ArticleJournal of dental research2013
Bis-enoxacin inhibits bone resorption and orthodontic tooth movement.
Article in Journal of dental research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 17 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
- Experimental evidence of pharmacological management of anchorage in Orthodontics: A systematic review.Dental press journal of orthodontics · 2015Pooled it
- Inhibition of osteoclastogenesis after bisphosphonate therapy discontinuation: an in vitro approach.Journal of molecular histology · 2022Article
- The New Face of a Well-Known Antibiotic: A Review of the Anticancer Activity of Enoxacin and Its Derivatives.Cancers · 2022Review
- Bisphosphonate-enoxacin inhibit osteoclast formation and function by abrogating RANKL-induced JNK signalling pathways during osteoporosis treatment.Journal of cellular and molecular medicine · 2021Article
- The V-ATPaseInternational journal of molecular sciences · 2021Review
- Selective toxicity of antibacterial agents-still a valid concept or do we miss chances and ignore risks?Infection · 2021Review
- Membrane Transport Proteins in Osteoclasts: The Ins and Outs.Frontiers in cell and developmental biology · 2021Review
- Specialized Roles for Actin in Osteoclasts: Unanswered Questions and Therapeutic Opportunities.Biomolecules · 2019Review
- Enoxacin and bis-enoxacin stimulate 4T1 murine breast cancer cells to release extracellular vesicles that inhibit osteoclastogenesis.Scientific reports · 2018Article
- Vacuolar HBiotarget · 2017Article
- Exosomes: novel regulators of bone remodelling and potential therapeutic agents for orthodontics.Orthodontics & craniofacial research · 2017Review
- Key Triggers of Osteoclast-Related Diseases and Available Strategies for Targeted Therapies: A Review.Frontiers in medicine · 2017Review
- The Beneficial Effects of Bisphosphonate-enoxacin on Cortical Bone Mass and Strength in Ovariectomized Rats.Frontiers in pharmacology · 2017Article
- The Potential Use of Pharmacological Agents to Modulate Orthodontic Tooth Movement (OTM).Frontiers in physiology · 2017Review
- Covalent Immobilization of Enoxacin onto Titanium Implant Surfaces for Inhibiting Multiple Bacterial Species Infection and In Vivo Methicillin-Resistant Staphylococcus aureus Infection Prophylaxis.Antimicrobial agents and chemotherapy · 2017Article
- Periodontitis in rats induces systemic oxidative stress that is controlled by bone-targeted antiresorptives.Journal of periodontology · 2015Article
- Article
Corrections and comments
- Erratum issuedGuiterrez, A [Corrected to Gutierrez, A]
Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
Abstract
unlabelledEnoxacin inhibits binding between the B-subunit of vacuolar H(+)-ATPase (V-ATPase) and microfilaments, and also between osteoclast formation and bone resorption in vitro. We hypothesized that a bisphosphonate derivative of enoxacin, bis-enoxacin (BE), which was previously studied as a bone-directed antibiotic, might have similar activities. BE shared a number of characteristics with enoxacin: It blocked binding between the recombinant B-subunit and microfilaments and inhibited osteoclastogenesis in cell culture with IC50s of about 10 µM in each case. BE did not alter the relative expression levels of various osteoclast-specific proteins. Even though tartrate-resistant acid phosphatase 5b was expressed, proteolytic activation of the latent pro-enzyme was inhibited. However, unlike enoxacin, BE stimulated caspase-3 activity. BE bound to bone slices and inhibited bone resorption by osteoclasts on BE-coated bone slices in cell culture. BE reduced the amount of orthodontic tooth movement achieved in rats after 28 days. Analysis of these data suggests that BE is a novel anti-resorptive molecule that is active both in vitro and in vivo and may have clinical uses. ABBREVIATIONS: BE, bis-enoxacin; V-ATPase, vacuolar H(+)-ATPase; TRAP, tartrate-resistant acid phosphatase; αMEM D10, minimal essential media, alpha modification with 10% fetal bovine serum; SDS-PAGE, sodium dodecyl sulfate-polyacrylamide gel electrophoresis; RANKL, receptor activator of nuclear factor kappa B-ligand; NFATc1, nuclear factor of activated T-cells; ADAM, a disintegrin and metalloprotease domain; OTM, orthodontic tooth movement.
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Identifiers
What OpenQuestion holds
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.