Engineered In vitro Models for Pathological Calcification: Routes Toward Mechanistic Understanding

Physiological calcification plays an essential part in the development of the skeleton and teeth; however, the occurrence of calcification in soft tissues such as the brain, heart, and kidneys associates with health impacts, creating a massive social and economic burden. The current paradigm for pathological calcification focuses on the biological factors responsible for bone-like mineralization, including osteoblast-like cells and proteins inducing nucleation and crystal growth. However, the exact mechanism responsible for calcification remains unknown. Toward this goal, this review dissects the current understanding of structure–function relationships and physico-chemical properties of pathologic calcification from a materials science point of view. We will discuss a range of potential mechanisms of pathological calcification, with the purpose of identifying universal mechanistic pathways that occur across multiple organs/tissues at multiple length scales. The possible effect of extracellular components in signaling and templating mineralization, as well as the role of intrinsically disordered proteins in calcification, is reviewed. The state-of-the-art in vitro models and strategies that can recreate the highly dynamic environment of calcification are identified

Evaluation of HTLV-1 in Human Subgingival Plaque of Seropositive Patients

Objective: The aim of this study was to investigate the existence of human T-lymphotropic virus type 1 (HTLV-1) in subgingival plaque of HTLV-1 seropositive pa-tients.Materials and Methods: A total of 18 patients including 13 females and fivemales, with a mean age of 37 years participated in this descriptive study. Half of them were HTLV-1 carriers and the others were in HTLV-1 associated myelopathy tropical spastic paraparesia (HAM/TSP) stage.Subgingival dental plaque samples were taken using sterile paper points and examined to detect HTLV-1 using polymerase chain reaction (PCR).Results: None of the carrier stage patients revealed HTLV-1 virus, while only one patient in the HAM/TSP group was found with the virus.Conclusion: This study showed that the existence of HTLV-1 virus in subgingival plaque of patients suffering from HTLV-1 in carrier and HAM/TSP stages with healthy periodon-tium is rare. Studies with larger samples are recommended

Minimum wage legislation, work conditions and employment

SIGLEAvailable from British Library Document Supply Centre-DSC:3597.9512(CEPR-DP--1524) / BLDSC - British Library Document Supply CentreGBUnited Kingdo

New deal for young people Introducing a more 'tailored' approach

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Periodontal changes following molar intrusion with miniscrews

BACKGROUND: With the introduction of skeletal anchorage system, recently it is possible to successfully intrude molar teeth. On the other hand, there have been concerns about periodontal changes associated with intrusion and there are few studies on this topic, especially for posterior teeth. MATERIALS AND METHODS: Ten female patients were enrolled in this study. Maxillary molar intrusion was achieved by inserting two miniscrews and a 17 × 25 titanium molybdenum alloy spring. Crestal height changes were evaluated at three intervals including: Baseline (T0), end of active treatment (T1) and 6 months after retention (T2). Other variables including probing depth, gingival recession, attachment level and bleeding on probing were evaluated by clinical measurements in the three above mentioned intervals. One-sample Kolmogrov-Smirnov test ascertained the normality of the data. For all patients, the changes in tooth position and crestal height were evaluated using one-sample t-test. (P < 0.05). RESULTS: Supra-erupted molars were successfully intruded a mean of 2.1 ± 0.9 mm during active treatment (T0-T1). A mean bone resorption of 0.9 ± 0.9 mm in mesial crest and 1 ± 0.8 mm in distal crest had occurred in total treatment (T0-T2). A mean of 0.6 ± 1.4 mm bone was deposited on mesial crest during the retention period (T1-T2) following tooth relapse. On average, 0.8 ± 0.4 mm attachment gain was obtained. Gingival margin coronalized a mean of 0.8 ± 0.6 mm throughout the entire treatment. Probing depth showed no significant change during treatment. CONCLUSION: Within the limitations of this study, these results suggest that not only periodontal status was not negatively affected by intrusion, but also there were signs of periodontal improvement including attachment gain and shortening of clinical crown height

The role of inflammation and genetics in periodontal disease

Periodontitis is a complex disease: (a) various causative factors play a role simultaneously and interact with each other; and (b) the disease is episodic in nature, and bursts of disease activity can be recognized, ie, the disease develops and cycles in a nonlinear fashion. We recognize that various causative factors determine the immune blueprint and, consequently, the immune fitness of a subject. Normally, the host lives in a state of homeostasis or symbiosis with the oral microbiome; however, disturbances in homeostatic balance can occur, because of an aberrant host response (inherited and/or acquired during life). This imbalance results from hyper- or hyporesponsiveness and/or lack of sufficient resolution of inflammation, which in turn is responsible for much of the disease destruction seen in periodontitis. The control of this destruction by anti-inflammatory processes and proresolution processes limits the destruction to the tissues surrounding the teeth. The local inflammatory processes can also become systemic, which in turn affect organs such as the heart. Gingival inflammation also elicits changes in the ecology of the subgingival environment providing optimal conditions for the outgrowth of gram-negative, anaerobic species, which become pathobionts and can propagate periodontal inflammation and can further negatively impact immune fitness. The factors that determine immune fitness are often the same factors that determine the response to the resident biofilm, and are clustered as follows: (a) genetic and epigenetic factors; (b) lifestyle factors, such as smoking, diet, and psychosocial conditions; (c) comorbidities, such as diabetes; and (d) local and dental factors, as well as randomly determined factors (stochasticity). Of critical importance are the pathobionts in a dysbiotic biofilm that drive the viscious cycle. Focusing on genetic factors, currently variants in at least 65 genes have been suggested as being associated with periodontitis based on genome-wide association studies and candidate gene case control studies. These studies have found pleiotropy between periodontitis and cardiovascular diseases. Most of these studies point to potential pathways in the pathogenesis of periodontal disease. Also, most contribute to a small portion of the total risk profile of periodontitis, often limited to specific racial and ethnic groups. To date, 4 genetic loci are shared between atherosclerotic cardiovascular diseases and periodontitis, ie, CDKN2B-AS1(ANRIL), a conserved noncoding element within CAMTA1 upstream of VAMP3, PLG, and a haplotype block at the VAMP8 locus. The shared genes suggest that periodontitis is not causally related to atherosclerotic diseases, but rather both conditions are sequelae of similar (the same?) aberrant inflammatory pathways. In addition to variations in genomic sequences, epigenetic modifications of DNA can affect the genetic blueprint of the host responses. This emerging field will yield new valuable information about susceptibility to periodontitis and subsequent persisting inflammatory reactions in periodontitis. Further studies are required to verify and expand our knowledge base before final cause and effect conclusions about the role of inflammation and genetic factors in periodontitis can be made