This review describes the mechanical and biological signalling pathways during orthodontic tooth movement and provides an update of the current literature. A theoretical model is introduced to elucidate the complex cascade of events after the application of an orthodontic force to a tooth. In this model, the events are divided into four stages: matrix strain and fluid flow, cell strain, cell activation and differentiation, and remodelling. Each stage is explained in detail and discussed using recent literature.

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RESUMOEste trabalho propõe um parâmetro anatômico, a incidência pélvica, como fator chave para a compreensão do alinhamento da coluna vertebral. Existe estreita relação, tanto para indivíduos normais como para indivíduos com deformidades da coluna, entre o parâmetro anatômico de incidência pélvica e a inclinação sacral, determinantes da lordose lombar. O ângulo de Cobb e a rotação vertebral apical servem de instrumento para o entendimento do aspecto tridimensional da coluna vertebral e das relações entre a pelve e a coluna. Uma equação preditiva para lordose é apresentada. A incidência pélvica parece ser o fator determinante do equilíbrio sagital da coluna. Ela determina as curvas da coluna vertebral, variando conforme outros parâmetros.Descritores: Pelve; Lordose; Escoliose; Equilíbrio sagital; Postura. ABSTRACT this paper proposes an anatomical parameter, the pelvic incidence, as the key factor for managing the spinal balance. there is a close relationship for both normal individuals and those with spinal deformities between the anatomical parameter of pelvic incidence and the sacral slope, which determine lumbar lordosis. the Cobb angle and the apical vertebral rotation serve as a tool for understanding the three-dimensional aspect of the spine and its relationships with the pelvis. A predictive equation of lordosis is postulated. the pelvic incidence seems to be the determining factor of the sagittal balance of the spine. It determines spinal curves and varies according to other parameters.

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The data indicate that long-lived collagen fibers do not exist in the soft tissues of the periodontium, and are probably not responsible for relapse. The differences in collagen half-life might be caused by local variations in compressive strain induced by normal function.