Evaluation of relapse after orthodontic therapy combined with orthognathic surgery in the treatment of skeletal class III

Introduction

Multidisciplinary treatment of skeletal malocclusion by orthognathic surgery in addition to orthodontics is a routine strategy believed to offer good functional and esthetic outcomes. Postoperative relapse is, however, a problem. The present study was conducted to analyze the stability of outcomes achieved by surgical treatment of skeletal class III patients in terms of the rate and extent of relapses.

Patients and methods

A total of 30 patients who had undergone orthodontic treatment combined with orthognathic surgery were included. The primary inclusion criterion was a skeletal class III treated by mandibular setback (Obwegeser/Dal Pont) surgery alone or combined with maxillary advancement (Le Fort I) surgery. Analysis was based on one preoperative and two postoperative cephalograms per patient.

Results

We observed relapse (defined, in accordance with Proffit, as changes >2 mm or 2°) at a rate of 24% after bimaxillary procedures, compared to a lower rate of 21% after mandibular setback procedures only. The relapse rate was 21% among patients who had undergone upper-jaw surgery versus 27% among those who had undergone lower-jaw surgery, which was statistically significant.

Conclusion

The majority of patients exhibited stable treatment outcomes. Maxillary advancement procedures were found to be less susceptible to relapse—resulting in more stable outcomes—and mandibular setback distances correlated positively with the degree of the relapse. No statistically significant differences were observed between the procedures conducted in both jaws versus in the lower jaw only, or in the extent of upper-jaw repositioning.     

The 5-Year Course of Obsessive-Compulsive Symptoms and Obsessive-Compulsive Disorder in First-Episode Schizophrenia and Related Disorders

Objective: To determine the course of obsessive-compulsive symptoms (OCS) and obsessive-compulsive disorder (OCD) in first-episode schizophrenia and related disorders and their relationship with clinical characteristics. Methods: Consecutively, admitted patients with a first-episode of schizophrenia, schizophreniform disorder, or schizoaffective disorder were screened for OCS, and these were measured with the Yale-Brown Obsessive-Compulsive Scale. Positive and Negative Syndrome Scale and Montgomery Åsberg Depression Rating Scale were used to assess severity of other symptoms. The course of 3- and 5-year symptoms, psychotic relapse, substance use, remission, full recovery, suicide, and social functioning were assessed. Results: One hundred and eighty-six consecutively admitted and consenting patients were included. Five years after admission, OCS could be assessed in 172 patients. Ninety-one patients (48.9%) reported no OCS symptoms on any of the assessments. OCS restricted to the first assessments occured in 15.1%, 13.4% had persistent OCS, 7.0% had no OCS at first assessment but developed OCS subsequently, and 15.6% had intermittent OCS. The proportion of patients with comorbid OCD varied between 7.3% and 11.8% during follow-up. OCD was associated with more severe depressive symptoms and poorer premorbid functioning and social functioning at follow-up. Conclusions: The 5-year course of OCS/OCD in patients with first-episode schizophrenia or related disorders is variable. OCS/OCD comorbidity was not associated with a more severe course of psychotic symptoms and relapse. Comorbid OCD was associated with more severe depressive symptoms, social dysfunction and worse premorbid functioning. Specific treatment options for schizophrenia patients with comorbid OCD are needed.     

Transition to first episode psychosis in ultra high risk populations: Does baseline functioning hold the key?

BackgroundBaseline functioning has been found to be a strong predictor of transition to psychosis in ultra high risk populations. However, the time course of functioning may enhance prediction. We investigated whether there were different patterns of functioning over time and whether particular temporal patterns were related to baseline characteristics and psychosis outcome.MethodFunctional data was assessed at baseline and after 3 to 6 year follow-up in an ultra high risk sample (n = 158; 92 female, mean age = 19.28 (SD = 3.33), range = 14–29). Using the median score of the GAF and the QLS scale, a ‘High’ and ‘Low’ group (comprising of subjects functioning above or below median at both baseline and follow-up) and a ‘Deterioration’ group and ‘Improving’ group were created.ResultsChi-square analyses showed that the Low and Deteriorating functioning groups were the most likely to develop first-episode psychosis (FEP). Importantly, UHR individuals with deteriorating functioning were at higher risk of transition than those whose functioning was low at baseline but improved over time (GAF: X² = 5.10, df = 1, p = .02; QLS: X² = 9.13, df = 1, p = .003). Binary logistic regression analyses showed that a decline in functioning was more strongly associated with FEP (GAF: p = < .0001; QLS: p < .0001) than the level of baseline functioning (GAF: p = .005; QLS: p = .09). The deteriorating group could not be distinguished from the High group in terms of baseline symptomatology.DiscussionWith the addition of the ‘low functioning’ criterion to the UHR criteria, we may miss out on some true positive cases. Limiting our attention to baseline poor functioning may therefore distort the picture in terms of risk for psychosis.     

The role of metabolism in the developmental toxicity of polycyclic aromatic hydrocarbon-containing extracts of petroleum substances

In vitro assays presently used for prenatal developmental toxicity (PDT) testing only assess the embryotoxic potential of parent substances and not that of potentially embryotoxic metabolites. Here we combined a biotransformation system, using hamster liver microsomes, with the ES-D3 cell differentiation assay of the embryonic stem cell test (EST) to compare the in vitro PDT potency of two 5-ring polycyclic aromatic hydrocarbons (PAHs), benzo[a]pyrene (BaP) and dibenz[a,h]anthracene (DBA), and dimethyl sulfoxide extracts from five PAH-containing petroleum substances (PS) and a gas-to-liquid base oil (GTLb), with and without bioactivation. In the absence of bioactivation, DBA, but not BaP, inhibited the differentiation of ES-D3 cells into beating cardiomyocytes in a concentration-dependent manner. Upon bioactivation, BaP induced in vitro PDT, while its major metabolite 3-hydroxybenzo[a]pyrene was shown to be active in the EST as well. This means BaP needs biotransformation to exert its embryotoxic effects. GTLb extracts tested negative in the EST, with and without bioactivation. The PS-induced PDT in the EST was not substantially changed following bioactivation, implying that metabolism may not play a crucial role for the PS extracts under study to exert the in vitro PDT effects. Altogether, these results indicate that although some PAH require bioactivation to induce PDT, some do not and this latter appears to hold for the (majority of) the PS constituents responsible for the in vitro PDT of these complex substances.     

Human islets and dendritic cells generate post‐translationally modified islet autoantigens

The initiation of type 1 diabetes (T1D) requires a break in peripheral tolerance. New insights into neoepitope formation indicate that post‐translational modification of islet autoantigens, for example via deamidation, may be an important component of disease initiation or exacerbation. Indeed, deamidation of islet autoantigens increases their binding affinity to the T1D highest‐risk human leucocyte antigen (HLA) haplotypes HLA‐DR3/DQ2 and ‐DR4/DQ8, increasing the chance that T cells reactive to deamidated autoantigens can be activated upon T cell receptor ligation. Here we investigated human pancreatic islets and inflammatory and tolerogenic human dendritic cells (DC and tolDC) as potential sources of deamidated islet autoantigens and examined whether deamidation is altered in an inflammatory environment. Islets, DC and tolDC contained tissue transglutaminase, the key enzyme responsible for peptide deamidation, and enzyme activity increased following an inflammatory insult. Islets treated with inflammatory cytokines were found to contain deamidated insulin C‐peptide. DC, heterozygous for the T1D highest‐risk DQ2/8, pulsed with native islet autoantigens could present naturally processed deamidated neoepitopes. HLA‐DQ2 or ‐DQ8 homozygous DC did not present deamidated islet peptides. This study identifies both human islets and DC as sources of deamidated islet autoantigens and implicates inflammatory activation of tissue transglutaminase as a potential mechanism for islet and DC deamidation.     

Chronic colitis due to an epithelial barrier defect: the role of kindlin-1 isoforms

Kindlin-1 is an epithelium-specific phosphoprotein and focal adhesion adaptor component. Mutations in the corresponding gene (KIND1) cause Kindler syndrome (KS), which is manifested by skin blistering, poikiloderma, photosensitivity and carcinogenesis. Some patients also exhibit gastrointestinal symptoms, but it has remained unclear whether these represent a feature of Kindler syndrome or a coincidence. We examined kindlin-1 in human gastrointestinal epithelia and showed that it is involved in the aetiopathology of Kindler syndrome-associated colitis. Kindlin-1 expression was assessed by indirect immunofluorescence, western blot and RT-PCR. Kindlin-1 is expressed in oral mucosa, colon and rectum. Both the full-length 74 kDa kindlin-1 protein and a 43 kDa isoform were detected in CaCo2 cells, the latter resulting from alternative splicing. In the first months of life, patients (homozygous for null mutations) had severe intestinal involvement with haemorrhagic diarrhoea and showed morphological features of severe ulcerative colitis. Later in childhood, histopathology demonstrated focal detachment of the epithelium in all segments of the colon, chronic inflammation and mucosal atrophy. These findings define an intestinal phenotype for Kindler syndrome as a consequence of a primary epithelial barrier defect. The different clinical intestinal manifestations in Kindler syndrome patients may be explained by partial functional compensation of kindlin-1 deficiency by the intestinal isoform or by the presence of truncated mutant kindlin-1.     

The carbohydrate-binding plant lectins and the non-peptidic antibiotic pradimicin A target the glycans of the coronavirus envelope glycoproteins

OBJECTIVES: Many enveloped viruses carry carbohydrate-containing proteins on their surface. These glycoproteins are key to the infection process as they are mediators of the receptor binding and membrane fusion of the virion with the host cell. Therefore, they are attractive therapeutic targets for the development of novel antiviral therapies. Recently, carbohydrate-binding agents (CBA) were shown to possess antiviral activity towards coronaviruses. The current study further elucidates the inhibitory mode of action of CBA. METHODS: Different strains of two coronaviruses, mouse hepatitis virus and feline infectious peritonitis virus, were exposed to CBA: the plant lectins Galanthus nivalis agglutinin, Hippeastrum hybrid agglutinin and Urtica dioica agglutinin (UDA) and the non-peptidic mannose-binding antibiotic pradimicin A. RESULTS AND CONCLUSIONS: Our results indicate that CBA target the two glycosylated envelope glycoproteins, the spike (S) and membrane (M) protein, of mouse hepatitis virus and feline infectious peritonitis virus. Furthermore, CBA did not inhibit virus-cell attachment, but rather affected virus entry at a post-binding stage. The sensitivity of coronaviruses towards CBA was shown to be dependent on the processing of the N-linked carbohydrates. Inhibition of mannosidases in host cells rendered the progeny viruses more sensitive to the mannose-binding agents and even to the N-acetylglucosamine-binding UDA. In addition, inhibition of coronaviruses was shown to be dependent on the cell-type used to grow the virus stocks. All together, these results show that CBA exhibit promising capabilities to inhibit coronavirus infections.     

Identifying viable theoretical frameworks with essential parameters for real-time and real world alcohol craving research: a systematic review of craving models

Background: Substance use is known to be episodic, dynamic, complex, and highly influenced by the environment, therefore a situational and momentary focus to alcohol craving research is appropriate. Current advances in mobile and wearable technology provide novel opportunities for craving research. However, the lack of consensus within craving theory impedes the identification and prioritization of parameters to be monitored. The aim of this study is to critically review current craving models in order to determine viable theoretical frameworks of alcohol craving and its essential parameters.

Methods: Eighteen models of craving were reviewed by applying a literature search with a five-step strategy that accounted for the momentary nature of craving and included a snowballing search and a key term extraction algorithm. Based on this review, multiple decision criteria were defined upon which to evaluate the models.

Results: Six models for alcohol craving were supported by sufficient empirical research to be eligible. The inferences drawn on these six models resulted in three decision criteria: the model should (1) incorporate negative affect as a predictor of relapse; (2) explain that dependent drinkers have a higher attentional bias towards alcohol cues than nondependent drinkers; (3) incorporate increased risk of relapse with heightened stress levels.

Conclusions: The affective processing model of negative reinforcement, the cognitive processing model, the incentive sensitization theory of addiction and the theory of neural opponent motivation are classified as viable theoretical frameworks, resulting in negative affect and stress as relevant parameters to include in real-time craving monitoring research.