# Effects of Occlusal Hypofunction on Osteoclastogenesis Induced by Periodontal Ligament Cells

**Authors:** Tomomi Takahashi, Tadashi Iizuka

PMC · DOI: 10.1155/ijod/9926168 · International Journal of Dentistry · 2025-10-14

## TL;DR

This study shows that reduced chewing activity leads to changes in PDL cells that promote more and larger osteoclasts, which can affect bone structure.

## Contribution

The study demonstrates for the first time how occlusal hypofunction alters PDL cell function to enhance osteoclastogenesis.

## Key findings

- PDL tissue showed atrophy on the non-occlusal side.
- N-Oc side PDL cells produced fewer OPG and more osteoclasts.
- Reduced OPG promotes larger osteoclast formation when combined with RANKL.

## Abstract

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.

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.

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.

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.

## Linked entities

- **Genes:** TNFSF11 (TNF superfamily member 11) [NCBI Gene 8600], BTF3P11 (basic transcription factor 3 pseudogene 11) [NCBI Gene 690]

## Full-text entities

- **Genes:** Tnfsf11 (tumor necrosis factor (ligand) superfamily, member 11) [NCBI Gene 21943] {aka Ly109l, ODF, OPGL, RANKL, Trance}, Tnfrsf11b (tumor necrosis factor receptor superfamily, member 11b (osteoprotegerin)) [NCBI Gene 18383] {aka OCIF, Opg, TR1}
- **Diseases:** Occlusal Hypofunction (MESH:D000309), atrophic (MESH:D020966)
- **Cell lines:** RAW 264.7 — Mus musculus (Mouse), Mouse leukemia, Cancer cell line (CVCL_0493)

## Full text

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## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12539991/full.md

## References

43 references — full list in the complete paper: https://tomesphere.com/paper/PMC12539991/full.md

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Source: https://tomesphere.com/paper/PMC12539991