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Yakından Mobil Ödeme (YMÖ) uygulamalarının kullanımı, geleneksel ödeme yöntemlerine göre birçok avantaj sağlaması nedeniyle giderek yaygınlaşmaktadır. Güney Kore'de YMÖ büyük bir yayılma gösterse de Almanya’da henüz yaygınlaşmadığı söylenebilir. Bu farklılığı anlamak için çalışma, her iki ülkede de YMÖ kullanma niyetiyle ilgili kabul faktörlerini incelemektedir. Kapsamlı bir literatür analizi ile YMÖ kullanım niyetini açıklamak için bir araştırma modeli geliştirilmiştir. Çevrimiçi bir anket yapılmış, araştırmaya 186 Alman ve 146 Güney Koreli katılmıştır. Sonuçlar, her iki ülkede de algılanan fayda, algılanan risk, algılanan uyumluluk ve kişisel yenilikçiliğin bireylerin davranışsal niyetini belirleyen faktörler olduğunu göstermiştir. Ayrıca sonuçlar, sosyal etkinin yalnızca Almanya'da YMÖ kullanma niyeti üzerinde bir etkisinin olduğunu, algılanan kullanım kolaylığı ve güven faktörlerinin her iki ülkede de anlamlı bir etkisinin olmadığını ortaya koymuştur. Son olarak, YMÖ kullanmaya yönelik davranışsal niyette, algılanan uyumluluk ve sosyal etki faktörlerinin etkilerinin kültür baz alınarak yapılan incelemede anlamlı olarak farklılaştığı bulunmuştur. Çalışma, teorik ve yönetimsel çıkarımların yanı sıra izleyen araştırmalar için bazı bilgiler sunmaktadır., The use of Proximity Mobile Payment (PMP) applications with several advantages over traditional payment methods is becoming more common. While a large diffusion of PMP is already apparent in South Korea, Germany is still lagging behind. The study examines the acceptance factors regarding the intention to use PMP in the mentioned countries to understand this divergence. A research model was developed to explain the behavioral intention, with an extensive literature analysis. An online survey was conducted, 186 Germans and 146 South Koreans participated the research. Results show that in both countries perceived usefulness, perceived risk, perceived compatibility, and personal innovativeness are the factors that determine the individuals’ intention to use PMP. In addition, the social influence has an impact on the intention only in Germany, while the factors perceived ease of use and trust had no influence in both countries. Lastly, the influence of factors perceived compatibility and social influence on intention varies due to cultural differences. The study provides theoretical and managerial implications as well as an insight for further research.

Objectives This open, single-cohort, multicenter, prospective study investigated the efficacy of immediately provisionalized tapered conical connection implant for single-tooth restorations in the anterior and premolar regions of the maxilla after 5 years of function. Materials and methods All implants were placed in healed sites and immediately provisionalized. MBLs, soft-tissue parameters, and oral-health impact profile (OHIP) were evaluated at implant insertion, 6, 12, 24, 36, and 60 months. Paired Wilcoxon signed-rank tests and Kaplan–Meier survival analysis was used for statistical and implant survival/success analyses, respectively. Results Seventy-seven patients (81 implants) completed the 5-year follow-up. The 5-year cumulative survival and success rates were 97.8%, and the mean MBL change from implant insertion to 5 years was − 0.80 ± 1.13 mm. Optimal papilla index scores were observed at 90.1% of sites at 5 years compared with 32.8% of sites at insertion. Pink esthetic score, modified bleeding and plaque indices, and OHIP showed statistically significant improvement at the 5-year follow-up. Conclusions Immediately provisionalized tapered conical connection implants promote marginal bone stability and excellent esthetic outcomes after 5 years of function. Clinical relevance This treatment is a viable option for patients requiring immediately provisionalized single-tooth restorations in the esthetic zone and shows favorable long-term clinical outcomes, including marginal bone stability and excellent esthetics.

This multicenter prospective clinical trial investigated immediately provisionalized, anodized, conical connection, tapered implants with platform shifting in maxillary anterior and premolar sites. Patients requiring single-tooth implant-supported restorations in maxillary anterior and premolar sites were enrolled. Implants were immediately provisionalized and evaluated at insertion, 6 months, and annually thereafter. Outcome measures were marginal bone level change (ΔMBL), cumulative survival rate (CSR), and success rate, soft-tissue parameters, and oral health impact profile (OHIP). ΔMBL and Pink Esthetic Score were analyzed using Wilcoxon signed-rank tests. CSR was calculated using life table analysis. Other soft-tissue parameters were analyzed using sign tests. Of 94 enrolled patients (99 implants), 84 (88 implants) attended the 3-year follow-up. After an initial bone loss between implant insertion and 6 months (− 0.92 ± 1.23 mm), bone levels stabilized from 6 months to 3 years (0.13 ± 0.94 mm) with no significant change. The 3-year CSR was 98.9%, and the cumulative success rate was 96.9%. Papilla index scores of 2 or 3 were observed at 88.6% of sites at the 3-year visit compared with 32.8% at implant insertion. Improvements were observed for all other outcomes, including bleeding on probing, esthetics, plaque, and OHIP. This restorative protocol was associated with high primary stability, patient satisfaction, stable bone levels, and an overall improvement of the soft tissue outcomes over a 3-year period. The presented treatment is a viable option for single-tooth restorations of maxillary anterior teeth and premolars with successful short- to mid-long-term clinical outcomes.

Objectives The aim of this multicenter prospective clinical study was to evaluate anodized tapered implants with a conical connection and integrated platform shifting placed in the anterior and premolar maxilla. Materials and methods The study enrolled patients requiring single-tooth restorations in healed sites of maxillary anterior and premolar teeth. All implants were immediately temporized. Clinical and radiographic evaluations were conducted at implant insertion, 6 months, and 1 year. Outcome measures included bone remodeling, cumulative survival rate (CSR), success rate, soft-tissue health and esthetics, and patient satisfaction. Bone remodeling and pink esthetic score were analyzed using Wilcoxon signed-rank tests. CSR was calculated using life table analysis. Other soft-tissue outcomes were analyzed using sign tests. Results Out of 97 enrolled patients (102 implants), 87 patients (91 implants) completed the 1-year visit. Marginal bone remodeling was −0.85 ± 1.36 mm. After the expected initial bone loss, a mean bone gain of 0.11 ± 1.05 mm was observed between 6 months and 1 year. The CSR was 99.0%, and the cumulative success rate was 97.0%. Partial or full papilla was observed at 30.8% of sites at baseline, 87.2% at 6 months, and 90.5% at 1 year. Soft-tissue response, esthetics, and patient satisfaction all improved during the study period. Conclusions Bone gain was observed following the expected initial bone loss, and soft-tissue outcomes improved suggesting favorable tissue response using anodized tapered conical connection implants. Clinical relevance Rapid stabilization of bone remodeling and robust papilla regeneration indicate favorable tissue healing promoted by the conical connection, platform-shift design. Trial registration clinicaltrials.gov NCT02175550

AIM Pharmacological inhibitors of prolyl hydroxylases, also termed hypoxia-mimetic agents (HMAs), when repeatedly injected can support angiogenesis and bone regeneration. However, the possible role of HMA loaded onto bone substitutes to support angiogenesis and bone regeneration under diabetic condition is unknown. The capacity of HMA loaded onto deproteinized bovine bone mineral (DBBM) to support angiogenesis and bone formation was examined in diabetic Wistar rats. METHODS Diabetes was induced by intraperitoneal injection of streptozotocin. The HMA dimethyloxalylglycine (DMOG) and desferrioxamine (DFO) were lyophilized onto DBBM. Calvarial defects were created with a trephine drill and filled with the respective bone substitutes. After 4 weeks of healing, the animals were subjected to histological and histomorphometric analysis. RESULTS In this report, we provide evidence that DMOG loaded onto DBBM can support angiogenesis in vivo. Specifically, we show that DMOG increased the vessel area in the defect site to 2.4% ± 1.3% compared with controls 1.1% ± 0.48% (P = 0.012). There was a trend toward an increased vessel number in the defect site with 38.6 ± 17.4 and 31.0 ± 10.3 in the DMOG and the control group (P = 0.231). The increase in angiogenesis, however, did not translate into enhanced bone formation in the defect area with 9.2% ± 7.1% and 8.4% ± 5.6% in DMOG and control group, respectively. No significant changes were caused by DFO. CONCLUSIONS The results suggest that DMOG loaded onto DBBM can support angiogenesis, but bone formation does not increase accordingly in a type 1 diabetic rat calvarial defect model at the indicated time point.

Aim Vitamin D deficiency is highly prevalent in the population and associated with impaired peri-implant bone regeneration. Yet, there is a gap in understanding the impact of vitamin D supplementation on the process of osseointegration. In this study, the effect of vitamin D supplementation on peri-implant bone regeneration was investigated. Methods Fifty ovariectomized Sprague–Dawley rats were divided into three groups. The depletion group was fed a vitamin D-free diet for 8 weeks. The repletion group received vitamin D-free diet for 6 weeks, before animals were switched to standard diet containing 2400 IU/kg vitamin D. The control group was fed the standard diet. Two titanium mini-implants were placed in the tibia. All groups remained on their previous diet until sacrifice. Blood sample testing and histomorphometric analysis were performed. Results Vitamin D depletion caused a significant reduction in 25-hydroxvitamin D in rat serum that returned to control levels in the repletion group. This vitamin deficiency was associated with a decrease in bone-to-implant contact in the cortical area, which was leveled to controls in the repletion group. No significant changes by vitamin D depletion were noticed in the medullar compartment. Moreover, also the peri-implant bone area and the mineral apposition rate remained unchanged upon vitamin D depletion. Conclusion These results indicate that vitamin D deficiency has a negative impact on cortical peri-implant bone formation in ovariectomized rats, which can be compensated by vitamin D supplementation. This study provides first insight into the potential beneficial effect of vitamin D supplementation in implant dentistry.

INTRODUCTION: The demand for new therapeutic approaches to treat bone defects and fractures is increasing in trauma surgery and orthopaedics because the number of patients with degenerative diseases is continuously growing. "Tissue Engineering" offers promising new technologies that combine the three components - cells, growth factors and matrix. Efforts are targeted at improving and accelerating recovery, especially for long bone fractures, and reducing the risk of delayed bone healing or pseudoarthrosis. Adult human adipose-derived stem cells (ASC) can differentiate into osteoblasts in an osteogenic surrounding. Bone morphogenetic protein-2 (BMP-2) accelerates and initiates this differentiation. Fibrin, a matrix that promotes wound healing, is a promising carrier for ASCs and BMP-2.MATERIALS AND METHODS: In this study, a 2mm transcortical drill hole in the femur of male rats served as a small non-critical size defect model for fracture simulation. In vivo bone healing was investigated upon administration of the growth factor BMP-2 embedded with ASCs in a locally applied fibrin matrix. Groups with the components alone were also investigated. After 2 and 4 weeks, μCT and histology were performed to determine the bone and callus volume.RESULTS AND DISCUSSION: After only a short period of time (2 and 4 weeks), this animal model discloses comparative information about the osteogenetic potential and bone regeneration with little effort (no osteosynthesis necessary). The most significant result found in this model is that the combination of ASCs and BMP-2 in a fibrin matrix significantly reduces callus formation after 2 weeks compared to BMP-2 alone. BMP-2 alone significantly increased callus formation. ASCs embedded alone in the fibrin matrix did not lead to increased bone regeneration.CONCLUSION: Transplantation of ASC modulated the callus induction by BMP-2 to a normal volume.

Intravenous application of bisphosphonates (BP) represents an established therapeutic strategy of tumor-associated bone metastasis and severe hypercalcemia. Patients can develop osteonecrosis of the jaw (ONJ) as a side effect of this therapy. The diagnosis of ONJ is based on three criteria: a) patients have been or are currently treated with BP; b) a deficiency in wound healing, which is in 70-80% associated with necrotic alveolar bone, characteristically exposed, is present for at least 8 weeks and c) no radiotherapy of the head and neck was performed. The suppression of bone turnover, concomitant with high functional load of the alveolar bone, and the subsequent accumulation of microfractures are considered the main pathologic factors of this disease. The cumulative incidence of ONJ lies approximately between 1 and 10% in oncologic patients, being associated with the antiresorptive potency and the respective molecular structure of the BPs. Patients with multiple myeloma develop ONJ more frequently than patients with other oncological diseases such as metastasizing breast- and prostate cancer, a fact that may also be due to the higher transfusion/injection frequency of BP in these patients. Dental treatment strategies are responsible for the occurrence of ONJ in approximately 80% of cases. Based on a clinical staging, patients can be grouped into three categories and should receive the corresponding treatment regime. Prospective clinical studies are required for a better understanding of etiology and pathogenesis of ONJ to make treatment, risk estimation and prognosis of ONJ more accurate.

AIM Vitamin D deficiency is considered to diminish bone regeneration. Yet, raising the serum levels takes months. A topic application of the active vitamin D metabolite, calcitriol, may be an effective approach. Thus, it becomes important to know the effect of vitamin D deficiency and local application on alveolar bone regeneration. MATERIAL AND METHODS Sixty rats were divided into three groups; two vitamin depletion groups and a control group. Identical single defects (2 mm diameter) were created in the maxilla and mandible treated with calcitriol soaked collagen in one deficiency group while in the other two groups not. Histomorphometric analysis and micro CTs were performed after 1 and 3 weeks. Serum levels of 25(OH)D3 and PTH were determined. RESULTS Bone formation rate significantly increased within the observation period in all groups. Bone regeneration was higher in the maxilla than in the mandible. However, bone regeneration was lower in the control group compared to vitamin depletion groups, with no significant effects by local administration of calcitriol (micro CT mandible p = 0.003, maxilla p

AIM Pharmacological inhibitors of prolyl hydroxylases, also termed hypoxia-mimetic agents (HMAs), when repeatedly injected can support angiogenesis and bone regeneration. However, the possible role of HMA loaded onto bone substitutes to support angiogenesis and bone regeneration under diabetic condition is unknown. The capacity of HMA loaded onto deproteinized bovine bone mineral (DBBM) to support angiogenesis and bone formation was examined in diabetic Wistar rats. METHODS Diabetes was induced by intraperitoneal injection of streptozotocin. The HMA dimethyloxalylglycine (DMOG) and desferrioxamine (DFO) were lyophilized onto DBBM. Calvarial defects were created with a trephine drill and filled with the respective bone substitutes. After 4 weeks of healing, the animals were subjected to histological and histomorphometric analysis. RESULTS In this report, we provide evidence that DMOG loaded onto DBBM can support angiogenesis in vivo. Specifically, we show that DMOG increased the vessel area in the defect site to 2.4% ± 1.3% compared with controls 1.1% ± 0.48% (P = 0.012). There was a trend toward an increased vessel number in the defect site with 38.6 ± 17.4 and 31.0 ± 10.3 in the DMOG and the control group (P = 0.231). The increase in angiogenesis, however, did not translate into enhanced bone formation in the defect area with 9.2% ± 7.1% and 8.4% ± 5.6% in DMOG and control group, respectively. No significant changes were caused by DFO. CONCLUSIONS The results suggest that DMOG loaded onto DBBM can support angiogenesis, but bone formation does not increase accordingly in a type 1 diabetic rat calvarial defect model at the indicated time point.

Age-related changes in periodontal bone regeneration, osseointegration of dental implants, and graft consolidation are increasingly considered in treatment planning. This study was intended to show whether aging is associated with a diminished responsiveness of osteoprogenitor cells to growth and differentiation factors.We compared the capacity of bone marrow stromal cells harvested from young and adult rats to proliferate, migrate, and differentiate into the osteogenic lineage following exposure to platelet-released supernatant (PRS) or bone morphogenetic protein-6 (BMP-6). Bone marrow stromal cells were isolated from 12 young rats aged 6 weeks and 12 adult rats aged 9 months. Proliferation was assessed by 3[H]thymidine incorporation, migration was evaluated with the Boyden chamber assay, and osteogenic differentiation was deduced from alkaline phosphatase activity.Irrespective of the donor age, bone marrow stromal cells showed increased mitogenic activity and chemotactic motility when exposed to PRS. Adult bone marrow stromal cells had higher alkaline phosphatase activities at baseline and upon incubation with BMP-6 than cells obtained from young animals. There was no difference between the two groups in the slope of the alkaline phosphatase activity curve following stimulation with BMP-6.The data demonstrate that, irrespective of their age, bone marrow stromal cells respond similarly to PRS and BMP-6 under in vitro conditions. These findings suggest that osteoprogenitor cells within the bone marrow of adult rats retain their juvenile potential to respond to growth and differentiation factors, which are released naturally or are applied therapeutically at sites of bone regeneration.

Delivery of DNA mixed with a degradable matrix carrier was supposed to improve transgene expression. Using a rabbit hind-limb ischemia model, we tested the angiogenic potency of plasmid encoding human vascular endothelial growth factor (pSG5-VEGF165) entrapped in fibrin sealant. Animals were injected intramuscularly with 500 μg of pSG5-VEGF165 or control plasmid, dissolved in saline (PBS) or fibrin glue. After 14 days, presence of delivered constructs and expression of transgene was confirmed in injected muscles of all animals. There were no significant differences in the levels of human VEGF mRNA and protein between VEGF-PBS and VEGF-fibrin groups (Mann-Whitney test). Accordingly, pSG5-VEGF165 regardless of the way of delivery, induced similar increases in capillary density within treated muscles (ANOVA). Control plasmid did not show any effects. In conclusion, injection of pSG5-VEGF165 into ischemic adductor muscle leads to synthesis of human VEGF and increases the number of capillaries. Fibrin carrier does not influence its angiogenic potential.

Background: Peroxisome proliferator-activated receptor-γ (PPARγ) ligands were shown to induce the vascular endothelial growth factor (VEGF) synthesis in several cell types. We tested the effect of ciglitazone, one of the most specific PPARγ agonists, on the angiogenic activity of VEGF. Methods: Experiments were performed on human umbilical vein endothelial cell (HUVEC), incubated for 12 to 48 h with human VEGF165 (30 ng/ml) in the presence or absence of ciglitazone (1–10 µM). Cell proliferation was tested by BrdU incorporation. Migration was measured in modified Boyden chambers. Morphogenesis and capillary outgrowth were assessed by tube formation assay and spheroid cell culture, respectively. Results: Treatment with ciglitazone inhibited by about 50 % VEGF-induced proliferation, migration, morphogenesis, and sprouting of capillaries. Conclusions: Thus we conclude that, despite augmentation of VEGF generation, ciglitazone may act as an antiangiogenic agent attenuating VEGF activity by directly influencing endothelial cells.

Background: Ischaemia/reperfusion (I/R) injury is characterized by the production of oxygen free radicals and the loss of high energy phosphates. α-Tocopherol (vitamin E) has been reported to play a protective role against free radical damage. Therefore, its i. v. supplementation prior to onset of ischaemia was investigated in an established I/R injury model. Methods: New Zealand white rabbits were subjected to a bilateral hind limb ischaemia/reperfusion of 2.5 h/2 h without any treatment (IR group), whereas in the VE group the vitamin E emulsion Tocovenos® was given i. v. for 10 min in a dose of 3 mg/kg bw. A SHAM group served as a control. Intramuscular phosphocreatine (PCr) and adenosine triphosphate (ATP), muscle interfibre area (MIFA), and microvessel cross-sectional area (MVCSA) were determined and electron microscopy was performed. Results: In the IR group, PCr decreased by 65 % of the initial level after 2.5 h of ischaemia and a further depletion was noticed after 2 h of reperfusion (20.9±1.1 vs 6.3±3.0 µmol/g wet wt,P

AIM Vitamin D deficiency is considered to diminish bone regeneration. Yet, raising the serum levels takes months. A topic application of the active vitamin D metabolite, calcitriol, may be an effective approach. Thus, it becomes important to know the effect of vitamin D deficiency and local application on alveolar bone regeneration. MATERIAL AND METHODS Sixty rats were divided into three groups; two vitamin depletion groups and a control group. Identical single defects (2 mm diameter) were created in the maxilla and mandible treated with calcitriol soaked collagen in one deficiency group while in the other two groups not. Histomorphometric analysis and micro CTs were performed after 1 and 3 weeks. Serum levels of 25(OH)D3 and PTH were determined. RESULTS Bone formation rate significantly increased within the observation period in all groups. Bone regeneration was higher in the maxilla than in the mandible. However, bone regeneration was lower in the control group compared to vitamin depletion groups, with no significant effects by local administration of calcitriol (micro CT mandible p = 0.003, maxilla p

Nitric oxide (NO) is a mediator involved in bone regeneration. We therefore examined the effect of the novel NO donor, S-nitroso human serum albumin (S-NO-HSA) on bone formation in a rabbit calvaria augmentation model. Circular grooves (8 mm diameter, two per animal) were created by a trephine drill in the cortical bone of 40 rabbits and titanium caps were placed on the rabbit calvaria bone filled with a collagen sponge soaked with either 100 μL S-NO-HSA (5%, 20%) or human albumin (5%, 20%). After 4 weeks the titanium hemispheres were subjected to histological and histomorphometric analysis. Bone formation and the volume of the residual collagen sponge were evaluated. S-NO-HSA treatment groups had a significantly higher volume of newly formed bone underneath the titanium hemispheres compared to the albumin control groups (5%: 15.5 ± 4.0% versus 10.6 ± 2.9%; P < 0.05; 20%: 14.0 ± 4.6% versus 6.0 ± 3.8%; P < 0.01). The volume of residual collagen sponge was also significantly lower in the S-NO-HSA groups compared to the control groups (5%: 0.4 ± 0.5% versus 2.6 ± 2.4%; P < 0.05 and 20%: 1.5 ± 2.7% versus 13.0 ± 18.7%; P < 0.01). This study demonstrates for the first time that S-NO-HSA promotes bone formation by slow NO release. Additionally, S-NO-HSA increases collagen sponge degradation.

Background. A prospective randomized multicenter trial was performed to compare knitted gelatin-coated Dacron bifurcation grafts, knitted collagen-coated Dacron grafts, and stretch polytetrafluoroethylene (PTFE) grafts. Methods. Between 1991 and 1998, 315 elective patients were randomized by age, gender, diabetes, runoff, indication (aneurysm, aortoiliac occlusive disease), and nicotine consumption at 3 centers of vascular surgery in Austria. The patients received gelatin-coated Dacron (GEL-D) grafts (n = 109), collagen-coated Dacron (COL-D) grafts (n = 100), or stretch PTFE grafts (n = 106). Results. No intraoperative deaths occurred. The 30-day mortality was 3%. No difference was found between the 3 graft materials in long-term patency. The primary 5-year patency rates were 92% for GEL-D, 89% for COL-D, and 91% for stretch PTFE (P =.6001). The secondary 5-year patency rates also differed: 97% for GEL-D, 100% for COL-D, and 97% for stretch PTFE (P =.2062). Early occlusions were observed overall in 3% and late occlusions in 5% of patients. When both Dacron grafts were compared collectively with stretch PTFE, a difference was found in infection rate: Dacron 3% (6/209) versus PTFE 0% (0/106); P

Nitric oxide (NO) is a mediator involved in bone regeneration. We therefore examined the effect of the novel NO donor, S-nitroso human serum albumin (S-NO-HSA) on bone formation in a rabbit calvaria augmentation model. Circular grooves (8 mm diameter, two per animal) were created by a trephine drill in the cortical bone of 40 rabbits and titanium caps were placed on the rabbit calvaria bone filled with a collagen sponge soaked with either 100 μL S-NO-HSA (5%, 20%) or human albumin (5%, 20%). After 4 weeks the titanium hemispheres were subjected to histological and histomorphometric analysis. Bone formation and the volume of the residual collagen sponge were evaluated. S-NO-HSA treatment groups had a significantly higher volume of newly formed bone underneath the titanium hemispheres compared to the albumin control groups (5%: 15.5 ± 4.0% versus 10.6 ± 2.9%; P < 0.05; 20%: 14.0 ± 4.6% versus 6.0 ± 3.8%; P < 0.01). The volume of residual collagen sponge was also significantly lower in the S-NO-HSA groups compared to the control groups (5%: 0.4 ± 0.5% versus 2.6 ± 2.4%; P < 0.05 and 20%: 1.5 ± 2.7% versus 13.0 ± 18.7%; P < 0.01). This study demonstrates for the first time that S-NO-HSA promotes bone formation by slow NO release. Additionally, S-NO-HSA increases collagen sponge degradation.

Intravenous application of bisphosphonates (BP) represents an established therapeutic strategy of tumor-associated bone metastasis and severe hypercalcemia. Patients can develop osteonecrosis of the jaw (ONJ) as a side effect of this therapy. The diagnosis of ONJ is based on three criteria: a) patients have been or are currently treated with BP; b) a deficiency in wound healing, which is in 70-80% associated with necrotic alveolar bone, characteristically exposed, is present for at least 8 weeks and c) no radiotherapy of the head and neck was performed. The suppression of bone turnover, concomitant with high functional load of the alveolar bone, and the subsequent accumulation of microfractures are considered the main pathologic factors of this disease. The cumulative incidence of ONJ lies approximately between 1 and 10% in oncologic patients, being associated with the antiresorptive potency and the respective molecular structure of the BPs. Patients with multiple myeloma develop ONJ more frequently than patients with other oncological diseases such as metastasizing breast- and prostate cancer, a fact that may also be due to the higher transfusion/injection frequency of BP in these patients. Dental treatment strategies are responsible for the occurrence of ONJ in approximately 80% of cases. Based on a clinical staging, patients can be grouped into three categories and should receive the corresponding treatment regime. Prospective clinical studies are required for a better understanding of etiology and pathogenesis of ONJ to make treatment, risk estimation and prognosis of ONJ more accurate.

Ischemia/reperfusion (I/R) injury is characterized by the production of oxygen-free radicals leading to disturbances in vasomotility (microvascular constriction) and microvascular permeability (interstitial edema formation). The objective was to evaluate the effect of the combined antioxidative and enzymatic preparation Phlogenzym on I/R injury of skeletal muscle.A rabbit hindlimb model of I/R (2.5/2 h) was used (IR group). Phlogenzym, containing rutin, trypsin, and bromelain, was applied enterally (60 mg/kg body weight) as a bolus 30 min prior to ischemia (Ph group). Sham-operated animals served as controls (CO group). Plasma malondialdehyde, potassium, and microvascular perfusion (monitored by laser flowmetry) were assessed. Histomorphometry and electron microscopy were performed from major adductor muscles.Two hours after reperfusion, potassium levels were significantly elevated in IR compared to Ph group (6.7 +/- 1.2 versus 4.9 +/- 0.9 mmol/l, P0.006). Enhanced lipid peroxidation, apparent by increased plasma malondialdehyde levels, was ameliorated in the Ph group (1.0 +/- 0.1 versus 0.7 +/- 0.1 nmol/ml, P0.0001). No-reflow (reduction of blood flow by 62% in IR group) was not observed in the Ph group (P0.004). Phlogenzym treatment prevented microvascular constriction (17.6 +/- 2.3 versus 12.6 +/- 1.1 microm(2), P0.0001) and mollified interstitial edema (21.5 +/- 2.0 versus 26.0 +/- 3.7%, P0.017), resulting in mild ultrastructural alterations in contrast to pronounced sarcolemmal and mitochondrial damage in untreated rabbits.Phlogenzym had a protective effect on skeletal muscle during I/R injury expressed by prevention of no-reflow and preservation of muscle tissue.

Background: Arterial intimal hyperplasia and following restenosis may be inhibited by estrogens. We investigated the effect of a synthetic steroid hormone, Tibolon: (a) on intima hyperplasia and restenosis in vivo, and (b) on production of endothelial nitric oxide synthase (eNOS), vascular endothelial growth factor (VEGF), endothelial cell proliferation and apoptosis in vitro. Methods: Influence of Tibolon treatment (0.1 mg/kg body weight, during 3 days before and 3 weeks after the operation as a drinking solution once daily) on neointimal formation (measured by morphometry) and arterial wall damage (by qualitative histology) were investigated in vivo using an animal model of balloon injury of carotid artery. In human umbilical vein endothelial cells (HUVEC) and human microvascular endothelial cells (HMEC-1), the effect of Tibolon (0.1 µg/ml) on eNOS and VEGF was assessed by ELISA. Cell proliferation was induced by VEGF165 and measured by BrdU incorporation assay, cell apoptosis was detected colorimetrically measuring DNA fragmentation. Results: Balloon injury resulted in neointima formation and prominent damage of the carotid artery wall. Treatment with Tibolon increased luminal area, decreased intimal area and intima to media ratio, and promoted better reparation of damaged vessel wall. In vitro, Tibolon treatment did not influence the expression of eNOS protein in HUVEC as well as cell proliferation rate but reduced apoptosis of endothelial cells by about 40%. Additionally, this treatment suppressed basal and IL-1β-stimulated synthesis of VEGF in HMEC-1. Conclusions: Tibolon treatment suppressed neointimal formation and promoted better reparation of damaged vessel wall in carotid artery after balloon injury. This positive effect seems to be associated with improved endothelial cell survival resulting possibly in increased NO production. It might be also related to the decrease of VEGF generation.

Background. Cell membrane rupture by oxygen-derived free radicals is a systematic feature of ischemia/reperfusion (I/R) injury. High taurine concentration gradients in skeletal muscle prompted us to evaluate whether plasma taurine levels (pTau) are a useful marker of I/R injury after different periods of ischemia. Methods. Rabbits were randomly assigned to either 1 or 2.5 hours of hind-limb ischemia followed by 2 hours of reperfusion (groups IR1 [n = 12] and IR2.5 [n = 13], respectively). Corresponding sham groups (SHAM1 [n = 8] and SHAM2.5 [n = 9]) were used as controls. Analyzed parameters included histomorphometry and electron microscopy of skeletal muscle biopsies, pTau, and plasma level of malondialdehyde. Skeletal muscle function was assessed 3 weeks after I/R injury. Results. No significant morphologic changes were detectable at the end of ischemia. After reperfusion, mild interstitial edema with intact muscle cell membranes developed in IR1 group; pTau was not increased. IR2.5 group, by contrast, showed severe interstitial edema formation (interfiber area increased by 112%, P

Background — Peroxynitrite generated from nitric oxide (NO) and superoxide (O 2 − ) contributes to ischemia/reperfusion (I/R) injury. Feedback inhibition of endothelial NO synthase by NO may inhibit O 2 − production generated also by endothelial NO synthase at diminished local l -arginine concentrations accompanying I/R. Methods and Results — During hindlimb I/R (2.5 hours/2 hours), in vivo NO was monitored continuously (porphyrinic sensor), and high-energy phosphates, reduced and oxidized glutathione (chromatography), and I/R injury were measured intermittently. Rabbits receiving human serum albumin (HSA) (controls) were compared with those receiving S -nitroso human serum albumin (S-NO-HSA) beginning 30 minutes before reperfusion for 1 hour or 30 minutes before ischemia for 3.5 hours (0.1 μmol · kg −1 · h − 1 ). The onset of ischemia led to a rapid increase of NO from its basal level (50±12 nmol/L) to 120±20 and 220±15 nmol/L in the control and S-NO-HSA–treated groups, respectively. In control animals, NO dropped below basal levels at the end of ischemia and to undetectable levels (P P P < 0.00001). Conclusions — Long-lasting release of NO by S-NO-HSA provides significant protection of skeletal muscle from I/R injury.