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      Influencia de la diabetes mellitus en el tratamiento ortodóncico. Revisión de la literatura Translated title: Influence of diabetes mellitus in orthodontic treatment. A review of the literature

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          Abstract

          RESUMEN Introducción: Actualmente, un creciente número de pacientes con diabetes mellitus (DM) busca tratamiento ortodóncico, lo que hace necesario conocer las implicancias de la DM en dicho tratamiento. La presente revisión bibliográfica tiene como propósito evaluar la influencia de DM en el tratamiento ortodóncico. Revisión: Existen escasos estudios clínicos acerca del comportamiento de diabéticos ante fuerzas ortodóncicas, siendo realizados mayoritariamente en modelos animales. La DM altera la respuesta inmune, por tanto, la inflamación y síntesis de matriz extracelular. La fuerza ortodóncica produce desequilibrio entre las metaloproteinasas de la matriz extracelular y sus inhibidores, alterando la actividad fibroblástica. Este desequilibrio afecta más rápida y prolongadamente a diabéticos. La remodelación del colágeno en animales diabéticos causa retardo en la regeneración ósea, debilitamiento del ligamento periodontal (PL) y microangiopatías gingivales. Los altos niveles de citoquinas y quimioquinas pro-inflamatorias presentes en diabéticos amplifican la inflamación, lo que puede explicar el mayor número de osteoclastos en comparación con pacientes sin DM. En la DM, los osteoclastos actúan más prolongadamente tras fuerzas ortodóncicas, causando altos niveles de destrucción ósea y degradación del PL. La DM no controlada puede retardar el tratamiento ortodóncico, por lo que en este caso estaría contraindicado. Se ha observado que glicemias normales, transforman a diabéticos en sanos frente a fuerzas ortodóncicas, normalizando las respuestas periodontal y alveolar. Conclusiones: En animales, la DM ha mostrado aumento de destrucción del PL y hueso alveolar, y disminución de efectividad del movimiento ortodóncico. Para realizar un tratamiento ortodóncico, es fundamental que la DM esté controlada.

          Translated abstract

          ABSTRACT Introduction: An increasing number of patients with diabetes mellitus (DM) are now seeking orthodontic treatment. It is necessary to know the influence of DM on orthodontic treatment.This literature review aims to evaluate the influence of DM on orthodontic treatment. Review: There are few clinical studies on the behavior of diabetics under orthodontic forces, being performed on animal models. DM alters the immune response, thus inflammation and extracellular matrix synthesis. The orthodontic force produces an imbalance between extracellular matrix metalloproteinases and their inhibitors, altering the activity of fibroblasts. This imbalance affects diabetics faster and longer. Collagen remodeling in diabetic animals slows down bone regeneration, weakening of the periodontal ligament (PL)and gingival microangiopathies. High levels of cytokines and pro-inflammatory chemokines present in diabetics amplify inflammation, which may explain the greater number of osteoclasts relative to patients without DM. In DM, osteoclasts show longer action after orthodontic forces, causing high levels of bone destruction and LP degradation. Uncontrolled DM can delay orthodontic treatment, so in this case it would be contraindicated. It has been observed that normal glycemia transforms diabetics into healthy ones when faced with orthodontic forces, normalizing periodontal and alveolar responses. Conclusions: In animals, DM has shown increased destruction of PL and alveolar bone and decreased effectiveness of orthodontic movement. To perform orthodontic treatment, it is essential that the DMis controlled.

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          Most cited references31

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          Mechanisms of tooth eruption and orthodontic tooth movement.

          Teeth move through alveolar bone, whether through the normal process of tooth eruption or by strains generated by orthodontic appliances. Both eruption and orthodontics accomplish this feat through similar fundamental biological processes, osteoclastogenesis and osteogenesis, but there are differences that make their mechanisms unique. A better appreciation of the molecular and cellular events that regulate osteoclastogenesis and osteogenesis in eruption and orthodontics is not only central to our understanding of how these processes occur, but also is needed for ultimate development of the means to control them. Possible future studies in these areas are also discussed, with particular emphasis on translation of fundamental knowledge to improve dental treatments.
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            Diabetes mellitus related bone metabolism and periodontal disease

            Diabetes mellitus and periodontal disease are chronic diseases affecting a large number of populations worldwide. Changed bone metabolism is one of the important long-term complications associated with diabetes mellitus. Alveolar bone loss is one of the main outcomes of periodontitis, and diabetes is among the primary risk factors for periodontal disease. In this review, we summarise the adverse effects of diabetes on the periodontium in periodontitis subjects, focusing on alveolar bone loss. Bone remodelling begins with osteoclasts resorbing bone, followed by new bone formation by osteoblasts in the resorption lacunae. Therefore, we discuss the potential mechanism of diabetes-enhanced bone loss in relation to osteoblasts and osteoclasts.
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              Advanced Glycation End Products, Diabetes, and Bone Strength

              Diabetic patients have a higher fracture risk than expected by their bone mineral density (BMD). Poor bone quality is the most suitable and explainable cause for the elevated fracture risk in this population. Advanced glycation end products (AGEs), which are diverse compounds generated via a non-enzymatic reaction between reducing sugars and amine residues, physically affect the properties of the bone material, one of a component of bone quality, through their accumulation in the bone collagen fibers. On the other hand, these compounds biologically act as agonists for these receptors for AGEs (RAGE) and suppress bone metabolism. The concentrations of AGEs and endogenous secretory RAGE, which acts as a “decoy receptor” that inhibits the AGEs-RAGE signaling axis, are associated with fracture risk in a BMD-independent manner. AGEs are closely associated with the pathogenesis of this unique clinical manifestation through physical and biological mechanisms in patients with diabetes mellitus.
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                Author and article information

                Journal
                odonto
                Avances en Odontoestomatología
                Av Odontoestomatol
                Ediciones Avances, S.L. (Madrid, Madrid, Spain )
                0213-1285
                2340-3152
                September 2021
                : 37
                : 3
                : 118-124
                Affiliations
                [2] Maule orgnameUniversidad de Talca Chile
                [3] Talca Maule orgnameUniversidad de Talca orgdiv1Escuela de Graduado orgdiv2Facultad de Ciencias de la Salud Chile
                [1] Santiago de Chile orgnameUniversidad Mayor Chile
                Article
                S0213-12852021000300002 S0213-1285(21)03700300002
                0dd844b0-2852-49b3-b48e-17130e6de4fc

                This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 International License.

                History
                : 25 February 2020
                : 16 January 2020
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 30, Pages: 7
                Product

                SciELO Spain

                Categories
                Artículos

                Orthodontics,Diabetes Mellitus,Bone Remodeling
                Orthodontics, Diabetes Mellitus, Bone Remodeling

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