Outcomes of clear aligner treatment with and without Dental Monitoring: A retrospective cohort study.

INTRODUCTION: The effects of Invisalign clear aligner treatment with and without Dental Monitoring (DM) were compared for treatment duration, number of appointments, refinements and refinement aligners, and accuracy of Invisalign in achieving predicted tooth positions (aligner tracking). The null hypothesis was that there are no differences between Invisalign with and without DM in these parameters. METHODS: A sample of 90 consecutively treated Invisalign patients (45 control, 45 DM) fitted the inclusion and exclusion criteria. Treatment duration, number of refinements, number of refinement aligners, time to first refinement, number of appointments, number of emergency visits, and accuracy of predicted tooth movement were observed for differences. RESULTS: The 2 groups were homogeneous (P >0.05) for sample size, age, gender, Angle classification, maxillary and mandibular irregularity index, and the number of initial aligners. There was a significant (P = 0.001) reduction in the number of appointments by 3.5 visits (33.1%) in the DM group. There was also a significant (P = 0.001) reduction in the time to the first refinement (1.7 months) in the DM group. Compared with Invisalign predicted tooth positions, actual tooth positions were statistically (P <0.05) more accurate for the DM group for the maxillary anterior dentition in rotational movements and mandibular anterior dentition for buccal-lingual linear movement. Invisalign therapy without DM was closer to predicted tooth positions for the maxillary posterior dentition for the tip. None of these differences surpassed the clinically significant thresholds (>0.5 mm or >2°); however, the DM group achieved this in 1.7 fewer months. CONCLUSIONS: DM with Invisalign therapy resulted in a reduced number of appointments by 3.5 visits (33.1%). The DM group also achieved a clinically similar accuracy in obtaining predicted tooth movements compared with the control group in 1.7 fewer months, indicating improved aligner tracking in the DM group.

Has Invisalign improved? A prospective follow-up study on the efficacy of tooth movement with Invisalign.

INTRODUCTION: The purpose of this research was to provide an update on the accuracy of tooth movement with Invisalign (Align Technology, Santa Clara, Calif). METHODS: This prospective clinical study included 38 patients treated with Invisalign Full or Invisalign Teen. All teeth, from the central incisor to the second molar, were measured on digital models created from intraoral scans. Predicted values were determined by superimposing the initial and final ClinCheck models, and achieved values were determined by superimposing the initial ClinCheck models and the digital models from the posttreatment scans. Individual teeth were superimposed with a best-fit analysis and measured using Compare software (version 8.1; GeoDigm, Falcon Heights, Minn). The types of tooth movements studied were a mesial-distal crown tip, buccal-lingual crown tip, extrusion, intrusion, and mesial-distal rotation. RESULTS: The mean accuracy of Invisalign for all tooth movements was 50%. The highest overall accuracy was achieved with a buccal-lingual crown tip (56%), whereas the lowest overall accuracy occurred with rotation (46%). The accuracies for mesial rotation of the mandibular first molar (28%), distal rotation of the maxillary canine (37%), and intrusion of the mandibular incisors (35%) were particularly low. CONCLUSIONS: There was a marked improvement in the overall accuracy; however, the strengths and weaknesses of tooth movement with Invisalign remained relatively the same.

A nonpyrrolysine member of the widely distributed trimethylamine methyltransferase family is a glycine betaine methyltransferase.

COG5598 comprises a large number of proteins related to MttB, the trimethylamine:corrinoid methyltransferase. MttB has a genetically encoded pyrrolysine residue proposed essential for catalysis. MttB is the only known trimethylamine methyltransferase, yet the great majority of members of COG5598 lack pyrrolysine, leaving the activity of these proteins an open question. Here, we describe the function of one of the nonpyrrolysine members of this large protein family. Three nonpyrrolysine MttB homologs are encoded in Desulfitobacterium hafniense, a Gram-positive strict anaerobe present in both the environment and human intestine. D. hafniense was found capable of growth on glycine betaine with electron acceptors such as nitrate or fumarate, producing dimethylglycine and CO2 as products. Examination of the genome revealed genes for tetrahydrofolate-linked oxidation of a methyl group originating from a methylated corrinoid protein, but no obvious means to carry out corrinoid methylation with glycine betaine. DSY3156, encoding one of the nonpyrrolysine MttB homologs, was up-regulated during growth on glycine betaine. The recombinant DSY3156 protein converts glycine betaine and cob(I)alamin to dimethylglycine and methylcobalamin. To our knowledge, DSY3156 is the first glycine betaine:corrinoid methyltransferase described, and a designation of MtgB is proposed. In addition, DSY3157, an adjacently encoded protein, was shown to be a methylcobalamin:tetrahydrofolate methyltransferase and is designated MtgA. Homologs of MtgB are widely distributed, especially in marine bacterioplankton and nitrogen-fixing plant symbionts. They are also found in multiple members of the human microbiome, and may play a beneficial role in trimethylamine homeostasis, which in recent years has been directly tied to human cardiovascular health.

Isolation and characterization of a tetramethylammonium-degrading Methanococcoides strain and a novel glycine betaine-utilizing Methanolobus strain.

Two novel strains of methanogens were isolated from an estuarine sediment with the capability to utilize quaternary amines. Based on the 16S rRNA analysis, strain B1d shared 99 % sequence identity with Methanolobus vulcani PL-12/M(T) and strain Q3c shared 99 % identity with Methanococcoides sp. PM1 and PM2, but our current isolates display clearly different capabilities of growth on quaternary amines and were isolated based on these capabilities. Strain Q3c was capable of growth on tetramethylammonium and choline, while strain B1d was capable of growth on glycine betaine. Ml. vulcani PL-12/M(T) was incapable of growth on glycine betaine, indicating an obvious distinction between strains B1d and PL-12/M(T). Strain Q3c now represents the only known tetramethylammonium-utilizing methanogen in isolation. Strain B1d is the first quaternary amine-utilizing methanogen from the genus Methanolobus. This study suggests that quaternary amines may serve as ready precursors of biological methane production in marine environments.

MicroRNA 21 (miR-21) and miR-181b couple with NFI-A to generate myeloid-derived suppressor cells and promote immunosuppression in late sepsis.

The sepsis initial hyperinflammatory reaction, if not treated early, shifts to a protracted state of immunosuppression that alters both innate and adaptive immunity and is associated with elevated mortality. Myeloid-derived suppressor cells (MDSCs) are myeloid progenitors and precursors that fail to differentiate into mature innate-immunity cells and are known for their potent immunosuppressive activities. We previously reported that murine MDSCs expand dramatically in the bone marrow during late sepsis, induced by cecal ligation and puncture, and demonstrated that they contribute to late-sepsis immunosuppression. However, the molecular mechanism responsible for generating these immature Gr1(+) CD11b(+) myeloid cells during sepsis remains unknown. We show here that sepsis generates a microRNA (miRNA) signature that expands MDSCs. We found that miRNA 21 (miR-21) and miR-181b expression is upregulated in early sepsis and sustained in late sepsis. Importantly, we found that simultaneous in vivo blockade of both miRNAs via antagomiR (a chemically modified miRNA inhibitor) injection after sepsis initiation decreased the bone marrow Gr1(+) CD11b(+) myeloid progenitors, improved bacterial clearance, and reduced late-sepsis mortality by 74%. Gr1(+) CD11b(+) cells isolated from mice injected with antagomiRs were able to differentiate ex vivo into macrophages and dendritic cells and produced smaller amounts of the immunosuppressive interleukin 10 (IL-10) and transforming growth factor ß (TGF-ß) after stimulation with bacterial lipopolysaccharide, suggesting that immature myeloid cells regained their maturation potential and have lost their immunosuppressive activity. In addition, we found that the protein level of transcription factor NFI-A, which plays a role in myeloid cell differentiation, was increased during sepsis and that antagomiR injection reduced its expression. Moreover, knockdown of NFI-A in the Gr1(+) CD11b(+) cells isolated from late-septic mice increased their maturation potential and reduced their production of the immunosuppressive mediators, similar to antagomiR injection. These data support the hypothesis that sepsis reprograms myeloid cells and thus alters the innate immunity cell repertoire to promote immunosuppression, and they demonstrate that this process can be reversed by targeting miR-21 and miR-181b to improve late-sepsis survival.

Scavenger receptor class a plays a central role in mediating mortality and the development of the pro-inflammatory phenotype in polymicrobial sepsis.

Sepsis is a frequent complication in critical illness. The mechanisms that are involved in initiation and propagation of the disease are not well understood. Scavenger receptor A (SRA) is a membrane receptor that binds multiple polyanions such as oxidized LDL and endotoxin. Recent studies suggest that SRA acts as a pattern recognition receptor in the innate immune response. The goal of the present study was to determine the role of SRA in polymicrobial sepsis. SRA deficient (SRA(-/-)) and C57BL/6JB/6J (WT) male mice were subjected to cecal ligation and puncture (CLP) to induce polymicrobial sepsis. NFκB activity, myeloperoxidase activity, and co-association of SRA with toll like receptor (TLR) 4 and TLR2 was analyzed in the lungs. Spleens were analyzed for apoptosis. Serum cytokines and chemokines were assayed. Blood and peritoneal fluid were cultured for aerobic and anaerobic bacterial burdens. Long-term survival was significantly increased in SRA(-/-) septic mice (53.6% vs. 3.6%, p < 0.05) when compared to WT mice. NFκB activity was 45.5% lower in the lungs of SRA(-/-) septic mice versus WT septic mice (p < 0.05). Serum levels of interleukin (IL)-5, IL-6, IL-10 and monocyte chemoattractant protein -1 were significantly lower in septic SRA(-/-) mice when compared to septic WT mice (p < 0.05). We found that SRA immuno-precipitated with TLR4, but not TLR2, in the lungs of WT septic mice. We also found that septic SRA(-/-) mice had lower bacterial burdens than WT septic mice. SRA deficiency had no effect on pulmonary neutrophil infiltration or splenocyte apoptosis during sepsis. We conclude that SRA plays a pivotal, and previously unknown, role in mediating the pathophysiology of sepsis/septic shock in a murine model of polymicrobial sepsis. Mechanistically, SRA interacts with TLR4 to enhance the development of the pro-inflammatory phenotype and mediate the morbidity and mortality of sepsis/septic shock.

The phosphocholine-binding pocket on C-reactive protein is necessary for initial protection of mice against pneumococcal infection.

Human C-reactive protein (CRP) protects mice from lethal Streptococcus pneumoniae infection when injected into mice within the range of 6 h before to 2 h after the administration of pneumococci. Because CRP binds to phosphocholine-containing substances and subsequently activates the complement system, it has been proposed that the antipneumococcal function of CRP requires the binding of CRP to phosphocholine moieties present in pneumococcal cell wall C-polysaccharide. To test this proposal experimentally, in this study, we utilized a new CRP mutant incapable of binding to phosphocholine. Based on the structure of CRP-phosphocholine complexes, which showed that Phe(66), Thr(76), and Glu(81) formed the phosphocholine-binding pocket, we constructed a CRP mutant F66A/T76Y/E81A in which the pocket was blocked by substituting Tyr for Thr(76). When compared with wild-type CRP, mutant CRP bound more avidly to phosphoethanolamine and could be purified by affinity chromatography using phosphoethanolamine-conjugated Sepharose. Mutant CRP did not bind to phosphocholine, C-polysaccharide, or pneumococci. Mutant CRP was free in the mouse serum, and its rate of clearance in vivo was not faster than that of wild-type CRP. When either 25 µg or 150 µg of CRP was administered into mice, unlike wild-type CRP, mutant CRP did not protect mice from lethal pneumococcal infection. Mice injected with mutant CRP had higher mortality rates than mice that received wild-type CRP. Decreased survival was due to the increased bacteremia in mice treated with mutant CRP. We conclude that the phosphocholine-binding pocket on CRP is necessary for CRP-mediated initial protection of mice against lethal pneumococcal infection.

MicroRNA-146a and RBM4 form a negative feed-forward loop that disrupts cytokine mRNA translation following TLR4 responses in human THP-1 monocytes.

Within hours after its initiation, the severe systemic inflammatory response of sepsis shifts to an adaptive anti-inflammatory state with coincident immunosuppression. This anti-inflammatory phenotype is characterized by diminished proinflammatory cytokine gene expression in response to toll-like receptor (TLR) stimulation with bacterial endotoxin/lipopolysaccharide (LPS), also known as endotoxin tolerance/adaptation. Our and other studies have established that gene-specific reprogramming following TLR4 responses independently represses transcription and translation of proinflammatory genes such as tumor necrosis factor alpha (TNFα). We also previously demonstrated that TNFα and interleukin (IL)-6 mRNA translation is repressed in endotoxin-adapted THP-1 human monocytes by an miRNA-based mechanism involving the argonaute family protein argonaute 2 (Ago2). Here, we further define the molecular nature of reprogramming translation by showing that TLR4-induced microRNA-146 promotes a feed-forward loop that modifies the subcellular localization of the RNA-binding protein RBM4 (RNA-binding motif protein 4) and promotes its interaction with Ago2. This interaction results in the assembly of a translation-repressor complex that disrupts TNFα and IL-6 cytokine synthesis in endotoxin-adapted THP-1 monocytes. This novel molecular path prevents the phosphorylation of RBM4 on serine-309 by p38 MAPK (mitogen-activated protein kinase), which leads to RBM4 accumulation in the cytosol and interaction with Ago2. We further find that microRNA-146a knockdown by antagomirs or protein phosphatase inhibition by okadaic acid increases p38 MAPK phosphorylation and results in RBM4 serine-309 phosphorylation and nuclear relocalization, which disrupts RBM4 and Ago2 interactions and restores TLR4-dependent synthesis of TNFα and IL-6. We conclude that miR-146a has a diverse and critical role in limiting an excessive acute inflammatory reaction.

The effect of alpha binaural beat music on orthodontic pain after initial archwire placement: A randomized controlled trial.

OBJECTIVE: The objective of this article was to evaluate the effect of alpha binaural beat music on pain level after initial placement of a maxillary fixed appliance, compared to music without binaural beats (placebo) and no music (control). METHODS: 60 patients undergoing maxillary fixed orthodontic appliance and initial archwire placement were randomly allocated into the three aforementioned groups. The pain level experienced was monitored for the following seven days, using the short-form McGill pain questionnaire (SF-MPQ). RESULTS / DESCRIPTORS: Intensity of both sensory and psychological aspects of pain reduced significantly in the binaural beat music (BBM) group, compared to the control, after the 5th day. Statistically significant lower affective and total pain scores were also found on day 6 for the placebo group, compared to the control. Present Pain Intensity (PPI): Statistically significant lower scores were found between the BBM group and the control group from days 3 to 7. Statistically significant lower scores were also found between the placebo and the control groups on days 4, 5 and 6. Visual Analog Scale (VAS): Compared to the control group, the placebo group had a lower VAS score on day 4, and the BBM group had lower scores on days 6 and 7. CONCLUSIONS: There was a significant reduction of pain demonstrated in the BBM group, compared to the control, toward the end of the first week of treatment. There was no difference in reported pain between the BBM and placebo groups for any of the scores.

Myeloid-derived suppressor cells evolve during sepsis and can enhance or attenuate the systemic inflammatory response.

Myeloid-derived suppressor cells (MDSCs) are a heterogeneous Gr1(+) CD11b(+) population of immature cells containing granulocytic and monocytic progenitors, which expand under nearly all inflammatory conditions and are potent repressors of T-cell responses. Studies of MDSCs during inflammatory responses, including sepsis, suggest they can protect or injure. Here, we investigated MDSCs during early and late sepsis. To do this, we used our published murine model of cecal ligation and puncture (CLP)-induced polymicrobial sepsis, which transitions from an early proinflammatory phase to a late anti-inflammatory and immunosuppressive phase. We confirmed that Gr1(+) CD11b(+) MDSCs gradually increase after CLP, reaching ∼88% of the bone marrow myeloid series in late sepsis. Adoptive transfer of early (day 3) MDSCs from septic mice into naive mice after CLP increased proinflammatory cytokine production, decreased peritoneal bacterial growth, and increased early mortality. Conversely, transfer of late (day 12) MDSCs from septic mice had the opposite effects. Early and late MDSCs studied ex vivo also differed in their inflammatory phenotypes. Early MDSCs expressed nitric oxide and proinflammatory cytokines, whereas late MDSCs expressed arginase activity and anti-inflammatory interleukin 10 (IL-10) and transforming growth factor ß (TGF-ß). Late MDSCs had more immature CD31(+) myeloid progenitors and, when treated ex vivo with granulocyte-macrophage colony-stimulating factor (GM-CSF), generated fewer macrophages and dendritic cells than early MDSCs. We conclude that as the sepsis inflammatory process progresses, the heterogeneous MDSCs shift to a more immature state and from being proinflammatory to anti-inflammatory.

Hematopoietic stem-progenitor cells restore immunoreactivity and improve survival in late sepsis.

Sepsis progresses from an early/acute hyperinflammatory to a late/chronic hypoinflammatory phase with immunosuppression. As a result of this phenotypic switch, mortality in late sepsis from persistent primary infection or opportunistic new infection often exceeds that in acute sepsis. Emerging data support that persistence of the hypoinflammatory (hyporesponsive) effector immune cells during late sepsis might involve alterations in myeloid differentiation/maturation that generate circulating repressor macrophages that do not readily clear active infection. Here, we used a cecal ligation and puncture (CLP) murine model of prolonged sepsis to show that adoptive transfer of CD34(+) hematopoietic stem-progenitor cells after CLP improves long-term survival by 65%. CD34(+) cell transfer corrected the immunosuppression of late sepsis by (i) producing significantly higher levels of proinflammatory mediators upon ex vivo stimulation with the Toll-like receptor 4 (TLR4) agonist lipopolysaccharide, (ii) enhancing phagocytic activity of peritoneal macrophages, and (iii) clearing bacterial peritonitis. Improved immunity by CD34(+) cell transfer decreased inflammatory peritoneal exudate of surviving late-sepsis mice. Cell tracking experiments showed that the transferred CD34(+) cells first appeared in the bone marrow and then homed to the spleen and peritoneum. Because CD34(+) cells did not affect the early-phase hyperinflammatory response, it is likely that the newly incorporated pluripotent CD34(+) cells differentiated into competent immune cells in blood and tissue, thereby reversing or replacing the hyporesponsive endotoxin-tolerant cells that occur and persist after the initiation of early sepsis.

Adoptive transfer of CD34(+) cells during murine sepsis rebalances macrophage lipopolysaccharide responses.

Effective treatment of the acute systemic inflammatory response associated with sepsis is lacking, but likely will require new ways to rebalance dysregulated immune responses. One challenge is that human sepsis often is diagnosed too late to reduce the hyperinflammation of early sepsis. Another is that the sequential response to sepsis inflammation rapidly generates an adaptive and immunosuppressive state, which by epigenetic imprint may last for months or years. Emerging data support that the immunosuppressive phase of sepsis can both directly reprogram gene expression of circulating and tissue cells, and disrupt development and differentiation of myeloid precursor cells into competent immunocytes. We recently reported that adoptive transfer of bone marrow CD34(+) cells into mice after sepsis induction by cecal ligation and puncture significantly improves late-sepsis survival by enhancing bacterial clearance through improved neutrophil and macrophage phagocytosis. That study, however, did not examine whether CD34(+) transfer can modify noninfectious acute systemic inflammatory responses. Here, we report that CD34(+) cell transfer mice that have survived late sepsis also resist lethal lipopolysaccharide (LPS)-induced inflammatory shock (88% lived vs 0% of naive mice). The CD34(+) cell-recipient survivor mice administered LPS had globally reduced levels of circulating inflammatory mediators compared with naive mice, but their peritoneal and bone marrow-derived macrophages (BMDMs), unlike those from naïve mice, remained LPS responsive ex vivo. We further found that CD34(+) cell transfer into LPS-challenged naïve mice had diminished immunosuppression, as assessed by ex vivo responses of peritoneal and BMDMs to LPS challenge. We conclude that CD34(+) cell adoptive transfer rebalances dysregulated immune responses associated with sepsis and endotoxin shock.

Isolation and characterization of a novel choline degrading Citrobacter amalonaticus strain from the human gut.

Gut microbiota metabolism can have profound effects on human health. Choline, a quaternary amine (QA) highly abundant in our diet, is canonically cleaved by a glycyl radical enzyme, choline trimethylamine lyase (CutC), and its SAM-dependent radical activator, CutD. CutC cleaves choline to form trimethylamine (TMA) and acetaldehyde. TMA is oxidized to TMAO by FMO3 in the liver, which plays a role in causing atherosclerosis. We hypothesized that alternative pathways for choline degradation occur within gut microbes and that certain gut microbiota can anaerobically respire or ferment QAs, such as choline. Based on this prediction we established QA-supplemented enrichment cultures using fecal material from healthy volunteers as the inocula. We have isolated, from a choline-supplemented enrichment of a human fecal sample, a strain of Citrobacter amalonaticus, that we have designated CJ25. This strain is capable of anaerobically utilizing choline as its sole carbon and energy source. Its genome does not contain the cutCD genes or genes encoding any COG5598 methyltransferases. We have confirmed the degradation of choline and production of acetate by the organism during growth of the strain. However, we used multiple analytical methods to confirm that no TMA accumulated in the medium during growth. Hence, strain CJ25 is a unique bacterium that degrades choline without the production of the proatherogenic metabolite TMA.

Maxillary Expansion: A Comparison of Damon Self-Ligating Bracket Therapy with MARPE and PAOO.

Purpose: The aim of this study was to investigate arch parameters and dentoalveolar changes from pretreatment to posttreatment by comparing the Miniscrew Assisted Rapid Palatal Expansion (MARPE), Periodontally Accelerated Osteogenic Orthodontics (PAOO), and Damon self-ligating bracket therapies. Materials and Methods: Seventy-nine patients underwent maxillary expansion followed by or in conjunction with Damon (n = 23), PAOO (n = 28), and MARPE (n = 28) therapies. Nine maxillary dental arch parameters were compared at pretreatment, posttreatment as well as, increments of treatment change. Measurements were made on STL study casts using 3Shape Ortho Analyzer 3D scanner software. Results: All groups showed significant posterior width increase in the molar area. The mean increase in inter-molar distance was more than 8X greater in MARPE group compared to Damon and more than 4X greater compared to PAOO. MARPE showed significantly greater increments of change in inter-molar width and palatal vault area. Conclusions: All groups showed a significant width increase in the canine and molar area. MARPE showed the greatest increase in inter-molar width, followed by PAOO and Damon. MARPE was the only group to show a significant increase in palatal vault area.

Structure of the alpha2epsilon2 Ni-dependent CO dehydrogenase component of the Methanosarcina barkeri acetyl-CoA decarbonylase/synthase complex.

Ni-dependent carbon monoxide dehydrogenases (Ni-CODHs) are a diverse family of enzymes that catalyze reversible CO:CO(2) oxidoreductase activity in acetogens, methanogens, and some CO-using bacteria. Crystallography of Ni-CODHs from CO-using bacteria and acetogens has revealed the overall fold of the Ni-CODH core and has suggested structures for the C cluster that mediates CO:CO(2) interconversion. Despite these advances, the mechanism of CO oxidation has remained elusive. Herein, we report the structure of a distinct class of Ni-CODH from methanogenic archaea: the alpha(2)epsilon(2) component from the alpha(8)beta(8)gamma(8)delta(8)epsilon(8) CODH/acetyl-CoA decarbonylase/synthase complex, an enzyme responsible for the majority of biogenic methane production on Earth. The structure of this Ni-CODH component provides support for a hitherto unobserved state in which both CO and H(2)O/OH(-) bind to the Ni and the exogenous FCII iron of the C cluster, respectively, and offers insight into the structures and functional roles of the epsilon-subunit and FeS domain not present in nonmethanogenic Ni-CODHs.

The effect of vestibular, lingual, and aligner appliances on the quality of life of adult patients during the initial stages of orthodontic treatment.

BACKGROUND: Patient quality of life (QoL) during orthodontic treatment is an important consideration that requires greater academic investigation as greater focus is placed on enhancing patient experience. Quality of life (QoL) was assessed in three orthodontic appliance groups, i.e., vestibular, lingual, and aligners during the initial stages of treatment. The sample was comprised of 117 adult patient-subjects distributed into 3 groups: vestibular (n = 41), lingual (n = 37), and aligner (n = 39). A WHOQOL-BREF questionnaire surveyed four domains (physical health, psychological health, social relationships, and environment). RESULTS: Mean scores for domain 1, physical health, showed that the aligner group (28.1) had significantly greater scores than that of the vestibular (22.7) or lingual (22) groups. Domain 2, psychological health, demonstrated significant differences (P < 0.001) between all groups, with the aligner group scoring the highest (23.2), followed by the lingual (18.4) and vestibular (15.2) groups. Domain 3, social relationship, showed that aligner (10.9) and lingual (10.2) scores were significantly greater (P < 0.001) than those of the vestibular group (7.8). Domain 4, environment, displayed significant differences between all groups, with the aligner group scoring highest (32.1), followed by the lingual group (29.3), and lastly the vestibular group (26.4). Overall, the highest mean score was obtained by the aligner group (23.1) and the lowest mean score was by the vestibular group (18). The mean domain scores for all three groups were significantly different (P ≤ 0.005) from each other (Table 2). CONCLUSIONS: Overall, patients undergoing Aligner therapy reported the overall highest QoL scores, followed by lingual and vestibular groups.

Effect of clear aligner wear protocol on the efficacy of tooth movement.

OBJECTIVES: To compare the efficacy of orthodontic tooth movement with three aligner wear protocols: 7 day, 10 day, and 14 day. MATERIALS AND METHODS: Eighty patients were randomly allocated into three groups: group A (7-day changes), group B (10-day changes), and group C (14-day changes). The posttreatment scans were compared with the final virtual treatment simulations through digital superimposition. The differences between predicted and actual achieved treatment outcomes were computed in six angular and six linear dimensions. Differences >0.5 mm for linear measurements and >2° for angular measurements were considered clinically relevant. RESULTS: Within groups, and irrespective of wear protocol, all linear discrepancies in both jaws were deemed clinically insignificant (<0.5 mm) while nearly all angular discrepancies were considered clinically significant (>2.0°). When the three groups were compared, group C (14-day changes) showed significantly greater accuracy in the posterior segment for maxillary intrusion, distal-crown tip and buccal-crown torque, and mandibular intrusion and extrusion. The mean treatment duration in the 7-day aligner change group was nearly half that of the 14-day aligner change group (5 months vs 9 months). CONCLUSIONS: Fourteen-day changes were statistically significantly more accurate in some posterior movements. However, this difference in accuracy did not exceed the threshold for clinical significance (>0.5 mm/>2.0°). Achieving a clinically similar accuracy between the 7-day protocol and 14-day protocol in half the treatment time suggests a 7-day protocol as an acceptable treatment protocol. Clinicians may consider slowing down to a 14-day protocol if challenging posterior movements are desired.