MDPI Acta Medica Okayama 2079-4991 13 9 2023 Long-Term Antibacterial Efficacy of Cetylpyridinium Chloride-Montmorillonite Containing PMMA Resin Cement 1495 EN Kumiko Yoshihara Department of Pathology & Experimental Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University Noriyuki Nagaoka Advanced Research Center for Oral and Craniofacial Science, Okayama University Dental School Yoji Makita National Institute of Advanced Industrial Science and Technology (AIST), Health and Medical Research Institute Yasuhiro Yoshida Department of Biomaterials and Bioengineering, Faculty of Dental Medicine, Hokkaido University Bart Van Meerbeek Department of Oral Health Sciences, BIOMAT & UZ Leuven (University Hospitals Leuven), Dentistry, KU Leuven (University of Leuven) Despite being able to adhesively restore teeth, adhesives and cement do not possess any anticariogenic protection potential, by which caries recurrence may still occur and reduce the clinical lifetime of adhesive restorations. Several antibacterial agents have been incorporated into dental adhesives and cement to render them anticariogenic. Due to an additional therapeutic effect, such materials are classified as 'dental combination products' with more strict market regulations. We incorporated cetylpyridinium chloride (CPC), often used for oral hygiene applications, into montmorillonite (CPC-Mont), the latter to serve as a carrier for controlled CPC release. CPC-Mont incorporated into tissue conditioner has been approved by the Pharmaceuticals and Medical Devices Agency (PmontMDA) in Japan. To produce a clinically effective dental cement with the antibacterial potential to prevent secondary caries, we incorporated CPC-Mont into PMMA resin cement. We measured the flexural strength, shear bond strength onto dentin, CPC release, and the biofilm-inhibition potential of the experimental CPC-Mont-containing PMMA cement. An 8 and 10 wt% CPC-Mont concentration revealed the antibacterial potential without reducing the mechanical properties of the PMMA cement. No potential conflict of interest relevant to this article was reported.

Okayama University Medical School Acta Medica Okayama 0386-300X 55 6 2001 Effects of zinc deficiency/zinc supplementation on ammonia metabolism in patients with decompensated liver cirrhosis. 349 355 EN Yasuhiro Yoshida Toshihiro Higashi Kazuhiro Nouso Harushige Nakatsukasa Shin-ichiro Nakamura Akiharu Watanabe Takao Tsuji Article 10.18926/AMO/32003 <p>Hepatic encephalopathy is one of the major complications in decompensated liver cirrhosis. The current study was conducted to clarify the mechanisms of zinc deficiency in liver cirrhosis and its involvement in hepatic encephalopathy via ammonia metabolism. Ten patients each with compensated or decompensated liver cirrhosis and 11 healthy volunteers were enrolled in the study. Serum zinc levels and its daily urinary excretion were measured, an oral zinc-tolerance test was performed to examine zinc malabsorption, and the effects of diuretics on zinc excretion and of zinc supplementation on ammonia metabolism in the skeletal muscle were studied. The mean serum zinc levels in patients with decompensated liver cirrhosis were found to be significantly lower than the levels in controls and patients with compensated liver cirrhosis. The serum zinc levels were inversely correlated with blood ammonia in the fasting state. In the oral zinc-tolerance test, the percent increase in serum zinc levels 120 and 180 min after ingestion was less in cirrhotic patients than in controls. A diuretic administration resulted in a significant reduction in serum zinc levels. An increased uptake of ammonia by and an increased release of glutamine from leg skeletal muscle after oral supplementation of zinc sulfate were evident. Taken together, zinc deficiency in decompensated cirrhotic patients appears to be due to low absorption and to high urinary excretion, for which excessive diuretic administration is, in part, responsible, and zinc supplementation might play an important role in the prevention of hepatic encephalopathy by activating glutamine synthetase.</p> No potential conflict of interest relevant to this article was reported.