ArticleArthritis research & therapy2025
Akt2 inhibition alleviates temporomandibular joint osteoarthritis by preventing subchondral bone loss.
Article in Arthritis research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Research progress on cellular senescence in the pathogenesis and treatment of osteoarthritis and temporomandibular joint osteoarthritis.Journal of oral & facial pain and headache · 2026Review
- Dental Pulp Stem Cell-Derived Extracellular Vesicles Attenuated Chondrocyte Apoptosis in Early Temporomandibular Joint Osteoarthritis via Regulating Hexokinase 2.Biomolecules · 2026Article
- Dental Pulp Stem Cell-Derived Intracellular Vesicles Promote Cartilage Regeneration and Alleviate Pain in Temporomandibular Joint Osteoarthritis.International dental journal · 2026Article
- The gut‑bone‑cartilage triad: Microbial regulation of the Wnt/β‑catenin signaling pathway in osteoarthritis joint remodeling (Review).Molecular medicine reports · 2026Review
- Senescent bone marrow mesenchymal stem cells exacerbate subchondral bone sclerosis and osteoarthritis via the senescence-associated secretory phenotype.Stem cell research & therapy · 2025Article
- Combined multi-omics approach to identify the key metabolites, key microorganisms and biomarkers correlated with the neutrophil extracellular traps-associated gene TIMP1 in osteoarthritis.Frontiers in pharmacology · 2025Article
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6 authors.
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Abstract
backgroundThis study aimed to investigate the role and mechanism of the Akt2 pathway in different stages of anterior disc displacement (ADD)-induced temporomandibular joint osteoarthritis (TMJOA).
methodsA rat model for TMJOA that simulates anterior disc displacement was established. For inhibit Akt2 expression in subchondral bone, rats were intravenously injected with adeno-associated virus carrying Akt2 shRNA at a titer of 1 × 10
resultsIn the rat model of ADD-induced TMJOA, rapid condylar bone loss occurred with increased phosphorylation of Akt2 in subchondral bone macrophages within 1 week post-surgery. At 8 weeks after surgery, abnormal remodeling of subchondral bone and degenerative changes in cartilage were observed. Inhibiting Akt2 reduced condylar bone resorption following ADD surgery while improving condylar bone morphology at 8 weeks post-surgery. Additionally, inhibition of Akt2 alleviated cartilage degeneration characterized by a decreased number of apoptotic chondrocytes, reduced expression of matrix metalloproteinases, and increased collagen type II expression in cartilage tissue.
conclusionsThe Akt2 pathway is activated mainly in subchondral bone macrophages during the early stage of ADD and plays an important role in regulating subchondral bone remodeling. Inhibition of Akt2 could serve as a prophylactic treatment to slow the progression of ADD-induced TMJOA.
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