Mechanical force orchestrates inflammatory and apoptosis-associated signaling in periodontal tissues during orthodontic tooth movement using complementary in vivo and in vitro models
5 affiliations
- 1Department of Histology and Embryology, Nihon University Graduate School of Dentistry at Matsudo, Matsudo, Chiba, 271-8587, Japan
- 2Research Institute of Oral Science, Nihon University School of Dentistry at Matsudo, 2-870-1 Sakae-cho Nishi, Matsudo, Chiba, 271-8587, Japan
- 3Department of Anesthesiology, Nihon University School of Dentistry, 1-8-13 Kanda-Surugadai, Chiyoda-ku, Tokyo, 101-8310, Japan
- 4Department of Oral Pathology and Microbiology, Faculty of Dentistry, Jamia Millia Islamia, New Delhi, 110025, India
- 5Department of Orthodontics & Dentofacial Orthopedics, Faculty of Dentistry, Jamia Millia Islamia, New Delhi, 110025, India
Abstract
Objectives: To investigate the relationship between force-induced inflammation and intrinsic mitochondrial apoptosis-associated signaling in periodontal ligament (PDL) tissues during orthodontic tooth movement (OTM) using complementary in-vivo and in-vitro models.
Materials and methods: OTM was induced in six C57BL/6 mice using a nickel-titanium coil spring delivering approximately 30–35 g of force for 14 days. The contralateral side served as the untreated control. Micro-computed tomography (micro-CT) assessed tooth displacement. Histological and immunohistochemical analyses evaluated TNF-α, phosphorylated NF-κB, cytochrome c, and apoptotic protease activating factor 1 (APAF1). Human PDL fibroblasts were exposed to 2.0 g/cm2 compressive force for 2, 4, 6, and 24 h. TNF-α, IL-6, and IL-8 mRNA expression was quantified using RT-PCR.
Results: Micro-CT revealed significantly greater inter-molar distance on the force-applied side than on the control side (0.2350 ± 0.0274 mm vs. 0.0750 ± 0.0187 mm; n = 6; paired p < 0.001). Immunohistochemistry showed increased TNF-α, phosphorylated NF-κB, cytochrome c, and APAF1 immunoreactivity in force-applied PDL tissues. In-vitro, TNF-α and IL-8 mRNA expression increased at 4, 6, and 24 h, while IL-6 expression was elevated at all time points, peaking at 4 h.
Conclusions: Orthodontic force induces inflammatory responses and alters mitochondrial apoptosis-associated signaling in periodontal tissues. These findings highlight potential interactions between inflammatory pathways and apoptosis-related molecular events during OTM. Further studies are required to establish whether these molecular changes result in apoptotic cell death.
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BibTeX
@article{suzuki2026mechanical,
title = {{Mechanical force orchestrates inflammatory and apoptosis-associated signaling in periodontal tissues during orthodontic tooth movement using complementary in vivo and in vitro models}},
author = {Yoshino Suzuki and Ujjal K. Bhawal and Shunichi Oka and Aman Chowdhry and Priyanka Kapoor},
journal = {Journal of Oral Biology and Craniofacial Research},
year = {2026},
month = oct,
doi = {10.1016/j.jobcr.2026.101563},
url = {https://doi.org/10.1016/j.jobcr.2026.101563},
note = {CC BY-NC-ND 4.0},
}
RIS
TY - JOUR
TI - Mechanical force orchestrates inflammatory and apoptosis-associated signaling in periodontal tissues during orthodontic tooth movement using complementary in vivo and in vitro models
AU - Yoshino Suzuki
AU - Ujjal K. Bhawal
AU - Shunichi Oka
AU - Aman Chowdhry
AU - Priyanka Kapoor
PY - 2026
DA - 2026/10/28
JO - Journal of Oral Biology and Craniofacial Research
DO - 10.1016/j.jobcr.2026.101563
UR - https://doi.org/10.1016/j.jobcr.2026.101563
AB - Objectives: To investigate the relationship between force-induced inflammation and intrinsic mitochondrial apoptosis-associated signaling in periodontal ligament (PDL) tissues during orthodontic tooth movement (OTM) using complementary in-vivo and in-vitro models. Materials and methods: OTM was induced in six C57BL/6 mice using a nickel-titanium coil spring delivering approximately 30–35 g of force for 14 days. The contralateral side served as the untreated control. Micro-computed tomography (micro-CT) assessed tooth displacement. Histological and immunohistochemical analyses evaluated TNF-α, phosphorylated NF-κB, cytochrome c, and apoptotic protease activating factor 1 (APAF1). Human PDL fibroblasts were exposed to 2.0 g/cm2 compressive force for 2, 4, 6, and 24 h. TNF-α, IL-6, and IL-8 mRNA expression was quantified using RT-PCR. Results: Micro-CT revealed significantly greater inter-molar distance on the force-applied side than on the control side (0.2350 ± 0.0274 mm vs. 0.0750 ± 0.0187 mm; n = 6; paired p < 0.001). Immunohistochemistry showed increased TNF-α, phosphorylated NF-κB, cytochrome c, and APAF1 immunoreactivity in force-applied PDL tissues. In-vitro, TNF-α and IL-8 mRNA expression increased at 4, 6, and 24 h, while IL-6 expression was elevated at all time points, peaking at 4 h. Conclusions: Orthodontic force induces inflammatory responses and alters mitochondrial apoptosis-associated signaling in periodontal tissues. These findings highlight potential interactions between inflammatory pathways and apoptosis-related molecular events during OTM. Further studies are required to establish whether these molecular changes result in apoptotic cell death.
SN - 2212-4268
SN - 2212-4276
ER -