Erschienen in:
01.04.2021 | Original Article
Effect of non-steroidal anti-inflammatory drugs on pulpal and periapical inflammation induced by lipopolysaccharide
verfasst von:
Fernanda Regina Ribeiro-Santos, Maya Fernanda Manfrin Arnez, Marcio Santos de Carvalho, Raquel Assed Bezerra da Silva, Marília Pacífico Lucisano Politi, Alexandra Mussolino de Queiroz, Paulo Nelson-Filho, Léa Assed Bezerra da Silva, Lúcia Helena Faccioli, Francisco Wanderley Garcia Paula-Silva
Erschienen in:
Clinical Oral Investigations
|
Ausgabe 11/2021
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Abstract
Objectives
The 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 methods
A 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.
Results
Inoculation 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.
Conclusions
NSAIDs 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.