Therefore, even if Candida does not proliferate to high levels, oral candidiasis can develop as a result of the alterations in the human host defenses, such as hyposalivation, which increases the risk of Candida colonization. There is an inverse relationship between salivary flow and oral Candida colonization [43], [44] and [45]. www.selleckchem.com/products/cobimetinib-gdc-0973-rg7420.html A similar relationship between salivary flow and candidiasis was observed in the Dry Mouth Clinic at Tsurumi

University Dental Hospital. Out of 2678 patients (male:female = 446:2232, mean age = 66.8), 1548 (57.8%) had oral colonization by Candida. To examine the relationship between salivary flow and Candida colonization at our institution, study subjects were divided into 5 groups according to their level of salivation ( Table 4). We measured the WRS and WSS, and hyposalivation was defined as a WRS less than 1.5 ml/15 min and/or WSS less than 10 ml/10 min. The highest CFU for Candida was observed in patients with Sjögren’s

syndrome (Group I), followed by non-Sjögren’s syndrome patients with decreased WRS and WSS (Group II), patients with only decreased WRS (Group III), patients with only decreased WSS (Group IV), and a group with WRS and WSS within the normal limits (Group V). These results suggest that hyposalivation is INK1197 in vitro a risk factor for an increase of Candida CFU, especially in Sjögren’s syndrome patients. Although the reason why Sjögren’s syndrome patients showed the highest CFU has not yet been elucidated, alterations in the salivary composition might be related to the observed Candida colonization [46] and [47]. The results also suggest that unstimulated saliva flow contributed more to an increase of Candida CFU than the stimulated saliva flow, because there were more Candida colonies in Group III than Group IV. An increase of Candida CFU due to hyposalivation may possibly lead to the onset of oral candidiasis. Oral candidiasis is classified into three major variants based on the clinical manifestation; pseudomembranous, erythematous (atrophic) and hyperplastic [48]. A diagnosis of candidiasis is based on the clinical findings and is supported by the identification of blastospores and pseudohyphae

in staining smears from a lesion, identification of colonies by culture on Sabouraud’s medium, or by histological 6-phosphogluconolactonase examination [49]. Although an interpretation of the results of a microbial examination is often complicated because Candida is present as a commensal organism in the oral cavities of up to 40% of individuals [48], fungal examination is helpful to distinguish candidiasis from non-specific stomatitis due to the hyposalivation. The occurrence of signs of erythematous candidiasis, such as atrophy of lingual papilla and redness of the oral mucosa was significantly higher in patients who had Candida detected in their mouths than in those that did not [50]. Such a relationship has been recognized previously in the literature [51]. A fungal examination is then needed to support the diagnosis.