Tooth loss, chewing efficiency and cognitive impairment in geriatric patients.

BACKGROUND Patients with dementia have poorer oral health and fewer teeth than their peers without cognitive impairment. OBJECTIVE The hypothesis of this study is that the number of natural teeth and the chewing efficiency are associated with cognitive functioning. METHODS This cross-sectional study included 29 patients diagnosed with dementia aged 75 years or older and 22 controls who were either cognitively normal (n = 19) or with mild cognitive impairment (n = 3). Neuropsychological, nutritional and dental assessments were performed. The chewing efficiency was evaluated with a two-colour mixing test. RESULTS Demented patients and controls presented with a mean of 4.9 and 6.5 teeth, respectively (n.s.). The number of natural teeth was not associated with dementia (p = 0.553). Same results were found for age (p = 0.746) and sex (p = 0.901). The chewing efficiency by visual inspection proved worse in participants with dementia than in the controls (p < 0.011) and explained 9.3% of the variance in the diagnosis of dementia. Neither dental state nor chewing efficiency was related to the nutritional state. CONCLUSION Chewing efficiency seems stronger associated with cognitive impairment than the number of teeth. Hence, in a more holistic approach for the geriatric assessment, the dental examination may be complemented by a chewing efficiency test.

Characterization of healing tissue in a tooth extraction socket in a rabbit model

The histology of healing in a tooth extraction socket has been described in many studies. The focus of research in bone biology and healing is now centered on molecular events that regulate repair of injured tissue. Rapid progress in cellular and molecular biology has resulted in identification of many signaling molecules (growth factors and cytokines) associated with formation and repair of skeletal tissues. Some of these include members of the transforming growth factor-β superfamily (including the bone morphogenetic proteins), fibroblast growth factors, platelet derived growth factors and insulin like growth factors. ^ Healing of a tooth extraction socket is a complex process involving tissue repair and regeneration. It involves chemotaxis of appropriate cells into the wound, transformation of undifferentiated mesenchymal cells to osteoprogenitor cells, proliferation and differentiation of committed bone forming cells, extracellular matrix synthesis, mineralization of osteoid, maturation and remodeling of bone. Current data suggests that these cellular events are precisely controlled and regulated by specific signaling molecules. A plethora of cytokines; have been identified and studied in the past two decades. Some of these like transforming growth factor beta (TGF-β), vascular endothelial growth factor (VEGF), platelet derived growth factor (PDGF) and fibroblast growth factors (FGFs) are well conserved proteins involved in the initial response to injury and repair in soft and hard tissue. ^ The purpose of this study was to characterize the spatial and temporal localization of TGF-βl, VEGF, PDGF-A, FGF-2 and BMP-2, and secretory IgA in a tooth extraction socket model, and evaluate correlation of spatial and temporal changes of these growth factors to histological events. The results of this study showed positive correlation of histological events to spatial and temporal localization of TGF-β1, BMP-2, FGF-2, PDGF-A, and VEGF in a rabbit tooth extraction model. ^

Novel molecular insights into human tooth agenesis

The development of dentition is a fascinating process that involves a complex series of epithelial-mesenchymel signaling interactions. That such a precise process frequently goes awry is not surprising. Indeed, tooth agenesis is one of the most commonly inherited disorders in humans that affects up to twenty percent of the population and imposes significant functional, emotional and financial burdens on patients. Mutations in the paired box domain containing transcription factor PAX9 result in autosomal dominant tooth agenesis that primarily involves posterior dentition. Despite these advances, little is known about how PAX9 mediates key signaling actions in tooth development and how aberrations in PAX9 functions lead to tooth agenesis. As an initial step towards providing evidence for the pathogenic role of mutant PAX9 proteins, I performed a series of molecular genetic analyses aimed at resolving the structural and functional defects produced by a number of PAX9 mutations causing non-syndromic posterior tooth agenesis. It is likely that the pathogenic mechanism underlying tooth agenesis for the first two mutations studied (219InsG and IIe87Phe) is haploinsufficiency. For the six paired domain missense mutations studied, the lack of functional defects observed for three of the mutant proteins suggests that these mutations altered PAX9 function through alternate mechanisms. Next, I explored further the nature of the partnership between Pax9 and the Msx1 homeoprotein and their role in the expression of a downstream effector molecule, Bmp4. When viewed in the context of events occurring in dental mesenchyme, the results of these studies indicate that the Pax9-Msx1 protein interaction involves the localized up-regulation of Bmp4 activity that is mediated by synergistic interactions between the two transcription factors. Importantly, these assays corroborate in vivo data from mouse genetic studies and support reports of Pax9-dependent expression of Bmp4 in dental mesenchyme. Taken together, these results suggest that PAX9 mutations cause an early developmental defect due to an inability to maintain the inductive potential of dental mesenchyme through involvement in a pathway involving Msx1 and Bmp4. ^

Major, trace element and XRF data for sediments and fish tooth samples, from a shallow marine setting with varying redox conditions (Site U1356, Wilkes Land Margin, E.Antarctica)

Fossil fish teeth from pelagic open ocean settings are considered a robust archive for preserving the neodymium (Nd) isotopic composition of ancient seawater. However, using fossil fish teeth as an archive to reconstruct seawater Nd isotopic compositions in different sedimentary redox environments and in terrigenous-dominated, shallow marine settings is less proven. To address these uncertainties, fish tooth and sediment samples from a middle Eocene section deposited proximal to the East Antarctic margin at Integrated Ocean Drilling Program Site U1356 were analyzed for major and trace element geochemistry, and Nd isotopes. Major and trace element analyses of the sediments reveal changing redox conditions throughout deposition in a shallow marine environment. However, variations in the Nd isotopic composition and rare earth element (REE) patterns of the associated fish teeth do not correspond to redox changes in the sediments. REE patterns in fish teeth at Site U1356 carry a typical mid-REE-enriched signature. However, a consistently positive Ce anomaly marks a deviation from a pure authigenic origin of REEs to the fish tooth. Neodymium isotopic compositions of cleaned and uncleaned fish teeth fall between modern seawater and local sediments and hence could be authigenic in nature, but could also be influenced by sedimentary fluxes. We conclude that the fossil fish tooth Nd isotope proxy is not sensitive to moderate changes in pore water oxygenation. However, combined studies on sediments, pore waters, fish teeth and seawater are needed to fully understand processes driving the reconstructed signature from shallow marine sections in proximity to continental sources. This article is protected by copyright. All rights reserved.

INFLUÊNCIA DO LASER DE BAIXA INTENSIDADE NA VELOCIDADE DA MOVIMENTAÇÃO ORTODÔNTICA

Este estudo investigou os efeitos do laser de baixa intensidade na velocidade da movimentação ortodôntica de caninos submetidos à retração inicial. A amostra constou de 26 caninos superiores e inferiores, submetidos à retração inicial realizada com mola Niti, com força de 150g. Um dos caninos foi irradiado com laser de diodo, seguindo o protocolo de aplicação: 780nm/20mW/5Jcm2/0,2J por ponto/Et=2J, nos dias 0, 3 e 7 pós-ativação, sendo que o contralateral foi considerado placebo. A retração durou em média 4 meses, num total de 9 aplicações de laser. Os modelos de cada mês foram escaneados com scanner 3D (3Shape) e as imagens tridimensionais foram analisadas por meio do Software Geomagic Studio 5, para a mensuração da quantidade de movimentação dos caninos retraídos. Foi empregada a Análise de Variância a três critérios, seguida pelo teste de Tukey (p<0,05). Para verificação da integridade tecidual, foram efetuadas radiografias periapicais iniciais e finais dos caninos retraídos e dos molares, nas quais foram avaliados uma possível reabsorção na crista alveolar, por meio da distância da crista óssea alveolar até a junção cemento-esmalte e os níveis de reabsorção radicular, por meio do índice de Levander e Malmgreen, sendo este último avaliado somente nos caninos retraídos. Para isto, foi empregado o teste não paramétrico de Wilcoxon (p<0,05). Os resultados indicaram que houve um aumento estatisticamente significante na velocidade da movimentação dos caninos irradiados comparados ao seu contralateral, em todos os tempos avaliados, como também a preservação da integridade tecidual. Com isso, concluiu-se que o laser de diodo pode acelerar a movimentação ortodôntica, podendo contribuir para a diminuição do tempo de tratamento.(AU)

INFLUÊNCIA DO LASER DE BAIXA INTENSIDADE NA VELOCIDADE DA MOVIMENTAÇÃO ORTODÔNTICA

Este estudo investigou os efeitos do laser de baixa intensidade na velocidade da movimentação ortodôntica de caninos submetidos à retração inicial. A amostra constou de 26 caninos superiores e inferiores, submetidos à retração inicial realizada com mola Niti, com força de 150g. Um dos caninos foi irradiado com laser de diodo, seguindo o protocolo de aplicação: 780nm/20mW/5Jcm2/0,2J por ponto/Et=2J, nos dias 0, 3 e 7 pós-ativação, sendo que o contralateral foi considerado placebo. A retração durou em média 4 meses, num total de 9 aplicações de laser. Os modelos de cada mês foram escaneados com scanner 3D (3Shape) e as imagens tridimensionais foram analisadas por meio do Software Geomagic Studio 5, para a mensuração da quantidade de movimentação dos caninos retraídos. Foi empregada a Análise de Variância a três critérios, seguida pelo teste de Tukey (p<0,05). Para verificação da integridade tecidual, foram efetuadas radiografias periapicais iniciais e finais dos caninos retraídos e dos molares, nas quais foram avaliados uma possível reabsorção na crista alveolar, por meio da distância da crista óssea alveolar até a junção cemento-esmalte e os níveis de reabsorção radicular, por meio do índice de Levander e Malmgreen, sendo este último avaliado somente nos caninos retraídos. Para isto, foi empregado o teste não paramétrico de Wilcoxon (p<0,05). Os resultados indicaram que houve um aumento estatisticamente significante na velocidade da movimentação dos caninos irradiados comparados ao seu contralateral, em todos os tempos avaliados, como também a preservação da integridade tecidual. Com isso, concluiu-se que o laser de diodo pode acelerar a movimentação ortodôntica, podendo contribuir para a diminuição do tempo de tratamento.(AU)

Impaired osteoclastic bone resorption leads to osteopetrosis in cathepsin-K-deficient mice

Cathepsin K is a recently identified lysosomal cysteine proteinase. It is abundant in osteoclasts, where it is believed to play a vital role in the resorption and remodeling of bone. Pycnodysostosis is a rare inherited osteochondrodysplasia that is caused by mutations of the cathepsin-K gene, characterized by osteosclerosis, short stature, and acroosteolysis of the distal phalanges. With a view to delineating the role of cathepsin K in bone resorption, we generated mice with a targeted disruption of this proteinase. Cathepsin-K-deficient mice survive and are fertile, but display an osteopetrotic phenotype with excessive trabeculation of the bone-marrow space. Cathepsin-K-deficient osteoclasts manifested a modified ultrastructural appearance: their resorptive surface was poorly defined with a broad demineralized matrix fringe containing undigested fine collagen fibrils; their ruffled borders lacked crystal-like inclusions, and they were devoid of collagen-fibril-containing cytoplasmic vacuoles. Assaying the resorptive activity of cathepsin-K-deficient osteoclasts in vitro revealed this function to be severely impaired, which supports the contention that cathepsin K is of major importance in bone remodeling.

Defects in embryonic hindbrain development and fetal resorption resulting from vitamin A deficiency in the rat are prevented by feeding pharmacological levels of all-trans-retinoic acid

Vitamin A is required for reproduction and normal embryonic development. We have determined that all-trans-retinoic acid (atRA) can support development of the mammalian embryo to parturition in vitamin A-deficient (VAD) rats. At embryonic day (E) 0.5, VAD dams were fed purified diets containing either 12 μg of atRA per g of diet (230 μg per rat per day) or 250 μg of atRA per g of diet (4.5 mg per rat per day) or were fed the purified diet supplemented with a source of retinol (100 units of retinyl palmitate per day). An additional group was fed both 250 μg of atRA per g of diet in combination with retinyl palmitate. Embryonic survival to E12.5 was similar for all groups. However, embryonic development in the group fed 12 μg of atRA per g of diet was grossly abnormal. The most notable defects were in the region of the hindbrain, which included a loss of posterior cranial nerves (IX, X, XI, and XII) and postotic pharyngeal arches as well as the presence of ectopic otic vesicles and a swollen anterior cardinal vein. All embryonic abnormalities at E12.5 were prevented by feeding pharmacological amounts of atRA (250 μg/g diet) or by supplementation with retinyl palmitate. Embryos from VAD dams receiving 12 μg of atRA per g of diet were resorbed by E18.5, whereas those in the group fed 250 μg of atRA per g of diet survived to parturition but died shortly thereafter. Equivalent results were obtained by using commercial grade atRA or atRA that had been purified to eliminate any potential contamination by neutral retinoids, such as retinol. Thus, 250 μg of atRA per g of diet fed to VAD dams (≈4.5 mg per rat per day) can prevent the death of embryos at midgestation and prevents the early embryonic abnormalities that arise when VAD dams are fed insufficient amounts of atRA.

Dissociation between bone resorption and bone formation in osteopenic transgenic mice

Bone mass is maintained constant in vertebrates through bone remodeling (BR). BR is characterized by osteoclastic resorption of preexisting bone followed by de novo bone formation by osteoblasts. This sequence of events and the fact that bone mass remains constant in physiological situation lead to the assumption that resorption and formation are regulated by each other during BR. Recent evidence shows that cells of the osteoblastic lineage are involved in osteoclast differentiation. However, the existence of a functional link between the two activities, formation and resorption, has never been shown in vivo. To define the role of bone formation in the control of bone resorption, we generated an inducible osteoblast ablation mouse model. These mice developed a reversible osteopenia. Functional analyses showed that in the absence of bone formation, bone resorption continued to occur normally, leading to an osteoporosis of controllable severity, whose appearance could be prevented by an antiresorptive agent. This study establishes that bone formation and/or bone mass do not control the extent of bone resorption in vivo.