The atrophy of the periodontal ligament places the tooth very close to the bone or another tooth, as occurs in unerupted teeth. The absent interdental bone and the lack of functional periodontal stimulus may lead to the fusion of the appositional layers of cement between the roots of the teeth. Concrescence almost always occurs in the region of the maxillary molars. Asymptomatic, it should always be remembered when the proper response to orthodontic movement is not obtained, and there is no apparent explanation. When surgically extracting a tooth and there is resistance, insisting will not be the best strategy. Moving the teeth with concrescence is not convenient, as it requires very intense forces. Once separated, these teeth can be considered normal for movement. It is possible to separate two teeth presenting concrescence, but it depends on the extension of the area, the surgical access and, especially, the clinical convenience. The tooth to be extracted will be repaired with new cement deposited in the sectioned area. The simple separation with the maintenance of the proximity and the lack of function of one of the teeth will cause a new concrescence. After a period of 1 to 3 months, the separated teeth are biologically prepared to be moved. The most important detail in this separation of teeth presenting concrescence is that the diagnosis should be made in advance, and not at the time of the intervention.

Introduction: The third molars are forgotten because they are the last in the dental arch, they do not directly influence the smile and they appear only in adolescence, when they do. Objectives: 1) to provide the clinician with a “checklist” to assess and diagnose changes to be screened in the third molar region in new patients; 2) to reveal the importance of not discharging the patient submitted to any dental treatment without first analyzing the third molars region clinically and on imaging examinations, since many diseases are associated to them. Result: A list of 10 situations that cover all diagnostic possibilities involving the third molars is presented. Conclusion: Adopting this protocol is a matter of habit, since the need is fundamental. The next professional assisting your patient may ask: “Did he not request examinations for the third molars?”.

Introduction: Teeth frequently fail to erupt and situations arise that prevent the canines from reaching the occlusal plane. Objective: Discourse about the three situations in which the canine does not reach the occlusal plane, and remains unerupted; and at the same time, point how to make a safe diagnosis of alveolodental ankylosis - one of the three causes -, based on tomography. Conclusions: Ankylosis occurs in impacted teeth by atrophy of the periodontal ligament, including the epithelial rests of Malassez. The tomographic signs of alveolodental ankylosis in unerupted canines are the interruption of hypodense periodontal space, discontinuity of the lamina dura and its continuity with the root surface, which gradually loses its regular shape.

Os toros palatino e mandibular são distúrbios do desenvolvimento do tipo anomalia de forma, com manifestação tardia no crescimento e maturação dos maxilares. Os casos familiares e a persistência dos toros com a idade e em desdentados lhes atribuem uma origem genética, que começa a ser desvendada. Há uma dificuldade para interpretar os toros como uma resposta adaptativa à sobrecarga oclusal, bruxismo e outros fatores externos, pois os toros não são hiperplasias e hipertrofias adaptativas. Os toros são protuberâncias ósseas sem cápsula fibrosa, o que os diferencia dos osteomas e lhes tira a natureza neoplásica, mesmo que benigna, especialmente porque também não apresentam crescimento contínuo e sem controle por parte do organismo. O tamanho dos toros se estabiliza ao final do crescimento dos maxilares, por volta dos 22 a 24 anos de idade. Os toros são constituídos de osso normal, do ponto de vista funcional e estrutural, e podem ser utilizados como sítio de origem de transplante ósseo autógeno para outros locais ou como sede de implantes osseointegráveis, se houver conveniência clínica para tais procedimentos. A sua remoção pode ser feita quando impedem procedimentos odontológicos terapêuticos.

Aberrant synthesis of mitochondrial proteins impairs cardiac function and causes heart disease. However, the mechanism of regulation of mitochondria encoded protein expression during cardiac disease remains underexplored. Here, we have shown that multiple pathogenic cardiac stressors induce the expression of miR-574 guide and passenger strands (miR-574-5p/3p) in both humans and mice. miR-574 knockout mice exhibit severe cardiac disorder under heart disease-triggering stresses. miR-574-5p/3p mimics that are delivered systematically using nanoparticles reduce cardiac pathogenesis under disease insults.Transcriptome analysis of miR-574-null hearts uncovers FAM210A as a common target mRNA for both strands of miR-574. The interactome capture and translational state analyses suggest that FAM210A interacts with mitochondrial translation factors and regulates the protein expression of mitochondrial encoded electron transport chain genes. Using a human cardiomyocyte cell culture system, we discover that miR-574 regulates FAM210A expression and modulates mitochondrial encoded protein expression, which influences cardiac remodeling in heart failure.Abbreviations of key terms: ACM, adult cardiomyocytes; CF, cardiac fibroblasts; CM, cardiomyocytes; ETC, electron transport chain; FAM210A, family with sequence similarity 210 member A; HF, heart failure; ISO, isoproterenol; MEG, mitochondrial encoded gene; MI, myocardial infarction; NEMG, nuclear-encoded mitochondrial gene; RBP, RNA-binding protein; RISC, RNA-induced silencing complex; TAC, transverse aortic constriction; UTR, untranslated region Results Cardiac stress induces miR-574-5p and miR-574-3p in human and mouse heartsFrom data mining of unbiased screening data from four laboratories, the guide strand miR-574-5p has been identified as a miRNA that is robustly induced in the heart in response to pathological cardiac remodeling, which included the cardiac tissues of patients during the initial stages following MI onset 33 , a mouse model of left coronary artery occlusion-derived MI 24 , and aged murine hearts ( Fig. 1a) 26 . On the other hand, the passenger strand miR-574-3p is increased in the human hearts after MI and more remarkably induced by exercise training in murine hearts 34 . The cardiac functions of complementary strands of miR-574-5p and miR-574-3p remain unknown. miR-574 is conserved in 43 animal species (10 primates and 33 mammals, UCSC Genome Browser). In mammals, miR-574 is located in intron 1 of the host gene FAM114A1 (Family with sequence similarity 114 member A1) ( Fig. 1b). We confirmed that both miR-574-5p and miR-574-3p were significantly induced in heart tissues of chronic HF patients, with the expression level of miR-574-5p even higher than that of miR-574-3p (Fig. 1c). Northern blot analysis showed that both miR-574-5p and miR-574-3p were expressed in the normal murine heart ( Supplementary Fig. 1a). miR-574-5p and miR-574-3p were both significantly induced in isoproterenol (ISO)-or transverse aortic constriction (TAC)-treated mouse hearts, compar...