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PubMed · 6960693

Orthodontic force systems: technical refinements for increased efficiency.

R A Hocevar
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Abstract

The efficiency of the Begg technique suffers because Class II elastics overwhelm anchor bends, which normally do not yield enough force for vertical control of maxillary incisors. This can be improved by attention to detail and modifications. Bite-opening bends in the arch wires distal to canines and lateral incisors, long (6.5 mm.) mesiogingivally angulated molar tubes, and placement of intermaxillary elastics at the distal ends of the tubes are all helpful. Intermaxillary "check elastics," having one end over the posterior end of the maxillary arch wire, both strands under the end of the mandibular arch wire, and the other end up to the maxillary anterior teeth, reinforce anchor bends and extrude upper and lower molars while keeping them upright. They augment bite opening in Stage I and counteract the adverse affects of the auxiliaries in Stage III.

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Biomechanical PhenomenaEquipment DesignHumansIncisorMalocclusionMalocclusion, Angle Class IIMolarOrthodontic AppliancesTooth Movement TechniquesJournal Article

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R A Hocevar. 1982. Orthodontic force systems: technical refinements for increased efficiency.. https://doi.org/10.1016/0002-9416(82)90282-2

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Characterization of the unique mechanism mediating the shear-dependent binding of soluble von Willebrand factor to platelets.

We have studied the mechanism of interaction between soluble von Willebrand factor (vWF), labeled with fluorescein isothiocyanate (FITC), and platelets exposed to shear in a cone-and-plate viscometer. A flow cytometer calibrated with fluorescent bead standards was used to calculate the number of molecules associated with each platelet in suspension. To validate the methods and reagents used, binding of the same labeled vWF was assessed in the presence of ristocetin or alpha-thrombin and found to be saturable, with a narrow and symmetric distribution on > 90% of the platelets. As expected, essentially all bound ligand interacted exclusively with platelet membrane glycoprotein (GP) Ib alpha in the presence of ristocetin and with GP IIb-IIIa after stimulation with alpha-thrombin. In contrast, only a minor proportion (< 20%) of the platelets exposed to shear were found to bind vWF, with no evidence for saturation and markedly decreased interaction when the platelet count was below 100,000 microliters. Moreover, shear-induced vWF binding was blocked equally effectively by selected monoclonal antibodies against either GP Ib alpha or GP IIb-IIIa or against the respective binding sites in vWF. Thus, both receptors are involved in the process, possibly through initial transient interactions mediated by GP Ib alpha that lead to platelet activation and subsequent irreversible binding supported by GP IIb-IIIa. While the levels of shear stress theoretically applied to platelets in these experiments are above those thought to occur in the normal circulation, our findings demonstrate a unique vWF binding mechanism that is not mimicked by other known modulators and correlates with platelet aggregation. Similar processes may occur in response to lower shear stress when platelets are exposed to thrombogenic surfaces and agonists generated at sites of vascular injury during thrombus formation.

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