Implant-supported fixed and removable prostheses in the fibular mandible

Abstract Background To restore the health-related quality of life (HRQoL) of patients who underwent jaw resection and reconstruction surgery, dental rehabilitation is an essential procedure and also one of the most challenging for oral and maxillofacial surgeons. Even though recent studies have reported the possibility and reliability of dental implant rehabilitation with the fibula free flap (FFF), clinical reports of long-term follow-up cases are scarce. We herein reported seven cases of FFF reconstruction and implant rehabilitation. We also discussed implant planning strategy and surgical techniques. Methods From 2012 to 2019, seven patients were treated with FFF reconstructive jaw surgery combined with dental implant installation and fabrication of implant-supported prostheses at Seoul National University Dental Hospital, Seoul, Korea. Patient characteristics and FFF treatment results were collected. Records of dental implants were analyzed clinically and radiologically. Results Among the seven patients in this report, there were three males and four females, with an average age of 54.4 years. A total of 39 implants were placed in the fibular bone. The mean follow-up period after implant installation was 24 months. Five implants failed and were removed 3 months after installation. The implant success rate was 87.2%. Marginal bone loss at 12 months after loading was 0.23 ± 0.18 mm on the mesial side and 0.25 ± 0.26 mm on the distal side. Conclusion With the challenges present in FFF-reconstructed patients, an implant-supported prosthesis is a reliable option for stable and functional oral rehabilitation. The implant-supported prosthesis on the FFF has great results regarding restoration of function (mastication, swallowing, and speaking), appearance, and overall HRQoL. Collaboration between surgeons and prosthodontists is essential for a satisfying outcome

Clinical feasibility and benefits of a tapered, sand-blasted, and acid-etched surfaced tissue-level dental implant

Abstract Background It has been 50 years since Brånemark first introduced the concept of osseointegration. Since then, numerous ongoing research, developments, and optimization of implant properties have been conducted. Despite the high survival and success rates of dental implants, failures still occur in a small number of patients that are being rehabilitated by implants. The purpose of this study was to evaluate the survival and success rate of the Stella® implants that incorporate sand-blasted and acid-etched (S&E) surface treatment and tapered body design to confirm their clinical feasibility and benefits after placement. Methods We reviewed 61 partially and fully edentulous patients who underwent a tapered, S&E surfaced tissue-level implant placement between May 2013 and February 2016 in the Department of Oral and Maxillofacial Surgery in the Seoul National University Dental Hospital. Patient characteristics and treatment results were collected, and records of dental implants were analyzed clinically and radiologically. Results A total of 105 implant fixtures were placed in these patients. The mean age at the time of the surgery was 63.7 years with a range of 31 to 88 years. In total, 4.0-mm and 4.5-mm diameter implants were the most frequently used dental implants (40%, 49%) in this study. Implants 8.5 mm in length were predominantly used (60%). Seventy dental implants were placed in the mandible (70%), and only one dental implant was placed in the maxillary anterior region. At the end of the 5-year observation period, the success rate of the Stella® implants was 98.1%. Among the 105 implants placed, 2 were considered to be failures. Summarizing the clinical and radiographic results, the remaining 103 implants were considered successfully integrated. Conclusion The overall success rate was 98.1%. The tapered, S&E surfaced tissue-level implant system exhibited great performance in a variety of clinical situations including failed implant sites that enabled predictable and successful treatment outcomes. The effectives of a tapered design of tissue level, not a parallel design, are shown in this clinical report

Soy protein supplementation does not cause lymphocytopenia in postmenopausal women

BACKGROUND: The health benefits of soy isoflavones have been widely investigated; however, there are some concerns as to whether soy isoflavones, similar to ipriflavone, a synthetic isoflavone, cause lymphocytopenia in postmenopausal women. Hence, the purpose of this study was to investigate the extent to which 12-month supplementation of 25 g soy protein containing 60 mg isoflavones alters lymphocyte counts or other hematological parameters in postmenopausal women who were not on hormone replacement therapy. METHODS: Eighty-seven postmenopausal women were randomly assigned to receive either soy protein or an equivalent amount of control protein devoid of isoflavones. Fasting venous blood was collected at baseline and at the end of twelve month study period for complete blood count analyses. RESULTS: Between the two treatment groups, the percent changes in hematological parameters, including lymphocytes, were not different. While women consuming the soy supplement had an increase in mean corpuscular hemoglobin concentration (MCHC) and red cell distribution width index (RDW; a marker of reticulocytes), women consuming the control diet had higher percentage of only MCHC. CONCLUSION: Overall, the results of the present study indicate that consumption of 25 g soy protein containing 60 mg isoflavones daily for one year does not cause lymphocytopenia

Mouse Odf2 localizes to centrosomes and basal bodies in adult tissues and to the photoreceptor primary cilium

Odf2 (outer dense fiber 2) is the major protein of the cytoskeleton of the sperm tail. In somatic cells, it is a component of the centrosome in which it is located in the appendages of the mother centriole. Additionally, as shown previously by forced expression in cultured cells, Odf2 localizes to centrioles, basal bodies, and primary cilia, which are all structurally and functionally interconnected. The importance of Odf2 has become obvious by the absence of primary cilia in Odf2-deficient cells and by the embryonic lethality of the Odf2 gene trap insertional mouse. However, nothing is known about the endogenous localization of Odf2 in the tissues of adult mice. We show here that Odf2 protein localizes to centrosomes, to photoreceptor primary cilia, and to basal bodies of ciliated cells of the respiratory epithelium and of the kidney. Our results thus suggest that Odf2 contributes to assorted ciliopathies

STK295900, a Dual Inhibitor of Topoisomerase 1 and 2, Induces G<inf>2</inf> Arrest in the Absence of DNA Damage

STK295900, a small synthetic molecule belonging to a class of symmetric bibenzimidazoles, exhibits antiproliferative activity against various human cancer cell lines from different origins. Examining the effect of STK295900 in HeLa cells indicates that it induces G2 phase arrest without invoking DNA damage. Further analysis shows that STK295900 inhibits DNA relaxation that is mediated by topoisomerase 1 (Top 1) and topoisomerase 2 (Top 2) in vitro. In addition, STK295900 also exhibits protective effect against DNA damage induced by camptothecin. However, STK295900 does not affect etoposide-induced DNA damage. Moreover, STK295900 preferentially exerts cytotoxic effect on cancer cell lines while camptothecin, etoposide, and Hoechst 33342 affected both cancer and normal cells. Therefore, STK295900 has a potential to be developed as an anticancer chemotherapeutic agent. © 2013 Kim et al

N-Glycosylation of ß4 Integrin Controls the Adhesion and Motility of Keratinocytes

α6ß4 integrin is an essential component of hemidesmosomes and modulates cell migration in wound healing and cancer invasion. To elucidate the role of N-glycosylation on ß4 integrin, we investigated keratinocyte adhesion and migration through the re-expression of wild-type or N-glycosylation-defective ß4 integrin (ΔNß4) in ß4 integrin null keratinocytes. N-glycosylation of ß4 integrin was not essential for the heterodimer formation of ß4 integrin with α6 integrin and its expression on a cell surface, but N-glycosylation was required for integrin-mediated cell adhesion and migration. Concomitantly with the reduction of ß4 integrin in the membrane microdomain, the intracellular signals of Akt and ERK activation were decreased in cells expressing ΔNß4 integrin. Forced cross-linking of ß4 integrin rescued the decreased ERK activation in ΔNß4 integrin-expressing cells to a similar extent in wild-type ß4 integrin-expressing cells. Surprisingly, compared with cells expressing wild-type ß4 integrin, an alternation in N-glycan structures expressed on epidermal growth factor receptor (EGFR), and the induction of a stronger association between EGFR and ß4 integrin were observed in ΔNß4 integrin-expressing cells. These results clearly demonstrated that N-glycosylation on ß4 integrin plays an essential role in keratinocyte cellular function by allowing the appropriate complex formation on cell surfaces

Oncogenic CagA Promotes Gastric Cancer Risk via Activating ERK Signaling Pathways: A Nested Case-Control Study

Background: CagA cellular interaction via activation of the ERK signaling pathway may be a starting point in the development of gastric cancer. This study aimed to evaluate whether genes involved in ERK downstream signaling pathways activated by CagA are susceptible genetic markers for gastric cancer. Methods: In the discovery phase, a total of 580 SNPs within +/-5 kbp of 30 candidate genes were genotyped to examine an association with gastric cancer risk in the Korean Multi-center Cancer Cohort (100 incident gastric cancer case-control sets). The most significant SNPs (raw or permutated p value??0.02) identified in the discovery analysis were re-evaluated in the extension phase using unconditional logistic regression model (400 gastric cancer case-control sets). Combined analyses including pooled-and meta-analysis were conducted to summarize all the results. Results: 24 SNPs in eight genes (ERK, Dock180, C3G, Rap1, Src, CrkL, Mek and Crk) were significantly associated with gastric cancer risk in the individual SNP analyses in the discovery phase (p??0.05). In the extension analyses, ERK rs5999749, Dock180 rs4635002 and C3G rs7853122 showed marginally significant gene-dose effects for gastric cancer. Consistently, final combined analysis presented the SNPs as significantly associated with gastric cancer risk (OR = 1.56, [95% CI: 1.19-2.06], OR = 0.61, [95% CI: 0.43-0.87], OR = 0.59, [95% CI: 0.54-0.76], respectively). Conclusions: Our findings suggest that ERK rs5999749, Dock180 rs4635002 and C3G rs7853122 are genetic determinants in gastric carcinogenesis

Genetic Susceptibility on CagA-Interacting Molecules and Gene-Environment Interaction with Phytoestrogens: A Putative Risk Factor for Gastric Cancer

OBJECTIVES: To evaluate whether genes that encode CagA-interacting molecules (SRC, PTPN11, CRK, CRKL, CSK, c-MET and GRB2) are associated with gastric cancer risk and whether an interaction between these genes and phytoestrogens modify gastric cancer risk. METHODS: In the discovery phase, 137 candidate SNPs in seven genes were analyzed in 76 incident gastric cancer cases and 322 matched controls from the Korean Multi-Center Cancer Cohort. Five significant SNPs in three genes (SRC, c-MET and CRK) were re-evaluated in 386 cases and 348 controls in the extension phase. Odds ratios (ORs) for gastric cancer risk were estimated adjusted for age, smoking, H. pylori seropositivity and CagA strain positivity. Summarized ORs in the total study population (462 cases and 670 controls) were presented using pooled- and meta-analysis. Plasma concentrations of phytoestrogens (genistein, daidzein, equol and enterolactone) were measured using the time-resolved fluoroimmunoassay. RESULTS: SRC rs6122566, rs6124914, c-MET rs41739, and CRK rs7208768 showed significant genetic effects for gastric cancer in both the pooled and meta-analysis without heterogeneity (pooled OR = 3.96 [95% CI 2.05-7.65], 1.24 [95% CI = 1.01-1.53], 1.19 [95% CI = 1.01-1.41], and 1.37 [95% CI = 1.15-1.62], respectively; meta OR = 4.59 [95% CI 2.74-7.70], 1.36 [95% CI = 1.09-1.70], 1.20 [95% CI = 1.00-1.44], and 1.32 [95% CI = 1.10-1.57], respectively). Risk allele of CRK rs7208768 had a significantly increased risk for gastric cancer at low phytoestrogen levels (p interaction<0.05). CONCLUSIONS: Our findings suggest that SRC, c-MET and CRK play a key role in gastric carcinogenesis by modulating CagA signal transductions and interaction between CRK gene and phytoestrogens modify gastric cancer risk