ArticlePloS one2026
Single-cell RNA sequencing of healthy and diseased rat temporomandibular joint condyle cartilage.
Article in PloS one, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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6 authors.
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Abstract
Osteoarthritis is a degenerative joint disease that disrupts the cellular homeostasis within cartilage tissues, promoting further disease progression that can lead to debilitating pain. Cartilage of the temporomandibular joint (TMJ) is unique among diarthrodial joints because they are of neural crest origin, rather than the mesoderm germ layer. TMJ cartilage also has different cellular architecture, where it is composed of a superficial fibrous layer, a proliferative layer, and a fibrocartilage layer overlying subchondral bone. Understanding of the cytopathological changes that occur during TMJ osteoarthritis (TMJOA) could potentiate therapies to mitigate disease progression and repair diseased tissues. Here, we analyzed the unique cell populations present in healthy and OA-induced condylar cartilage of adult rats through single-cell RNA-sequencing. TMJOA was established via our previous rat model to study the changes in the cellular composition of the condyle in response to OA. Several cell types could be uniquely identified, and the prominent matrix producing cells were fibroblasts and chondrocyte subsets. Our trajectory and pseudotime analysis revealed three cell fates stemming from a fibrochondrocyte-like population and two chondrocyte cell fates that stem from a shared progenitor population. We also found that Pleiotrophin is uniquely expressed in the proliferative zone by cells with a chondrocyte progenitor phenotype. In OA cartilage, differential gene expression in the fibroblast group revealed responses to inflammation, possibly through activation of chondrocyte differentiation. The chondrocyte group was highly metabolically active, indicative of rapid repair or remodeling. Cell-cell signaling analysis revealed that chondrocyte and chondrocyte progenitor communication became highly activated. Additionally, intracellular pathways that may contribute to cellular dysfunction and tissue remodeling were highly active, while pathways related to tissue catabolism appeared less active.
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