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Background and objectives: Cytotoxic T-lymphocyte (CTL)-mediated inflammatory response to tumors plays a crucial role in preventing the progression of some cancers. Programmed cell death ligand 1 (PD-L1), a cell-surface glycoprotein, has been reported to repress T-cell-mediated immune responses against tumors. However, the clinical significance of PD-L1 in colorectal cancer (CRC) remains unclear. Our aim was to elucidate the prognostic significance of PD-L1 expression and CD8+ CTL density in CRC. Materials and methods: CD8 and PD-L1 immunostaining was conducted on 157 pathologic specimens from patients with CRC. The CD8+ CTL density and PD-L1 expression within the tumor microenvironment were assessed by immunohistochemistry. Results: Tumor invasion (pT) was significantly correlated with intratumoral (p = 0.011) and peritumoral (p = 0.016) CD8+ CTLs density in the tumor microenvironment. In addition, there was a significant difference in the intensity of CD8+ CTLs between patients with and without distant metastases (intratumoral p = 0.007; peritumoral p = 0.037, T-test). Lymph node metastasis (pN) and TNM stage were significantly correlated with PD-L1 expression in CRC cells (p = 0.015, p = 0.029, respectively). Multivariate analysis revealed a statistically significant relationship between the intratumoral CD8+ CTL density and disease-free survival (DFS) (hazard ratio [HR] 2.06; 95% confidence interval [CI]: 1.01–4.23; p = 0.043). The DFS was considerably shorter in patients with a high expression of PD-L1 in cancer cells than those with a low expression (univariate HR 2.55; 95% CI 1.50–4.34; p = 0.001; multivariate HR 0.48; 95% CI 0.28–0.82; p = 0.007). Conversely, patients with high PD-L1 expression in tumor-infiltrating lymphocytes had a longer DFS in both univariate analysis (HR 0.25; 95% CI: 0.14–0.44; p < 0.001) and multivariate analysis (HR 3.42; 95% CI: 1.95–6.01; p < 0.001). Conclusion: The CD8+ CTL density and PD-L1 expression are prognostic biomarkers for the survival of patients with CRC.

The aim of this study was to compare the effects of hydroxyapatite (HA), deproteinized bovine bone (DPB), human-derived allogenic bone (HALG), and calcium sulfate (CAP) graft biomaterials used with titanium barriers for bone augmentation to treat peri-implant defects in rat calvarium treated by guided bone regeneration (GBR). Thirty-two female Sprague-Dawley rats were divided into four groups: DPB, HALG, HA, and CAP. One titanium barrier was fixed to each rat's calvarium after the titanium implants had been fixed. In total, 32 titanium implants and barriers were used. Ninety days after the surgical procedure, all the barriers were removed. After decalcification of bone tissue, the titanium implants were removed gently, and new bone regeneration in the peri-implant area was analyzed histologically. Immunohistochemical staining of vascular endothelial growth factor (VEGF) was also performed. There were no statistically significant between-group differences in new bone regeneration or VEGF expression after 3 months. According to the results of the histological and immunohistochemical analyses, none of the grafts used in this study showed superiority with respect to new bone formation.

The topography, chemical features, surface charge, and hydrophilic nature of titanium implant surfaces are crucial factors for successful osseointegration. This study aimed to investigate the bone implant contact (BIC) ratio of titanium dental implants with different surface modification techniques using the rat femoral bone model. Sandblasted and acid washed (SL-AW), sandblasted (SL), resorbable blast material (RBM), microarc (MA), and sandblasted and microarc (SL-MA) surfaces were compared in this study. Forty male Sprague-Dawley rats were used in this study. The rats were divided into 5 equal groups (n = 8), and totally 40 implants were integrated into the right femoral bones of the rats. The rats were sacrificed 12 weeks after the surgical integration of the implants. The implant surface-bone tissue interaction was directly observed by a light microscope, and BIC ratios were measured after the nondecalcified histological procedures. Bone implant contact ratios were determined as follows: SL-AW: 59.26 ± 14.36%, SL: 66.01 ± 9.63%, RBM: 63.53 ± 11.23%, MA: 65.51 ± 10.3%, and SL-MA: 68.62 ± 6.6%. No statistically significant differences were found among the 5 different surfaced titanium implant groups (P > 0.05). Our results show that various implant surface modification techniques can provide favorable bone responses to the BIC of dental implants.

The aim of this experimental animal study was to evaluate the effects of systemic propranolol on new bone formation in peri-implant bone defects. Material and Methods: Implant slots were created 4 mm long and 2.5 mm wide. After the titanium implants were placed in the sockets, 2 mm defects were created in the neck of the implants. Bone grafts were placed in these defects. Then the rats were randomly divided into three equal groups: control (n = 8), propranolol dose-1 (PRP-1) (n = 8), and propranolol dose-2 (PRP-2) (n = 8) groups. In the control group, the rats received no further treatment during the eight-week experimental period after the surgery. The rats in the PRP-1 and PRP-2 groups were given 5 mg/kg and 10 mg/kg propranolol, respectively, every three days for the eight-week experimental period after the surgery. At the end of the experimental period, the rats were euthanized. Blood serum was collected for biochemical analysis, and the implants and surrounding bone tissues were used for the histological analysis. Results: There were no significant differences in the histological analysis results and the biochemical parameters (alkaline phosphatase, calcium, creatinine and phosphorus) of the groups (P > 0.05). Also, in the test groups, there was numerically but not statistically more new bone formation detected compared with the controls. Conclusions: Within the limitations of this study, propranolol did not affect the new bone formation in peri-implant defects.