Comparison of Macro-and Micro-porosity of a Titanium Mesh for Guided Bone Regeneration: An In Vivo Experimental Study.

BACKGROUND/AIM: Guided bone regeneration (GBR) is one of the surgical methods used for vertical ridge augmentation prior to dental implant placements. Titanium meshes have been used for osteogenic space maintenance in GBR sites by clinicians. We aimed to compare the influence of micropores and macropores in a titanium mesh on bone regeneration in a rat calvarial vertical GBR model. MATERIALS AND METHODS: The calvaria of nine rats were exposed, and plastic cylinders were set bilaterally. Eighteen surgical sites were randomly allocated into three groups according to the materials of titanium lid and bone substitutes: microporous titanium lid+deproteinized bovine bone mineral (DBBM), macroporous titanium lid +DBBM, microporous titanium lid+carbonate apatite. Newly generated bone inside the cylinders was evaluated using micro-computed tomography (micro-CT). Furthermore, bone regeneration and angiogenesis were evaluated histologically at 12 weeks. RESULTS: Quantitative volumetric analyses using micro-CT showed a gradual increase in bone volume inside the cylinders in all three groups. Histological observation confirmed vigorous bone regeneration in the microporous groups compared to that in the macroporous group. In the upper part of the cylinders, soft tissue invaded the GBR site by passing through the pores of the macroporous mesh. The blood vessels in the upper part of the cylinders were smaller in the microporous groups than in the macroporous group. There was no difference in bone formation between cylinders filled with DBBM or carbonate apatite. CONCLUSION: Microvasculature penetrates 50-µm diameter micropores and accelerates bone formation inside the cylinder, which was set on rat calvaria. The microporous titanium mesh can facilitate angiogenesis from both the dura mater and periosteal in vertical ridge augmentation. Our data showed superiority of microporous titanium vascular permeability and osteoconductivity, supporting bone growth.

Real-time assessment of guided bone regeneration in critical size mandibular bone defects in rats using collagen membranes with adjunct fibroblast growth factor-2.

BACKGROUND/PURPOSE: Fibroblast growth factor-2 (FGF-2) regulates bone formation. The concept of guided bone regeneration using a resorbable collagen membrane (RCM) is generally accepted in implant dentistry. This study aimed to investigate the bone healing pattern in rat mandibular bone defects in real-time with and without RCM containing FGF-2 (RCM/FGF-2). MATERIALS AND METHODS: Critical-size circular bone defects (4.0 mm diameter) were created on both sides of the rat mandibular bone. The defects were randomly divided into the following groups: control, RCM alone, RCM containing low (0.5 µg) or high (2.0 µg) concentration of FGF-2. We performed real-time in vivo micro-computerized tomography scans at the baseline and at 2, 4, and 6 weeks, and measured the volume of newly formed bone (NFB), bone mineral density (BMD) of NFB, and the closure percentage of the NFB area. At 6 weeks, the mandibular specimens were assessed histologically and histomorphometrically to evaluate the area of new bone regeneration. RESULTS: Real-time assessment revealed a significant increase in the volume, BMD, and closure percentage of the NFB area in the RCM/FGF-2-treated groups than that in the control and RCM groups. In the H-FGF-2 group, the volume and BMD of NFB exhibited a significant increase at 6 weeks than that at the baseline. Histological evaluation revealed the presence of osteoblasts, osteocytes, and blood vessels within the NFB. CONCLUSION: The real-time in vivo experiment demonstrated that RCM/FGF-2 effectively promoted bone regeneration within the critical-size mandibular defects in rats and verified new bone formation starting in the early postoperative phase.

Pedicle Periosteum as a Barrier for Guided Bone Regeneration in the Rabbit Frontal Bone.

BACKGROUND/AIM: For alveolar ridge reconstruction prior to dental implant placement, a barrier membrane is placed to create space over the bone defect. Although periosteum possesses osteogenic capacity, direct contact between defects and periosteum has been avoided. The present study aimed to investigate whether pedicle periosteum could be used as a barrier membrane. MATERIALS AND METHODS: Twelve rabbits were used. A U-shaped incision was made in the frontal bone, and the skin-periosteum over the frontal bone was stripped. Two trephine-drilled holes with a diameter of 5 mm were prepared in the frontal bone. One hole was covered with pedicle periosteum (periosteum side), and the periosteum was secured to the contralateral side. The other defect was covered with an occlusive membrane (membrane side). RESULTS: The histological observation showed that both defects, which were covered either by the periosteum or by the membrane, were closed almost completely after 12 weeks of healing. No statistically significant difference was observed in the bone defect closure rates between the two sides at 4 and 12 weeks. CONCLUSION: This study demonstrated that the pedicle periosteum possesses regenerative effects equivalent to those of occlusive membrane. The periosteum contributes to new bone formation by acting as a mechanical barrier and a source of osteogenic components.

Inhibitory effects of a tryptamine derivative on ultraviolet radiation-induced apoptosis in MC3T3-E1 mouse osteoblasts.

MS-IPA1 is a new synthetic compound that is synthesized from tryptamine. Recently, our group demonstrated that SST-VED-I-1, which has a similar chemical structure to MS-IPA1, inhibits starvation-induced apoptosis in osteoblasts. However, the effects of MS-IPA1 on apoptosis in osteoblasts have not yet been examined. Therefore, this study examined the effects of this compound on apoptosis in osteoblasts. In this study, MC3T3-E1 mouse osteoblasts were used and apoptosis was induced by ultraviolet radiation (UV). We investigated the effect of MS-IPA1 on apoptosis by analyzing caspase3/7 activity, translocation of phosphatidylserine (PS), and mRNA expression levels of Bcl-2 and Bax. In addition, it was investigated whether MS-IPA1 affects cell proliferation and cell cycle progression. We found that MS-IPA1 had no effect on cell proliferation or cell cycle progression. However, MS-IPA1 suppressed UV-induced cell death in a dose-dependent manner, which was accompanied with the inhibition of caspase activation and translocation of PS. Furthermore, after UV exposure, Bcl-2 expression was increased in the MS-IPA1-treated cells as compared to that in the vehicle-treated cells. In contrast, Bax expression was decreased in the MS-IPA1-treated cell as compared to that in the vehicle-treated cells. These results suggest that MS-IPA1 has an inhibitory effect on apoptosis in osteoblasts through a Bcl-2 family-dependent signaling pathway.

Inhibitory Effects of a Tryptamine Derivative on Ultraviolet Radiation-Induced Apoptosis in MC3T3-E1 Mouse Osteoblasts.

MS-IPA1 is a new synthetic compound that is synthesized from tryptamine. Recently, our group demonstrated that SST-VED-I-1, which has a similar chemical structure to MS-IPA1, inhibits starvation-induced apoptosis in osteoblasts. However, the effects of MS-IPA1 on apoptosis in osteoblasts have not yet been examined. Therefore, this study examined the effects of this compound on apoptosis in osteoblasts. In this study, MC3T3-E1 mouse osteoblasts were used and apoptosis was induced by ultraviolet radiation (UV). We investigated the effect of MS-IPA1 on apoptosis by analyzing caspase3/7 activity, translocation of phosphatidylserine (PS), and mRNA expression levels of Bcl-2 and Bax. In addition, it was investigated whether MS-IPA1 affects cell proliferation and cell cycle progression. We found that MS-IPA1 had no effect on cell proliferation or cell cycle progression. However, MS-IPA1 suppressed UV-induced cell death in a dose-dependent manner, which was accompanied with the inhibition of caspase activation and translocation of PS. Furthermore, after UV exposure, Bcl-2 expression was increased in the MS-IPA1-treated cells as compared to that in the vehicle-treated cells. In contrast, Bax expression was decreased in the MS-IPA1-treated cell as compared to that in the vehicle-treated cells. These results suggest that MS-IPA1 has an inhibitory effect on apoptosis in osteoblasts through a Bcl-2 family-dependent signaling pathway.