ArticleClinical oral investigations2021
Effect of non-steroidal anti-inflammatory drugs on pulpal and periapical inflammation induced by lipopolysaccharide.
Article in Clinical oral investigations, 2021. 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, 15 citations in OpenAlex.
- The effect of low-dose aspirin on aspirin triggered lipoxin, interleukin 1 beta, and prostaglandin E2 levels in periapical fluid: a double-blind randomized clinical trial.BMC oral health · 2023Trial
- Apical Periodontitis May Exacerbate Ulcerative Colitis via Neutrophil Extracellular Trap-Mediated Systemic Inflammation and Intestinal Barrier Disruption in Mice.International endodontic journal · 2026Article
- Inflammation-responsive biomimetic hybrid nanovesicles reverse stem cell senescence by up-regulating SIRT1 to treat periodontitis.Journal of nanobiotechnology · 2026Article
- Bilayer gelatin-methacryloyl scaffold for pulp inflammation suppression and dentin-like tissue regeneration.Journal of controlled release : official journal of the Controlled Release Society · 2026Article
- Genetic insights into the relationship between anti-inflammatory drug target genes and oral diseases.Inflammopharmacology · 2025Article
- Expression patterns of mechanosensitive ion channel PIEZOs in irreversible pulpitis.BMC oral health · 2024Article
- Systemic inhibition of 5-lipoxygenase by MK-886 exacerbates apical periodontitis bone loss in a mouse model.BMC oral health · 2023Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesThe objective of this study was to evaluate the effect of non-steroidal anti-inflammatory drugs (NSAIDs) in controlling pulpal and periapical inflammation in vivo as a potential coadjutant systemic therapy for pulpitis. MATERIALS AND
methodsA suspension containing E. coli lipopolysaccharide (LPS; 1.0 μg/μL) was inoculated into the pulp chamber of the first molars of C57BL/6 mice (n = 72), and the animals were treated daily with indomethacin or celecoxib throughout the experimental periods. After 7, 14, 21, and 28 days, the tissues were removed for histopathological, histoenzymology, histometric, and immunohistochemical evaluation.
resultsInoculation of LPS into the pulp chamber induced the synthesis of the enzyme cyclooxygenase-2 (COX-2) in dental pulp and periapical region. Indomethacin and celecoxib treatment changed the profile of inflammatory cells recruited to dental pulp and to the periapex, which was characterized by a higher mononuclear cell infiltrate, compared to LPS inoculation alone which recruited a higher amount of polymorphonuclear neutrophils. Administration of indomethacin for 28 days resulted in the development of apical periodontitis and increased osteoclast recruitment, unlike celecoxib.
conclusionsNSAIDs indomethacin and celecoxib changed the recruitment of inflammatory cells to a mononuclear profile upon inoculation of LPS into the pup chamber, but indomethacin enhanced periapical bone loss whereas celecoxib did not. CLINICAL RELEVANCE: Celecoxib, a selective COX-2 inhibitor, can change the profile of inflammatory cells recruited to the dental pulp challenged with LPS and might a be potential systemic coadjutant for treatment of pulpitis.
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