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Introducción: las lesiones cervicales no cariosas (NCCL, por sus siglas en inglés) son un grupo de lesiones que afectan el área cervical del órgano dental causando hipersensibilidad dentinaria y defectos estéticos. Objetivo: analizar la literatura sobre las lesiones cervicales no cariosas, su etiología, consideraciones anatómicas, características morfológicas de la lesión y tratamientos no restaurativos. Material y métodos: se realizó una búsqueda en la base de datos PubMed, utilizando las palabras clave: non-carious cervical lesions OR noncarious cervical lesions OR tooth wear OR tooth erosion OR dental abfraction OR abfraction, recopilando un total de 78 artículos. Resultados: es necesario determinar la etiología antes de seleccionar las estrategias de tratamiento para las lesiones cervicales no cariosas. Conocer los distintos tipos de tejidos que componen al órgano dentario facilita la comprensión de los factores que participan en el desarrollo de las lesiones cervicales no cariosas. Esto permite que el tratamiento se enfoque más en la causa del problema que en los síntomas. Con esto podemos modificar diversos factores de manera interceptiva, los tratamientos de terapia con láser y compuestos tópicos son una estrategia mínimamente invasiva. Conclusiones: la mejor manera de describir a las lesiones cervicales no cariosas sería como una enfermedad multifactorial. Se debe prestar especial atención en los métodos de diagnóstico, identificando cofactores que propicien el avance de la lesión, como son la fricción y la biocorrosión. Esta revisión brinda datos que asocian a los factores oclusales como una de las principales causas de una enfermedad que afecta a más de la mitad de la población adulta (AU)

Introduction: non-carious cervical lesions (NCCL) are a group of lesions that affect the cervical area of the dental organ causing dentin hypersensitivity and cosmetic defects. Objective: to know, through a systematic review, the current state of non-carious cervical lesions. Material and methods: a search was conducted in the PubMed database, using the keywords: non-carious cervical lesions OR noncarious cervical lesions OR tooth wear OR tooth erosion OR dental abfraction OR abfraction, compiling a total of 78 articles. Results: determining etiology is necessary before selecting treatment strategies for non-carious cervical lesions (NCCL). Know the different types of tissues that make up the dentary organ, facilitate the understanding of the factors involved in the development of noncarious al cervical lesions. This allows treatment to focus more on the cause of the problem than on symptoms. With this we can modify various factors in an interceptive way, laser therapy treatments and topical compounds, are a minimally invasive strategy. Conclusions: the best way to describe non-carious al cervical lesions would be as a multifactorial disease to which special attention should be paid to both diagnostic methods, identifying cofactors that promote the progression of injury, such as friction and biocorrosion. This review provides data that associates occlusal factors as one of the main causes of a disease that affects more than half of the adult population (AU)

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JUSTIFICATION: Canines represent corners in the dental arch, and are important features in facial esthetics, as they support the upper lip, wing of the nose, and influence the nasolabial fold and the appearance of facial aging. In the laterality movements, the canines guidance coordinate the opening and closing of the teeth, saving the TMJ from sudden movements. DISCUSSION: As a result of the lack of eruption or the inadequate positioning of the maxillary canine, the loss of the laterality guide may occur, which will then occur in the maxillary lateral incisor, inducing lesions of "occlusal trauma", such as inflammatory root resorption. Likewise, without well positioned canines, there may be premature aging and change in facial esthetics. CONCLUSION: In order to avoid problems with eruption and positioning of the maxillary canines, early diagnosis is made by analyzing their position and their relationship with the other teeth, and in the three-dimensional context of the maxilla, between 8-10 years of age. Preventive measures can create bone space and direction so that the maxillary canines can occupy their position in the dental arch.

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Temporomandibular joint (TMJ) disorder caused by occlusal trauma is one of the most controversial topics in dentistry. Experimental traumatic occlusion (ETO) induced by metal crowns cemented to mandibular first molars in rats causes a long-lasting nociceptive response. This study aimed to elucidate whether ETO generates an increase in inflammatory mediators in the TMJ. In addition, the impact of ETO on trigeminal ganglia, neurotransmitter release, and satellite glial cell (SGC) activation was investigated. ELISA revealed enhanced inflammatory mediators, including TNF-α, IL-1ß, IL-6, CX3CL1, and ADAM-17 by Western blotting, in periarticular TMJ tissue after 28 d of ETO. In the trigeminal ganglia, ETO groups increased the release of the neurotransmitters substance P and glutamate. Overexpression of the AMPA receptor and upregulation of NMDA were observed in the 0.4- and 0.7-mm ETO groups, respectively, highlighting enhanced neuronal excitation. Increased IL-1ß and COX-2 mRNA levels in the 0.7-mm ETO group confirmed trigeminal ganglia SGC activation. Immunofluorescence and electrophoresis of SGC revealed increased pERK expression in the 0.7-mm ETO group. ERK phosphorylation was shown to be nociceptive specific, with its upregulation occurring in cases of chronic inflammatory pain. Increased PKA mRNA levels were observed in the 0.4-mm ETO group, while CREB mRNA levels were upregulated for both ETO groups. Electrophoresis showed overexpression of sodium channel Nav 1.7 in the 0.7-mm ETO group, while immunofluorescence revealed that Nav 1.7 is expressed in sensory trigeminal ganglia cells. The results of this study suggest that occlusal trauma induces neuroimmune crosstalk, with synthesis of proinflammatory/pronociceptive mediators, which increases neuronal activity in trigeminal ganglia via the activation of an inflammatory response cascade to develop a persistent neuroinflammatory state that leads to central sensitization.

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BACKGROUND: Excessive occlusal forces and occlusal trauma have been implicated as co-destructive factors for periodontitis in animal models. The objective of this study was to assess the association between occlusal trauma and periodontitis. METHODS: A total of 167 cases and 205 controls were included for analysis. Occlusal trauma was the exposures of interest and was registered for cases and controls. Additional clinical co-variables were registered as well for further analysis. The association of the exposure and periodontitis was determined by the odds ratio and logistic regression analysis adjusted for confounders. RESULTS: Amalgam restorations, pathogenic occlusion and occlusal trauma were more frequent in cases as compared to controls (P ≤ 0.05). The distribution of pathogenic occlusion and occlusal trauma was similar according to the stage and class of periodontitis. Logistic regression analysis showed a significant association for cigarette smoking, systemic conditions, amalgam restorations, pathogenic occlusion, and occlusal trauma with periodontitis (P ≤ 0.05). After adjusting for confounding variables in the model, amalgam restorations and occlusal trauma remained strongly associated with periodontitis (P ≤ 0.05). CONCLUSIONS: Occlusal trauma is strongly associated with periodontitis. Additional long-term prospective studies are necessary to further understand the impact of the occlusal condition and periodontitis.

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ABSTRACT: Many orthodontic treatments alone cannot reestablish an ideal occlusion, requiring correction through orthognathic surgery. An adequate surgical planning, execution and case follow-up can provide surgical stability between the maxilla and the mandible. Soft tissue conservation and proper correction during a healing phase are important to achieving this goal. Patient C.L.B.S, 38 years old, female, presented with Angle Class I occlusion, facial profile class II, maxilla with mobility, chin surgically advanced and anterior open bite. She was submitted to orthognathic surgery 10 years ago. In the panoramic radiography the absence of bone formation in the maxilla was observed, causing an open bite. For the surgery conventional radiographs were used, as well as the dental cast in articulator for model surgery and preparation of surgical guide. With the surgery an improvement in the patient's aesthetics profile and an ideal occlusion, static and functional were expected. The treatment was orthodontic-surgical, with correction of the dento-facial deformity with counter-clockwise rotation of the maxilla, lowering repositioning in 3 mm of its posterior portion through Le Fort I osteotomy, advancement of the 4 mm mandible with bilateral sagittal osteotomy, and genioplasty for posterior repositioning with a Z-osteotomy, to improve mentual harmony. There was an improvement in the profile and aesthetics of the patient, which developed an Angle Class I profile, a decrease in the mentual projection, and an aesthetic and functional improvement. The orthognathic surgery allowed the advancement of the mandible, the repositioning of the maxilla and the mentual posterior repositioning, obtaining the correction of the Angle class II profile and the anterior open bite, resulting in an important improvement of facial profile and esthetics, presence of skeletal stability, restoration of function, self-esteem and quality of life.

RESUMEN: En muchos casos, el tratamiento ortodóntico por si solo no puede restablecer una oclusión ideal, siendo necesaria una cirúrgia ortognática. Una buena planificación quirúrgica, ejecución y seguimiento del caso, pueden proporcionar estabilidad entre los maxilares. La preservación de los tejidos blandos y una fijación adecuada son esenciales para ese objetivo. La paciente CLBS, 38 años, se presentó con oclusión Clase I de Angle, teniendo perfil clase II, maxilar con movilidad, mentón quirúrgicamente avanzado y mordida abierta anterior. La paciente fue sometida a cirugía ortognática 10 años antes. En radiografía panorámica, se nota la ausencia de formación ósea debido a una fijación maxilar realizada erróneamente, lo que causó la mordida abierta. Durante la planificación, fueron utilizadas radiografías convencionales, modelos de yeso en articulador para cirugía de modelo y confección de guía quirúrgica. Con el procedimento quirúrgico se esperaba obtener una mejora en el perfil de la paciente y una oclusión ideal, estática y funcional. El tratamiento fue ortodóntico-quirúrgico, con corrección de la deformidad dento-facial con giro antihorario de la mandíbula, con reposicionamiento inferior de 3 mm de su parte posterior, por medio de osteotomía Le Fort I, avance de la mandíbula de 4 mm con osteotomía sagital bilateral, y retroceso del mentón en su posición original con osteotomía en Z, mejorando la armonía del mentón. Hubo una mejora en perfil y en la estética de la paciente, como también una mejora en el perfil, estética y funcionalidade, con diminución del mentón. La cirúrgia ortognática permitió el movimiento de la mandíbula, reposicionamiento maxilar y además fue posible retroceder el mentón, obteniendo la corrección del perfil Clase II y de la mordida abierta anterior. El resultado representa una mejora del perfil y de la estética facial, además se nota una estabilidad esquelética, con restablecimiento de la función, autoestima y calidad de vida.

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Observational studies have indicated that crestal bone level changes at implants are typically associated with clinical signs of inflammation, but still mechanical overload has been described as possible factor leading to hard-tissue deficiencies at implant sites without mucosal inflammation. The aim of this paper was systematically review the literature regarding the possible effect of traumatic occlusal forces on the peri-implant bone levels. Literature search was conducted using PubMed, Scielo and Lilacs, including the following terms: oral OR dental AND implant$ AND (load OR overload OR excessive load OR force$ OR bruxism) AND (bone loss OR bone resorption OR implant failure$). Databases were searched for the past 10 years of publications, including: clinical human studies, either randomized or not, cohort studies, case control studies, case series and animal research. Exclusion criteria were review articles, guidelines and in vitro and in silico (finite element analysis) research, as well as retrospective studies. The PICO questions formulated was: "does traumatic occlusal forces lead to peri-implant bone loss?" The database searches as well as additional hand searching, resulted in 807 potentially relevant titles. After inclusion/exclusion criteria assessment 2 clinical and 4 animal studies were considered relevant to the topic. The included animal studies did not reveal an association between overload and peri-implant bone loss when lower overloads were applied, whereas in the presence of excessive overload it seemed to generate peri-implant bone loss, even in the absence of inflammation. The effect of traumatic occlusal forces in peri-implant bone loss is poorly reported and provides little evidence to support a cause-and-effect relationship in humans, considering the strength of a clinically relevant traumatic occlusal force.

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This article deals with establishing a new link between trauma from occlusion and periodontal pockets based on the know-how and background gradually developed. To provide a better understanding to the reader, a historical perspective is firstly presented. The main features on the controversy of the role played by trauma from occlusion on the physiologic behavior of the periodontal structures are shown, together with how deviations from the normal characteristics of this relationship itself affect the integrity of the periodontal tissues when or associated with dental biofilm in the presence or not of periodontal pockets have arisen. The literature provides evidence showing that the very first publication to establish a strong correlation between trauma from occlusion and periodontal pockets in humans was of Latin-American origin. However, subsequently, trauma from occlusion was mostly evaluated by an American group, followed by a Scandinavian group, yet with some contributions from the Latin-American group. Basically trauma from occlusion has been correlated with periodontal pockets in view of the fact that these would render the periodontal supporting tissues more amenable to the spread of inflammation of biofilm-related periodontal pockets. This would facilitate the fast deepening of periodontal pockets, influencing the generation of infrabony periodontal pockets or suprabony periodontal pockets that are deeper than in areas without trauma from occlusion. The factors related to these different behaviors are discussed. Several clinical cases are presented showing evidence that corroborates the possibility of an actual interrelationship between trauma from occlusion and periodontitis. Theoretical evaluations based on recent advances of the mechanisms involving molecular modulation in physiological and altered occlusal functions, as well as on research data, and evaluations from data of clinical cases, support the assumption that trauma from occlusion and periodontitis may embrace the unique pathologic condition of the associated lesion trauma from occlusion plus periodontitis or act independently even if both co-exist simultaneously in a particular case. The link between both conditions that was emphasized as definitively necessary in order for an associated lesion to develop is that both lesions, namely trauma from occlusion and periodontitis, occur in their destructive stage at exactly the same time. This involvement would explain why so many different data are presented in the literature and hopefully will shed some light for development of new methodologies of research. Clinical cases were selected to present a treatment philosophy on the subject.

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OBJECTIVES: The goal of this study is to propose a standard protocol of experimental occlusal trauma to evaluate the inflammatory hyperalgesia induced by metallic crowns on orofacial tissues of rats. MATERIALS AND METHODS: Thirty animals were randomly divided into six groups (n = 5 per group). Detailed methodology on the manufacturing of metallic crowns is described. The inflammatory hyperalgesia induced by occlusal interference was evaluated by intra-articular injection of a low dose of 0.5% formalin (30 µl) or vehicle (saline) into temporomandibular joint, 21 or 28 days after metallic crown cementation. Posteriorly, pro-inflammatory cytokines were evaluated by enzyme-linked immunosorbent assay to assess the effect of occlusal interference on periodontium. RESULTS: The cementation of metallic crowns with dental anatomy on the lower molar of rats does not show signs of stress and lack of feeding. Metallic crown-induced occlusal trauma results in a temporomandibular joint inflammatory hyperalgesia (P < 0.05: ANOVA, Tukey's test). Otherwise, it was observed that occlusal trauma results in the increase of protein level of pro-inflammatory cytokines TNF-alpha and IL-1beta in the gingival tissues (P < 0.05). CONCLUSION: This study demonstrates in detail a methodology of occlusal trauma resulting from the cementation of metallic crowns in the lower molars of rats, mimicking occlusal interferences commonly evaluated in the dental clinic. This methodology makes new studies to better understand the mechanisms involved in the occlusal trauma of orofacial tissues possible. CLINICAL RELEVANCE: The standardization of an experimental occlusal interference model will allow us to understand the deleterious effect and mechanisms that affect the orofacial tissues.

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Abstract Observational studies have indicated that crestal bone level changes at implants are typically associated with clinical signs of inflammation, but still mechanical overload has been described as possible factor leading to hard-tissue deficiencies at implant sites without mucosal inflammation. The aim of this paper was systematically review the literature regarding the possible effect of traumatic occlusal forces on the peri-implant bone levels. Literature search was conducted using PubMed, Scielo and Lilacs, including the following terms: oral OR dental AND implant$ AND (load OR overload OR excessive load OR force$ OR bruxism) AND (bone loss OR bone resorption OR implant failure$). Databases were searched for the past 10 years of publications, including: clinical human studies, either randomized or not, cohort studies, case control studies, case series and animal research. Exclusion criteria were review articles, guidelines and in vitro and in silico (finite element analysis) research, as well as retrospective studies. The PICO questions formulated was: "does traumatic occlusal forces lead to peri-implant bone loss?" The database searches as well as additional hand searching, resulted in 807 potentially relevant titles. After inclusion/exclusion criteria assessment 2 clinical and 4 animal studies were considered relevant to the topic. The included animal studies did not reveal an association between overload and peri-implant bone loss when lower overloads were applied, whereas in the presence of excessive overload it seemed to generate peri-implant bone loss, even in the absence of inflammation. The effect of traumatic occlusal forces in peri-implant bone loss is poorly reported and provides little evidence to support a cause-and-effect relationship in humans, considering the strength of a clinically relevant traumatic occlusal force.

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OBJECTIVE: This study aims to systematically evaluate the effects of traumatic occlusion on the periodontal tissue of rats. The set of questions to be answered were-Can traumatic occlusion acting on a healthy and an unhealthy periodontium cause periodontal destruction? DESIGN: The protocols for systematic review were all developed, following the Preferred Reporting Items for Systematic reviews and Meta-Analyses statement and applied to animal research. Reporting of In vivo experiment guidelines for reporting animal research to assess the risk of bias of the studies. MATERIALS AND METHODS: A literature search was conducted using MEDLINE through PubMed and manual search from the reference lists of main articles related to the theme. RESULTS: This search strategy identified 65 references, of which 33 were considered inappropriate. The full texts of 32 articles were read, 31 of which did not meet the eligibility criteria and were excluded. The final selection included 1 article for which data was extracted for further evaluation. The article included shows a strongest reaction in the periodontium in front of a secondary occlusal trauma as inflammation and apical migration of the junctional epithelium, bone degradation, and decrease in the quantity of collagen fiber. However, primary occlusal trauma also presents these alterations, with the exception of apical migration of the junctional epithelium. CONCLUSIONS: Although only one study was included in the systematic review of traumatic occlusion, there is some evidence from experimental studies on animals that shows a coherent picture of the effects of traumatic occlusion on the periodontium. However, new studies are needed to fully answer the questions posed by this systematic review.

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