ArticleBioMed research international2017
Decreased Expression of Semaphorin3A/Neuropilin-1 Signaling Axis in Apical Periodontitis.
Article in BioMed research international, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 43 citations in OpenAlex.
- Probiotic Potential of Lactobacillus and Enterococcus Strains Isolated From the Faecal Microbiota of Critically Endangered Hangul Deer (Cervus hanglu hanglu): Implications for Conservation Management.Probiotics and antimicrobial proteins · 2025Article
- Identification of JNK-JUN-NCOA axis as a therapeutic target for macrophage ferroptosis in chronic apical periodontitis.International journal of medical sciences · 2025Article
- Neuro-bone tissue engineering: emerging mechanisms, potential strategies, and current challenges.Bone research · 2023Review
- Neuronal Guidance Molecules in Bone Remodeling and Orthodontic Tooth Movement.International journal of molecular sciences · 2022Review
- Semaphorin 3A mitigates lipopolysaccharide-induced chondrocyte inflammation, apoptosis and extracellular matrix degradation by binding to Neuropilin-1.Bioengineered · 2021Article
- Plasma Rich in Growth Factors in the Treatment of Endodontic Periapical Lesions in Adult Patients: A Narrative Review.Pharmaceuticals (Basel, Switzerland) · 2021Review
- A Potential Role of Semaphorin 3A during Orthodontic Tooth Movement.International journal of molecular sciences · 2021Article
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apical periodontitis (AP) is a chronic infection of endodontic origin accompanied with bone destruction around the apical region. Semaphorin3A (Sema3A) and neuropilin-1 (Nrp1) are regarded as a pair of immune regulators in bone metabolism. In this study, we firstly investigated the expression pattern of Sema3A/Nrp1 in apical periodontitis and its correlation with bone destruction. Using rat animal model, we analysed the level of mandibular bone destruction and the expression of Sema3A/Nrp1 on days 0, 7, 14, 21, 28, and 35 after pulp exposure. In addition, clinical samples from apical periodontitis patients were obtained to analyse the expression of Sema3A/Nrp1. These results indicated that the bone destruction level expanded from days 7 to 35. The number of positive cells and level of mRNA expression of Sema3A/Nrp1 were significantly decreased from days 7 to 35, with a negative correlation with bone destruction. Moreover, expression of Sema3A/Nrp1 in the AP group was reduced compared to the control group of clinical samples. In conclusion, decreased expression of Sema3A/Nrp1 was observed in periapical lesions and is potentially involved in the bone resorption of the periapical area, suggesting that Sema3A/Nrp1 may contribute to the pathological development of apical periodontitis.
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