An ultrastructural study of the effects of bisphosphonate administration on osteoclastic bone resorption during relapse of experimentally moved rat molars.

This study was designed to clarify the effects of systemic administration of bisphosphonate, pamidronate, on the bone resorbing activity of osteoclasts during relapse of rat molars, after experimental movement. An elastic band was inserted between the upper first and second molars of 7-week-old rats and removed 21 days later. At 1 day before elastic band removal, bisphosphonate was administered via a tail vein. After elastic band removal, the rats were further maintained for 0, 5, or 10 days. The relapse of the first molars was studied by means of light and scanning-electron and transmission-electron microscopy. When an elastic band was removed, the mean interdental distance between the first and second molars in all rats was approximately 435 micrometer. In the control rats, it had decreased to 108 micrometer by day 5 and 57 micrometer by day 10. In these control rats, numerous osteoclasts appeared along the alveolar bone surface in the compressed side of the periodontal ligament of first molars. Administration of bisphosphonate significantly inhibited the prominent decrease in interdental distance. In these rats, it averaged 313 micrometer at day 5 and 115 micrometer at day 10. In bisphosphonate-treated rats, osteoclasts aggregated mainly in vascular canals of alveolar bone but were occasionally observed along the alveolar bone surfaces facing the periodontal ligament. Administration of bisphosphonate also induced structural changes, such as disappearance of ruffled borders and cytoplasmic polarity, in osteoclasts. A degenerated osteoclast was also observed in a bisphosphonate-treated rat. However, bisphosphonate induced no structural changes in osteoblasts, osteocytes, or periodontal ligament fibroblasts. These results suggest that a single systemic administration of bisphosphonate decreases the extent of initial relapse in experimentally moved rat molars via a mechanism involving impairment of the structure and resorptive functions of osteoclasts.