Do oral conditions influence the incidence of bloodstream infection after hematopoietic stem cell transplantation? A retrospective study in Japan.

PURPOSE: This study aimed to evaluate the incidence of bloodstream infection (BSI) among patients undergoing hematopoietic stem cell transplantation (HSCT) for teeth indicated for extraction. METHODS: Patients who underwent HSCT at Toranomon Hospital (Tokyo, Japan) between January 2017 and December 2019 were retrospectively evaluated. The incidence of BSI among patients with teeth indicated for extraction who did not undergo extraction (oral high-risk group) and patients who did not have this risk (oral low-risk group) was compared. RESULTS: Among the 191 consecutive patients included in this study, 119 patients were classified as undergoing high-risk transplantation. BSI after HSCT was observed in 32 out of 60 (53.3%) patients and 56 out of 131 (42.7%) patients in the oral low-risk and oral high-risk groups, respectively (p = 0.173). Multivariable analyses revealed that the presence of > 3 teeth as intraoral sources of infection and age over 50 years were determinants of BSI originating from the oral cavity after engraftment (odds ratio [OR], 9.11; 95% confidential interval [CI] 2.27-36.61]; p = 0.002; OR, 3.22; CI [1.47-7.08], p = 0.004, respectively). CONCLUSION: In patients undergoing HSCT, the presence of less than three intraoral sources of infection did not affect the incidence of BSI after HSCT.

Masticatory function after unilateral distal extension removable partial denture treatment: intra-individual comparison with opposite dentulous side.

Due to large individual differences of masticatory function, an inter-individual comparison between denture patients and complete dentate people would be insufficient. This cross-sectional study aimed to evaluate patients' masticatory performance (determined by Mixing Ability Index, MAI) and bite force (determined by maximum bite force, MBF) after removable partial denture (RPD) treatment by comparing those of the RPD replaced side with those of their own opposite dentulous side, and to evaluate influence of bite force on masticatory performance in different dentitions. Subjects included patients with unilateral distal extension RPDs (n=28). Apart from the RPD replaced area on one-side, all subjects had intact dentitions. Both masticatory parameters were evaluated separately on each chewing side. MAls and MBFs obtained from the RPD replaced side (0.65 +/- 0.50 and 220 +/- 155 N, mean +/- SD) were significantly lower than those from the dentulous side (1.06 +/- 0.64 and 450 +/- 268 N; Wilcoxon signed-ranks, P < 0.001). MBF significantly influenced MAI in both RPD replaced (Univariate linear regression; R2 = 0.17, P < -0.001) and dentulous sides (R2 = 0.51, P < 0.001). After RPD treatment, masticatory performance and bite force of RPD replaced side were lower than those of their own dentulous side. The influence of the bite force on masticatory performance in RPD replaced side was less significant than that in the dentulous side.

Microbial metabolite of dimethylarsinic acid is highly toxic and genotoxic.

Dimethylarsinic acid [DMA, (CH(3))(2)AsO(OH)] causes cancer in the urinary bladder of rats. However, its mechanism of cancer or the ultimate carcinogenic form is not yet known. Rats administered dimethylarsinic acid excrete three unknown arsenic compounds (termed M-1, M-2, and M-3) in urine or feces, and these compounds are presumed to be produced by intestinal bacteria. Escherichia coli A3-6 isolated from a rat yielded two unknown arsenic compounds (M-2 and M-3) from dimethylarsinic acid and M-1 from trimethylarsine oxide (TMAO) in the presence of cysteine (Cys). Contents of M-2 and M-3 varied with cysteine concentration. The cytotoxicity and genotoxicity of the bacteria-free solution of dimethylarsinic acid or trimethylarsine oxide metabolized by E. coli A3-6 were studied using V79 cells. Dimethylarsinic acid (1 mM) metabolized by E. coli A3-6 in the presence of cysteine (1 mM) was highly cytotoxic (50% survival reduction concentration; 2.1 microM As) in V79 cells, and the toxic substance appeared to be M-2. The metabolite solution (at 2.5-10 microM total As) induced c-mitosis and tetraploids, and caused mitotic arrest, since it increased mitotic cells at the cytotoxic dose. The metabolite solution also significantly increased sister chromatid exchange (SCE) and chromosomal aberrations, most of which were chromatid gaps and chromatid breaks. A3-6 converted 96.1% of trimethylarsine oxide to M-1 in the presence of cysteine. This metabolite solution did not exhibit cytotoxicity or genotoxicity. The reported M-2 concentration in urine of rats administered levels of DMA via drinking water known to cause bladder tumors was sufficient to exhibit cytotoxic and genotoxic effects in urinary bladder. Thus, we hypothesize that intestinal bacteria play an important role in carcinogenicity of dimethylarsinic acid.