ReviewFrontiers in cell and developmental biology2026
Periodontium-derived fibroblasts as a model to evaluate inflammation and pharmacological modulation of osteogenesis and osteoclast formation.
Review in Frontiers in cell and developmental biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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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Who cites it
2 citing papers in PubMed.
- Osteogenic differentiation of gingival and periodontal ligament fibroblasts inhibits osteoclast formation in 2D and 3D fibrin cultures.Bone reports · 2026Article
- Natural Polysaccharide-Mediated Nano-Delivery Systems for Osteoporosis Therapy From a Gut-Bone Axis Regulatory Perspective.Advanced healthcare materials · 2026Review
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Authors and funding
4 authors.
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Abstract
Two anatomically and functionally distinct populations of periodontium-derived fibroblasts can be identified: gingiva fibroblasts (GFs), which originate from the soft connective tissue of the gingiva and support epithelial attachment and tissue integrity, and periodontal ligament fibroblasts (PDLFs), which produce collagenous fibers that anchor teeth within the alveolar bone socket. Both cell types can contribute to osteogenesis when cultured in the presence of mineralization medium, and both cell types can drive osteoclast formation when co-cultured with osteoclast precursors. Under inflammatory conditions such as periodontitis, this balance is disturbed, leading to more osteoclast-driven bone resorption. The model system of osteogenesis and osteoclastogenesis can be used to further dissect the contributing factors of periodontitis by incorporating bacteria or their components like TLR agonists. Chronic inflammation can further be mimicked by using inflammatory cytokines such as IL-1β, TNF-α and Activin-A. Furthermore, bone anabolic and (anti-)catabolic medications such as parathyroid hormone (PTH), anti-TGF-β, sclerostin and anti-sclerostin can be used to investigate their effects on both osteogenesis and osteoclastogenesis. This platform is ideal for studying the effect of medication used in comorbidities of periodontitis, such as rheumatoid arthritis (RA; e.g., anakinra, infliximab) and diabetes (e.g., metformin), which have all been shown to inhibit osteoclast formation. The osteogenesis culture system can be manipulated over time, making it an ideal system for studying how the osteogenic stage of periodontium-derived fibroblasts affects subsequent osteoclast formation. Finally, fibroblast-based three-dimensional (3D) culture systems provide physiologically relevant environments that capture spatial cell-matrix interactions essential for hard and soft tissue repair in periodontal tissue regeneration. Collectively, these models help bridge
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