The development of white spot demineralization associated with fixed appliance orthodontic treatment is a significant clinical problem. Both established and experimental methods for prevention of such lesions in day-to-day clinical practice are presented and discussed.Key words: White spot lesions, orthodontics, prevention.Abbreviations and acronyms: ACP = amorphous calcium phosphate; CPP = casein phosphopeptide; CPP-ACP = casein phosphopeptide-amorphous calcium phosphate.(Accepted for publication 28 March 2006.) Overall management of white spot lesions involves consideration of methods of preventing demineralization and also methods of encouraging remineralization of existing lesions. Preventive measures take precedence, due to the challenging nature of treating patients who do develop significant numbers of white spot lesions. In addition to regular professional oral hygiene visits and the application of appropriate preventive medicaments, successful preventive strategies involve oral health promotion, patient education and patient compliance. This article reviews the relevant historical and contemporary literature regarding methods available to prevent the formation of these white spot lesions during orthodontic treatment. Aetiology of demineralizationWhite spot lesions develop as a result of a dietary carbohydrate and saliva modified bacterial infection, resulting in an imbalance between demineralization and remineralization of the enamel.5 This is an interrupted process, with periods of remineralization and demineralization occurring, depending on the state of the oral environment in terms of the prolonged accumulation and retention of bacterial plaque on the enamel surface, the standard of individual oral hygiene and the inherent resistance of that person.5-7 A white spot lesion is the precursor of frank enamel caries. The white appearance of early enamel caries is due to an optical phenomenon which is caused by mineral loss in the surface or subsurface enamel. Enamel crystal dissolution begins with subsurface demineralization, creating pores between the enamel rods. The resultant alteration of the refractive index in the affected area is then a consequence of both surface roughness and loss of surface shine and alterations in internal reflection, all resulting in greater visual enamel opacity, as porous enamel scatters more light than sound enamel. 2,8 The demineralization process may encompass the full thickness of the enamel and some of the dentine before the relatively hypermineralized surface layer is actually lost.It is generally accepted that the insertion of fixed orthodontic appliances creates stagnation areas for plaque and makes tooth cleaning more difficult. The irregular surfaces of brackets, bands, wires and other INTRODUCTIONThe demineralization of enamel adjacent to orthodontic brackets is a significant clinical problem. White spot lesions develop as a result of prolonged plaque accumulation on the affected surface, commonly due to inadequate oral hygiene. It has been reported th...

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Recent research has examined associations between inflammation and mental health, and has increasingly focused on utilising younger samples to characterise the temporal relationship between inflammatory responses and the emergence of other symptoms. These studies have typically used blood to measure inflammation, although rates of detection for many inflammatory markers appear to be low. Saliva is a safe and low-cost alternative, and adult research has shown that levels of some salivary markers correlate well with those in serum. However, no research has examined this association in young people. This study examined 16 inflammatory markers in serum and saliva in 17 depressed adolescents and 18 healthy controls, aged 13-18 years. In general, detection rates were higher in saliva compared to in serum. When non-detectable levels were excluded, serum levels of C-reactive protein (CRP) correlated with salivary CRP (r=0.424, p=0.015), and this correlation appeared to only exist for those individuals with high levels of serum CRP (r=0.599, p=0.014). However, when non-detectable levels were included as zero, salivary levels of CRP, interleukin (IL)-2, IL-12p70, and interferon (IFN)-γ correlated with their serum counterparts. No significant clinical group differences in any acute phase proteins or cytokines were present. This study suggests that saliva can be used to measure inflammation in studies with adolescent participants, especially CRP, as it appears to correlate with systemic inflammation for those individuals who are expected to have high levels of inflammation. Implications for future directions in research on salivary inflammatory markers are discussed.

c-Kit tyrosine receptor kinase, a well-established stem cell marker, is expressed in a variety of tissues including the pancreas. The involvement of c-Kit in fetal rat and human endocrine pancreatic development, survival, and function has been well characterized but primarily using in vitro experimental approaches. Therefore, the aim of the current study was to examine whether deficiency of a functional c-Kit receptor would have physiological and functional implications in vivo. We characterized the c-Kit mutant mouse, c-Kit(W-v/+), to evaluate the in vivo role of c-Kit in beta-cell growth and function. Here we report that male c-Kit(W-v/+) mice, at 8 wk of age, showed high fasting blood glucose levels and impaired glucose tolerance, which was associated with low levels of insulin secretion after glucose stimulation in vivo and in isolated islets. Morphometric analysis revealed that beta-cell mass was significantly reduced (50%) in male c-Kit(W-v/+) mice when compared with controls (c-Kit(+/+)) (P < 0.05). In parallel, a reduction in pancreatic duodenal homeobox-1 and insulin gene expression in whole pancreas as well as isolated islets of c-Kit(W-v/+) male mice was noted along with a decrease in pancreatic insulin content. Furthermore, the reduction in beta-cell mass in male c-Kit(W-v/+) mice was associated with a decrease in beta-cell proliferation. Interestingly, these changes were not observed in female c-Kit(W-v/+) mice until 40 wk of age. Our results clearly demonstrate that the c-Kit receptor is involved in the regulation of glucose metabolism, likely through an important role in beta-cell development and function.

Aim Existing literature links poor sleep and anxiety symptoms in adolescents. This pilot study aimed to develop a practical method through which a program to improve sleep could reach adolescents in need and to examine the feasibility of a mindfulness‐based, multi‐component group sleep intervention using sleep and anxiety as outcome measures. Methods Sixty‐two grade 9 students (aged 13–15) at a girls’ school were screened with the Pittsburgh Sleep Quality Index (PSQI) and Spence Children's Anxiety Scale (SCAS). Ten participants with self‐reported poor sleep were enrolled into a six‐session program based on Bootzin & Stevens, with added stress/anxiety‐specific components. Sessions covered key aspects of basic mindfulness concepts and practice, sleep hygiene, sleep scheduling, evening/daytime habits, stimulus control, skills for bedtime worries and healthy attitudes to sleep. Treatment changes were measured by pre‐post scores on the PSQI, SCAS and 7‐day actigraphy‐measured sleep. Results The program demonstrated high acceptability, with a completion rate of 90%. Based on effect‐size analysis, participants showed significant improvement on objective sleep onset latency (SOL), sleep efficiency and total sleep time; actigraphy data also showed significantly earlier bedtime, rise time and smaller day‐to‐day bedtime variation. Post‐intervention global PSQI scores were significantly lower than that of pre‐intervention, with significant improvement in subjective SOL, sleep quality and sleep‐related daytime dysfunction. There were small improvements on some subscales of the SCAS, but change on its total score was minimal. Conclusions A mindfulness‐based, multi‐component, in‐school group sleep intervention following brief screening is feasible, and has the potential to improve sleep. Its impact on anxiety needs further investigation.

Normal sleep has a profound effect on the cardiovascular system, reducing cardiovascular activity throughout non-rapid eye movement sleep; changes that are modified and augmented by circadian system influence. There is also evidence that sleep-initiated changes in autonomic balance may in turn modify the development of sleep within a night, particularly the development of slow wave sleep. It is assumed that the cardiovascular changes that accompany sleep reflect a functional aspect of sleep, although the precise functional role has not been agreed upon. Nevertheless, there is good evidence that the cardiovascular changes that occur during normal sleep are beneficial for the cardiovascular system. Arousals from sleep, which are common even in normal sleep, are associated with a surge in activity in cardiorespiratory systems, with marked effects on the sleep-related pattern of cardiovascular activity when they occur frequently. Despite the importance of this aspect of sleep, controversy remains as to both the nature of the activation response and the circumstances under which it is elicited. The concept that sleep-related changes in cardiovascular activity are beneficial leads to the corollary that sleep disturbance would result in adverse cardiovascular consequences. While there is strong empirical evidence for such a relationship, it remains unclear whether this is a direct effect or, as has been suggested recently, the effect of disturbed sleep is mediated via stress-related modification of neuroendocrine systems.

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This study explored whether short sleep duration and sleep quality mediate the relationship between age and depressive symptoms. For comparison, we also explored whether depressive symptoms mediate the relationship between age and short sleep duration and sleep quality. The sample comprised 741 adolescents (63.5% female, mean age 15.78 years, range 11.92-19.67 years) in grades 7-12 from 11 secondary schools in metropolitan Melbourne, Australia. Students completed the Pittsburgh Sleep Quality Index (PSQI) and Center for Epidemiologic Studies Depression Scale (CES-D). Path analyses suggested that short sleep duration significantly mediated the relationship between age and depressive symptoms. Poor sleep quality also significantly mediated this relationship when sleep quality was defined by subjective judgement, but not sleep disturbance, sleep efficiency, or sleep onset latency. Depressive symptoms significantly mediated the relationship between age and short sleep duration and sleep quality (subjective judgement, sleep disturbance, sleep efficiency, and sleep onset latency). These findings suggest that the population-wide increase in depressive symptoms across adolescence is partially mediated by sleep-related developmental changes. They also highlight the importance of examining specific sleep problems when investigating the relationship between sleep and mood in this age group.