factors |
---|---|
Altered physiological status | Mucosal barrier alterations |
Infancy/old age | Exogenous epithelial change |
Altered hormonal status | Trauma |
Diabetes | Loss of occlusion |
Hypothyroidism/Hypoparathyroidism | Maceration |
Cushing’s syndrome | Endogenous epithelial changes |
Altered hematinic or nutritional status | Atrophy |
Iron deficiency | Hyperplasia |
Hypovitaminosis, Vit B12, folic acid | Dysplasia/Oral cancer |
Malnutrition | Saliva quantitative changes |
Altered immune status | Xerostomia |
Defects in cell-mediated immunity | Sjogren’s syndrome |
Reduced numbers of phagocytes | Radiotherapy/Cytotoxic therapy |
Lymphopenia or leukopenia | Saliva qualitative changes |
Decreased CD4 count | pH/glucose concentration |
Due to infective states/ HIV | Poor oral or denture hygiene |
Blood dyscrasias/ malignancies | High carbohydrate diet |
Immunosuppressant/ chemotherapy | Heavy smoking/ Betel nut chewing |
Broad spectrum antibiotics | Inhaled steroid |
Virulence Factors | Effects |
---|---|
Adherence | Promote retention in the mouth |
Expression of cell surface adhesins | Specific adhesion |
Cell surface hydrophobicity | Nonspecific adhesion |
Invasion and destruction of host tissue | Enhance pathogenicity |
Hyphae development/thigmotropism | Promote invasion/active penetration |
Secret hydrolytic enzymes | Cytotoxicity to oral epithelium |
Secret acidic metabolites | Degrade basement membrane/matrix |
Endocytosis | Passive penetration of epithelium |
Evasion of host defense | Reduce phagocytosis/help retention |
Phenotypic switching | Antigenic modification |
Proteolytic degrading immune factors | Destroy sIgA/ antimicrobial peptides |
Binding of complement | Antigenic masking |
Synergism with bacteria | Promote mixed-species retention |
Acute/Chronic Candidosis | Hyperplastic Candidosis |
Pseudomembranous candidosis | Plaque-like |
Erythematous candidosis | Nodular-like |
Candida-associated lesions | Granular or papillary-like * |
Denture stomatitis | Keratinized primary lesions superinfected with Candida |
Localized simple inflammation | Leukoplakia |
Diffuse erythematous type | Oral lichen planus |
Granular type (inflammatory papillary hyperplasia) * | Lupus erythematosus |
Median rhomboid glossitis (MRG) | Chronic mucocutaneous candidosis (CMC) |
Angular cheilitis | Congenital/ Familial CMC, diffuse type |
Cheilocandidosis | Acquired CMC, focal, or diffuse type |
Juxtavermillion candidosis | Endocrinopathy associated |
Oropharyngeal candidosis | Hypothyroidism, hypoparathyroidism, |
Dangerous sign of immunosuppression | MG-thymoma, Addison’s disease, etc. |
Suppurative oral candidosis | Immunosuppression associated |
Focal necrotizing ulcerative mucositis or osteomyelitis | Diabetes, iron deficiency, HIV/AIDS, neutropenia, etc. |
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Lu, S.-Y. Oral Candidosis: Pathophysiology and Best Practice for Diagnosis, Classification, and Successful Management. J. Fungi 2021, 7, 555. https://doi.org/10.3390/jof7070555
Lu S-Y. Oral Candidosis: Pathophysiology and Best Practice for Diagnosis, Classification, and Successful Management. Journal of Fungi. 2021; 7(7):555. https://doi.org/10.3390/jof7070555
Chicago/Turabian StyleLu, Shin-Yu. 2021. "Oral Candidosis: Pathophysiology and Best Practice for Diagnosis, Classification, and Successful Management" Journal of Fungi 7, no. 7: 555. https://doi.org/10.3390/jof7070555