Correlation between Primary Stability of Dental Implants and Bone Density: A Retrospective Analysis.

Dental implants have gained popularity in recent years. The most important variable in determining the effectiveness of the implant's primary stability is bone density. The success of the implant depends on proper procedure and implant stability. With this background, the aim of the present study was to study the correlation between primary stability and bone density. The present retrospective study was conducted among 2,440 patients who had undergone implant treatment in the Department of Implantology, Saveetha Dental College and Hospitals, Chennai, from June 2021 to February 2022. Data regarding patient's age, gender, implant location, bone density, and primary stability were taken into consideration. Association between primary stability and bone density was assessed using the Chi-square test. Of the subjects, 33.42% had D2 bone density in the lower posterior region; 13.98% had D3 density in the lower posterior region. Primary stability of 30-40 Ncm was seen in the majority of the subjects; 32.64% who had primary stability of 30-40 Ncm had D2 bone density. There was a statistically significant association between implant site and bone density (p = 0.04) and primary stability and bone density (p = 0.03). Within the limitations of the study, it can be concluded that there is a strong association between implant primary stability and bone density.

Elevated Electrochemical Performance of LiNi0.1Mg0.1Co0.8O2 and LiFePO4 Cathodes with Tris(2,2,2-trifluoroethyl) Phosphite as an Efficient Electrolyte Additive.

The significant role of Tris(2,2,2-trifluoroethyl) phosphite (TTFP) as an efficient additive during cycling of the layered nanostructured LiNi0.1Mg0.1Co0.8O2 and olivine LiFePO4 cathode materials in EC/DMC and 1M LiPF6 electrolyte for Li-ion battery are extensively investigated in this work. The electrochemical characterization techniques such as cyclic voltammetry, galvanostatic charge/discharge, and electrochemical impedance spectroscopy show that TTFP improves cycling stability and reduces the irreversible capacity of LiNi0.1Mg0.1Co0.8O2 and LiFePO4 electrodes. Also, the presence of TTFP in electrolyte solution reduces the impedance in LiNi0.1Mg0.1Co0.8O2 and LiFePO4 cathode materials at room temperature. A family of Nyquist plots was obtained from LiNi0.1Mg0.1Co0.8O2 and LiFePO4 electrodes for various potentials during the course of charging. The addition of TTFP in the electrolyte reduces the surface impedance of lithiated LiNi0.1Mg0.1Co0.8O2 and LiFePO4 which can be attributed to the reaction of the additive on the electrode's surface. Also, the presence of the additive TTFP in LiNi0.1Mg0.1Co0.8O2 and LiFePO4 cell enhances the lithium diffusion rate and improves the electronic conductivity of the cathode material.

Carcinogen-Induced Model of Proangiogenesis in Zebrafish Embryo-Larvae.

Tumor angiogenesis is the main target in cancer drug development. Discovery of antiangiogenic agents targeting different mechanisms of action is the major area of research to control tumor growth and metastasis. Zebrafish (in the embryo-larvae stage) acts as an essential preclinical efficacy-toxicity model for antiangiogenic drug discovery. We aimed to develop a carcinogen-induced model of proangiogenesis in zebrafish embryo-larvae using the carcinogens lindane and benzo[a]pyrene. Zebrafish were randomly selected for mating. Postspawning, healthy embryos were staged, dispensed in reverse-osmosis water in a 12-well plate, and incubated at 28.5 °C, wherein 24 h postfertilization they were exposed to sublethal concentrations of the carcinogens. Three days postexposure, embryos were stained with alkaline phosphatase, and the angiogenic basket was imaged using a bright-field microscope. The number of subintestinal vessels, their length from somite to the basket, and other proangiogenic parameters were measured and analyzed. The effective concentrations causing a 30% increase in subintestinal vessels for benzo[a]pyrene and lindane were 2.69 and 2.24 µM, respectively, thus proving their proangiogenic potency. The carcinogen-induced model of proangiogenesis in zebrafish embryo-larvae can be used as an effective high-throughput screening tool to assess the proangiogenic potential of carcinogenic compounds and to screen antiangiogenic drugs for better therapeutic intervention. Environ Toxicol Chem 2021;40:447-453.© 2020 SETAC.

Biohazards associated with materials used in prosthodontics.

Dental materials for permanent restorations are manufactured with the intent to be stable and insoluble, but they do not fully achieve this goal. The amount of dissolved components is small and their detection sometimes requires sophisticated analytical equipment. The minute amounts of components that leach out of permanent dental restorative materials are most unlikely to cause toxic reactions, locally or systemically. Reliable research information using robust methodology is thus needed to clarify the various safety issues and frequency of adverse reactions in general dentistry, including prosthodontic treatment.

Force Finishing and Centering to Balance a Removable Complete Denture Prosthesis Using the T-Scan III Computerized Occlusal Analysis System.

Obtaining bilateral balance of removable complete denture prostheses is the occlusal goal of the restorative dentist or prosthodontist. Despite our best clinical efforts, and the using of advanced mechanical devices like semi-adjustable articulators and face bow transfer mounting of dental casts, it is a struggle to provide accurate occlusal force balance. Some of the advocated reasons for the clinical difficulty of obtaining reliable occlusal balance are that stone casts lack soft tissue resiliency, and articulators only approximate human occlusal functional movements. However, modern technology offers clinicians a digital answer to this clinical force balance problem. It is known as computerized occlusal analysis. The T-Scan III system can be employed with complete removable denture prostheses to perform computer-guided occlusal force-finishing corrective adjustments that measurably improve the installed prosthetic occlusal balance.

Protective effect of curcumin during selenium induced toxicity on dehydrogenases in hepatic tissue.

Selenium administration resulted in a marked decrease in the activity levels of the liver succinate dehydrogenase, malate dehydrogenase, and lactate dehydrogenase while pyruvate dehydrogenase increased significantly (P<0.001) in the wistar rat. The degree of decrease of these enzymes was significantly less (P<0.001) when rats were treated with curcumin, a natural constituent Curcuma longa. Curcumin seems to prevent oxidative damage mediated through selenium and protect the dehydrogenases possibly through its anti-oxidative property.

Antioxidant effect of curcumin in selenium induced cataract of Wistar rats.

Wistar rat pups treated with curcumin, a natural constituent of Curcuma longa before being administered with selenium showed no opacities in the lens. The lipid peroxidation, xanthine oxidase enzyme levels in the lenses of curcumin and selenium co-treated animals were significantly less when compared to selenium treated animals. The superoxidase dismutase and catalase enzyme activities of curcumin and selenium co-treated animal lenses showed an enhancement. Curcumin co-treatment seems to prevent oxidative damage and found to delay the development of cataract.

Central retinal vein occlusion due to herpes zoster as the initial presenting sign in a patient with acquired immunodeficiency syndrome (AIDS).

Central retinal vein occlusion (CRVO) due to herpes zoster has rarely been reported. Varicella zoster virus is a common opportunistic infection in patients with AIDS. This case report is about a 40-year-old man with herpes zoster ophthalmicus and central retinal vein occlusion of the right eye who is HIV-positive. Although the lesion resolved following treatment with intravenous acyclovir and oral steroid, the patient subsequently developed florid disc neovascularization and vitreous hemorrhage. The paper highlights CRVO as the initial presentation in an AIDS patient with herpes zoster ophthalmicus.

Inactivation of glutathione peroxidase by peroxynitrite.

Glutathione peroxidase (GSH-Px) is inactivated on exposure to peroxynitrite under physiologically relevant conditions. Stopped-flow kinetic studies show that the reaction between peroxynitrite and GSH-Px is first-order in each of the reactants, with an apparent second-order rate constant of 4.5 +/- 0.2 x 10(4) M-1 s-1 per monomer unit of enzyme. In good agreement with this value, GSH-Px inactivation experiments afford an apparent second-order rate constant of 1.8 +/- 0.1 x 10(4) M-1 s-1 per monomer unit of enzyme. The hydroxyl radical scavengers mannitol, DMSO, and benzoate (at 100 mM) afford only 8-12% protection of the enzyme, while addition of 25 mM bicarbonate results in 55% protection. The minimal protection by hydroxyl radical scavengers indicates, as expected, that hydroxyl radicals are not involved in the inactivation. Protection by bicarbonate occurs because peroxynitrite is rapidly trapped by CO2 to form the adduct nitrosoperoxycarbonate (ONOOCO2-), and/or other reactive species that preferentially decompose to nitrate rather than react with GSH-Px. The close agreement between the rate constants obtained from enzyme inactivation and from stopped-flow kinetics experiments suggests that the mechanism of the reaction between peroxynitrite and GSH-Px involves the oxidation of the ionized selenol of the selenocysteine residue in the enzyme's active site (E-Se-) by peroxynitrite. This reaction does not simply involve formation of the selenenic acid, E-SeOH, because E-SeOH is an intermediate in the catalytic cycle of the enzyme, and thus its formation cannot explain the inactivation we observe. Thus, the ionized selenol in the active site is transformed into a form of selenium that cannot easily be reduced back to the selenol.

Carbon dioxide modulation of hydroxylation and nitration of phenol by peroxynitrite.

We have examined the formation of hydroxyphenols, nitrophenols, and the minor products 4-nitrosophenol, benzoquinone, 2,2'-biphenol, and 4,4'-biphenol from the reaction of peroxynitrite with phenol in the presence and absence of added carbonate. In the absence of added carbonate, the product yields of nitrophenols and hydroxyphenols have different pH profiles. The rates of nitration and hydroxylation also have different pH profiles and match the trends observed for the product yields. At a given pH, the sum of the rate constants for nitration and hydroxylation is nearly identical to the rate constant for the spontaneous decomposition of peroxynitrite. The reaction of peroxynitrite with phenol is zero-order in phenol, both in the presence and absence of added carbonate. In the presence of added carbonate, hydroxylation is inhibited, whereas the rate of formation and yield of nitrophenols increase. The combined maximum yield of o- and p-nitrophenols is 20 mol% (based on the initial concentration of peroxynitrite) and is about fourfold higher than the maximal yield obtained in the absence of added carbonate. The o/p ratio of nitrophenols is the same in the presence and absence of added carbonate. These results demonstrate that hydroxylation and nitration occur via two different intermediates. We suggest that the activated intermediate formed in the isomerization of peroxynitrous acid to nitrate, ONOOH*, is the hydroxylating species. We propose that intermediate 1, O=N-OO-CO2-, or secondary products derived from it, is (are) responsible for the nitration of phenol. The possible mechanisms responsible for nitration are discussed.

Peroxynitrite-mediated oxidation of D,L-selenomethionine: kinetics, mechanism and the role of carbon dioxide.

Peroxynitrite oxidizes D,L-selenomethionine (MetSe) by two competing mechanisms, a one-electron oxidation that leads to ethylene and a two-electron oxidation that gives methionine selenoxide (MetSeO). Kinetic modeling of the experimental data suggests that both peroxynitrous acid and the peroxynitrite anion react with MetSe to form MetSeO with rate constants of 20,460 +/- 440 M-1 s-1 and 200 +/- 170 M-1 s-1, respectively at 25 degrees C. The enthalpy (delta H++) and entropy (delta S++) of activation for the reaction of peroxynitrous acid with MetSe at pH 4.6 are 2.55 +/- 0.08 kcal mol-1 and -30.5 +/- 0.3 cal mol-1 K-1, respectively. With increasing concentrations of MetSe at pH 7.4, the yield of ethylene decreases and that of MetSeO increases, suggesting, as with methionine, the reactions leading to ethylene and MetSeO have different kinetic orders. We propose that the activated form of peroxynitrous acid, HOONO*, is the one-electron oxidant and ground-state peroxynitrite is the two-electron oxidant in the reaction of peroxynitrite with MetSe. The peroxynitrite anion rapidly adds to CO2 to form an adduct, O = N-OO-CO2- (1), capable of generating potent reactive species, and we therefore examined the role of CO2 in the peroxynitrite/MetSe system. In presence of added bicarbonate, the yield of ethylene obtained from the reaction of 0.4 mM peroxynitrite with 1.0 mM MetSe increases slightly with an increase in the concentration of bicarbonate from 0 to 5.0 mM and remains constant with a further increase of bicarbonate up to 20 mM. The yield of MetSeO, from the reaction of 10 mM peroxynitrite with 10 mM MetSe, decreases by 35% with an increase in the concentration of bicarbonate from 0 to 25 mM. Kinetic simulations show that the decrease in the yield of MetSeO is due to reaction of the peroxynitrite anion with CO2. These results suggest that CO2 partially protects MetSe from peroxynitrite-mediated oxidation and that 1 or its derivatives do not mediate the oxidation of MetSe to MetSeO.

Rapid oxidation of DL-selenomethionine by peroxynitrite.

Peroxynitrite, the reaction product of nitric oxide and superoxide, rapidly oxidizes DL-selenomethionine (MetSe) with overall second-order kinetics, first-order in peroxynitrite and first-order in MetSe. The oxidation of MetSe by peroxynitrite goes by two competing mechanism. The first produces ethylene by what we propose to be a one-electron oxidation of MetSe. In the second mechanism, MetSe undergoes a two-electron oxidation that gives methionine selenoxide (MetSe = O); the apparent second-order rate constant, k2(app), for this process is (2.4 +/- 0.1) x 10(3) M-1s-1 at pH 7.4 and 25 degrees C. The kinetic modeling of the experimental data suggests that both peroxynitrous acid (k2 = 20,460 +/- 440 M-1s-1 at 25 degrees C) and the peroxynitrite anion (k3 = 200 +/- 170 M-1s-1 at 25 degrees C) are involved in the second-order reaction leading to selenoxide. These rate constants are 10- to 1,000-fold higher than those for the reactions of methionine (Met) with peroxynitrite. With increasing concentrations of MetSe at pH 7.4, the yield of ethylene decreases, while that of MetSe = O increases, suggesting that the reactions leading to ethylene and selenoxide have different kinetic orders. These results are analogous to those we previously reported for methionine and 2-keto-4-thiomethylbutanoic acid (KTBA),where ethylene is produced in a first-order reaction and sulfoxide in a second-order reaction. Therefore, we suggest that the reaction of peryoxynitrite with MetSe involves a mechanism similar to that we proposed for Met, in which an activated intermediate of peroxynitrous acid (HOONO) is the one-electron oxidant and reacts with first-order kinetics and ground-state peroxynitrite is the two-electron oxidant and reacts with second-order kinetics.

Nitration and hydroxylation of phenolic compounds by peroxynitrite.

The kinetics and products of the reaction of peroxynitrite with the phenolic compounds phenol, tyrosine, and salicylate were studied as a function of pH. All reactions are first-order in peroxynitrite and zero-order in the phenolic compound. Relative to the hydroxyl group, electrophilic substitution in the 2- and 4-positions (if available) leads to hydroxylated and nitrated products. The total yield of the products is proportional to the concentration of peroxynitrite. The sum of the rates of hydroxylation and nitration of phenol, determined by the stopped-flow technique, is approximately equal to the rate constant for the isomerization of peroxynitrite to nitrate. The rate vs pH profiles of the nitration and hydroxylation reactions parallel the yield vs pH profile with nitration maxima at pH 1.8 and 6.8, while hydroxylation is dominant between these two pH values. The activation energies for both hydroxylation and nitration are 18.8 +/- 0.3 kcal mol-1, identical to that of the isomerization of peroxynitrite to nitrate. Ethanol decreases the yield of hydroxylation, but has less effect on the nitration. The rate of reaction in the presence of metal complexes is first-order in metal complex and peroxynitrite and zero-order in the phenolic compound. The enhancement of the nitration of phenol by Fe(III)-edta and -nta is pH-dependent, with a maximum near pH 7, while Fe(III)-citrate, Cu(II)-edta, and CuSO4 affect the nitration much less. The second-order rate constants for Fe(III)-edta at pH 4.8 and 7.2 are 1.4 x 10(3) and 5.5 x 10(3) M-1 s-1, respectively, at 25 degrees C. The activation energies for the nitration reaction in the presence of Fe(III)-edta are 11.5 and 12.2 kcal mol-1 at pH 4.8 and 7.2, respectively. The nitration of tyrosine and salicylate by peroxynitrite is maximally enhanced by Fe(III)-edta.

Reaction of peroxynitrite with L-tryptophan.

The reaction between peroxynitrous acid (hydrogen oxoperoxonitrate) and L-tryptophan is 130 M(-1)s(-1) at 25°C. The pH dependence of the second-order rate constant shows a maximum at pH 5.1. The enthalpy and entropy of activation at pH 7.1 are 10.6 ± 0.4 kcal.mol(-1) and -16 ± 2 cal.mol(-1)K(-1) respectively. High-performance liquid chromatography analysis revealed a number of reaction products, two of which were identified as 5- and 6- nitrotryptophan. Hydroxytryptophans were not observed, even at low peroxynitrite concentrations where most of the peroxynitrite decays to nitrate via a first-order process. These results support the hypothesis that isomerization of protonated peroxynitrite to nitrate does not involve formation of the hydroxyl radical.

The reaction of nitric oxide with organic peroxyl radicals.

Nitric oxide and organic peroxyl radicals are key reactive radicals implicated in a wide range of biological processes. We have measured rate constants for the reactions of several organic peroxyl radicals with nitric oxide in aqueous solution and found that they are all fast, with k = 1-3 x 10(9) L mol-1 s-1. The reactions lead to the formation of an intermediate, identified as the organic peroxynitrite, which decayed with a rate constant of k = 0.1-0.3 s-1. Possible products of this decay include the more reactive alkoxyl and nitrogen dioxide free radicals, or the less reactive organic nitrate. In alcoholic solutions, the rate constants of the initial reactions were similar, but the product decay rates were about 200 times faster. Because of the ubiquity of both nitric oxide and organic peroxyl radicals, their interaction could make a significant contribution to many physiological processes.

The reaction of no with superoxide.

The rate constant for the reaction of NO with .O2- was determined to be (6.7 +/- 0.9) x 10(9) l mol-1 s-1, considerably higher than previously reported. Rate measurements were made from pH 5.6 to 12.5 both by monitoring the loss of .O2- and the formation of the product -OONO. The decay rate of -OONO, in the presence of 0.1 mol l-1 formate, ranges from 1.2 s-1 at pH 5 to about 0.2 s-1 in strong base, the latter value probably reflecting catalysis by formate.