Enamel colour changes following whitening with 10 per cent carbamide peroxide: a comparison of orthodontically-bonded/debonded and untreated teeth. (49/1061)

The purpose of this study was to determine if a colour difference exists between teeth that had orthodontic appliances bonded to and debonded from them and untreated controls subjected to whitening with 10 per cent carbamide peroxide. The sample consisted of 20 pairs of first and second premolars extracted for orthodontic reasons. The contralateral surfaces were divided into an experimental and control group. The experimental group underwent orthodontic bonding/debonding procedures. Both groups were subjected to 4 hour whitening and 20 hour hydration sessions for 30 days. The L*a*b* colour system was chosen to evaluate any colour change and these changes were calculated by determining the delta E from the L*a*b* values using a colorimeter. Colour change readings were taken before and after each 4 hour whitening. Additional readings were taken at 48 hour intervals for 30 days following the cessation of active whitening. The results were analysed using statistical (ANOVA) and graphical analyses (alpha = 0.05). A colour change difference of 2 CIELAB units was set as being clinically significant. A mean clinical colour difference was found for enamel surfaces subjected to orthodontic bonding/debonding of attachments relative to control sites after whitening. Bonding and debonding procedures resulted in a significant colour difference between orthodontic bonded and control sites at the end of the active period, which became insignificant at the end of the 30 day period of monitoring. Both the control and debonded sites responded to whitening; however, the control sites responded initially to a greater extent; the orthodontic debonded sites did not respond until after 2 weeks of continuous whitening. After the 2 week period the improved response of the debonded sites decreased the colour difference between the two groups.  (+info)

An approach to enhance the interface adhesion between an orthodontic plastic bracket and adhesive. (50/1061)

For the purpose of improving the degree of success of plastic bracket bonding, based on the analysis of the chemical components of plastic brackets, a systematic method for the treatment of the adhesive surface of plastic brackets was introduced in this study. After sandblasting the adhesive surfaces of two commercially available plastic brackets (Spirit and Clear Bracket), a favourable surface treatment was obtained with the application of a silane coupling agent, gamma-methacryloxy propyl trimethoxy silane. The findings showed that (i) the fillers added to the plastic brackets were glass fillers with Si-OH groups distributed on their surfaces; (ii) sandblasting of the bracket surface resulted in exposure of the glass fillers; (iii) combined with sandblasting, silane coupling treatment significantly increased the bond strength (P < 0.05), which was adequate to withstand the forces generated during orthodontic therapy; and (iv) treatment with sandblasting and silane coupling 24 hours before direct bonding did not cause a significant reduction in bond strength. It is concluded that sandblasting and silane coupling treatment offers the benefit of increasing the in vitro bond strength of plastic brackets for orthodontic application.  (+info)

Dental enamel formation and its impact on clinical dentistry. (51/1061)

The nature of tooth enamel is of inherent interest to dental professionals. The current-day clinical practice of dentistry involves the prevention of enamel demineralization, the promotion of enamel remineralization, the restoration of cavitated enamel where demineralization has become irreversible, the vital bleaching of dental enamel that has become discolored, and the diagnosis and treatment of developmental enamel malformations, which can be caused by environmental or genetic factors. On a daily basis, dental health providers make diagnostic and treatment decisions that are influenced by their understanding of tooth formation. A systemic condition during tooth development, such as high fever, can produce a pattern of enamel defects in the dentition. Knowing the timing of tooth development permits estimates about the timing of the disturbance. The process of enamel maturation continues following tooth eruption, so that erupted teeth can become less susceptible to decay over time. Mutations in the genes encoding enamel proteins lead to amelogenesis imperfecta, a collection of inherited diseases having enamel malformations as the predominant phenotype. Defects in the amelogenin gene cause X-linked amelogenesis imperfecta, and genes encoding other enamel proteins are candidates for autosomal forms. Here we review our current understanding of dental enamel formation, and relate this information to clinical circumstances where this understanding may be particularly relevant.  (+info)

Bacterial colonization associated with fixed orthodontic appliances. A scanning electron microscopy study. (52/1061)

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.  (+info)

The developmental biology of cementum. (53/1061)

In conclusion, we have reviewed an extensive literature on early cementogenesis and performed a detailed morphological and molecular analysis to illustrate and verify key issues in the current debate about epithelial and mesenchymal contributions to root cementum. We have demonstrated that prior to cementogenesis, Hertwig's epithelial root sheath disintegrates and dental follicle cells penetrate the epithelial layer to invade the root surface. Our studies confirmed that HERS became disrupted or disintegrated prior to cementum deposition. We visualized how mesenchymal cells from the dental follicle penetrated the HERS bilayer and deposited initial cementum, while immediately adjacent epithelial cells were separated from the root surface by a basal lamina and did not secrete any cementum. Human specimen from the Gottlieb collection indicated that HERS was removed from the root surface prior to cementum deposition. Our in situ hybridization and immolocalization data revealed that both amelogenin mRNAs and enamel proteins were restricted to the crown enamel and were absent from the root surface and from the cervical-most ameloblasts adjacent to the root margin. On Western blots, cementum protein extracts did not cross-react with amelogenin antibodies. Our studies in conjunction with our literature review together confirmed the classical theory of cementum as a dental follicle derived connective tissue that forms subsequent to HERS disintegration.  (+info)

Inherited risks for susceptibility to dental caries. (54/1061)

Dental caries incidence is affected by host factors that may be related to the structure of dental enamel, immunologic response to cariogenic bacteria, or the composition of saliva. Genetic variation of the host factors may contribute to increased risks for dental caries. This systematic review examined the literature to address the question, "Is the risk for dental decay related to patterns of genetic inheritance?" Numerous reports have described a potential genetic contribution to the risk for dental caries. Studies on twins have provided strong evidence for the role of inheritance. Establishing a basis for a genetic contribution to dental caries will provide a foundation for future studies utilizing the human genome sequence to improve understanding of the disease process. Inherited disorders of tooth development with altered enamel structure increase the incidence of dental caries. Specific genetic linkage has not been determined for all of the syndromes of altered tooth development. Consequently, genetic screens of large populations for genes or mutations associated with increased caries susceptibility have not been done. Altered immune response to the cariogenic bacteria may also increase the incidence of caries. Association between specific patterns of HLA genetic inheritance and dental caries risk is weak and does not provide a predictable basis for predicting future decay rates. The evidence supporting an inherited susceptibility to dental caries is limited. Genetic linkage approaches on well-characterized populations with clearly defined dental caries incidence will be required to further analyze the relationship between inheritance and dental caries.  (+info)

Exposure to metal ions and susceptibility to dental caries. (55/1061)

Results from several epidemiologic studies have shown that there are large differences in the prevalence of dental caries from one region to another within the United States as well as in other countries. It has been postulated that the observed differences may be attributed in part at least to exposure to trace elements such as selenium, vanadium, molybdenum, strontium, and lead. Although data from epidemiologic studies usually support this hypothesis, direct evidence is sparse with the possible exception of exposure to lead. Data from several epidemiologic studies and animal-based research support the concept that lead is a caries-promoting element. Lead mimics calcium in several respects and may affect development of teeth and salivary glands, clearly enhancing susceptibility to dental caries. Elevated blood levels are found most commonly in persons residing in inner cities, particularly among the poor. Many states require blood lead level to be monitored in young children. Where feasible, these records should form part of health history and be available to the treating dental practitioner to ensure that extra preventive procedures may be implemented.  (+info)

Possible role of heat shock protein (Hsp) 25 in the enamel organ during amelogenesis in the rat molar. (56/1061)

The postnatal expression of heat shock protein (Hsp) 25 during the amelogenesis of rat molars was investigated by immunocytochemistry and confocal microscopy. The localization pattern of Hsp 25-immunoreactivity in the inner enamel epithelium and ameloblast cell layer of the rat molars was almost identical to that in the rat incisors which we have previously reported: an intense Hsp25-immunoreactivity, which first appeared in the preameloblasts, was recognized in secretory ameloblasts and ruffle-ended ameloblasts with stage-specific immunointensity. Confocal microscopy with Hsp 25-antibody and rhodamine-labeled phalloidin clearly demonstrated the co-localization of Hsp 25 and actin filaments in the ameloblast layer, supporting our hypothesis that this molecule might serve to reinforce the ameloblast layer during enamel formation as well as the formation and maintenance of the ruffled border in ruffle-ended ameloblasts. Interestingly, the enamel free area cells, which essentially lack the ability for enamel formation, showed the Hsp 25-immunoreactivity during 4-11 days when they developed a ruffled border, but decreased in that immunoreactivity after postnatal 15 days following apoptosis. Since Hsp 25 has been shown to be a specific inhibitor of apoptosis, the enamel-free area cells contribute to determine the outline of dentin at the cusped area. These data support our previous hypothesis on the diverse functions of Hsp 25 in amelogenesis.  (+info)