The “taste” of foods is perceived as a flavor formed from integrating multimodal information such as olfaction, temperature of foods and the sense of touch on the oral mucosa, with gustation. However, the mechanisms for the flavor information processing are still controversial. In this review, it will be described where and how the taste and odor information are integrated into the flavor in the brain on the basis of recent our knowledge. As part of the review, I will also introduce recent our research for this issue. We observed the cortical responses for the taste and/or odor stimulation in the experimental rats and mouse brain under the anesthetized condition using in vivo flavin protein autofluorescence imaging technique. When the animals were stimulated by odor alone, corresponding responses were observed only in the piriform cortex（PC）. Similarly, taste-alone stimulation elicited the responses in the gustatory area（GC）in the insular cortex（IC）. Interestingly, simultaneous stimulation by odor and taste induced the additional response in the agranular insular cortex（AI）. Moreover, in mice trained to learn the association between a taste and an odor, the response area evoked by stimulation with odor or taste alone was altered. In these mice we observed that the odor-alone stimulation evoked the responses not only in the PC but also in the GC, and that taste-alone stimulation evoked the responses in the PC in addition to the GC. These results suggest that the PC, IC including the AI, and surrounding brain region are involved in the formation of associative learning of taste and odor, as “the flavor formation”, and in the representation of the flavor in the brain.

Patient`s with Sjögren’s syndrome（SS）are prone to the development of dental caries as a result of reduced salivary flow. As no studies to date have reported on the association between improved salivary flow in patients with SS and caries prevention, we conducted a retrospective study on the influence of salivary secretion on the number of decayed/missing/filled（DMF）teeth. This study involved a total of 165 patients with a mean observation period of 57.7±8.62 months. The results showed a significant negative correlation between the change in the number of missing teeth from baseline to end point and the mean stimulated whole salivary flow（SWSF）, which was based on the mean baseline and end point SWSF（r＝−0.155, P＝0.047）. In addition, an increase in the number of missing teeth in patients with a mean SWSF not exceeding 6 mL/10min was observed compared to patients with a mean SWSF of more than 6 mL/10min. Logistic regression analysis showed SWSF to be a risk factor for increased number of missing teeth（OR＝0.905, 95 ％ CI＝0.832–0.985, P＝0.021）. During the observation period, although SWSF increased between baseline and end point, increase in SWSF did not prevent an increase of DMF. As this study showed that SS patients were susceptible to missing teeth with no clear evidence of reduced number of DMF teeth associated with increased salivation, the results suggest that SS patients require all available caries prevention interventions, including

not only salivary secretagogue, but also topical measures such as fluoride, antimicrobials and non-fluoride re-mineralizing agents.

Methotrexate（MTX）is a structural analog of folate used as an antirheumatic drug and anticancer drug, and is classified as an antifolate. Recently, the occurrence of methotrexate-associated lymphoproliferative disorders（MTX-LPD）in the oral cavity have been reported. We describe a 62-year-old woman（Case 1）and a 76-year-old man（Case 2）. The diagnosis was MTX-LPD. The lesion disappeared after the withdrawal of MTX. We reviewed reports documenting 42 cases of oral MTX-LPD in Japan. The age of onset was 40-86 years old. There were 13 males and 29 females, with an average age of 69.1 years.