Autotransplantation of impacted maxillary canines into surgically modified sockets and orthodontic treatment: a 4-year follow-up case report.

The permanent maxillary canine is the second most frequently impacted or displaced tooth. The standard treatment for an impacted canine includes, among other things, surgical exposure and orthodontic alignment. Surgical techniques for this procedure vary depending on whether the tooth is labially or palatally impacted, while orthodontic techniques vary according to clinical judgment and experience. Autotransplantation is a treatment alternative for impacted canines with complete root formation. The success of tooth transplantation depends on the vitality of the periodontal ligament (PDL) attached to the donor tooth, and its viability decreases when it is exposed extraorally. This article reports on maxillary canine autotransplantations combined with connective tissue grafts (CTGs) and orthodontics. The recipient mesiodistal space was created orthodontically and the recipient socket was prepared using dental implant drills. Following transplantation, bone defects were grafted using guided bone regeneration (GBR). At 4 years post-transplantation, the soft tissue level was stable and periapical radiographs showed a practically normal contour of the alveolar crest around teeth 13 and 23. The two permanent canines presented no root resorption and ankylosis, and no signs of inflammation or bleeding were observed. The procedure used in this case report demonstrates that canine transplantation combined with GBR, plastic surgery procedures, and orthodontic treatment may yield acceptable and predictable esthetic results.

Neural plasticity and proliferation in the generation of antidepressant effects: hippocampal implication.

It is widely accepted that changes underlying depression and antidepressant-like effects involve not only alterations in the levels of neurotransmitters as monoamines and their receptors in the brain, but also structural and functional changes far beyond. During the last two decades, emerging theories are providing new explanations about the neurobiology of depression and the mechanism of action of antidepressant strategies based on cellular changes at the CNS level. The neurotrophic/plasticity hypothesis of depression, proposed more than a decade ago, is now supported by multiple basic and clinical studies focused on the role of intracellular-signalling cascades that govern neural proliferation and plasticity. Herein, we review the state-of-the-art of the changes in these signalling pathways which appear to underlie both depressive disorders and antidepressant actions. We will especially focus on the hippocampal cellularity and plasticity modulation by serotonin, trophic factors as brain-derived neurotrophic factor (BDNF), and vascular endothelial growth factor (VEGF) through intracellular signalling pathways-cAMP, Wnt/ ß -catenin, and mTOR. Connecting the classic monoaminergic hypothesis with proliferation/neuroplasticity-related evidence is an appealing and comprehensive attempt for improving our knowledge about the neurobiological events leading to depression and associated to antidepressant therapies.