ArticleJournal of nanobiotechnology2025
Porphyromonas gingivalis extracellular vesicles exacerbated osteoporosis by disrupting osteoblast mitochondrial dynamics and inhibiting Cpt2-regulated fatty acid oxidation.
Article in Journal of nanobiotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed.
- Lysine-specific demethylase 3A (KDM3A) protects against ovarian dysfunction in premature ovarian insufficiency by transcriptional activation of ATP-binding cassette sub-family A member 7 (ABCA7)-mediated mitochondrial homeostasis.Molecular biomedicine · 2026Article
- ApiRegenin, an Animal-Derived Platelet-Rich Plasma Extract, Accelerates Wound Healing of Chronic Diabetic Ulcer in Mice.Pharmaceutics · 2026Article
- Marrow fatty acids in osteoporosis: metabolic insights, emerging therapeutic targets.Journal of bone and mineral metabolism · 2026Review
- Porphyromonas gingivalis-derived extracellular vesicles aggravate bone destruction in rheumatoid arthritis by promoting Syk-dependent osteoclastogenesis.International journal of oral science · 2026Article
- Biological properties and potential pathogenic mechanisms of oral bacterial-derived extracellular vesicles in oral and systemic diseases.Extracellular vesicles and circulating nucleic acids · 2026Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
backgroundRecent studies have implicated periodontitis (PD) as a potential risk factor for osteoporosis; however, the precise mechanisms remain unclear. Porphyromonas gingivalis (Pg), a key pathogen associated with PD, can secrete extracellular vesicles (EVs). However, whether Pg EVs can be transported to the bone marrow and influence osteoporosis-related osteoblast differentiation warrants exploration. This study compares Pg EVs with EVs from Porphyromonas endodontalis (Pe), which is a less virulent congener but the evidence for its pathogenicity in PD is weak.
resultsPg EVs can be translocated into the marrow of mice and be internalized by osteoblasts through clathrin- and lipid raft-mediated endocytosis, thereby exacerbating osteoporosis. Pg EVs promote mitochondrial fission and inhibit mitochondrial fusion, leading to mitochondrial fragmentation, impaired mitochondrial activity and suppressed osteogenic differentiation. Furthermore, Pg EVs downregulate the protein level of carnitine palmitoyl transferase 2 (Cpt2) and inhibit fatty acid oxidation (FAO) by disrupting mitochondrial dynamics, which impairs osteoblast ATP production and exacerbates osteoporosis. The effects of Pe EVs are similar but weaker than those of Pg EVs.
conclusionsThis study elucidates that Pg EVs exacerbate osteoporosis by disrupting osteoblast mitochondrial dynamics and suppressing Cpt2-regulated FAO. This study contributes to understanding of the etiological mechanisms through which Pg contributes to the progression of osteoporosis and highlights the pivotal role of EVs in the association between periodontal disease and systemic diseases.
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