ArticleFrontiers in oral health2023
The protective role of CD73 in periodontitis: preventing hyper-inflammatory fibroblasts and driving osteoclast energy metabolism.
Article in Frontiers in oral health, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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.
The trial behind it
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
6 citing papers in PubMed, 6 citations in OpenAlex.
- Palmitate drives mitochondrial and ER stress through disruption of the CD73-Adenosine axis.Research square · 2026Article
- Patients with periodontal disease demonstrates changes in purinergic and inflammatory markers in PBMCs, serum and saliva.Purinergic signalling · 2025Article
- Article
- Hypoxia-inducible Factor 1α Contributes to Matrix Metalloproteinases 2/9 and Inflammatory Responses in Periodontitis.Cell biochemistry and biophysics · 2025Article
- Mitochondrial function in oral health and disease.Journal of immunological methods · 2024Review
- CD73: agent development potential and its application in diabetes and atherosclerosis.Frontiers in immunology · 2024Review
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Introduction: Periodontitis is an immune-mediated inflammatory disease affecting almost half of the adult population and is the leading cause of tooth loss in the United States. The role of extracellular nucleotide signaling including nucleotide metabolizing enzyme CD73 adds an important layer of interaction of purine mediators capable of orchestrating inflammatory outcomes. CD73 is able to catabolize 5'-adenosine monophosphate into adenosine at the extracellular level, playing a critical role in regulating many processes under physiological and pathological conditions. Here, we explored the role of CD73 in ligature-induced periodontitis Methods: We assessed gingival levels of inflammatory cytokines Results: Our results in mice show that lack of CD73 resulted in increased inflammatory cytokines and chemokines such as IL-1β, IL-17, Cxcl1 and Cxcl2 in diseased gingiva relative to the healthy-controls and in comparison with the wild type. CD73-deficient gingival fibroblasts also manifested a defective healing response with higher MMP-13 levels. CD73-deficient animals also showed increased osteoclastogenesis Conclusion: In conclusion, CD73 appears to play a protective role in the gingival periodontal tissue and bone homeostasis, regulating hyper-inflammatory state of stromal fibroblasts and osteoclast energy metabolism and being an important candidate for future target therapies to prevent or control immune-mediated inflammatory and osteolytic diseases.
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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.