Relationship between tooth loss/probing depth and systemic disorders in periodontal patients

During the last decades, many published studies have focused on the associations between periodontal disease and different systemic disorders. The purpose of the present investigation was to study the relationship between occurrence of systemic disorders and the two variables mean number of teeth and periodontal probing pocket depth after stratification according to smoking habits. The study was conducted as a retrospective study based on consecutive selection of patients at a specialist clinic of Periodontology. The study population consisted of 1854 individuals. Of these, 797 were males, and 1057 were females. Multiple regression analyses were adopted in order to calculate the partial correlations between the number of remaining teeth/the relative frequency of periodontal probing depths > or = 5 mm and presence of systemic disease for different strata according to sex and smoking habits with age included as an independent variable. Non-smoking men with cardiovascular disease, diabetes and rheumatoid disease had significantly fewer teeth compared to non-smoking men without systemic disorder. In conclusion, cardio-vascular disease, diabetes and rheumatoid disease may be regarded as risk indicators of tooth loss in men. However, in order to investigate hypotheses concerning potential risk factors, emerging from cross-sectional studies, being true risk factors of tooth loss, longitudinal prospective studies including established risk factors along with new exposures of interest as covariates are required.     

Synthesis and Characterisation of Nanocomposite Mo-Fe-B Thin Films Deposited by Magnetron Sputtering

Several ternary phases are known in the Mo-Fe-B system. Previous ab initio calculations have predicted that they should exhibit a tempting mix of mechanical and magnetic properties. In this study, we have deposited Mo-Fe-B films with a Fe-content varying from 0–37 at.% using non-reactive DC (direct current) magnetron sputtering. The phase composition, microstructure, and mechanical properties were investigated using X-ray diffraction, scanning transmission electron microscopy, and nanoindentation measurements. Films deposited at 300 °C and with >7 at.% Fe are nanocomposites consisting of two amorphous phases: a metal-rich phase and a metal-deficient phase. Hardness and elastic modulus were reduced with increasing Fe-content from ~29 to ~19 GPa and ~526 to ~353 GPa, respectively. These values result in H³/E² ratios of 0.089–0.052 GPa, thereby indicating brittle behaviour of the films. Also, no indication of crystalline ternary phases was observed at temperatures up to 600 °C, suggesting that higher temperatures are required for such films to form.     

Mycoplasma antibodies in rheumatoid arthritis.

Sera of 100 patients under examination at the Outpatient Department of the Rheumatism Foundation Hospital were studied by the indirect hemagglutination technique, using both mycoplasma reference strains, and isolates from RA and SLE as antigens. The series consisted of five groups: I, definite RA (49 patients); II, probable RA (11); III, possible RA or nonspecific inflammatory arthritis (34); IV, osteoarthrosis (2); V, Reiter's disease (4). Mycoplasma antibodies in titres of 16 or higher were encountered in groups I-IV in 26, 8, 19, and one case respectively. Twenty-one out of 106 blood donors had antibodies against an isolate from RA and/or M. arthritidis strain PG 6. The titres found were 16 or 32, except in two cases, 128. In the definite RA group, 21 out of 26 patients possessing mycoplasma antibodies, showed titres of 16 or higher against isolates from RA and/or SLE, 12 against M. arthritidis strain PG 6 and/or Campo, 8 against M. fermentans, and 6 against a T-strain from NGU. Antibodies against M. arthritidis strain Campo were found more often than against strain PG 6. The longer the duration of the arthritic symptoms was, the more frequent seemed also to be the occurrence of mycoplasma antibodies.     

Recombinant antibodies to an oxidized low-density lipoprotein epitope induce rapid regression of atherosclerosis in apobec-1(-/-)/low-density lipoprotein receptor(-/-) mice.

OBJECTIVES: The present study tested the hypothesis that treatment with human recombinant immunoglobulin G1 (IgG1) antibodies against a specific oxidized low-density lipoprotein (oxLDL) epitope will induce regression of existing atherosclerotic lesions in LDL receptor-deficient mice expressing apolipoprotein B-100 (apoB-100) (Apobec-1(-/-)/LDLR(-/-)). BACKGROUND: Oxidized LDL plays an essential role in the pathogenesis of atherosclerosis. We previously showed that an antibody against oxLDL reduces progression of atherosclerosis in mice. METHODS: Apobec-1(-/-)/LDLR(-/-) mice were fed a high-fat diet until they were 24 weeks and were subsequently transferred to chow. Starting at 25 weeks, mice were given 3 weekly injections of either of 2 recombinant human IgG1 antibodies (IEI-E3 or 2D03) against a malondialdehyde-modified apoB-100 peptide sequence. RESULTS: At 25 weeks, atherosclerotic lesions covered 10.3 +/- 3.7% of the descending aorta. Transfer to chow diet resulted in a modest regression of atherosclerosis over a 5-week period (8.28 +/- 4.36%; p = NS). Antibody treatment induced additional regression of atherosclerosis by 50% (2D03; p = 0.001) and 36% (IEI-E3; p = 0.004) compared with control IgG1. The 2D03 treatment also reduced plaque inflammation, enhanced plaque expression of the adenosine triphosphate-binding cassette transporter A1, and inhibited expression of monocyte chemoattractant protein-1 in cultured monocytes. CONCLUSIONS: Human IgG1 against a specific oxLDL epitope can induce rapid and substantial regression of atherosclerotic lesions, possibly by stimulating lipid efflux and inhibiting macrophage recruitment. These recombinant human antibodies could represent a novel strategy for rapid regression/stabilization of atherosclerotic lesions.     

Liver-derived insulin-like growth factor-I is involved in the regulation of blood pressure in mice

IGF-I has been suggested to be of importance for cardiovascular structure and function, but the relative role of locally produced and liver-derived endocrine IGF-I remains unclear. Using the Cre-LoxP recombination system, we have previously created transgenic mice with a liver-specific, inducible IGF-I knockout (LI-IGF-I-/-). To examine the role of liver-derived IGF-I in cardiovascular physiology, liver-derived IGF-I was inactivated at 4 wk of age, resulting in a 79% reduction of serum IGF-I levels. At 4 months of age, systolic blood pressure (BP) was increased in LI-IGF-I-/- mice. Echocardiography showed increased posterior wall thickness in combination with decreased stroke volume and cardiac output, whereas other systolic variables were unchanged, suggesting that these cardiac effects were secondary to increased peripheral resistance. Acute nitric oxide-synthase inhibition increased systolic BP more in LI-IGF-I-/- mice than in control mice. LI-IGF-I-/- mice showed impaired acetylcholine-induced vasorelaxation in mesenteric resistance vessels and increased levels of endothelin-1 mRNA in aorta. Thus, the increased peripheral resistance in LI-IGF-I-/- mice might be attributable to endothelial dysfunction associated with increased expression of endothelin-1 and impaired vasorelaxation of resistance vessels. In conclusion, our findings suggest that liver-derived IGF-I is involved in the regulation of BP in mice.     

Cost-Effectiveness Models for Chronic Obstructive Pulmonary Disease: Cross-Model Comparison of Hypothetical Treatment Scenarios

ObjectivesTo compare different chronic obstructive pulmonary disease (COPD) cost-effectiveness models with respect to structure and input parameters and to cross-validate the models by running the same hypothetical treatment scenarios.MethodsCOPD modeling groups simulated four hypothetical interventions with their model and compared the results with a reference scenario of no intervention. The four interventions modeled assumed 1) 20% reduction in decline in lung function, 2) 25% reduction in exacerbation frequency, 3) 10% reduction in all-cause mortality, and 4) all these effects combined. The interventions were simulated for a 5-year and lifetime horizon with standardization, if possible, for sex, age, COPD severity, smoking status, exacerbation frequencies, mortality due to other causes, utilities, costs, and discount rates. Furthermore, uncertainty around the outcomes of intervention four was compared.ResultsSeven out of nine contacted COPD modeling groups agreed to participate. The 5-year incremental cost-effectiveness ratios (ICERs) for the most comprehensive intervention, intervention four, was €17,000/quality-adjusted life-year (QALY) for two models, €25,000 to €28,000/QALY for three models, and €47,000/QALY for the remaining two models. Differences in the ICERs could mainly be explained by differences in input values for disease progression, exacerbation-related mortality, and all-cause mortality, with high input values resulting in low ICERs and vice versa. Lifetime results were mainly affected by the input values for mortality. The probability of intervention four to be cost-effective at a willingness-to-pay value of €50,000/QALY was 90% to 100% for five models and about 70% and 50% for the other two models, respectively.ConclusionsMortality was the most important factor determining the differences in cost-effectiveness outcomes between models.