The periodontium is exposed to physical forces in vivo in response to mastication, speech and orthodontic tooth movement. Experiments carried out in humans, as well as in animals, have produced evidence indicating that, in the context of a healthy dental alveolar environment, the trauma from occlusion cannot induce periodontal tissue breakdown. The specialized tissue responsible for this protective effect is known as the periodontal ligament (PDL). The PDL distributes the applied forces to the contiguous alveolar bone, therefore, dissipating the otherwise traumatic stimulus and converting it into a remodeling feedback mechanism. Although the histological and some of the biochemical effects of orthodontic force application have been described, the mechanism by which the PDL maintains the integrity of the periodontium is poorly understood. Previously, it has been shown that mechanical force induces cellular dynamic changes in the PDL that lead to characteristic gene expression patterns. Particularly interesting is the spacio-temporal distribution of a protein called Periostin. A divergent change in Periostin mRNA expression occurs between the compression and tension sites of the PDL. In addition to its expression in the periosteum, the exclusive localization of periostin in the PDL suggests a relevant function of this molecule in the PDL dynamics as a force-distributing system. This project was focused on the in vivo function of Periostin in the PDL, as it may play a major role in buffering the mechanical stress that is generated during normal occlusal function. The central hypothesis of this project was that Periostin plays a key role in maintaining the integrity of the periodontium in response to occlusal load. To test this hypothesis, in vivo and in vitro approaches were used in order to identify the significance of Periostin in the periodontium during occlusal function. Our results have provided novel insights into the regulation of PDL function and its biological response to mechanical stress to allow normal dental and alveolar adaptation. The data generated have major implications for our understanding of periodontal biology and highlight novel pathways that determine periodontitis susceptibility that could be targeted in the treatment of metabolic periodontal diseases.