ArticleScientific reports2025
Anti-VEGF neutralizing antibody delays osteomucosal healing by reducing collagen formation in mice.
Article in Scientific reports, 2025. 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.
- Comments on 'Bisphosphonate and statin: adverse effects of co-medication on wound healing in in vitro models of periodontal tissues'.Acta odontologica Scandinavica · 2026Article
- Plasma-Activated Water as a Novel Irrigation Strategy for Seawater-Immersed Burn Wounds: Antibacterial Activity and Healing Promotion in Rats.Biomedicines · 2026Article
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Authors and funding
12 authors.
Funding
Abstract
Medication-related osteonecrosis of the jaw (MRONJ) is a detrimental side effect in patients undergoing treatment with antiresorptive agents. The anti-angiogenic agent, bevacizumab (anti-VEGF antibody (Ab)), has also been reported to be associated with MRONJ. However, the role of anti-VEGF Ab in MRONJ development, especially under conditions of pre-existing inflammation, remains elusive. This study examined anti-VEGF Ab effects on bone necrosis and osteomucosal healing, with or without pre-inflammation. Forty mice received biweekly i.p. injections of anti-VEGF Ab (10 mg/kg) or saline (Veh). For the tooth extraction (TE) model (n = 10), maxillary first molars were extracted. For the ligature-induced periodontitis and tooth extraction (LIP-TE) model (n = 10), maxillary second molars were ligated with 5-0 silk for 8 weeks before extraction. Mice were euthanized after 3 weeks of post-extraction healing. In both TE and LIP-TE models, anti-VEGF Ab-treated mice showed delayed osteomucosal healing with diminished bone formation, lower CD31 and collagen III expression, and increased osteoclast numbers than Veh-treated mice. There was no significant difference in necrotic bone areas. IL-23- or IL-17-producing cell numbers remained unchanged in both Veh- and anti-VEGF Ab-treated mice. Anti-VEGF Ab delayed osteomucosal healing by reducing collagen production in the presence or absence of pre-inflammatory conditions, without causing bone necrosis. Our data suggest anti-VEGF Ab delays osteomucosal wound healing but does not cause bone necrosis alone.
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