Long-term results of mandibular implants supporting an overdenture: implant survival, failures, and crestal bone level changes

The present study summarizes the long-term clinical observations of edentulous patients treated with mandibular implant-supported overdentures.

Syntrophin mutation associated with long QT syndrome through activation of the nNOS-SCN5A macromolecular complex.

Mutations in 11 genes that encode ion channels or their associated proteins cause inherited long QT syndrome (LQTS) and account for approximately 75-80% of cases (LQT1-11). Direct sequencing of SNTA1, the gene encoding alpha1-syntrophin, was performed in a cohort of LQTS patients that were negative for mutations in the 11 known LQTS-susceptibility genes. A missense mutation (A390V-SNTA1) was found in a patient with recurrent syncope and markedly prolonged QT interval (QTc, 530 ms). SNTA1 links neuronal nitric oxide synthase (nNOS) to the nNOS inhibitor plasma membrane Ca-ATPase subtype 4b (PMCA4b); SNTA1 also is known to associate with the cardiac sodium channel SCN5A. By using a GST-fusion protein of the C terminus of SCN5A, we showed that WT-SNTA1 interacted with SCN5A, nNOS, and PMCA4b. In contrast, A390V-SNTA1 selectively disrupted association of PMCA4b with this complex and increased direct nitrosylation of SCN5A. A390V-SNTA1 expressed with SCN5A, nNOS, and PMCA4b in heterologous cells increased peak and late sodium current compared with WT-SNTA1, and the increase was partially inhibited by NOS blockers. Expression of A390V-SNTA1 in cardiac myocytes also increased late sodium current. We conclude that the A390V mutation disrupted binding with PMCA4b, released inhibition of nNOS, caused S-nitrosylation of SCN5A, and was associated with increased late sodium current, which is the characteristic biophysical dysfunction for sodium-channel-mediated LQTS (LQT3). These results establish an SNTA1-based nNOS complex attached to SCN5A as a key regulator of sodium current and suggest that SNTA1 be considered a rare LQTS-susceptibility gene.

SCN4B-encoded sodium channel beta4 subunit in congenital long-QT syndrome.

BACKGROUND Congenital long-QT syndrome (LQTS) is potentially lethal secondary to malignant ventricular arrhythmias and is caused predominantly by mutations in genes that encode cardiac ion channels. Nearly 25% of patients remain without a genetic diagnosis, and genes that encode cardiac channel regulatory proteins represent attractive candidates. Voltage-gated sodium channels have a pore-forming alpha-subunit associated with 1 or more auxiliary beta-subunits. Four different beta-subunits have been described. All are detectable in cardiac tissue, but none have yet been linked to any heritable arrhythmia syndrome. METHODS AND RESULTS We present a case of a 21-month-old Mexican-mestizo female with intermittent 2:1 atrioventricular block and a corrected QT interval of 712 ms. Comprehensive open reading frame/splice mutational analysis of the 9 established LQTS-susceptibility genes proved negative, and complete mutational analysis of the 4 Na(vbeta)-subunits revealed a L179F (C535T) missense mutation in SCN4B that cosegregated properly throughout a 3-generation pedigree and was absent in 800 reference alleles. After this discovery, SCN4B was analyzed in 262 genotype-negative LQTS patients (96% white), but no further mutations were found. L179F was engineered by site-directed mutagenesis and heterologously expressed in HEK293 cells that contained the stably expressed SCN5A-encoded sodium channel alpha-subunit (hNa(V)1.5). Compared with the wild-type, L179F-beta4 caused an 8-fold (compared with SCN5A alone) and 3-fold (compared with SCN5A + WT-beta4) increase in late sodium current consistent with the molecular/electrophysiological phenotype previously shown for LQTS-associated mutations. CONCLUSIONS We provide the seminal report of SCN4B-encoded Na(vbeta)4 as a novel LQT3-susceptibility gene.

Precision of fit and retention force of cast non-precious-crowns on standard titanium implant-abutment with different design and height

OBJECTIVE The cost-effectiveness of cast nonprecious frameworks has increased their prevalence in cemented implant crowns. The purpose of this study was to assess the effect of the design and height of the retentive component of a standard titanium implant abutment on the fit, possible horizontal rotation and retention forces of cast nonprecious alloy crowns prior to cementation. MATERIALS AND METHODS Two abutment designs were examined: Type A with a 6° taper and 8 antirotation planes (Straumann Tissue-Level RN) and Type B with a 7.5° taper and 1 antirotation plane (SICace implant). Both types were analyzed using 60 crowns: 20 with a full abutment height (6 mm), 20 with a medium abutment height (4 mm), and 20 with a minimal (2.5 mm) abutment height. The marginal and internal fit and the degree of possible rotation were evaluated by using polyvinylsiloxane impressions under a light microscope (magnification of ×50). To measure the retention force, a custom force-measuring device was employed. STATISTICAL ANALYSIS one-sided Wilcoxon rank-sum tests with Bonferroni-Holm corrections, Fisher's exact tests, and Spearman's rank correlation coefficient. RESULTS Type A exhibited increased marginal gaps (primary end-point: 55 ± 20 μm vs. 138 ± 59 μm, P < 0.001) but less rotation (P < 0.001) than Type B. The internal fit was also better for Type A than for Type B (P < 0.001). The retention force of Type A (2.49 ± 3.2 N) was higher (P = 0.019) than that of Type B (1.27 ± 0.84 N). Reduction in abutment height did not affect the variables observed. CONCLUSION Less-tapered abutments with more antirotation planes provide an increase in the retention force, which confines the horizontal rotation but widens the marginal gaps of the crowns. Thus, casting of nonprecious crowns with Type A abutments may result in clinically unfavorable marginal gaps.