scholarly journals Alveolar bone healing process in spontaneously hypertensive rats (SHR): A radiographic densitometry study

2012 ◽  
Vol 20 (2) ◽  
pp. 222-227 ◽  
Author(s):  
Natalia Manrique ◽  
Cassiano Costa Silva Pereira ◽  
Lourdes Maria Gonzáles Garcia ◽  
Samuel Micaroni ◽  
Antonio Augusto Ferreira de Carvalho ◽  
...  
2015 ◽  
Vol 19 (6) ◽  
pp. 1319-1327 ◽  
Author(s):  
Natalia Manrique ◽  
Cassiano Costa Silva Pereira ◽  
Eloá Rodrigues Luvizuto ◽  
Maria Del Pilar Rodriguez Sánchez ◽  
Tetuo Okamoto ◽  
...  

2019 ◽  
Vol 14 (1) ◽  
pp. 311-317
Author(s):  
Wei Liu ◽  
Ben Chen ◽  
Youyang Zheng ◽  
Yuehua Shi ◽  
Zhuojin Shi

AbstractPlatelet-rich plasma (PRP) has been shown to be a beneficial growth factor for bone tissue healing and is used in implantology. The aim of this study was to investigate the effects of PRP on bone defects in rabbits. Twenty rabbits were used to establish the implant bone defect model in this study. An intrabony defect (5mm × 5mm × 3mm) was created in alveolar bone in the lower jar of each rabbit. The wound was treated with PRP. The expression of platelet-derived growth factor BB (PDGFBB) was assessed by enzyme-linked immunosorbent assay (ELISA). Focal adhesion kinase (FAK) and related phosphatidylinositol 3-kinase (PI3K)/AKT (protein kinase B) levels were measured by Western blot. The results show that PRP could significantly improve the bone healing process when compared with control, and 10% PRP could markedly increase fibroblast proliferation 48-h post treatment. PDGFBB was higher in the PRP group than that in the control group. PRP treatment also could elevate the phosphorylation of FAK and PI3K/AKT, although the inhibitor of PDGFR could reverse this trend. These results suggest that PRP treatment improves the bone healing process through the FAK/PI3K/AKT pathway.


PLoS ONE ◽  
2021 ◽  
Vol 16 (3) ◽  
pp. e0247372
Author(s):  
Victor Gustavo Balera Brito ◽  
Mariana Sousa Patrocinio ◽  
Maria Carolina Linjardi Sousa ◽  
Ayná Emanuelli Alves Barreto ◽  
Sabrina Cruz Tfaile Frasnelli ◽  
...  

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-α, IL-6, IL-1β, 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.


2014 ◽  
Vol 72 (12) ◽  
pp. 2569-2581 ◽  
Author(s):  
Walter Cristiano Gealh ◽  
Cassiano Costa Silva Pereira ◽  
Eloa Rodrigues Luvizuto ◽  
Idelmo Rangel Garcia-Júnior ◽  
Cristina Antoniali ◽  
...  

2013 ◽  
Vol 27 (5) ◽  
pp. 423-430 ◽  
Author(s):  
Veronica Kei Len Chin ◽  
Adriana Shinagawa ◽  
Maria da Graca Naclerio-Homem

2010 ◽  
Vol 24 (2) ◽  
pp. 170-176 ◽  
Author(s):  
Marta Ferreira Bastos ◽  
Felipe Vilhena Brilhante ◽  
Joyce Pinho Bezerra ◽  
Carlos Alberto Silva ◽  
Poliana Mendes Duarte

2021 ◽  
Vol 12 ◽  
Author(s):  
Michelle de Campos Soriani Azevedo ◽  
Angélica Cristina Fonseca ◽  
Priscila Maria Colavite ◽  
Jéssica Lima Melchiades ◽  
André Petenuci Tabanez ◽  
...  

Host inflammatory immune response comprises an essential element of the bone healing process, where M2 polarization allegedly contributes to a favorable healing outcome. In this context, immunoregulatory molecules that modulate host response, including macrophage polarization, are considered potential targets for improving bone healing. This study aims to evaluate the role of the immunoregulatory molecules VIP (Vasoactive intestinal peptide) and PACAP (Pituitary adenylate cyclase activating polypeptide), which was previously described to favor the development of the M2 phenotype, in the process of alveolar bone healing in C57Bl/6 (WT) mice. Experimental groups were submitted to tooth extraction and maintained under control conditions or treated with VIP or PACAP were evaluated by microtomographic (µCT), histomorphometric, immunohistochemical, and molecular analysis at 0, 3, 7, and 14 days to quantify tissue healing and host response indicators at the healing site. Gene expression analysis demonstrates the effectiveness of VIP or PACAP in modulating host response, evidenced by the early dominance of an M2-type response, which was paralleled by a significant increase in M2 (CD206+) in treated groups. However, despite the marked effect of M1/M2 balance in the healing sites, the histomorphometric analysis does not reveal an equivalent/corresponding modulation of the healing process. µCT reveals a slight increase in bone matrix volume and the trabecular thickness number in the PACAP group, while histomorphometric analyzes reveal a slight increase in the VIP group, both at a 14-d time-point; despite the increased expression of osteogenic factors, osteoblastic differentiation, activity, and maturation markers in both VIP and PACAP groups. Interestingly, a lower number of VIP and PACAP immunolabeled cells were observed in the treated groups, suggesting a reduction in endogenous production. In conclusion, while both VIP and PACAP treatments presented a significant immunomodulatory effect with potential for increased healing, no major changes were observed in bone healing outcome, suggesting that the signals required for bone healing under homeostatic conditions are already optimal, and additional signals do not improve an already optimal process. Further studies are required to elucidate the role of macrophage polarization in the bone healing process.


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