Tatsuo Fukuhara

Clinical application of prostaglandin E1 (PGE1) upon orthodontic tooth movement

Chemically produced prostaglandin E1 (PGE1) was administered in clinical cases of orthodontic tooth movement. In the first phase, lingual arch springs were applied on both sides of the maxilla to upper first premolars which were scheduled for extraction. One side received submucosal injections of PGE1 and the other received vehicle injections. The rate of tooth movement in the buccal direction approximately doubled on the side of several PGE1 injections as compared to the control side. In the second phase, the PGE1 injections were applied in canine-retraction cases for up to 3 weeks in first-premolar-extraction cases. The rate of distal canine movement was almost double on the side receiving PGE1 injections as compared to the vehicle-injected side. In the third phase, the PGE1 injections were applied on routine canine retraction in first-premolar-extraction cases. The rate of distal canine movement was almost 1.6-fold on the side of PGE1 injections as compared to the vehicle-injected side. Throughout this study, no side effects were observed macroscopically in the gingiva and roentgenographically in the alveolar bone, except for a slight pain reaction consistent with orthodontic tooth movement.

The Effect of Prostaglandins on Experimental Tooth Movement in Monkeys (Macaca fuscata)

Local administrations of prastaglandins E1 or E2 combined with orthodontic tooth movemerat can approximately double the rate of tooth movement in monkeys compared to that of the control. Macroscopically, no side-effect was observed in the gingiva and associated structures.

Behavior of Mast Cells in Periodontal Ligament Associated with Experimental Tooth Movement in Rats

Orthodontic mechanical stress reduced the frequency of the appearance of mast cells stainable with toluidine blue in the periodontal ligament on both the pressure and tension sides of rat molar teeth. This effect was seen immediately after insertion of elastic bands between the first and second molars, and the greatest reduction in the number of mast cells stainable with toluidine blue was observed 15 min after insertion.

A stable analogue of throm☐ane A2, 9,11-epithio-11,12-methanothrom☐ane A2, stimulates bone resorption in vitro and osteoclast-like cell formation in mouse marrow culture

Thromboxane A2 (TXA2) is a powerful promoter of platelet aggregation and smooth muscle contraction. However, this compound is highly unstable and is rapidly hydrated to a more stable metabolite, thromboxane B2 (TXB2). TXA2 has been considered to be involved in bone resorption, in particular bone loss caused by inflammatory diseases and by orthodontic treatment. However precise mechanisms of bone resorption caused by TXA2 have not yet been proved because of its highly unstable nature. Recently, a chemically stable analogue of TXA2, 9,11-epithio-11,12-methanothromboxane A2 (STA2), was successfully synthesized. Using this synthetic compound, we examined its in vitro bone resorbing activity and induction of osteoclast-like cells in a mouse marrow culture system in comparison with related compounds with bone resorbing activity. Like prostaglandin E2 (PGE2), a well-known bone resorbing agent, STA2 time- and dose-dependently stimulated the release of 45Ca from prelabelled mouse calvariae. Both STA2 and PGE2 induced the accumulation of cAMP in mouse calvariae. The TXA2 antagonist, ONO-3708, inhibited STA2-induced release of 45Ca. TXB2 induced neither bone resorption nor cAMP accumulation. When mouse marrow cells were cultured with STA2 for 8 days, osteoclast-like multinucleated cells appeared in parallel with the increase of the amount of STA2 added. Again TXB2 showed no effect on osteoclast-like cell formation. These results indicate a role for TXA2 in some form of bone resorption.