A digital technique for occlusal design of a posterior full crown based on physiological tooth displacement and occlusion of adjacent teeth.

This article presents a digital technique to construct a virtual occlusion in the maximal intercuspal position (MIP), considering physiological tooth displacement and reducing intermesh penetrations between occlusal surfaces, in order to design more precise and accurate occlusal contacts of a posterior full crown.

Effect of a novel interocclusal recording method on occlusal accuracy of implant-supported fixed prostheses: A randomized clinical trial.

OBJECTIVES: To investigate the effect of a novel interocclusal recording method on the occlusal accuracy of implant-supported fixed prostheses for partially dentate patients with distal extension. MATERIALS AND METHODS: Twenty patients with two or more adjacent teeth missing in the distal extension and scheduled to receive implant-supported fixed prostheses were enrolled. Two interocclusal recording methods were used: placing polyvinyl siloxane (PVS) on the interocclusal recording caps (test), and placing PVS on healing abutments (control). The intraoral occlusal contacts in maximal intercuspal position (MIP) were compared with those in the mounted casts to calculate sensitivity and positive predictive value (PPV). Then, patients were randomly allocated into two groups to determine which interocclusal record would be used. The implant prostheses' evaluations mainly included occlusal adjustment height, volume, and time, occlusal contact score based on articulating paper examination. Paired-samples t-test, Mann-Whitney U test, and least squares regression analyzed the statistic differences. RESULTS: The test method had higher sensitivity to detect intraoral occlusal contacts than the control method (p = .002), but similar PPV (p = .10). During the prostheses' evaluations, the occlusal adjustment height in the test group was significantly lower than that in the control group [99.4 (53.2, 134.2) vs. 159.0 (82.3, 247.8) µm, p = .03], while the occlusal contact score before adjustment was higher (p = .006). The groups had similar occlusal adjustment volume and time. CONCLUSIONS: The novel interocclusal recording method for implant-supported fixed prostheses was more accurate and could reduce the occlusal adjustment.

Assessment of physiological posterior-tooth displacement under habitual occlusal force by intraoral scanning using implant-supported crowns as the reference.

STATEMENT OF PROBLEM: Studies that have used digital methods to quantitatively evaluate physiological tooth displacement under occlusal force are sparse. PURPOSE: The purpose of this clinical study was to measure physiological posterior tooth displacement under occlusal force by intraoral scanning and reverse engineering technology by using implants as the reference. MATERIAL AND METHODS: A total of 14 participants received 15 implant-supported single mandibular first molar crowns. The surface data of maxillary and mandibular posterior teeth (U1 and L1) and the buccal occlusal data in the maximum intercuspal position (MIP) with habitual occlusal force were obtained by using an intraoral scanner (TRIOS 3, v20.1.2). The U1 and L1 data were segmented into single teeth, which were then aligned to the buccal occlusal data by using the "best-fit alignment" command to build the data under occlusal force (U2 and L2). U1 and L1 data were compared with U2 and L2 data to calculate the centroid and functional cusp vertex displacements and the long axis deflections of the second premolars and second molars, taking the first molar as the reference. The medians, and first quartile (Q1), third quartile (Q3) of the above data were reported, and the Shapiro-Wilk and Wilcoxon tests were used to analyze the differences (α=.05). RESULTS: Under occlusal force, the median (Q1, Q3) centroid displacements of posterior teeth ranged from 61 (52, 101) µm to 146 (80, 186) µm; the functional cusp vertex displacements ranged from 82 (62, 117) µm to 146 (98, 189) µm, and the long axis deflections ranged from 0.45 (0.25, 0.87) degrees to 1.03 (0.52, 1.41) degrees. Mandibular second premolars displaced lingually, mesially, and apically; mandibular second molars displaced distally and apically; and maxillary second premolars and second molars displaced lingually and apically. CONCLUSIONS: A digital method taking implant-supported single crowns as the reference was used to demonstrate physiological posterior-tooth displacement under habitual occlusal force.

Digitally designed occlusion of an implant-supported crown considering physiological tooth displacement under occlusal loading.

Physiological natural tooth displacement under occlusal loading can influence intraoral occlusal contacts. However, gypsum casts and digital scans cannot simulate the physiological tooth displacement under occlusal loading. The occlusal design of the implant-supported crowns has been based mainly on the experience of dental laboratory technicians, lacking accuracy and individualization. Therefore, a digital technique that considers physiological tooth displacement is presented to design the occlusion of implant-supported single crowns.

Desensitization of NMDA channels requires ligand binding to both GluN1 and GluN2 subunits to constrict the pore beside the activation gate.

N-methyl-D-aspartate (NMDA) receptor channels are activated by glutamate (or NMDA) and glycine. The channels also undergo desensitization, which denotes decreased channel availability, after prolonged exposure to the activating ligands. Glycine apparently has a paradoxical negative effect on desensitization, as the increase in ambient glycine in concentrations required for channel activation would increase sustained NMDA receptor currents. We hypothesized that this classical "glycine-dependent desensitization" could be glycine-dependent activation in essence. By performing electrophysiological recordings and biophysical analyses with rat brain NMDA receptors heterogeneously expressed in Xenopus laevis oocytes, we characterized that the channel opened by "only" NMDA (in nominally glycine-free condition probably with the inevitable nanomolar glycine) would undergo a novel form of deactivation rather than desensitization, and is thus fully available for subsequent activation. Moreover, external tetrapentylammonium ions (TPentA), tetrabutylammonium ions, and tetrapropylammonium ions (TPA, in higher concentrations) block the pore and prohibit channel desensitization with a simple "foot-in-the-door" hindrance effect. TpentA and TPA have the same voltage dependence but show different flow dependence in binding affinity, revealing a common binding site at an electrical distance of ~0.7 from the outside yet differential involvement of the flux-coupling region in the external pore mouth. The smaller tetraethylammonium ion and the larger tetrahexylammonium and tetraheptylammonium ions may block the channel but could not affect desensitization. We conclude that NMDA receptor desensitization requires concomitant binding of both glycine and glutamate, and thus movement of both GluN1 and GluN2 subunits. Desensitization gate itself embodies a highly restricted pore reduction with a physical distance of ~4 Å from the charged nitrogen atom of bound tetraalkylammonium ions, and is located very close to the activation gate in the bundle-crossing region in the external pore vestibule.

The differential contribution of GluN1 and GluN2 to the gating operation of the NMDA receptor channel.

The Ν-methyl-D-aspartate (NMDA) receptor channel is an obligatory heterotetramer formed by two GluN1 and two GluN2 subunits. However, the differential contribution of the two different subunits to channel operation is not clear. We found that the apparent affinity of glycine to GluN1 (K gly ∼ 0.6 µM) is much higher than NMDA or glutamate to GluN2 (K NMDA ∼ 36 µM, K glu ∼ 4.8 µM). The binding rate constant (derived from the linear regression of the apparent macroscopic binding rates) of glycine to GluN1 (∼9.8 × 10(6) M(-1) s(-1)), however, is only slightly faster than NMDA to GluN2 (∼4.1 × 10(6) M(-1) s(-1)). Accordingly, the apparent unbinding rates of glycine from activated GluN1 (time constant ∼2 s) are much slower than NMDA from activated GluN2 (time constant ∼70 ms). Moreover, the decay of NMDA currents upon wash-off of both glycine and NMDA seems to follow the course of NMDA rather than glycine unbinding. But if only glycine is washed off, the current decay is much slower, apparently following the course of glycine unbinding. The apparent binding rate of glycine to the fully deactivated channel, in the absence of NMDA, is roughly the same as that measured with co-application of both ligands, whereas the apparent binding rate of NMDA to the fully deactivated channel in the absence of glycine is markedly slower. In this regard, it is interesting that the seventh residue in the highly conserved SYTANLAAF motif (A7) in GluN1 and GluN2 are so close that they may interact with each other to control the dimension of the external pore mouth. Moreover, specific mutations involving A7 in GluN1 but not in GluN2 result in channels showing markedly enhanced affinity to both glycine and NMDA and readily activated by only NMDA, as if the channel is already partially activated. We conclude that GluN2 is most likely directly responsible for the activation gate of the NMDA channel, whereas GluN1 assumes a role of more global control, especially on the gating conformational changes in GluN2. Structurally, this intersubunit regulatory interaction seems to involve the SYTANLAAF motif, especially the A7 residue.

Modulation of NMDA channel gating by Ca2+ and Cd2+ binding to the external pore mouth.

NMDA receptor channels are characterized by high Ca2+ permeability. It remains unclear whether extracellular Ca2+ could directly modulate channel gating and control Ca2+ influxes. We demonstrate a pore-blocking site external to the activation gate for extracellular Ca2+ and Cd2+, which has the same charge and radius as Ca2+ but is impermeable to the channel. The apparent affinity of Cd2+ or Ca2+ is higher toward the activated (a steady-state mixture of the open and desensitized, probably chiefly the latter) than the closed states. The blocking effect of Cd2+ is well correlated with the number of charges in the DRPEER motif at the external pore mouth, with coupling coefficients close to 1 in double mutant cycle analyses. The effect of Ca2+ and especially Cd2+ could be allosterically affected by T647A mutation located just inside the activation gate. A prominent "hook" also develops after wash-off of Cd2+ or Ca2+, suggesting faster unbinding rates of Cd2+ and Ca2+ with the mutation. We conclude that extracellular Ca2+ or Cd2+ directly binds to the DRPEER motif to modify NMDA channel activation (opening as well as desensitization), which seems to involve essential regional conformational changes centered at the bundle crossing point A652 (GluN1)/A651(GluN2).