Desmocollin 3 (Dsc3) and desmoglein 3 (Dsg3) are both transmembrane glycoproteins that belong to the cadherin family of calcium-dependent cell adhesion molecules. beta-Catenin is a member of the cadherin-catenin complex that mediates homotypic cell-cell adhesion and is also an important molecule in the wnt signaling pathway. In this study, we examined the simultaneous expression level of Dsc3, Dsg3, and beta-catenin in oral squamous cell carcinomas (OSCCs) and normal oral epithelia using immunohistochemistry. There was a significant correlation (p < 0.05) among the following variables in OSCCs: reduced or loss of expression of Dsc3, Dsg3, and beta-catenin compared to normal oral epithelium, reduced or loss of expression of Dsc3 and histological grade (moderately or poorly differentiated), and reduced or loss of expression of beta-catenin and lymph node metastasis. Furthermore, a positive correlation was found between reduced or loss of beta-catenin staining and reduced or loss of Dsc3 staining in lymph node metastatic cancer tissue (r = 0.734, p < 0.05). These results suggest an abnormal expression of Dsc3, Dsg3, and beta-catenin induced in the progression of oral carcinomas and that the Dsc3 expression level might be related to the regulation of beta-catenin in lymph node metastasis and cell proliferation in OSCCs.

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Presepsin, a glycoprotein produced during bacterial phagocytosis, is used as a sepsis marker for bacterial infections. However, presepsin levels are affected by renal function, and the evaluation criteria according to kidney function or in chronic kidney diseases remain controversial. Furthermore, presepsin may be increased by sample stirring, but no studies have evaluated this effect.In this study, we excluded the effect of stirring by standardizing the blood collection conditions, analyzed the influence of kidney function on presepsin concentrations, and recalculated the reference range based on the findings. EDTA-whole blood from 47 healthy subjects and 85 patients with chronic kidney disease was collected to measure presepsin by PATHFAST. Presepsin was found to be significantly correlated with the levels of creatinine (r = 0.834), eGFRcreat (r = 0.837), cystatin-C (r = 0.845), and eGFRcys (r = 0.879). Furthermore, in patients with CKD, presepsin levels stratified by eGFRcys showed a significant increase in the CKD G2 patient group and with advancing glomerular filtration rate stage. The following values were obtained: Normal: 97.6 ± 27.4 pg/mL, CKD G1: 100.2 ± 27.6 pg/mL, CKD G2: 129.7 ± 40.7 pg/mL, CKD G3: 208.1 ± 70.2 pg/mL, CKD G4: 320.2 ± 170.1 pg/mL, CKD G5: 712.8 ± 336.3 pg/mL. The reference range, calculated by a nonparametric method using 67 cases of healthy volunteers and patients with chronic kidney disease G1, was found to be 59–153 pg/mL, which was notably lower than the standard reference range currently used. Presepsin concentrations were positively correlated with a few biomarkers of renal function, indicating the necessity to consider the effect of renal function in patients with renal impairment. Using the recalculated reference range considering kidney function may improve the accuracy of evaluating presepsin for diagnosis of sepsis compared to the standard reference currently in use.

Abstract— The purpose of the present study was to evaluate the influence of bacterial infection on the pulpal and periodontal tissues in replanted teeth using germ‐free and conventional rats. Forty maxillary and mandibular first molars from ten 6‐week‐old germ‐free male Wistar rats were used. The animals and all materials were maintained in a germ‐free environment inside vinyl isolators throughout the experimental periods. Twenty conventional male Wistar rats served as controls. The first molars were intentionally replanted immediately after extraction. At 3 days, and 1,2,4 and 8 weeks after replantation, animals were sacrificed and the re planted teeth were histopathologically evaluated. Diversity of pulp tissue response was notable in conventional rats, which initially showed various degrees of neutrophil infiltration and then display ed different types of response, including revascularization with reparative dentin formation and complete necrosis. Pulpal responses of germ‐free rats were less variable, being characterized by an almost complete lack of neutrophil infiltration and a high frequency of bone‐like tissue ingrowth. Typical inffammatory resorption was detected only in conventional rats, whereas a higher incidence of ankylosis was notable in germ‐free rats. The present results may corroborate the concept that bacterial infection is a major cause of serious healing complications following tooth replantation, such as pulp necrosis and inflammatory root resorption. The difficulty in optimally controlling bacterial infection seems to be highly relevant to the complexity and unpredictability of the outcome of this procedure. It should also be emphasized that extensive mechanical damage to the periodontal tissues may trigger the development of unfavorable healing complications as ankylosis, even under strictly aseptic conditions.

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