Mast cells contribute to alveolar bone loss in Spontaneously Hypertensive Rats with periodontal disease regulating cytokines production

Autor(es)

Balera Brito, Victor Gustavo ^{[1, 2]} ; Patrocinio, Mariana Sousa ^[1] ; Linjardi Sousa, Maria Carolina ^[1] ; Alves Barreto, Ayna Emanuelli ^{[1, 2]} ; Tfaile Frasnelli, Sabrina Cruz ^[1] ; Lara, Vanessa Soares ^[3] ; Santos, Carlos Ferreira ^[4] ; Penha Oliveira, Sandra Helena ^{[1, 2]}

Afiliação do(s) autor(es)

^[1] Sao Paulo State Univ, UNESP, Sch Dent, Dept Basic Sci, Aracatuba, SP - Brazil

^[2] Sao Paulo State Univ, UNESP, Sch Dent, SBFis, Programa Multicentr Posgrad Ciencias Fisiol, Aracatuba, SP - Brazil

^[3] Univ Sao Paulo, Bauru Sch Dent, Dept Biol Sci, Sao Paulo, SP - Brazil

^[4] Univ Sao Paulo, Bauru Sch Dent, Dept Stomatol, Sao Paulo, SP - Brazil

• Tipo de documento: Artigo Científico
• Fonte: PLoS One; v. 16, n. 3 MAR 4 2021.
• Citações Web of Science: 0

Resumo

Mast cells (MCs) play a pivotal role in inflammatory responses and had been studied in inflammatory bone disorders, however, their role in alveolar bone loss induced by periodontal disease (PD) is not yet fully understood. We, therefore, aimed to evaluate the effects of MCs depletion in the PD-induced alveolar bone loss in Wistar (W) and Spontaneously Hypertensive Rats (SHRs). PD was induced by ligating the lower first molars with silk thread one day after the MCs depletion, by the pre-treatment with compound 48/80 for 4 days. After 15 days of PD induction, the hemi-mandibles were surgically collected for qRT-PCR, histological analyses, immunostaining, and ELISA. Systolic blood pressure (SBP) was verified by tail plethysmography to confirm the hypertensive status, and SHR presented SBP >150 mmHg, and previous MC depletion alone or associated with PD did not alter this parameter. SHRs showed a more severe alveolar bone loss compared to W, and MC depletion significantly inhibited this response in both strains, with a more significant response in SHRs. MCs were less abundant in 48/80+PD groups, thus validating the previous MCs depletion in our model. PD increased the number of MC in the gingival tissue of SHR. Cytokine production (TNF-alpha, IL-6, IL-1 beta, and CXCL3) was constitutively higher in SHR and increased further after PD, which was also significantly reduced in the MCs-depleted animals. PD led to an increased expression of Opn, Rankl, Rank, Vtn, Itga5, Itgb5, Trap, and Ctsk in the mandible of W and SHRs, which was reversed in MCs-depleted animals. These results suggest that MCs significantly contributes to the PD-induced alveolar bone resorption, especially in the SHR, which is associated with a more severe PD progression compared to Wistar, partly explained by these cells contribution to the inflammatory status and mediator production, stimulating osteoclast-related response markers, which were reduced after MC depletion in our experimental model. (AU)

• Processo FAPESP: 18/23676-3 - Participação dos microRNAs nas alterações ósseas locais induzidas pela doença periodontal e pelo sistema renina-angiotensina local em ratos espontaneamente hipertensos
• Beneficiário: Victor Gustavo Balera Brito
• Modalidade de apoio: Bolsas no Brasil - Doutorado
• Processo FAPESP: 17/05873-3 - Análise in vitro do papel dos mastócitos e do sistema renina-angiotensina sobre osteoblastos e osteoclastos de animais espontaneamente hipertensos
• Beneficiário: Sabrina Cruz Tfaile Frasnelli
• Modalidade de apoio: Bolsas no Brasil - Pós-Doutorado
• Processo FAPESP: 17/07095-8 - Papel dos mastócitos sobre a diferenciação osteogênica in vitro de células mesenquimais estromais da medula óssea de camundongos
• Beneficiário: Maria Carolina Linjardi de Sousa
• Modalidade de apoio: Bolsas no Brasil - Iniciação Científica
• Processo FAPESP: 17/02271-2 - O papel do Telmisartan na diferenciação osteoblástica em animais espontaneamente hipertensos
• Beneficiário: Mariana Sousa Patrocinio
• Modalidade de apoio: Bolsas no Brasil - Iniciação Científica
• Processo FAPESP: 15/03965-2 - Papel do sistema renina-angiotensina em diferentes modelos inflamatórios orais: uma abordagem interdisciplinar experimental e clínica
• Beneficiário: Carlos Ferreira dos Santos
• Modalidade de apoio: Auxílio à Pesquisa - Temático