A review of the literature pertaining to the histological and ultrastructural changes related to orthodontic tooth movement reveals that much attention has been devoted to the fibrillar and cellular components of the periodontal ligament (PDL). Although the vascular response to experimental tooth movement has been investigated, specific morphological and morphometric data on changes in the tension zone of the PDL microvascular system are lacking. The present investigation was conducted to study the ultrastructural vascular response in the tension zone of the PDL following a short-term extrusive force. Six 12-week-old male Porton rats were anesthetized and cannulated via the aorta after applying a 1-N extrusive force for 30 min to the right maxillary first molar. The contralateral molar served as a control in all animals. The apical portion of both the control and experimental PDL was prepared for TEM examination. In the experimental PDL, degenerative changes in the endothelial cell wall and incipient nuclear shrinkage were observed in about 30% of the postcapillary venules and 18% of the capillaries, whereas the arterial components were generally spared. Compared to the control PDL, these degenerative changes were significantly marked in the experimental PDL (p<0.01). The results of this study suggest that the postcapillary venules are the most vulnerable segment in the PDL microvascular system.

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A case of complex odontoma, which contained melanin pigment in the ghost cells in a 53-year-old Japanese woman is reported. In addition to the characteristic histopathologic features of complex odontoma, ghost cells containing melanin pigment were widely distributed in and around the calcified masses. Furthermore, cytoplasmic processes of dendritic cells (melanocytes) were seen in some parts. The possible histogenesis of melanin pigment in odontogenic lesions was discussed, although no conclusion could be drawn from the present study as to its origin in complex odontoma.

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Tricalcium phosphate was implanted into standardized defects in the maxilla and mandible of beagles. The tricalcium phosphate provoked new bone formation in the defects, which healed 0.02 mm/day faster than the untreated controls.

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We examined the cerebral location of the readiness potential (hereinafter referred to as “RP”) upon activation of the masseter muscle by voluntary and unilateral jaw-biting movement. Four normal adults served as subjects. Five scalp electrodes were placed according to the international 10-20 method at CZ, C3, C4, T3 and T4. In addition, in one of the subjects, RPs were recorded by 12 scalp electrodes in order to study changes occurring in the distribution of RPs with time. The maximum amplitude of the RP was located at T4 in the temporal area, which was involved in the biting movement as a negative slow potential occurring 1.4-0.8 s before the beginning of the discharge to the masseter muscle. The maximum amplitude of the RP on the contralateral side was located at T3. This meant that the amplitude of the RP tended to be higher on the same side as the biting movement than on the contralateral side in all subjects. From scalp topography, the maximum amplitude of the RP was shown to be confined to T4, and was especially marked immediately before the beginning of discharge to the masseter muscle. From these results it is thought that in the case of voluntary biting movement, the RP reflects activities of the pyramidal cells in the masticatory area of the cortex, and that strong descending impulses from both sides then reach the masseter muscles.

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