The first experimental investigation of orthodontic tooth movement was published by Sandstedt in 1904-1905. After 100 years, there is a good understanding of the sequence of events at both tissue and cellular levels and now the current focus of research is at the molecular level. The techniques of reverse transcription-polymerase chain reaction and in situ hybridization to detect mRNAs of interest have revolutionized tooth movement studies and an expanding list of antibodies and enzyme-linked immunosorbent assays directed against human and animal proteins will facilitate their identification in tissue sections and/or culture supernatants. Nevertheless, although this technology has greatly simplified research for the clinical and laboratory investigator, message is not always translated into protein, and the presence of a protein does not necessarily mean it is biologically active. In vivo and in vitro methods have been widely used in tooth movement studies. However, data from in vitro models, in which the mechanical stimulus can be carefully controlled (tension versus compression; intermittent versus continuous), should be correlated with in vivo data from animal models. The current evidence suggests that downstream from the initial mechanotransduction event at focal adhesions which link the extracellular matrix to the cytoskeleton, mechanically induced remodelling is mediated by a complex feedback mechanism involving the synthesis of cytokines such as interleukin-1 (IL-1), IL-6, and receptor activator of nuclear factor k B ligand by cells of the osteoblast and/or fibroblast lineages. These in turn act in an autocrine/paracrine fashion to regulate the expression of transcription factors, cytokines, growth factors, enzymes, and structural molecules involved in the differentiation, proliferation, and function of mesenchymal and other cell types. Contrary to the impression gained from the literature, tooth movement is not confined to events within the periodontal ligament. Orthodontic tooth movement involves two interrelated processes: (1) deflection or bending of the alveolar bone and (2) remodelling of the periodontal tissues.

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The forces that orthodontic appliances apply to the teeth are transmitted through the periodontal ligament (PDL) to the supporting alveolar bone, leading to the deposition or resorption of bone, depending upon whether the tissues are exposed to a tensile or compressive mechanical strain. To evaluate the osteogenic potential of PDL cells, we applied a 12% uni-axial cyclic tensile strain to cultured human PDL cells and analyzed the differential expression of 78 genes implicated in osteoblast differentiation and bone metabolism by real-time RT-PCR array technology. Sixteen genes showed statistically significant changes in expression in response to alterations in their mechanical environment, including cell adhesion molecules and collagen fiber types. Genes linked to the osteoblast phenotype that were up-regulated included BMP2, BMP6, ALP, SOX9, MSX1, and VEGFA; those down-regulated included BMP4 and EGF. This study has expanded our knowledge of the transcriptional profile of PDL cells and identified several new mechanoresponsive genes.