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dc.contributor.authorHerrera, Bruno Schneider-
dc.contributor.authorCoimbra, Leila Santana-
dc.contributor.authorSilva, Agatha Ribeiro da-
dc.contributor.authorTeixeira, Simone Aparecida-
dc.contributor.authorCosta, Soraia Katia Pereira-
dc.contributor.authorWallace, John Lawrence-
dc.contributor.authorSpolidorio, Luis Carlos-
dc.contributor.authorMuscara, Marcelo Nicolas-
dc.identifier.citationMedical Gas Research, v. 5, n. 4, p. 1-9, 2015.-
dc.description.abstractBackground: In experimental periodontitis, non-steroidal antiinflammatory drugs (NSAIDs) effectively inhibit the resultant alveolar bone loss. However, their deleterious gastric effects, observed in both animals and humans, dramatically limit their long-term use. It has been proven that the addition of a hydrogen sulfide (H2S)-releasing moiety to classical NSAID structures results in antiinflammatory compounds with improved gastric safeness. In this way, we decided to compare the effects of naproxen with its H2S-releasing derivative ATB-346 on ligature-induced periodontitis in rats. Methods: Male Holtzman rats had a cotton ligature placed subgingivally around the lower right first molar during 7 days. During this period, groups of animals were daily treated with Na2S (a spontaneous H2S donor) or equimolar oral doses of naproxen (10 mg/kg) or ATB-346 (16 mg/kg). The mandibles were finally collected for histological analysis, radiographical measurements of alveolar bone loss and micro-computed tomography (μCT) analysis. Interleukin (IL)-1β, IL-6 and IL-10 were quantified in gingiva samples, and the stomachs were also collected for scoring of tissue damage and measurement of myeloperoxidase (MPO, a marker of granulocyte infiltration). Results: Ligature-induced bone loss was significantly inhibited by all the treatments, although only ATB-346 treatment resulted in significant inhibition of bone defect and other histological characteristics (such as flatness of the gingival epithelium, chronic inflammatory cell infiltration and loss of connective tissue in the gingival papillae). Both naproxen and ATB-346 inhibited the increase of gingival IL-1β and IL-6 secondary to periodontitis, but IL-10 was unaffected. Significant damage and increased MPO contents were only found in the stomachs of the naproxen-treated animals. Conclusion: The H2S-releasing moiety in the ATB-346 compound not only does not impair the effects of the parent naproxen on periodontitis, but also improves bone quality and prevents the gastric mucosa damage due to prostaglandin inhibition, thus configuring a potentially new adjuvant therapy for periodontal diseases.en
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)-
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)-
dc.sourceCurrículo Lattes-
dc.subjectBone lossen
dc.subjectH2S-releasing NSAIDen
dc.titleThe H2S-releasing naproxen derivative, ATB-346, inhibits alveolar bone loss and inflammation in rats with ligature-induced periodontitisen
dc.contributor.institutionUniversidade de São Paulo (USP)-
dc.contributor.institutionUniversidade Estadual Paulista (UNESP)-
dc.contributor.institutionUniversity of Toronto-
dc.description.affiliationUniversidade Estadual Paulista Júlio de Mesquita Filho, Departamento de Fisiologia e Patologia, Araraquara, RUA HUMAITA, 1680, CENTRO, CEP 14801903, SP, Brasil-
dc.description.affiliationDepartment of Pharmacology, Institute of Biomedical Sciences, University of Sao Paulo (USP), Sao Paulo, SP, Brazil-
dc.description.affiliationDepartment of Pharmacology and Toxicology, University of Toronto, Toronto, ON, Canada-
dc.description.affiliationUnespUniversidade Estadual Paulista Júlio de Mesquita Filho, Departamento de Fisiologia e Patologia, Araraquara, RUA HUMAITA, 1680, CENTRO, CEP 14801903, SP, Brasil-
dc.rights.accessRightsAcesso aberto-
dc.relation.ispartofMedical Gas Research-
Appears in Collections:Artigos, TCCs, Teses e Dissertações da Unesp

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