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TNF Accelerates Death of Mandibular Condyle Chondrocytes in Rats with Biomechanical Stimulation-Induced Temporomandibular Joint Disease
- Source :
- PLoS ONE, PLoS ONE, Vol 10, Iss 11, p e0141774 (2015)
- Publication Year :
- 2015
-
Abstract
- Objective To determine if temporomandibular joint chondrocyte apoptosis is induced in rats with dental biomechanical stimulation and what a role TNF takes. Methods Thirty-two rats were divided into 4 groups (n = 8/group) and exposed to incisor mal-occlusion induced by unilateral anterior crossbite biomechanical stimulation. Two groups were sampled at 2 or 4 weeks. The other two groups were treated with local injections of a TNF inhibitor or PBS into the temporomandibular joints area at 2 weeks and then sampled at 4 weeks. Twenty-four rats either served as unilateral anterior crossbite mock operation controls (n = 8/group) with sampling at 2 or 4 weeks or received a local injection of the TNF inhibitor at 2 weeks with sampling at 4 weeks. Chondrocytes were isolated from the temporomandibular joints of 6 additional rats and treated with TNF in vitro. Joint samples were assessed using Hematoxylin&eosin, Safranin O, TUNEL and immunohistochemistry staining, real-time PCR, fluorogenic activity assays and Western blot analyses. The isolated chondrocytes were also analyzed by flow cytometry. Results Unilateral anterior crossbite stimulation led to temporomandibular joint cartilage degradation, associated with an increase in TUNEL-positive chondrocytes number, caspase-9 expression levels, and the release of cytochrome c from mitochondria at 2 weeks without changes in TNF and caspase-8 levels until after 4 weeks. TNF stimulated apoptosis of the isolated chondrocytes and up-regulated caspase-8 expression, but did not change caspase-9 expression levels. Local injection of TNF inhibitor down-regulated caspase-8 expression and reduced TUNEL-positive cell number, but did not reverse cartilage thickness reduction, caspase-9 up-regulation or cytochrome c release. Conclusions Unilateral anterior crossbite stimulation induces mitochondrion-mediated apoptosis of articular chondrocytes. TNF accelerated the unilateral anterior crossbite induced chondrocytes apoptosis via death-receptor pathway. However, anti-TNF therapy does not prevent cartilage loss in this model of temporomandibular joint.
- Subjects :
- medicine.medical_specialty
Pathology
medicine.medical_treatment
H&E stain
lcsh:Medicine
Down-Regulation
Stimulation
Apoptosis
Osteoarthritis
Chondrocyte
Gene Expression Regulation, Enzymologic
Rats, Sprague-Dawley
Chondrocytes
Internal medicine
medicine
Animals
lcsh:Science
Cells, Cultured
Caspase 8
Multidisciplinary
Chemistry
Tumor Necrosis Factor-alpha
Cartilage
lcsh:R
Mandibular Condyle
Cytochromes c
Temporomandibular Joint Disorders
medicine.disease
Temporomandibular joint
TNF inhibitor
Rats
Endocrinology
medicine.anatomical_structure
lcsh:Q
Female
Research Article
Subjects
Details
- ISSN :
- 19326203
- Volume :
- 10
- Issue :
- 11
- Database :
- OpenAIRE
- Journal :
- PloS one
- Accession number :
- edsair.doi.dedup.....8bd6fa87cde27b38959a68b9dd4b76dd