including posaconazole, voriconazole, isavuconazole, and ravuconazole, exhibit greater activity against Candida species and include molds in their antifungal spectrum (Radulescu, 2016). The novel echinocandin antifungals, including caspofungin, micafungin, and anidulafungin, provide effective alternatives for azole-resistant fungal infections (Perlin, 2015; Riley, Muzny, Swiatlo, and Legendre, 2016). Echinocandins inhibit (1,3)-d-glucan synthase, an essential component of the cell wall of many fungi that is absent in mammalian cells. Echinocandins exhibit fungicidal activity against many Candida species, including azole-resistant isolates, and are also active against Aspergillus species. Some newer antifungal agents are reserved for candidemia and/or are unavailable for topical administration. The role of probiotics, prebiotics, and biogenics is currently being investigated as an alternative treatment for this condition (Ohshima, Kojima, Seneviratne, & Maeda, 2016; van de Veerdonk, & Netea, 2016). unaware of its presence. There have been patient reports of burning sensation, altered taste sensation, and soreness. The surrounding tissues are not erythematous or edematous (Hall et al., 2015; Greenspan, Greenspan, & Webster- Cyriaque, 2016). Specific treatment is not required in every case but may be indicated for symptoms attributable to the lesion or for cosmetic reasons. Several treatment options are available, including systemic antiviral therapy (acyclovir, valacyclovir, or famciclovir) that prevents the Epstein-Barr virus from replicating or topical therapy with podophyllin resin 25% solution or retinoic acid (tretinoin). tobacco use, long-term alcohol use, and other chronic irritants have been linked to its development (Abidullah et al., 2014; Villa, & Sonis, 2018; Lorenzo-Pouso, et al., 2022). A biopsy should be performed to rule out neoplastic change or cancer for persistent white or erythematous oral lesions. Because most leukoplakias are asymptomatic, the primary objective of treatment should be to prevent malignant transformation. However, evidence supporting effective treatment in preventing malignant transformation of leukoplakia is lacking (Abidullah et al., 2014). According to a recent Cochrane review there is still limited evidence indicating that intervention improves outcomes as compared to placebo (Lodi et al., 2016). Additional investigation in this area is warranted to determine appropriate intervention to prevent malignant transformation of this entity.
of 28 studies in HIV-infected adults and children with oropharyngeal candidiasis (n = 3,225) suggested that ketoconazole, fluconazole, itraconazole, and clotrimazole improved treatment outcomes (Pienaar, Young, & Holmes, 2010). Compared with nystatin, fluconazole favored clinical cure in adults (RR 1.69), but there was no difference with regard to clinical cure between fluconazole and ketoconazole (RR 1.27), itraconazole (RR 1.05), or clotrimazole (RR 1.14). Compared with clotrimazole, both fluconazole (RR 1.47) and itraconazole (RR 2.20) were better for mycological cure. Thus, well-absorbed drugs (fluconazole, ketoconazole, and itraconazole) appear to be more efficacious treatments in this population than those that were partially (clotrimazole) or poorly absorbed (nystatin). Subsequent reviews appear to substantiate these findings (Lyu, Zhao, Yan, & Hua, 2016). For infection unresponsive to these treatments, many other antifungal drugs are available. Newer azole antifungals, Hairy leukoplakia Oral hairy leukoplakia is associated with Epstein-Barr virus infections and mostly occurs in HIV-infected patients – both immunocompromised and immunocompetent – but may also be associated with the use of corticosteroids, cyclosporine, or other long-term immunosuppressive regimens (Hall, Eminger, Hesterman, & Heymann, 2015; Greenspan, Greenspan, & Webster-Cyriaque, 2016; Moosazadeh, Shafaroudi, Gorji, Barzegari, & Nasiri, 2021). Hairy leukoplakia may vary in appearance from smooth, flat, small lesions to irregular hairy lesions with prominent folds. The lesions typically involve the dorsum and lateral borders of the tongue and the floor of the mouth. Hairy leukoplakia is often asymptomatic, and many patients are Oral leukoplakia Oral leukoplakia is a white patch or plaque on the mucous membranes of the oral cavity that cannot be characterized clinically or pathologically as any other disease (Abidullah, Kiran, Gaddikeri, Raghoji, & Ravishankar, 2014; Villa, & Sonis, 2018; Lorenzo-Pouso, et al., 2022). It is therefore a diagnosis of exclusion from other oral white lesions, such as infective lesions (candidiasis and hairy leukoplakia), lichen planus, white sponge nevus, and carcinomas. Initial leukoplakic lesions typically manifest as a thin, homogeneous, grayish-white plaque, either well defined or blending with the surrounding tissue. Some lesions develop surface irregularities or mixed red and white lesions (speckled leukoplakia or erythroplakia). These patches are not easily scraped off. Oral leukoplakia is considered a premalignant lesion, and although the etiology of leukoplakia is not fully elucidated,
DRUG-RELATED CHANGES TO SALIVARY GLANDS
During unstimulated salivary flow, the submandibular glands contribute 65% to 70% of salivary fluid, followed by the parotid glands (20%), sublingual glands (7% to 8%), and minor salivary glands (<10%). However, in stimulated salivary flow the parotids contribute more than 50% of the total salivary secretion (Miranda-Rius, Brunet-Llobet, Lahor-Soler, & Farré, 2015). Salivary secretions may be serous, mucous, or mixed. Serous secretions are produced mainly by the parotids, whereas mucous secretions are produced primarily by the smaller glands. The salivary content depends on the proportion between the serous and mucous cells in the mixed glands, such as the submandibular and sublingual glands.
Salivary fluid consists of approximately 99% water, with the remaining 1% representing a variety of electrolytes (sodium, potassium, calcium, chloride, magnesium, bicarbonate, and phosphate) and proteins (enzymes, immunoglobulins and other antimicrobial factors, glycoproteins, traces of albumin, etc.), in addition to glucose and nitrogenous products, such as urea and ammonia (de Almeida, Grégio, Machado, de Lima, & Azevedo, 2008; Pereira & van der Bilt, 2016). In a healthy state, mean daily saliva production ranges from 1 L to 1.5 L, with a normal stimulated salivary flow rate from 1 mL/minute to 3 mL/minute and an unstimulated flow rate from 0.25 mL/minute to 0.35 mL/minute (Sharma, Somasundara, Prasanna Kumar, & Bhat, 2014). There is considerable intraindividual variation in salivary flow rate, and a normal or abnormal rate cannot be determined from one measurement alone.
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