Protective effects of low-intensity pulsed ultrasound on mandibular condylar cartilage exposed to mechanical overloading
Mutsumi Fujita, Minami Sato, Hiroki MoriiD, Akihiko IwasaiD, Nobuhiko KawaiiD, Ali Habiballah Hassan, Eiji I. TanakaiD
Abstract
The aim of this study was to examine the role of low-intensity pulsed ultrasound (LIPUS) exposure in the onset and early progression of temporomandibular joint (TMJ) osteoarthritis (TMJ-OA) induced by mechanical overloading. Fifteen-week-old male Wistar rats were divided into two experimental groups and a control group (n = 5 each). In the experimental groups, both TMJs were subjected to mechanical overloading by forced mouth opening using a jaw-opening device for 3 h/day for 5 continuous days. After mechanical overloading, TMJs in one experimental group were exposed to LIPUS for 20 min/day. After the experiments, mandibles were resected from the rats, and the condyles were processed. The bones were analyzed using high-resolution microcomputed tomography (micro-CT). The resected TMJs were also subjected to histological analysis and immunohistochemical staining. Micro-CT images of the mandibular condyle showed severe subchondral trabecular bone loss in the experimental group with overloading. Treatment with LIPUS after overloading resulted in decreased subchondral trabecular bone resorption. In TMJ sections from the experimental group with overloading, cell-free regions and proteoglycan loss characterized the cartilage degradation; LIPUS exposure restricted these changes in the mandibular condyle. Furthermore, the number of tartrate-resistant acid phosphatase-positive osteoclasts in the mineralized layer of the condylar cartilage increased after mechanical overloading and decreased after LIPUS treatment. Our findings suggest that LIPUS exposure after mechanical TMJ overloading downregulates subchondral trabecular bone resorption and proteoglycan loss in the mandibular condylar cartilage. Thus, it may prove to be protective effects of LIPUS exposure on onset and early progression of TMJ-OA induced by mechanical overloading.
02 /Specification & Classification
Click any tag to browse matching papers- Citations
- 11
- FWCI
- 1.14
- Field percentile
- top 23%
- Organism
- Assay
- Approach
Reproducibility ledger
Nobody has reported trying to reproduce this paper yet. Did you replicate an experiment or run the code? Your report saves the next lab a week.
Sign in to file a reproducibility report.
Related papers
- LOXL2 Deletion Triggers TMJ Osteoarthritis While Overexpression Protects Against NF-κB-Induced Chondrocyte Apoptosis
Rajnikant Dilip Raut, Chumki Choudhury, … Manish V. Bais·bioRxiv·May 12, 2025
- Leptin: A Potential Adipokine Bridging Systemic Endotoxemia and Sex-Divergent Temporomandibular Joint Osteoarthritis Development
Shipin Zhang, Siyi Chen, … David Fercher·bioRxiv·Oct 13, 2025
- Suppressed Osteocyte Perilacunar / Canalicular RemodelingPlays a Causal Role in Osteoarthritis
C. M. Mazur, J. J. Woo, … T. Alliston·bioRxiv·Jan 31, 2019
- Liproxstatin-1 alleviates cartilage degradation by inhibiting chondrocyte ferroptosis in temporomandibular joint
- A stimuli-responsive ex vivo model of osteoarthritis demonstrates TLR4-mediated cartilage degradation and a Rapamycin-induced fast matrix recovery
Roberto Di Gesù, Hagar Kenawy, … Riccardo Gottardi·bioRxiv·Jun 11, 2026
- Micromechanical characterisation of osteoarthritic subchondral bone by micropillar compression
Samuel McPhee, Marta Peña Fernández, … Uwe Wolfram·Acta BiomaterialiaPeer-reviewed·May 20, 2026