This investigation was undertaken to assess bacterial plaque accumulation adjacent to orthodontic brackets. Experiments were carried out on 11 subjects who were scheduled for orthodontic treatment including extraction of two or four premolars. Metal brackets were bonded to the premolars to be extracted using macro-filled bonding composite. A conventional elastomeric ring was placed around one bracket and a steel ligature wire around the bracket on the contralateral tooth. The subjects were told to continue their normal oral hygiene regimen. Teeth were extracted at 1, 2, or 3 weeks after bracket bonding. Scanning electron microscopic (SEM) examination of brackets, excess composite, and buccal enamel revealed that mature plaque was present on excess composite at 2 and 3 weeks after bonding, whereas plaque on the gingival enamel surface was still at an early stage of development. The results demonstrate that excess composite around the bracket base is the critical site for plaque accumulation due to its rough surface and the presence of a distinct gap at the composite-enamel interface. The method of ligation does not appear to influence the bacterial morphotypes on both composite and enamel surfaces.
The aim of the study was to assess the effect of a comprehensive prophylactic regimen in reducing the incidence of white spot lesions (WSL) and caries during orthodontic treatment. Eighty consecutive patients, scheduled for fixed appliance treatment in both jaws were compared with a non-orthodontic matched-control group. The oral hygiene regimen consisted of brushing two to three times daily, flossing, fluoride rinse, and plaque disclosing tablets. Patients were requested to avoid carbonated soft drinks/acidic juices and candies. The WSL index of Gorelick et al. (Gorelick L, Geiger A M, Gwinnett A J 1982 Incidence of white spot formation after bonding and banding. American Journal of Orthodontics 81: 93-98) was used. Caries were scored according to Amarante et al. (Amarante E, Raadal M, Espelid I 1998 Impact of diagnostic criteria on the prevalence of dental caries in Norwegian children aged 5, 12 and 18 years. Community Dental Oral Epidemiology 26: 87-94). We collected data from all finished cases. It comprised 40 subjects in the orthodontic group (mean age: 13.6 years, range: 12-16 years) and 40 matched controls. The average treatment time was 18 months (range: 9-25 months). The mean increase in WSL index in the orthodontic group was 1.9 and 0.4 in the control group (P = 0.001). The mean increase in dentine caries was 0.5 lesions and 0.7 lesions in the in the orthodontic group and control group, respectively (P = 0.62). Twenty-three per cent of treated patients showed good compliance, 68 per cent moderate compliance, and 9 per cent poor compliance. The mean increase in WSL was 1.0, 1.4, and 3.3 in the good, moderate, and poor compliance group, respectively (P = 0.155). Orthodontically treated patients have significantly higher risk for developing WSL than untreated patients, while there is no difference with respect to development of new dentinal caries lesions. This study showed that a possible relationship between compliance and WSL development existed.
The rat incisor is a commonly used model in studies of tooth eruption, amelogenesis and effects of mechanical loading on the dental and periodontal tissues. The purpose of this study was to assess the three-dimensional architecture of the microvascular bed of the rat incisor enamel organ, to describe the direction of blood flow, and to provide a histometric assessment of the vascular categories that can be statistically analyzed. Vascular corrosion casts were prepared and examined by scanning electron microscopy. The microvasculature of the labial periodontal space was arranged in three distinct layers. The inner layer in direct relation to the enamel organ consisted of a capillary network which was drained by short venules at the cemento-enamel junction. The intermediate layer consisted of arterioles oriented parallel to the long axis of the incisor mainly mid-labially, branching off smaller arterioles to the capillary network. The outer layer was formed by flattened sinusoid vessels of larger caliber. Blood supply was from the anterior superior alveolar artery branches through the arterioles into the capillary network. Drainage was postero-laterally along the cemento-enamel junction via short venules which emptied into the sinusoid vessels, finally to flow through Volkmann's canals into the alveolar bone via small venules. The findings demonstrate that the microvasculature of the rat incisor enamel organ has an exceptionally high level of physiologically-adapted structural organization.
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