High-fat Western diets contribute to tissue dysregulation of fatty acid and glucose intake, resulting in obesity and insulin resistance and their sequelae, including atherosclerosis. New therapies are desperately needed to interrupt this epidemic. The significant idea driving this research is that the understudied regulation of fatty acid entry into tissues at the endothelial cell (EC) interface can provide novel therapeutic targets that will greatly modify health outcomes and advance health-related knowledge. Dysfunctional endothelium, defined as activated, pro-inflammatory, and pro-thrombotic, is critical in atherosclerosis initiation, in modulating thrombotic events that could result in myocardial infarction and stroke, and is a hallmark of insulin resistance. Dyslipidemia from high-fat diets overwhelmingly contributes to the development of dysfunctional endothelium. CD36 acts as a receptor for pathological ligands generated by high-fat diets and in fatty acid uptake, and therefore, it may additionally contribute to EC dysfunction. We created EC CD36 knockout (CD36°) mice using cre-lox technology and a cre-promoter that does not eliminate CD36 in hematopoietic cells (Tie2e cre). These mice were studied on different diets, and crossed to the low density lipoprotein receptor (LDLR) knockout for atherosclerosis assessment. Our data show that EC CD36° and EC CD36°/LDLR° mice have metabolic changes suggestive of an uncompensated role for EC CD36 in fatty acid uptake. The mice lacking expression of EC CD36 had increased glucose clearance compared with controls when fed with multiple diets. EC CD36° male mice showed increased carbohydrate utilization and decreased energy expenditure by indirect calorimetry. Female EC CD36°/LDLR° mice have reduced atherosclerosis. Taken together, these data support a significant role for EC CD36 in systemic metabolism and reveal sex-specific impact on atherosclerosis and energy substrate use.

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Summary Background Reduction in orthodontic treatment time is gaining popularity due to patient demands. Several new techniques of acceleratory orthodontic treatment have been introduced to effectively treat the malocclusion in a shorter time period with minimal adverse effects. Objective The objective of this systematic review is to critically evaluate the potential effect of accelerated surgically assisted orthodontic techniques on periodontal tissues. Materials and methods Electronic databases used to perform the search were Medline (Ovid), EMBASE, PubMed, Scopus, Cochrane, Google Scholar, and hand searching of the literature was also performed. Selection criteria Only randomized control trials (RCTs) that assessed the relationship between accelerated surgically assisted orthodontic techniques and its effects on periodontium were included. Data collection and analysis The Joanna Briggs Institute (JBI) critical appraisal checklist tool (2016) was used to assess the finally selected studies. Among these studies, five evaluated corticotomy-facilitated orthodontics, two tested accelerated tooth movement with piezocision, one compared corticotomy-facilitated orthodontics with piezocision, and one studied the effects of periodontally accelerated osteogenic orthodontics. The duration of these studies was relatively short and had moderate to high risk of bias. Results Literature search identified 225 records from 5 databases and 50 articles from the partial grey literature (Google scholar) search. Finally, nine eligible RCTs were included in the review. Limitations Most of the included studies were of a high risk of bias due to high experimental heterogeneity and small sample size. Long-term follow-up of the periodontal response to these interventions was also lacking. Conclusions There is an absence of evidence considering the lack of long-term follow-up and small sample size therefore, the results of this review should be carefully interpreted. Implications Due to the need for more studies with less risk of bias, these techniques should be implemented in dental practice with caution. With stronger evidence, the study may be confirmed to provide quicker desired results for orthodontic patients. Registration This study protocol was not registered. Funding No funding was obtained for this systematic review.

SummaryLoricrin downregulation has been associated with age‐related changes as well as inherited and inflammatory skin diseases. We hypothesize that changes in loricrin could be more related to altered barrier function and consequently disorders that affect epithelial cells, such as psoriasis, atopic dermatitis (AD), erythrokeratoderma, loricrin keratoderma (LK) and periodontitis. The aim of this review is to summarize what is known about the association between loricrin downregulation and epithelial‐related disorders (ERDs). A search was performed on the following databases: Medline, Cochrane Library, PubMed, EMBASE, Lilacs, Scopus and Google Scholar, resulting in 16 included articles. Loricrin keratoderma was the ERD most frequently associated with loricrin mutations (730insG, 709insC and 578insG; 5/7 cases – 71.44 %). Atopic dermatitis was the ERD most frequently associated with loricrin downregulation (2/7 cases – 28.6 %). Mutilating palmoplantar keratoderma, progressive symmetrical erythrokeratoderma and a new type of erythrokeratoderma were not associated with any mutations. At the gene level, periodontitis patients showed the highest decrease (–6.89x), followed by AD (–6.5x) and psoriasis patients (–0.5x). In summary, loricrin mutation and downregulation were associated with several ERDs. The diversity in disease presentation is likely related to whether there is a total loss of loricrin, mislocalization and/or if the mutant form of loricrin causes dysfunction of other proteins and/or changes in cornification.

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