The sentinel node concept has been widely discussed, and the technique of sentinel navigation surgery has been advocated. However, in the oral environment, the study of the lymphatic architecture has been hampered by the presence of hard tissues such as teeth and bone. In this study, we examined the distribution of lymphatic vessels in the gingiva using an enzyme-histochemical method, 5'-nucleotidase staining. In the buccal free gingiva, the density of lymphatic vessels was 7.8±0.4 on the oral epithelium side and 4.8±2.4 on the sulcal epithelium side. In the lingual free gingiva, the density was 9.4±0.3 on the oral epithelium side and 3.3±0.2 on the sulcal epithelium side. As a result, we concluded that the lymphatic network within the sulcal epithelium intrinsically provides a much poorer flow than the lymphatic network of the oral epithelium, similar to the blood capillary network.
Although several methods have been developed to investigate thrombus or hemostatic plug formation in microvessels in vivo , our knowledge on platelet behavior during such a process is still limited. We, therefore, developed new instrumentation which enables us to induce interactions of individual platelets and to detect their behavior with endothelium in and around the growing thrombus. To evoke a platelet reaction, focal hemorrhage was induced with a nitrogen-dye laser focused through the microscope optics using mesenteric microcirculation of the rat. Platelet deposition at the site of injury was then observed during thrombus formation in real-time. The system was able to provide images with high spatial resolution at video-frame rate that could be used to reconstruct three-dimensional model of a thrombus. (Abstract movie) [MVRC 2 (1): 8-12,2008]
The dental pulp, which is surrounded by the hard tissue of the tooth, contains the vessels required for circulation in the tooth. Within this closed environment, inflammation progresses very rapidly. Morphologically, the vasculature of dental pulp is being elucidated, but characteristics of lymphatic vessels have not been well established. Therefore, detailed knowledge of the inflammatory defense mechanism in dental pulp is currently lacking. In the present study, vascular changes after pulpitis incident to experimental cavity formation were observed by resin casting and scanning electron microscopy. A standard cylindrical experimental cavity (2-mm diameter x 2-mm depth) was created on the tooth surfaces of the lower premolars of beagle dogs. The synthetic resin was injected 4 h or 1, 3, 7, 30, or 90 days after cavity formation. The blood vessels of the dental pulp exhibited the three-layered structure of main artery and vein in the central layer, arteriole and venule in the intermediate layer, and capillary network (CN) in the surface layer. Four hours after cavity formation, leakage of resin was observed under the CN. One day after cavity formation, resin lumps gathered beneath the CN. After 3 days, a constricted vessel that connects to the venule was observed. After 7 days, a constricted vessel was found to run along the main artery and venule in the axis direction. After 30 and 90 days, the dental pulp was necrotized along the experimental cavity. These results suggest that the newly formed constricted vessel functions similarly to a lymphatic vessel. [MVRC 2 (1) : 13-17, 2008]
To treat pulpitis, a pulpectomy, which surgically removes dental pulp, is generally used. Recently, antibiotic therapy has also been utilized. In the present study, the effect of metronidazole, incident to experimental pulpitis, was observed by the resin cast method and a scanning electron microscope (SEM). Beagle dogs with healthy periodontal tissue served as the experimental animals. A standard experimental cavity (2mm in diameter x 2 mm depth) was prepared on the surface of the tooth. Experimental cavities were exposed in the oral cavity for 1 day or for 7 days. Then, one side of the experimental cavities was filled with glass ionomer cement containing 3% metronidazole and observed after 30 days. The remaining side of the cavities was filled with glass ionomer cement as a control. After experimental cavity preparation, leaking resin was observed under the capillary network. In the metronidazole-treated group, the leakage of resin decreased. The vascular structure was regenerated in a manner quite similar to normal pulp. However a circulatory disturbance was caused in the pulpal vasculature. These results indicate that constricted vessels and metronidazole work together to recover the microcirculation of dental pulp, suggesting that metronidazole can be an effective treatment for pulpitis.[MVRC 2 (1) : 18-23 ,2008]
Hyperglycemia plays a more important role in the initiation and development of microangiopathy than in macroangiopathy among diabetes-induced complications. Platelet-endothelium interaction and thrombus formation might be accelerated in diabetic microcirculation. However, few in vivo studies have demonstrated thrombus formation in microcirculation of diabetic animal models. In this study, we conducted a photothrombotic vessel occlusion model in the mesenteric arterioles of normal rats or streptozotocin-induced diabetic rats. A photothrombosis, which is caused by production of active oxygen, was induced under the presence of a photosensitizing dye (Photofrin) and light irradiation. We measured the time from beginning of irradiation to initiation of platelet adhesion (Ti) and the time from beginning of irradiation to vessel occlusion (To). Then we conducted a photochemical platelet adhesion assay using platelets collected from healthy controls or diabetic patients with human cultured endothelial cells treated with normal glucose concentration, high glucose concentration or advanced glycation end products (AGE). We measured the area of platelet adhesion to endothelial cells. The in vivo experimental results showed that Ti and To in diabetic arterioles significantly decreased compared to those in normal arterioles. The in vitro results did not show any significant difference between adhesion of normal platelets and that of diabetic platelets to the cultured endothelial cells. However, platelet adhesion to the cultured endothelial cells treated with high glucose concentration and with AGE increased significantly compared to that with normal glucose concentration. From these results, it can be concluded that platelet-endothelium interaction and thrombus formation are accelerated in diabetic microcirculation.[MVRC 2 (1): 24-32,2008]
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