Cephalometric evaluation in different phases of Jasper jumper therapy

Introduction: The aim of this study was to evaluate the dentoskeletal and soft-tissue effects of Class II malocclusion treatment with the Jasper jumper followed by Class II elastics at the different stages of therapy. Methods: The sample comprised 24 patients of both sexes (11 boys, 13 girls) with an initial age of 12.58 years, treated for a mean period of 2.15 years. Four lateral cephalograms were obtained of each patient in these stages of orthodontic treatment: at pretreatment (T1), after leveling and alignment (T2), after the use of the Jasper jumper appliance and before the use of Class II intermaxillary elastics (T3), and at posttreatment (T4). Thus, 3 treatment phases could be evaluated: leveling and alignment (T1-T2), use of the Jasper jumper (T2-T3), and use of Class II elastics (T3-T4). Dependent analysis of variance (ANOVA) and Tukey tests were used to compare the durations of the 3 treatment phases and for intragroup comparisons of the 4 treatment stages. Results: The alignment phase showed correction of the anteroposterior relationship, protrusion and labial inclination of the maxillary incisors, and reduction of overbite. The Jasper jumper phase demonstrated labial inclination, protrusion and intrusion of the mandibular incisors, mesialization and extrusion of the mandibular molars, reduction of overjet and overbite, molar relationship improvement, and reduction in facial convexity. The Class II elastics phase showed labial inclination of the maxillary incisors; retrusion, uprighting, and extrusion of the mandibular incisors; and overjet and overbite increases. Conclusions: The greatest amount of the Class II malocclusion anteroposterior discrepancy was corrected with the Jasper jumper appliance. Part of the correction was lost during Class II intermaxillary elastics use after use of the Jasper jumper appliance. (Am J Orthod Dentofacial Orthop 2011;140:e77-e84)

Influence of Antiplatelet Drugs in the Pathogenesis of Experimental Periodontitis and Periodontal Repair in Rats

Background: Platelets contain an array of biologic mediators that can modulate inflammation and repair processes including proinflammatory mediators and growth factors. Previous studies have shown that periodontitis and periodontal repair are associated with platelet activation. We hypothesized that drug-induced platelet inactivation may interfere in the processes of inflammation and repair in experimental periodontitis in rats by suppressing the release of biologic mediators from platelets to the site of injury. Methods: To measure the effects on periodontitis, ligatures were placed around first molars, and aspirin (Asp, 30 mg/kg) or clopidogrel (Clo, 75 mg/kg) was given intragastrically once daily for 15 days. Interleukin-6 (IL-6), tumor necrosis factor-a (TNF-alpha), and thromboxane A(2) levels were measured by enzyme-linked immunosorbent assay. To evaluate the effects of antiplatelet drugs on periodontal repair, ligatures were removed after 15 days of periodontitis induction, and Asp or Clo were administered beginning the following day for 15 days. Periodontal repair was assessed by microcomputed tomography. Results: On periodontitis phase, Asp and Clo significantly reduced levels of TNF-alpha and II-6 (P < 0.05), but only Asp decreased thromboxane A(2) (P < 0.05). Asp and Clo decreased inflammatory infiltration; however, this reduction was more pronounced with Clo treatment (P < 0.05). Histometric analysis showed that Asp and Clo impaired alveolar bone resorption. During the repair phase and after removal of the ligatures, microcomputed tomography analysis demonstrated that treatment with Asp and Clo did not impair alveolar bone repair. Conclusion: Systemic administration of Asp and Clo attenuates the inflammation associated with periodontitis without affecting the repair process when stimulus is removed. J Periodontol 2011;82:767-777.

Evaluation of chronic omega-3 fatty acids supplementation on behavioral and neurochemical alterations in 6-hydroxydopamine-lesion model of Parkinson`s disease

Omega-3 polyunsaturated fatty acids (omega-3 PUFAs) have been widely associated to beneficial effects over different neuropathologies, but only a few studies associate them to Parkinson`s disease (PD). Rats were submitted to chronic supplementation (21-90 days of life) with fish oil, rich in omega-3 PUFAs, and were uni- or bilaterally lesioned with 4 mu g of the neurotoxin 6-hydroxydopamine (6-OHDA) in the medial forebrain bundle Although lipid incorporation was evidenced in neuronal membranes, it was not sufficient to compensate motor deficits induced by 6-OHDA. In contrast, omega-3 PUFAs were capable of reducing rotational behavior induced by apomorphine, suggesting neuroprotection over dyskinesia The beneficial effects of omega-3 PUFAs were also evident in the maintenance of thiobarbituric acid reactive substances index from animals lesioned with 6-OHDA similar to levels from SHAM and intact animals. Although omega-3 PUFAs did not modify the tyrosine hydroxylase immunoreactivity in the substantia nigra pars compacta and in the ventral tegmental area, nor the depletion of dopamine (DA) and its metabolites in the striatum, DA turnover was increased after omega-3 PUFAs chronic supplementation Therefore, it is proposed that omega-3 PUFAs action characterizes the adaptation of remaining neurons activity. altering striatal DA turnover without modifying the estimated neuronal population. (C) 2009 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved

Evaluation of estrogen neuroprotective effect on nigrostriatal dopaminergic neurons following 6-hydroxydopamine injection into the substantia nigra pars compacta or the medial forebrain bundle

Studies involving estrogen treatment of ovariectomized rats or mice have attributed to this hormone a neuroprotective effect on the substantia nigra pars compacta (SNpc) neurons. We investigated the effect of estradiol replacement in ovariectomized rats on the survival of dopaminergic mesencephalic cell and the integrity of their projections to the striatum after microinjections of 1 mu g of 6-hydroxydopamine (6-OHDA) into the right SNpc or medial forebrain bundle (MFB). Estradiol replacement did not prevent the reduction either in the striatal concentrations of DA and metabolites or in the number of nigrostriatal dopaminergic neurons following lesion with 1 mu g of 6-OHDA into the SNpc. Nevertheless, estradiol treatment reduced the decrease in striatal DA following injection of 1 mu g of 6-OHDA into the MFB. Results suggest therefore that estrogen protect nigrostriatal dopaminergic neurons against a 6-OHDA injury to the MFB but not the SNpc. This may be due to the distinct degree of lesions promoted in these different rat models of Parkinson`s disease.