968 resultados para tooth plaque
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Purpose: The purpose of this longitudinal study was to determine factors associated with mutans streptococci (MS) infection and development of caries lesions in a group of children 21 to 72 months old. Methods: The 63 caries-free children, recruited since birth, were divided into: (1) a study group of 24 children who were colonized with MS; and (2) a control group of 39 children without MS. The children were recalled every 3 months for approximately 24 months, and their social, medical, and dental histories were updated. At each recall, the teeth were checked for presence or absence of plaque, enamel hypoplasia, and caries lesions, and their MS status was assessed using a commercial test kit. Results: MS infection was associated with: (1) visible plaque (P < .01); (2) enamel hypoplasia (P < .05); (3) commencement of tooth-brushing after 12 months of age (P < .05); (4) lack of parental assistance with tooth-brushing (P < .025); and (5) increased hours of child care/school (P < .05). Four children (20%) were colonized at an age range of 21 to 36 months, 9 (45%) at 37 to 48 months, and 7 (35%) at 49 to 72 months (P < .001). Eight children who developed caries lesions: (1) had more hypoplastic teeth (P < .001); (2) ate sugar-containing snacks (P < .05); and (3) did not brush regularly with chlorhexidine gel (P < .01) compared to those who remained free of caries lesions. Conclusions: Lack of oral hygiene, consumption of sugar-containing snacks, and enamel hypoplasia are significant factors for both MS infection and caries lesion initiation.
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Adverse effects of corticosteroids on bone metabolism raise concerns as to whether steroid treatment may influence orthodontic movement. This study examined the effect of prednisolone on orthodontic movement using an established rat model. The corticosteroid treated group (N = 6) was administered prednisolone (1 mg/kg) daily, for a 12-day induction period; the control group (N = 6) received equivalent volumes of saline. On day 12, an orthodontic appliance was placed which exerted 30 g of mesial force to the maxillary first molar. Animals were sacrificed on day 24 and tooth movement was measured. Sagittal sections of the molars were stained with haematoxylin and eosin, and for tartrate-resistant acid phosphatase (TRAP) activity. While there were no significant differences in the magnitude of tooth movement between the 2 groups, steroid-treated rats displayed significantly less root resorption on the compression side and fewer TRAP-positive cells within the PDL space on the same side. This suggests steroid treatment suppressed elastic activity.
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There is a general perception that the problem of tooth wear is increasing due to elements of the modern diet and due to increased retention of dentition into older age. Tooth wear encompasses erosion, abrasion and attrition of dental tissues – these often co-exist – yet in general, erosion is of more significance to the young and attrition is of more significance to the older population. Diet plays a significant role in the aetiology of tooth wear and likewise advanced tooth wear in older age may impose dietary restrictions with consequences for dietary intake and nutritional status. There is a need to increase the awareness of the disease of tooth wear and the associated nutritional problems. At present, the aetiology of tooth wear is poorly understood – especially with respect to the role of diet. Clearer information on how best to measure and monitor the incidence and prevalence is needed in order to obtain longitudinal data on trends in tooth wear and to monitor the factors that contribute to this condition. These issues will be addressed in the following presentations: 1) What is tooth wear? Aetiology, measurement and monitoring, 2) The role of diet in the aetiology of dental erosion, 3) Groups at increased risk of tooth wear: Eating disorders, ‘dieters' sportsmen and those with impairments, 4) Tooth wear in older adults: nutritional implications. In summary this symposium seeks to: 1) increase awareness of the disease of tooth wear, and its associated nutritional problems 2) increase understanding of the aetiology of tooth wear, especially the dietary role, 3) provide information on how to measure and monitor tooth wear, 4) highlight future research requirements in the area of tooth wear and diet.
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The aged population have an increased susceptibility to infection, therefore function of the innate immune system may be impaired as we age. Macrophages, and their precursors monocytes, play an important role in host defence in the form of phagocytosis, and also link the innate and adaptive immune system via antigen presentation. Classically-activated 'M1' macrophages are pro-inflammatory, which can be induced by encountering pathogenic material or pro-inflammatory mediators. Alternatively activated 'M2' macrophages have a largely reparative role, including clearance of apoptotic bodies and debris from tissues. Despite some innate immune receptors being implicated in the clearance of apoptotic cells, the process has been observed to have a dominant anti-inflammatory phenotype with cytokines such as IL-10 and TGF-ß being implicated. The atherosclerotic plaque contains recruited monocytes and macrophages, and is a highly inflammatory environment despite high levels of apoptosis. At these sites, monocytes differentiate into macrophages and gorge on lipoproteins, resulting in formation of 'foam cells' which then undergo apoptosis, recruiting further monocytes. This project seeks to understand why, given high levels of apoptosis, the plaque is a pro-inflammatory environment. This phenomenon may be the result of the aged environment or an inability of foam cells to elicit an anti-inflammatory effect in response to dying cells. Here we demonstrate that lipoprotein treatment of macrophages in culture results in reduced capacity to clear apoptotic cells. The effect of lipoprotein treatment on apoptotic cell-mediated immune modulation of macrophage function is currently under study.
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Plasma transferrin binding in Down syndrome and Alzheimer's disease is significantly reduced compared with age matched controls and it was thought this may help elucidate a pathological time sequence for the onset of dementia in Down syndrome. In Down syndrome, there was a reduction in gallium and aluminium transferrin binding both with age and the onset of dementia. Non-transferrin bound gallium species were identified as non-transportable phosphate or silicate. Thus, the route of entry of metals into the brain must be via a transferrin mediated complex only. A clear sequence of pathological events has been demonstrated in Down syndrome which shows the pathway to development of plaques and dementia and this is believed to have an immunological origin.
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The objective of this study was to determine the possible relationships between the morphological types of plaque revealed in silver and immunostained sections of Alzheimer’s disease (AD) tissue. The density of cored and uncored senile plaques in Glees and Marsland preparations, and of diffuse, primitive, classic and compact beta/A4 deposits in immunostained preparations were estimated. A principal components analysis (PCA) of the data suggested that three uncorrelated principal components accounted for 80% of the variation in lesion density in the tissues. This suggested that thee processes lead independently to the formation of: (1) the uncored Glees plaques; (2) the primitive beta/A4 deposits and most of the classic beta/A4 deposits and (3) the compact beta/A4 deposits and the remaining classic deposits. Hence, the uncored plaques revealed by the Glees stain and the primitive beta/A4 deposits represented distinct plaque populations. In addition, the classic beta/A4 deposits did not appear to represent a uniform plaque population but to originate from at least two pathological processes. The uncored Glees plaques appeared to the only plaque population closely related to the diffuse beta/A4 deposits.
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Discrete, microscopic lesions are developed in the brain in a number of neurodegenerative diseases. These lesions may not be randomly distributed in the tissue but exhibit a spatial pattern, i.e., a departure from randomness towards regularlity or clustering. The spatial pattern of a lesion may reflect its development in relation to other brain lesions or to neuroanatomical structures. Hence, a study of spatial pattern may help to elucidate the pathogenesis of a lesion. A number of statistical methods can be used to study the spatial patterns of brain lesions. They range from simple tests of whether the distribution of a lesion departs from random to more complex methods which can detect clustering and the size, distribution and spacing of clusters. This paper reviews the uses and limitations of these methods as applied to neurodegenerative disorders, and in particular to senile plaque formation in Alzheimer's disease.
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Tooth enamel is the stiffest tissue in the human body with a well-organized microstructure. Developmental diseases, such as enamel hypomineralisation, have been reported to cause marked reduction in the elastic modulus of enamel and consequently impair dental function. We produce evidence, using site-specific transmission electron microscopy (TEM), of difference in microstructure between sound and hypomineralised enamel. Built upon that, we develop a mechanical model to explore the relationship of the elastic modulus of the mineral-protein composite structure of enamel with the thickness of protein layers and the direction of mechanical loading. We conclude that when subject to complex mechanical loading conditions, sound enamel exhibits consistently high stiffness, which is essential for dental function. A marked decrease in stiffness of hypomineralised enamel is caused primarily by an increase in the thickness of protein layers between apatite crystals and to a lesser extent by an increase in the effective crystal orientation angle. © 2009 Elsevier Ltd. All rights reserved.
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Sabrena O'Keefe giving speech while holding the time capsule plaque. Also pictured: Pablo Haspel, BBC SGA President, BBC Campus Laura Farinas, SGA President, MMC Campus The Annual FIU Student Leadership Summit is held each February on the Biscayne Bay Campus. The Summit is a one-day conference for current student leaders. The Summit offers our students the opportunity to learn from the vast expertise of our faculty and administrators, to share their leadership experiences with each other and to establish a network of support and cooperation within the university. On Feb. 2, 2013, we celebrated the 10th anniversary of holding the Student Leadership Summit. In honor of this occasion, we buried a time capsule containing materials from the day as well as messages from participants to the participants of 2023 when the time capsule is to be opened.
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Time capsule burial plaque before placed on burial site. The Annual FIU Student Leadership Summit is held each February on the Biscayne Bay Campus. The Summit is a one-day conference for current student leaders. The Summit offers our students the opportunity to learn from the vast expertise of our faculty and administrators, to share their leadership experiences with each other and to establish a network of support and cooperation within the university. On Feb. 2, 2013, we celebrated the 10th anniversary of holding the Student Leadership Summit. In honor of this occasion, we buried a time capsule containing materials from the day as well as messages from participants to the participants of 2023 when the time capsule is to be opened.