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Updated: Jan 14, 2026
Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils
Published on: January 21, 2020
Effects of Occlusal Hypofunction on Osteoclastogenesis Induced by Periodontal Ligament Cells
Tomomi Takahashi1, Tadashi Iizuka1
1Support Section for Education and Research, Faculty of Dental Medicine, Hokkaido University, Sapporo, Japan.
Background:
Periodontal ligament (PDL) cells express several osteoclastic cytokines, including receptor activator of nuclear factor kappa ligand (RANKL) and osteoprotegerin (OPG). They regulate the alveolar bone structure by influencing osteoclast activity. The structure of the PDL is affected by mechanical stress. However, few in vitro studies have examined the effects of hypofunctional occlusion in isolated PDL cells. This study aimed to elucidate the role of PDL cells in osteoclastogenesis under hypofunctional occlusal conditions.
Methods:
Left maxillary molars were extracted to eliminate the occlusal force. Three weeks later, the histology and cytology of the PDL tissue samples were analyzed. To investigate osteoclast formation, isolated PDL cells were cocultured with RAW 264.7 cells.
Results:
The PDL tissue demonstrated atrophic changes on the non-occlusal side (N-Oc side). Immunocytochemistry and western blotting indicated that the isolated PDL cells were positive for RANKL and OPG; however, OPG expression was lower on the N-Oc side compared with the occlusal side (Oc side). Coculturing of PDL and RAW 264.7 induced the formation of osteoclast-like cells in all experimental groups. The N-Oc side exhibited more and larger osteoclasts than the Oc side. Osteoclast-like cells supplemented with RANKL and anti-OPG antibodies were significantly larger than those supplemented with RANKL alone.
Conclusions:
These findings show that the biological functions of PDL cells are altered by occlusal hypofunction and that a reduction in OPG expression promotes osteoclast differentiation.
