ArticleOsteoarthritis and cartilage2016
Unilateral anterior crossbite induces aberrant mineral deposition in degenerative temporomandibular cartilage in rats.
Article in Osteoarthritis and cartilage, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.
- Effect of mechanical loading on the metabolic activity of cells in the temporomandibular joint: a systematic review.Clinical oral investigations · 2018Pooled it
- BAP31 Drives Cartilage Calcification through Disruption of Autophagosome-Lysosome Fusion in Osteoarthritis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- PF4 drives mechanical overload-induced temporomandibular joint osteoarthritis through TLR2-dependent activation of NF-κB.Journal of translational medicine · 2026Article
- FGF19 promotes cartilage destruction in the progress of temporomandibular joint osteoarthritis.Cell and tissue research · 2026Article
- Activation of SLIT2/ROBO1/LRP6 axis aggravates cartilage degradation via β-catenin signaling in TMJOA.JCI insight · 2026Article
- OX40L in endothelial cells promotes temporomandibular joint subchondral bone angiogenesis and osteoclastogenesis in mice.Bone & joint research · 2026Article
- RNF152-mediated, ubiquitin-dependent degradation of HSP27 activates the PI3K/AKT pathway, driving synovial inflammatory cascades in TMJOA.Arthritis research & therapy · 2025Article
- USP32 promotes temporomandibular joint osteoarthritis by modulating PKM2 stability and glycolytic metabolism in chondrocytes.Cell death & disease · 2025Article
- Preclinical perspectives on disorders of the temporomandibular joint: Tracing the past, navigating the present, and shaping the future.The journal of pain · 2025Review
- Orosomucoid 1 Ameliorates Temporomandibular Joint Osteoarthritis by Maintaining Cartilage Homeostasis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Targeted soluble epoxide hydrolase inhibits M1 macrophage polarization to improve cartilage injury in temporomandibular joint osteoarthritis.Journal of translational medicine · 2025Article
- Development of animal model for anterior open bite and mechanism of temporomandibular joint morphological change: an implication for MAC surgery.BMC oral health · 2025Article
- Comparative review: clinical and pathological heterogeneity in kneeFrontiers in bioengineering and biotechnology · 2025Review
- Adipose tissue-derived extracellular vesicles aggravate temporomandibular joint osteoarthritis associated with obesity.Clinical and translational medicine · 2024Article
- Lysosomal destabilization: A missing link between pathological calcification and osteoarthritis.Bioactive materials · 2024Article
- Critical signaling molecules in the temporomandibular joint osteoarthritis under different magnitudes of mechanical stimulation.Frontiers in pharmacology · 2024Review
- Expressions of parathyroid hormone-related protein (PTHrP) and parathyroid hormone receptor-1 (PTH1R) in the condylar cartilage of temporomandibular joint modulated by occlusal elevation.Journal of dental sciences · 2023Article
- Intra-articular treatment of temporomandibular joint osteoarthritis by injecting actively-loaded meloxicam liposomes with dual-functions of anti-inflammation and lubrication.Materials today. Bio · 2023Article
- Zonal interdependence in the temporomandibular joint cartilage.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- Spinal CCK1 Receptors Contribute to Somatic Pain Hypersensitivity Induced by Malocclusion via a Reciprocal Neuron-Glial Signaling Cascade.The journal of pain · 2022Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
Abstract
objectiveTo investigate whether mechanical stress induces mineral deposits that contribute to matrix degradation at the onset of osteoarthritis (OA) in temporomandibular joint (TMJ) cartilage.
designFemale Spraguee-Dawley rats were subjected to an unilateral anterior crossbite (UAC) procedure. Histology, electron microscopy, and energy dispersive spectrometer (EDS) were used to examine cartilage matrix structures and composition of mineral deposit in the affected TMJ cartilage. Protein and/or RNA expression of phenotypic markers and mineralization modulators and matrix degradation was analyzed by immunohistochemistry and/or real-time PCR. Synthetic basic calcium phosphate (BCP) and calcium pyrophosphate dehydrate (CPPD) crystals were used to stimulate ATDC5 cells for their impact on cell differentiation and gene expression.
resultsFragmented and disorganized collagen fibers, expanded fibrous spaces, and enhancement of matrix vesicle production and mineral deposition were observed in matrices surrounding hypertrophic chondrocytes in cartilage as early as 2-weeks post-UAC and exacerbated with time. The mineral deposits in TMJ cartilage at 12- and 20-weeks post-UAC had Ca/P ratios of 1.42 and 1.44, which are similar to the ratios for BCP. The expression of mineralization inhibitors, NPP1, ANK, CD73, and Matrix gla protein (MGP) was decreased from 2 to 8 weeks post-UAC, so were the chondrogenic markers, Col-2, Col-X and aggrecan. In contrast, the expression of tissue-nonspecific alkaline phosphatase (TNAP) and MMP13 was increased 4-weeks post-UAC. Treating ADTC5 cells with BCP crystals increased MMPs and ADAMTS5 expression, but reduced matrix production in a time-dependent manner.
conclusionUAC induces deposition of BCP-like minerals in osteoarthritic cartilage, which can stimulate matrix degradation by promoting the expression of cartilage-degrading enzymes to facilitate OA progression.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.