PURPOSE: This pilot study investigated the effect of surface roughness on osseointegration by comparing two types of commercial SLA-treated dental implants with different surface roughness levels: moderately rough (Sa = 1 – 2 µm) and rough surfaces (Sa > 2 µm). MATERIALS AND METHODS: Two implant groups were studied: TS (rough surface) and ADD (moderately rough surface) groups. Surface characteristics were analyzed using optical profilometry and SEM. In vitro studies using BRITER cells assessed cell adhesion, proliferation, and osteogenic differentiation through CCK-8 assay and qRT-PCR for osteopontin (OPN), osteocalcin (OCN), and alkaline phosphatase (ALP) expression. The in vivo study involved 12 implants (six per group) placed in mandibular defects of two beagle dogs. After 8 weeks, histomorphometric analysis evaluated bone to implant contact (BIC) and inter-thread bone density (ITBD). Statistical analysis used Student’s t-test and two-way ANOVA for in vitro data, and Mann-Whitney U test for in vivo data. RESULTS: Surface analysis revealed Sa values of 2.50 ± 0.27 µm for the TS group and 1.80 ± 0.06 µm for the ADD group. In vitro studies showed no significant differences in cell adhesion and proliferation between the groups (P > .05). However, gene expression patterns differed, with ADD group showing higher OPN expression (P < .001) and TS group showing higher ALP expression (P < .01). The in vivo study revealed no statistically significant differences in BIC and ITBD between the two groups (P > .05). CONCLUSION Surface roughness influenced osteoblast differentiation in vitro, but did not significantly affect osseointegration outcomes in vivo. Both moderately rough and rough surfaces appeared to support comparable levels of osseointegration. Larger studies are needed to confirm these findings and determine optimal implant surface characteristics.

Periodontal disease (PD) is strongly linked to increased risk of oral squamous cell carcinoma (OSCC); however, the specific mechanism through which the development of PD and OSCC is simultaneously promoted remains unclear.This study explored the impact of periodontal pathogens on OSCC progression and the contribution of periodontal pathogen-stimulated OSCC to PD development. The expression of osteoclastogenesis-inducing factors was assessed using quantitative reverse transcription polymerase chain reaction analysis following stimulation of OSCC with lipopolysaccharide (LPS) derived from the periodontal pathogen Porphyromonas gingivalis (Pg), a pathogen commonly responsible for PD. The cell counting kit-8 assay was used to determine the effects of Pg-LPS on OSCC proliferation and drug resistance to cisplatin and 5-fluorouracil. The effects of conditioned medium (CM) derived from Pg-LPS–stimulated OSCC on osteoclastogenesis was evaluated using tartrate-resistant acid phosphatase (TRAP) staining on bone marrow-derived macrophages (BMMs). Pg-LPS administration in SCC-25 and YD-8 OSCC cell lines induced a significant increase in receptor activator of nuclear factor kappa-B ligand mRNA expression; however, it did not affect cell proliferation. Treatment with CM derived from Pg-LPS–stimulated SCC-25 or YD-8 cells markedly enhanced the formation of TRAP-positive multinucleated cells during osteoclast differentiation of BMMs. Altogether, these findings demonstrate that Pg-LPS–stimulated OSCC promoted osteoclastogenesis through a paracrine mechanism.

PURPOSE: This pilot study investigated the effect of surface roughness on osseointegration by comparing two types of commercial SLA-treated dental implants with different surface roughness levels: moderately rough (Sa = 1 – 2 µm) and rough surfaces (Sa > 2 µm). MATERIALS AND METHODS: Two implant groups were studied: TS (rough surface) and ADD (moderately rough surface) groups. Surface characteristics were analyzed using optical profilometry and SEM. In vitro studies using BRITER cells assessed cell adhesion, proliferation, and osteogenic differentiation through CCK-8 assay and qRT-PCR for osteopontin (OPN), osteocalcin (OCN), and alkaline phosphatase (ALP) expression. The in vivo study involved 12 implants (six per group) placed in mandibular defects of two beagle dogs. After 8 weeks, histomorphometric analysis evaluated bone to implant contact (BIC) and inter-thread bone density (ITBD). Statistical analysis used Student’s t-test and two-way ANOVA for in vitro data, and Mann-Whitney U test for in vivo data. RESULTS: Surface analysis revealed Sa values of 2.50 ± 0.27 µm for the TS group and 1.80 ± 0.06 µm for the ADD group. In vitro studies showed no significant differences in cell adhesion and proliferation between the groups (P > .05). However, gene expression patterns differed, with ADD group showing higher OPN expression (P < .001) and TS group showing higher ALP expression (P < .01). The in vivo study revealed no statistically significant differences in BIC and ITBD between the two groups (P > .05). CONCLUSION Surface roughness influenced osteoblast differentiation in vitro, but did not significantly affect osseointegration outcomes in vivo. Both moderately rough and rough surfaces appeared to support comparable levels of osseointegration. Larger studies are needed to confirm these findings and determine optimal implant surface characteristics.

PURPOSE: This pilot study investigated the effect of surface roughness on osseointegration by comparing two types of commercial SLA-treated dental implants with different surface roughness levels: moderately rough (Sa = 1 – 2 µm) and rough surfaces (Sa > 2 µm). MATERIALS AND METHODS: Two implant groups were studied: TS (rough surface) and ADD (moderately rough surface) groups. Surface characteristics were analyzed using optical profilometry and SEM. In vitro studies using BRITER cells assessed cell adhesion, proliferation, and osteogenic differentiation through CCK-8 assay and qRT-PCR for osteopontin (OPN), osteocalcin (OCN), and alkaline phosphatase (ALP) expression. The in vivo study involved 12 implants (six per group) placed in mandibular defects of two beagle dogs. After 8 weeks, histomorphometric analysis evaluated bone to implant contact (BIC) and inter-thread bone density (ITBD). Statistical analysis used Student’s t-test and two-way ANOVA for in vitro data, and Mann-Whitney U test for in vivo data. RESULTS: Surface analysis revealed Sa values of 2.50 ± 0.27 µm for the TS group and 1.80 ± 0.06 µm for the ADD group. In vitro studies showed no significant differences in cell adhesion and proliferation between the groups (P > .05). However, gene expression patterns differed, with ADD group showing higher OPN expression (P < .001) and TS group showing higher ALP expression (P < .01). The in vivo study revealed no statistically significant differences in BIC and ITBD between the two groups (P > .05). CONCLUSION Surface roughness influenced osteoblast differentiation in vitro, but did not significantly affect osseointegration outcomes in vivo. Both moderately rough and rough surfaces appeared to support comparable levels of osseointegration. Larger studies are needed to confirm these findings and determine optimal implant surface characteristics.

Periodontal disease (PD) is strongly linked to increased risk of oral squamous cell carcinoma (OSCC); however, the specific mechanism through which the development of PD and OSCC is simultaneously promoted remains unclear.This study explored the impact of periodontal pathogens on OSCC progression and the contribution of periodontal pathogen-stimulated OSCC to PD development. The expression of osteoclastogenesis-inducing factors was assessed using quantitative reverse transcription polymerase chain reaction analysis following stimulation of OSCC with lipopolysaccharide (LPS) derived from the periodontal pathogen Porphyromonas gingivalis (Pg), a pathogen commonly responsible for PD. The cell counting kit-8 assay was used to determine the effects of Pg-LPS on OSCC proliferation and drug resistance to cisplatin and 5-fluorouracil. The effects of conditioned medium (CM) derived from Pg-LPS–stimulated OSCC on osteoclastogenesis was evaluated using tartrate-resistant acid phosphatase (TRAP) staining on bone marrow-derived macrophages (BMMs). Pg-LPS administration in SCC-25 and YD-8 OSCC cell lines induced a significant increase in receptor activator of nuclear factor kappa-B ligand mRNA expression; however, it did not affect cell proliferation. Treatment with CM derived from Pg-LPS–stimulated SCC-25 or YD-8 cells markedly enhanced the formation of TRAP-positive multinucleated cells during osteoclast differentiation of BMMs. Altogether, these findings demonstrate that Pg-LPS–stimulated OSCC promoted osteoclastogenesis through a paracrine mechanism.

PURPOSE: This pilot study investigated the effect of surface roughness on osseointegration by comparing two types of commercial SLA-treated dental implants with different surface roughness levels: moderately rough (Sa = 1 – 2 µm) and rough surfaces (Sa > 2 µm). MATERIALS AND METHODS: Two implant groups were studied: TS (rough surface) and ADD (moderately rough surface) groups. Surface characteristics were analyzed using optical profilometry and SEM. In vitro studies using BRITER cells assessed cell adhesion, proliferation, and osteogenic differentiation through CCK-8 assay and qRT-PCR for osteopontin (OPN), osteocalcin (OCN), and alkaline phosphatase (ALP) expression. The in vivo study involved 12 implants (six per group) placed in mandibular defects of two beagle dogs. After 8 weeks, histomorphometric analysis evaluated bone to implant contact (BIC) and inter-thread bone density (ITBD). Statistical analysis used Student’s t-test and two-way ANOVA for in vitro data, and Mann-Whitney U test for in vivo data. RESULTS: Surface analysis revealed Sa values of 2.50 ± 0.27 µm for the TS group and 1.80 ± 0.06 µm for the ADD group. In vitro studies showed no significant differences in cell adhesion and proliferation between the groups (P > .05). However, gene expression patterns differed, with ADD group showing higher OPN expression (P < .001) and TS group showing higher ALP expression (P < .01). The in vivo study revealed no statistically significant differences in BIC and ITBD between the two groups (P > .05). CONCLUSION Surface roughness influenced osteoblast differentiation in vitro, but did not significantly affect osseointegration outcomes in vivo. Both moderately rough and rough surfaces appeared to support comparable levels of osseointegration. Larger studies are needed to confirm these findings and determine optimal implant surface characteristics.

Periodontal disease (PD) is strongly linked to increased risk of oral squamous cell carcinoma (OSCC); however, the specific mechanism through which the development of PD and OSCC is simultaneously promoted remains unclear.This study explored the impact of periodontal pathogens on OSCC progression and the contribution of periodontal pathogen-stimulated OSCC to PD development. The expression of osteoclastogenesis-inducing factors was assessed using quantitative reverse transcription polymerase chain reaction analysis following stimulation of OSCC with lipopolysaccharide (LPS) derived from the periodontal pathogen Porphyromonas gingivalis (Pg), a pathogen commonly responsible for PD. The cell counting kit-8 assay was used to determine the effects of Pg-LPS on OSCC proliferation and drug resistance to cisplatin and 5-fluorouracil. The effects of conditioned medium (CM) derived from Pg-LPS–stimulated OSCC on osteoclastogenesis was evaluated using tartrate-resistant acid phosphatase (TRAP) staining on bone marrow-derived macrophages (BMMs). Pg-LPS administration in SCC-25 and YD-8 OSCC cell lines induced a significant increase in receptor activator of nuclear factor kappa-B ligand mRNA expression; however, it did not affect cell proliferation. Treatment with CM derived from Pg-LPS–stimulated SCC-25 or YD-8 cells markedly enhanced the formation of TRAP-positive multinucleated cells during osteoclast differentiation of BMMs. Altogether, these findings demonstrate that Pg-LPS–stimulated OSCC promoted osteoclastogenesis through a paracrine mechanism.

PURPOSE: This pilot study investigated the effect of surface roughness on osseointegration by comparing two types of commercial SLA-treated dental implants with different surface roughness levels: moderately rough (Sa = 1 – 2 µm) and rough surfaces (Sa > 2 µm). MATERIALS AND METHODS: Two implant groups were studied: TS (rough surface) and ADD (moderately rough surface) groups. Surface characteristics were analyzed using optical profilometry and SEM. In vitro studies using BRITER cells assessed cell adhesion, proliferation, and osteogenic differentiation through CCK-8 assay and qRT-PCR for osteopontin (OPN), osteocalcin (OCN), and alkaline phosphatase (ALP) expression. The in vivo study involved 12 implants (six per group) placed in mandibular defects of two beagle dogs. After 8 weeks, histomorphometric analysis evaluated bone to implant contact (BIC) and inter-thread bone density (ITBD). Statistical analysis used Student’s t-test and two-way ANOVA for in vitro data, and Mann-Whitney U test for in vivo data. RESULTS: Surface analysis revealed Sa values of 2.50 ± 0.27 µm for the TS group and 1.80 ± 0.06 µm for the ADD group. In vitro studies showed no significant differences in cell adhesion and proliferation between the groups (P > .05). However, gene expression patterns differed, with ADD group showing higher OPN expression (P < .001) and TS group showing higher ALP expression (P < .01). The in vivo study revealed no statistically significant differences in BIC and ITBD between the two groups (P > .05). CONCLUSION Surface roughness influenced osteoblast differentiation in vitro, but did not significantly affect osseointegration outcomes in vivo. Both moderately rough and rough surfaces appeared to support comparable levels of osseointegration. Larger studies are needed to confirm these findings and determine optimal implant surface characteristics.

Purpose: We aimed to refine the radiotherapy (RT) volume and dose for intracranial germinoma considering recurrences and long-term toxicities. Materials and Methods: Total 189 patients with intracranial germinoma were treated with RT alone (n=50) and RT with upfront chemotherapy (CRT) (n=139). All cases were confirmed histologically. RT fields comprised the extended-field and involved-field only for primary site. The extended-field, including craniospinal, whole brain (WB), and whole ventricle (WV) for cranial field, is followed by involved-field boost. The median follow-up duration was 115 months. Results: The relapses developed in 13 patients (6.9%). For the extended-field, cranial RT dose down to 18 Gy exhibited no cranial recurrence in 34 patients. In CRT, 74 patients (56.5%) showed complete response to chemotherapy and no involved-field recurrence with low-dose RT of 30 Gy. WV RT with chemotherapy for the basal ganglia or thalamus germinoma showed no recurrence. Secondary malignancy developed in 10 patients (5.3%) with a latency of 20 years (range, 4 to 26 years) and caused mortalities in six. WB or craniospinal field rather than WV or involved-field significantly increased the rate of hormone deficiencies, and secondary malignancy. RT dose for extended-field correlated significantly with the rate of hormone deficiencies, secondary malignancy, and neurocognitive dysfunction. Conclusion De-intensifying extended-field rather than involved-field or total scheme of RT will be critical to decrease the late toxicities. Upfront chemotherapy could be beneficial for the patients with complete response to minimize the RT dose down to 30 Gy. Prospective trials focused on de-intensification of the extended-field RT are warranted.

Objective: Human adipose tissue-derived mesenchymal stem cells (ASCs) have been reported to promote angiogenesis and tissue repair. However, poor survival and engraftment efficiency of transplanted ASCs are the major bottlenecks for therapeutic application. The present study aims to improve the therapeutic efficacy of ASCs for peripheral artery diseases. Methods: Hydrogen peroxide (H2O2) was used to induce apoptotic cell death in ASCs.To measure apoptosis, we used flow cytometry-based apoptosis analysis and terminal deoxynucleotidyl transferase dUTP nick end labeling staining. A murine hindlimb ischemia model was established to measure the ASC-mediated therapeutic angiogenesis and in vivo survival ability of ASCs. Results: We identified that the inhibitor of lamin A-progerin binding, JH4, protects ASCs against H2O2-induced oxidative stress and apoptosis. Co-administration of ASCs with JH4 improved ASC-mediated blood reperfusion recovery and limb salvage compared to that of the control group in a mouse hind limb ischemia model. Immunofluorescence showed that JH4 treatment potentiated ASC-mediated vascular regeneration via reducing ASC apoptosis post transplantation. Conclusion JH4 exerts anti-apoptotic effects in ASCs in conditions of oxidative stress, and contributes to the repair of ischemic hind limb injury by improving cell survival.