Oral and Maxillofacial Fungal Infections

Manfredi, Maddalena; Polonelli, Luciano; Giovati, Laura; Alnuaimi, Ali; McCullough, Michael

doi:10.1007/978-3-319-28100-1_1-1

Cited by 2 publications

(6 citation statements)

References 213 publications

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“…Chronic mucocutaneous candidiasis syndromes represent a group of several very rare heterogeneous immunologic disorders characterized by underlying immune deficiencies. Clinically, affected patients suffer from chronic and sometimes life-long persistent or recurrent mucocutaneous candidiasis involving the skin, nails, and genital mucosa; however, greater than 90% of patients present with oral involvement [80,81]. It is thought that the severity of the clinical manifestation correlates with the severity of the underlying immune defect.…”

Section: Chronic Mucocutaneous Candidiasis Syndromesmentioning

confidence: 99%

“…It is thought that the severity of the clinical manifestation correlates with the severity of the underlying immune defect. Many types of chronic mucocutaneous candidiasis syndromes exist that include the sporadic form, forms secondary to immunosuppressive therapies, diabetes, T-cell deficiency or HIV infection, inherited familial genetic forms, and autoimmune polyendocrinopathy candidiasis ectodermal dystrophy (APECED) [80,81]. These patients are often refractory to standard antifungal therapies and have an increased susceptibility to developing oral squamous cell carcinoma [70,81].…”

Section: Chronic Mucocutaneous Candidiasis Syndromesmentioning

confidence: 99%

“…The exact mechanism via which conventional tobacco cigarette smoking predisposes to OC development is yet to be definitively established, but a plausible theory suggests that the decreased salivary flow rate in cigarette smokers and, consequently, the lowered pH may result in an acidic environment that is likely to favor Candida colonization and growth [96]. Additionally, it was suggested that cigarette smoking may cause a decrease in salivary immunoglobulin A (IgA) and a depression of neutrophil function, encouraging oral colonization of Candida [80]. Intriguingly, it was further theorized that cigarette smoking can provide nutrition for Candida to produce carcinogens [80,97].…”

Section: Smokingmentioning

confidence: 99%

“…Additionally, it was suggested that cigarette smoking may cause a decrease in salivary immunoglobulin A (IgA) and a depression of neutrophil function, encouraging oral colonization of Candida [80]. Intriguingly, it was further theorized that cigarette smoking can provide nutrition for Candida to produce carcinogens [80,97].…”

Section: Smokingmentioning

confidence: 99%

“…Furthermore, HIV + patients have significantly lower protective levels of antimicrobial peptides, namely, histatin-5 (Hst-5); thus, these patients are reported to have increased rates of OC compared to matched healthy controls [87]. Interestingly, linear gingival erythema was identified as a specific Candida-associated clinical finding in HIV + patients [70]; linear gingival erythema clinically presents as a localized or generalized well-demarcated linear band of erythema along the free gingival margins [80]. Both antifungal therapy and adequate oral hygiene practices are required to eliminate this condition [78].…”

Section: Hiv Infection and Aidsmentioning

confidence: 99%

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Oral Candidiasis: A Disease of Opportunity

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Oral candidiasis, commonly referred to as “thrush,” is an opportunistic fungal infection that commonly affects the oral mucosa. The main causative agent, Candida albicans, is a highly versatile commensal organism that is well adapted to its human host; however, changes in the host microenvironment can promote the transition from one of commensalism to pathogen. This transition is heavily reliant on an impressive repertoire of virulence factors, most notably cell surface adhesins, proteolytic enzymes, morphologic switching, and the development of drug resistance. In the oral cavity, the co-adhesion of C. albicans with bacteria is crucial for its persistence, and a wide range of synergistic interactions with various oral species were described to enhance colonization in the host. As a frequent colonizer of the oral mucosa, the host immune response in the oral cavity is oriented toward a more tolerogenic state and, therefore, local innate immune defenses play a central role in maintaining Candida in its commensal state. Specifically, in addition to preventing Candida adherence to epithelial cells, saliva is enriched with anti-candidal peptides, considered to be part of the host innate immunity. The T helper 17 (Th17)-type adaptive immune response is mainly involved in mucosal host defenses, controlling initial growth of Candida and inhibiting subsequent tissue invasion. Animal models, most notably the mouse model of oropharyngeal candidiasis and the rat model of denture stomatitis, are instrumental in our understanding of Candida virulence factors and the factors leading to host susceptibility to infections. Given the continuing rise in development of resistance to the limited number of traditional antifungal agents, novel therapeutic strategies are directed toward identifying bioactive compounds that target pathogenic mechanisms to prevent C. albicans transition from harmless commensal to pathogen.

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Section: Chronic Mucocutaneous Candidiasis Syndromesmentioning

confidence: 99%