Investigation of periodontal ligament reaction upon excessive occlusal load--osteopontin induction among periodontal ligament cells.

Abstract

The purpose of the present study was to investigate the reaction of the periodontal ligament to excessive occlusal loading by observing the histological changes and osteopontin induction. The possibility of ligand for receptor activator of nuclear factor kappaB (RANKL) participation in osteopontin induction was also discussed.
The precise mechanism of periodontal ligament breakdown by excessive occlusal loading remains unclear. We established an experimental model for excessive occlusal loading in vivo. Osteopontin is known to be produced upon mechanical loading and is considered to induce the migration of osteoclasts to the resorption site. RANKL is one of the essential factors for osteoclast maturation and induces the constitutive induction of intracellular osteopontin in vitro.
The occlusal surface of the upper left first molars of rats was raised by steel wire bonding in order to induce occlusal trauma. The destruction of the periodontal ligament was observed and the production of osteopontin and RANKL by periodontal ligament cells was detected via immunohistochemistry.
Our model produced wide-ranging destruction of the periodontal ligament. From day 3 to day 7, prominent compression of the periodontal ligament and osteoclast migration were observed at the apical interradicular septum. Osteopontin was detected in some osteoclasts, surrounding fibroblasts, and osteoblasts adjacent to the compression area. RANKL was observed from day 1 to day 7 around the osteoblasts and osteoclasts.
Our model was useful for the detailed investigation of periodontal ligament breakdown during excessive occlusal loading. Although intracellular osteopontin was produced in osteoclasts with intermittent occlusal loading, the role of this protein in the cells was not clear. No correlation between RANKL distribution and osteopontin production in osteoclasts could be found.