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Celecoxib treatment dampens LPS‐induced periapical bone resorption in a mouse model

Petean, I. B. F. ; Almeida‐Junior, L. A. ; Arnez, M. F. M. ; Queiroz, A. M. ; Silva, R. A. B ; Silva, L. A. B. ; Faccioli, L. H. ; Paula‐Silva, F. W. G.

International endodontic journal, 2021-08, Vol.54 (8), p.1289-1299 [Periódico revisado por pares]

Chichester: Wiley Subscription Services, Inc

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  • Título:
    Celecoxib treatment dampens LPS‐induced periapical bone resorption in a mouse model
  • Autor: Petean, I. B. F. ; Almeida‐Junior, L. A. ; Arnez, M. F. M. ; Queiroz, A. M. ; Silva, R. A. B ; Silva, L. A. B. ; Faccioli, L. H. ; Paula‐Silva, F. W. G.
  • Assuntos: Acid phosphatase ; Acid phosphatase (tartrate-resistant) ; apical periodontitis ; bacterial lipopolysaccharide ; Bone resorption ; Cathepsin K ; Celecoxib ; ciclo‐oxygenase‐1 ; ciclo‐oxygenase‐2 ; Dentistry ; Gene expression ; Gum disease ; Immunohistochemistry ; Indomethacin ; Inhibitor drugs ; K gene ; Lipopolysaccharides ; Molars ; Osteoclasts ; Osteoprotegerin ; Periodontitis ; Polymerase chain reaction ; Prostaglandin endoperoxide synthase ; Reverse transcription ; Rodents ; Root canals ; TRANCE protein
  • É parte de: International endodontic journal, 2021-08, Vol.54 (8), p.1289-1299
  • Notas: ObjectType-Article-1
    SourceType-Scholarly Journals-1
    ObjectType-Feature-2
    content type line 23
  • Descrição: Aim To evaluate the efficacy of selective and nonselective inhibitors of cyclooxygenase‐2 enzymes in the treatment of experimental apical periodontitis induced by bacterial lipopolysaccharide (LPS) in vivo in a mouse model. Methodology Thirty‐six C57BL/6 mice were used. After access cavity preparation, a solution containing E. coli LPS (1.0 µg µL−1) was inoculated into the root canals of the mandibular and maxillary right first molars (n = 72) After 30 days, apical periodontitis was established and the animals were systemically treated with celecoxib, a selective COX‐2 inhibitor (15 mg kg−1), or indomethacin, a nonselective COX‐2 inhibitor (5 mg kg−1), for 7 and 14 days. Blocks containing teeth and bone were removed for histopathological and histometric analyses (haematoxylin and eosin), evaluation of osteoclasts numbers (tartrate‐resistant acid phosphatase enzyme – TRAP) and immunohistochemistry for RANK, RANKL and OPG. Gene expression was performed using reverse transcription and real‐time polymerase chain reaction (qRT‐PCR) for RANK, RANKL, OPG, TRAP, MMP‐9, cathepsin K and calcitonin receptor. Histopathological, histometric, TRAP, immunohistochemistry and qRT‐PCR data were evaluated using Kruskal–Wallis followed by Dunn’s test (α = 0.05). Results Systemic administration of celecoxib for 7 and 14 days prevented periapical bone resorption (P < 0.0001), differently from indomethacin that exacerbated bone resorption at 7 days (P < 0.0001) or exerted no effect at 14 days (P = 0.8488). Celecoxib treatment reduced osteoclast formation in apical periodontitis, regardless of the period of treatment (P < 0.0001 for 7 days and P = 0.026 for 14 days). Administration of celecoxib or indomethacin differentially modulated the expression of genes involved in bone resorption. At 7 days, celecoxib and indomethacin treatment significantly inhibited expression of mRNA for cathepsin K (P = 0.0005 and P = 0.016, respectively) without changing TRAP, MMP‐9 and calcitonin receptor gene expression. At 14 days, celecoxib significantly inhibited expression of mRNA for MMP‐9 (P < 0.0001) and calcitonin receptor (P = 0.004), whilst indomethacin exerted no effect on MMP‐9 (P = 0.216) and calcitonin receptor (P = 0.971) but significantly augmented cathepsin K gene expression (P = 0.001). Conclusions The selective COX‐2 inhibitor celecoxib reduced osteoclastogenic signalling and activity that dampened bone resorption in LPS‐induced apical periodontitis in mice, with greater efficacy than the nonselective inhibitor indomethacin.
  • Editor: Chichester: Wiley Subscription Services, Inc
  • Idioma: Inglês
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  • Realização: ABCD-USP USP   Logos de Redes Sociais: Freepik

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