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This article described research aimed at testing the hypothesis that tissue remodeling during orthodontic tooth movement is modulated, at least in part, by factors derived from the nervous and vascular (immune) systems.

Piezoelectric currents in mechanically stressed bone were implicated in the activation of bone cells. The objectives of this experiment were to determine the usefulness of exogenous electric currents in accelerating orthodontic tooth movement and to study the effect of electric-orthodontic treatment on periodontal cyclic nucleotides. Maxillary canines were tipped in five cats by 80 g force. Two groups of five cats each were treated by an electric-orthodontic procedure to one maxillary canine for 7 and 14 days, respectively. Teeth treated by force and electricity moved significantly faster than those treated by force alone. Enhanced bone resorption was observed near the anode (PDL compression site), while bone formation was pronounced near the cathode (PDL tension site). Staining for cyclic nucleotides was increased when electric stimulation was added to the mechanical force. These results suggest that orthodontic tooth movement may be accelerated by the use of locally applied electric currents.

During development of the mammalian secondary palate, medial-edge epithelia (MEE) from apposing palatal shelves adhere and undergo autolysis allowing palatal mesenchymal regions to unite. In a prior study (Greene & Pratt, 1979), we reported a transient increase in levels of cyclic AMP (cAMP) in the mouse and rat palate during epithelial adhesion and cell death. The objective of this study was to examine the distribution of cyclic AMP in the developing rodent secondary palate using immunohistochemistry to localize cyclic AMP. Staining for cAMP was observed in the epithelium just prior to and during epithelial fusion (day 16 in the rat; day 14 in the mouse). Cyclic AMP was distributed throughout the epithelial cytoplasm whereas no staining was seen in nuclei. Epithelial staining for cAMP was faint or absent 24 and 48 h prior to epithelial contact. Mesenchymal staining for cAMP was minimal and associated with the plasma membrane at all stages studied. These results demonstrate that elevated levels of cAMP in the rat and mouse palate during epithelial adhesion and cell death are mainly due to increases of the nucleotide in palatal epithelium. This observation suggests that a transient increase in epithelial cAMP may play a role in palatal epithelial differentiation.