Publications by authors named "Andressa Vilas Boas Nogueira"

24 Publications

  • Page 1 of 1

Effects of obesity on periodontal tissue remodeling during orthodontic movement.

Am J Orthod Dentofacial Orthop 2021 Apr 6;159(4):480-490. Epub 2021 Feb 6.

Department of Diagnosis and Surgery, School of Dentistry at Araraquara, São Paulo State University, Araraquara, São Paulo, Brazil. Electronic address:

Introduction: Orthodontic movement triggers a sequence of cellular and molecular events that may be affected by different systemic conditions. This study evaluated the effect of obesity on rat periodontal tissue remodeling induced by mechanical orthodontic force.

Methods: Thirty-two Holtzman rats were distributed into 4 groups: control, obesity induction (O), orthodontic movement (M), and obesity induction and orthodontic movement (OM). Obesity was induced by a high-fat diet for 90 days. After 15 days of orthodontic movement, the animals were killed. Obesity induction was confirmed by animal body weight, adipose tissue weight, and serologic analysis. Periodontal tissue remodeling was evaluated using microcomputed tomography and histologic analysis. The gene expression of adipokines and cytokines in gingival tissues was evaluated.

Results: An increase in body and adipose tissue weight was observed in the obesity induction groups. The O group presented an increase in lipids and blood glucose. The OM group showed a decrease in bone volume fraction and bone mineral density compared with all other groups and a tendency for more rapid tooth movement than the M group. The OM group showed a higher quantity of inflammatory cells and higher Mmp1 expression than the O group. The O and OM groups showed higher Nampt expression than the control group and lower Nampt expression than the M group.

Conclusions: Obesity modulates periodontal tissue remodeling during orthodontic movement and results in more inflammation and bone loss than in nonobese animals.
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http://dx.doi.org/10.1016/j.ajodo.2019.12.025DOI Listing
April 2021

and Tumor Necrosis Factor-Alpha Stimulate Synthesis of Visfatin by Human Macrophages.

Int J Mol Sci 2021 Jan 27;22(3). Epub 2021 Jan 27.

Department of Periodontology and Operative Dentistry, University Medical Center, University of Mainz, 55131 Mainz, Germany.

There is little known about the effect of the periodontopathogen on macrophages as key cells of the innate immune defense in the periodontium. Therefore, the aim of the present study was to investigate the effect of and additionally of the pro-inflammatory cytokine tumor necrosis factor-alpha (TNFα) on visfatin and other pro-inflammatory and proteolytic molecules associated with periodontitis in human macrophages. The presence of macrophage markers CD14, CD86, CD68, and CD163 was examined in gingival biopsies from healthy individuals and periodontitis patients. Human macrophages were incubated with and TNFα for up to 2 d. The effects of both stimulants on macrophages were determined by real-time PCR, ELISA, immunocytochemistry, and immunofluorescence. was able to significantly stimulate the synthesis of visfatin by human macrophages using TLR2 and MAPK pathways. In addition to visfatin, was also able to increase the synthesis of cyclooxygenase 2, TNFα, and matrix metalloproteinase 1. Like , TNFα was also able to stimulate the production of these proinflammatory and proteolytic molecules. Our results highlight the pathogenetic role of in periodontal diseases and also underline the involvement of visfatin in the aetiopathogenesis of periodontitis.
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http://dx.doi.org/10.3390/ijms22031235DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7865436PMC
January 2021

Regulation of Anti-Apoptotic SOD2 and BIRC3 in Periodontal Cells and Tissues.

Int J Mol Sci 2021 Jan 8;22(2). Epub 2021 Jan 8.

Department of Periodontology and Operative Dentistry, University Medical Center, University of Mainz, 55131 Mainz, Germany.

The aim of the study was to clarify whether orthodontic forces and periodontitis interact with respect to the anti-apoptotic molecules superoxide dismutase 2 (SOD2) and baculoviral IAP repeat-containing protein 3 (BIRC3). SOD2, BIRC3, and the apoptotic markers caspases 3 (CASP3) and 9 (CASP9) were analyzed in gingiva from periodontally healthy and periodontitis subjects by real-time PCR and immunohistochemistry. SOD2 and BIRC3 were also studied in gingiva from rats with experimental periodontitis and/or orthodontic tooth movement. Additionally, SOD2 and BIRC3 levels were examined in human periodontal fibroblasts incubated with and/or subjected to mechanical forces. Gingiva from periodontitis patients showed significantly higher SOD2, BIRC3, CASP3, and CASP9 levels than periodontally healthy gingiva. SOD2 and BIRC3 expressions were also significantly increased in the gingiva from rats with experimental periodontitis, but the upregulation of both molecules was significantly diminished in the concomitant presence of orthodontic tooth movement. In vitro, SOD2 and BIRC3 levels were significantly increased by , but this stimulatory effect was also significantly inhibited by mechanical forces. Our study suggests that SOD2 and BIRC3 are produced in periodontal infection as a protective mechanism against exaggerated apoptosis. In the concomitant presence of orthodontic forces, this protective anti-apoptotic mechanism may get lost.
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http://dx.doi.org/10.3390/ijms22020591DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7827060PMC
January 2021

In vivo and in vitro anti-inflammatory and pro-osteogenic effects of citrus cystatin CsinCPI-2.

Cytokine 2019 11 18;123:154760. Epub 2019 Jun 18.

Department of Diagnosis and Surgery, School of Dentistry at Araraquara, Sao Paulo State University - UNESP, Araraquara, São Paulo, Brazil. Electronic address:

Cystatins are natural inhibitors of cysteine peptidases. Recently, cystatins derived from plants, named phytocystatins, have been extensively studied. Among them, CsinCPI-2 proteins from Citrus sinensis were identified and recombinantly produced by our group. Thus, this study described the recombinant expression, purification, and inhibitory activity of this new phytocystatin against human cathepsins K and B and assessed the anti-inflammatory effect of CsinCPI-2 in vitro in mouse and in vivo in rats. In addition, the pro-osteogenic effect of CsinCPI-2 was investigated in vitro. The inflammatory response of mouse macrophage cells stimulated with P. gingivalis was modulated by CsinCPI-2. The in vitro results showed an inhibitory effect (p < 0.05) on cathepsin K, cathepsin B, IL-1β, and TNF-α gene expression. In addition, CsinCPI-2 significantly inhibited in vivo the activity of TNF-α (p < 0.05) in the blood of rats, previously stimulated by E. coli lipopolysaccharide (LPS). CsinCPI-2 had a pro-osteogenic effect in human dental pulp cells, demonstrated by the increase in alkaline phosphatase (ALP) activity, deposition of mineralized nodules, and the gene expression of the osteogenic markers as bone morphogenetic protein 2 (BMP-2), runt-related transcription factor 2 (Runx-2), ALP, osteocalcin, and bone sialoprotein (BSP). These preliminary studies suggested that CsinCPI-2 has a potential anti-inflammatory, and at the same time, a pro-osteogenic effect. This may lead to new therapies for the control of diseases where inflammation plays a key role, such as periodontal disease and apical periodontitis.
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http://dx.doi.org/10.1016/j.cyto.2019.154760DOI Listing
November 2019

Regulation of ghrelin receptor by microbial and inflammatory signals in human osteoblasts.

Braz Oral Res 2019 Apr 25;33:e025. Epub 2019 Apr 25.

University Medical Center, Johannes Gutenberg University, Department of Periodontology and Operative Dentistry, Mainz, Germany.

Recently, it has been suggested that the anti-inflammatory hormone ghrelin (GHRL) and its receptor GHS-R may play a pivotal role in periodontal health and diseases. However, their exact regulation and effects in periodontitis are not known. The aim of this in-vitro study was to investigate the effect of microbial and inflammatory insults on the GHS-R1a expression in human osteoblast-like cells. MG-63 cells were exposed to interleukin (IL)-1β and Fusobacterium nucleatum in the presence and absence of GHRL for up to 2 d. Subsequently, gene expressions of GHS-R1a, inflammatory mediators and matrix metalloproteinase were analyzed by real-time PCR. GHS-R protein synthesis and NF-κB p65 nuclear translocation were assessed by immunocytochemistry and immunofluorescence microscopy, respectively. IL-1β and F. nucleatum caused a significant upregulation of GHS-R1a expression and an increase in GHS-R1a protein. Pre-incubation with a MEK1/2 inhibitor diminished the IL-1β-induced GHS-R1a upregulation. IL-1β and F. nucleatum also enhanced the expressions of cyclooxygenase 2, CC-chemokine ligand 2, IL-6, IL-8, and matrix metalloproteinase 1, but these stimulatory effects were counteracted by GHRL. By contrast, the stimulatory actions of IL-1β and F. nucleatum on the GHS-R1a expression were further enhanced by GHRL. Our study provides original evidence that IL-1β and F. nucleatum regulate the GHS-R/GHRL system in osteoblast-like cells. Furthermore, we demonstrate for the first time that the proinflammatory and proteolytic actions of IL-1β and F. nucleatum on osteoblast-like cells are inhibited by GHRL. Our study suggests that microbial and inflammatory insults upregulate GHS-R1a, which may represent a protective negative feedback mechanism in human bone.
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http://dx.doi.org/10.1590/1807-3107bor-2019.vol33.0025DOI Listing
April 2019

Regulation of Ghrelin Receptor by Periodontal Bacteria and .

Mediators Inflamm 2017 29;2017:4916971. Epub 2017 Nov 29.

Section of Experimental Dento-Maxillo-Facial Medicine, Center of Dento-Maxillo-Facial Medicine, University of Bonn, Bonn, Germany.

Ghrelin plays a major role in obesity-related diseases which have been shown to be associated with periodontitis. This study sought to analyze the expression of the functional receptor for ghrelin (GHS-R1a) in periodontal cells and tissues under microbial conditions and . The GHS-R1a expression in human periodontal cells challenged with the periodontopathogen , in gingival biopsies from periodontally healthy and diseased individuals, and from rats with and without ligature-induced periodontitis was analyzed by real-time PCR, immunocytochemistry, and immunofluorescence. induced an initial upregulation and subsequent downregulation of GHS-R1a in periodontal cells. In rat experimental periodontitis, the GHS-R1a expression at periodontitis sites was increased during the early stage of periodontitis, but significantly reduced afterwards, when compared with healthy sites. In human gingival biopsies, periodontally diseased sites showed a significantly lower GHS-R1a expression than the healthy sites. The expression of the functional ghrelin receptor in periodontal cells and tissues is modulated by periodontal bacteria. Due to the downregulation of the functional ghrelin receptor by long-term exposure to periodontal bacteria, the anti-inflammatory actions of ghrelin may be diminished in chronic periodontal infections, which could lead to an enhanced periodontal inflammation and tissue destruction.
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http://dx.doi.org/10.1155/2017/4916971DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5727798PMC
August 2018

Suppressor of cytokine signaling 1 expression during LPS-induced inflammation and bone loss in rats.

Braz Oral Res 2017 Sep 28;31:e75. Epub 2017 Sep 28.

Universidade Estadual Paulista - UNESP, School of Dentistry at Araraquara, Department of Diagnosis and Surgery, Araraquara, SP, Brazil.

This study aimed to characterize the dynamics of suppressor of cytokine signaling (SOCS1) expression in a rat model of lipopolysaccharide-induced periodontitis. Wistar rats in the experimental groups were injected three times/week with LPS from Escherichia coli on the palatal aspect of the first molars, and control animals were injected with vehicle (phosphate-buffered saline). Animals were sacrificed 7, 15, and 30 days after the first injection to analyze inflammation (stereometric analysis), bone loss (macroscopic analysis), gene expression (qRT-PCR), and protein expression/activation (Western blotting). The severity of inflammation and bone loss associated with LPS-induced periodontitis increased from day 7 to day 15, and it was sustained through day 30. Significant (p < 0.05) increases in SOCS1, RANKL, OPG, and IFN-γ gene expression were observed in the experimental group versus the control group at day 15. SOCS1 protein expression and STAT1 and NF-κB activation were increased throughout the 30-day experimental period. Gingival tissues affected by experimental periodontitis express SOCS1, indicating that this protein may potentially downregulate signaling events involved in inflammatory reactions and bone loss and thus may play a relevant role in the development and progression of periodontal disease.
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http://dx.doi.org/10.1590/1807-3107BOR-2017.vol31.0075DOI Listing
September 2017

Inflammatory bowel disease and oral health: systematic review and a meta-analysis.

J Clin Periodontol 2017 Apr 6;44(4):382-393. Epub 2017 Mar 6.

Section of Experimental Dento-Maxillo-Facial Medicine, School of Dentistry, University of Bonn, Bonn, Germany.

Background: The objective of this systematic review was to systematically investigate whether there is an association between inflammatory bowel disease (IBD) and oral health.

Methods: Literature searches for randomized and non-randomized studies were performed up to January 2017. Risk of bias within studies was assessed with the Downs and Black checklist. Across-studies risk of bias was assessed with the GRADE framework. Quantitative synthesis was conducted with random-effects meta-analyses.

Results: A total of 9 cross-sectional studies including 1297 patients were included. IBD was associated with increased risk of periodontitis (332 more patients per 1000 patients; 95% confidence interval (CI): 257-388 patients; p < 0.001) compared to non-IBD patients. Additionally, the Decayed-Missing-Filled-Teeth index of IBD patients was significantly worse than non-IBD patients (mean difference: 3.85; 95% CI: 2.36-5.34; p = 0.005). Patients with ulcerative colitis had considerably worse oral health for most of the assessed factors, while the quality of overall evidence ranged from high to low, due to the observational nature of contributing studies.

Conclusions: Inflammatory bowel disease was associated with significantly higher risk of periodontitis and worse oral health compared to non-IBD patients. However, longitudinal studies are needed in order to establish a causality link between IBD and periodontal disease.
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http://dx.doi.org/10.1111/jcpe.12698DOI Listing
April 2017

Contribution of biomechanical forces to inflammation-induced bone resorption.

J Clin Periodontol 2017 01 16;44(1):31-41. Epub 2016 Dec 16.

Department of Diagnosis and Surgery, School of Dentistry at Araraquara, Univ Estadual Paulista (UNESP), Araraquara, São Paulo, Brazil.

Aim: This study aimed to evaluate the contribution of biomechanical loading to inflammation-induced tissue destruction.

Materials And Methods: A total of 144 adult Holtzman rats were randomly assigned into four experimental groups: control (C), ligature-induced periodontal disease (P), orthodontic movement (OM), and combination group (OMP). On days 1, 3, 7, and 15, following baseline, nine animals from each experimental group were killed. Bone volume fraction (BVF) and bone mineral density (BMD) were measured using micro-computed tomography. Expression and synthesis profile of cytokines and receptors of inflammation in gingival tissues were evaluated by PCR array assay and multiplex immunoassay.

Results: At 15 days, the OMP group presented a significantly (p < 0.05) lower BVF and BMD levels when compared to all the other groups. The OMP group presented the highest number of upregulated protein targets in comparison to the other groups. Furthermore, the gene expression and protein levels of CCL2, CCL3, IL-1β, IL1-α, IL-18, TNF-α, and VEGF were significantly (p < 0.05) higher in the OMP group when compared to the P group.

Conclusions: In summary, mechanical loading modulates the inflammatory response of periodontal tissues to periodontal disease by increasing the expression of several pro-inflammatory mediators and receptors, which leads to increased bone resorption.
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http://dx.doi.org/10.1111/jcpe.12636DOI Listing
January 2017

Treatment of periodontal disease with an Er,Cr:YSGG laser in rats exposed to cigarette smoke inhalation.

Lasers Med Sci 2015 Nov 27;30(8):2095-103. Epub 2015 Mar 27.

Araraquara Dental School-São Paulo University "Júlio de Mesquita Filho", Araraquara, São Paulo, Brazil.

The purpose of this study was to evaluate the erbium, chromium:yttrium-scandiumgallium-garnet (Er,Cr:YSGG) laser irradiation in the treatment of periodontitis in rats exposed to cigarette smoke inhalation (CSI). Ligatures were placed in the maxillary second molars. After a 15-day period, the ligatures were removed and 180 animals were randomly divided into six groups: (1) CSRP group--CSI and manual scaling and root planing (SRP) treatment; (2) CL group--CSI and Er,Cr:YSGG laser irradiation; (3) CSRP + L group-CSI, SRP, and Er,Cr:YSGG irradiation; (4) SRP group-manual SRP; (5) L group--Er,Cr:YSGG irradiation; (6) SRP + L group--SRP and Er,Cr:YSGG irradiation. At 7, 15, and 30 days after treatments, animals were euthanized and histologic, histometric, immunohistochemistry, and real-time PCR analyses were performed. Histometrically, no differences were observed in the SRP, L, and SRP + L groups exposed to CSI. The CSRP group showed more bone formation at 30 days than at 15 days (p < 0.01) but less bone at 30 days than the CL group at 30 days (p < 0.05). Immunohistochemical staining was positive for osteoblasts, fibroblasts, and osteoclasts. Real-time PCR showed more (vascular endothelial growth factor) VEGF expression in the L (p < 0.05) and SRP + L (p < 0.01) groups at 30 days than at 15 days and less VEGF expression in the CSRP group at 30 days than at 15 days (p < 0.05). There was no difference in fibroblast growth factor (FGF) expression. The Er,Cr:YSGG laser irradiation promotes favorable conditions for tissue repair even in animals exposed to CSI, with similar results as those achieved from manual scaling and root planing.
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http://dx.doi.org/10.1007/s10103-015-1731-8DOI Listing
November 2015

Leptin effects on the regenerative capacity of human periodontal cells.

Int J Endocrinol 2014 22;2014:180304. Epub 2014 Jul 22.

Experimental Dento-Maxillo-Facial Medicine, University of Bonn, 53111 Bonn, Germany ; Clinical Research Unit 208, University of Bonn, 53111 Bonn, Germany.

Obesity is increasing throughout the globe and characterized by excess adipose tissue, which represents a complex endocrine organ. Adipose tissue secrets bioactive molecules called adipokines, which act at endocrine, paracrine, and autocrine levels. Obesity has recently been shown to be associated with periodontitis, a disease characterized by the irreversible destruction of the tooth-supporting tissues, that is, periodontium, and also with compromised periodontal healing. Although the underlying mechanisms for these associations are not clear yet, increased levels of proinflammatory adipokines, such as leptin, as found in obese individuals, might be a critical pathomechanistic link. The objective of this study was to examine the impact of leptin on the regenerative capacity of human periodontal ligament (PDL) cells and also to study the local leptin production by these cells. Leptin caused a significant downregulation of growth (TGFβ1, and VEGFA) and transcription (RUNX2) factors as well as matrix molecules (collagen, and periostin) and inhibited SMAD signaling under regenerative conditions. Moreover, the local expression of leptin and its full-length receptor was significantly downregulated by inflammatory, microbial, and biomechanical signals. This study demonstrates that the hormone leptin negatively interferes with the regenerative capacity of PDL cells, suggesting leptin as a pathomechanistic link between obesity and compromised periodontal healing.
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http://dx.doi.org/10.1155/2014/180304DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4129942PMC
August 2014

Beneficial effects of adiponectin on periodontal ligament cells under normal and regenerative conditions.

J Diabetes Res 2014 13;2014:796565. Epub 2014 Jul 13.

Experimental Dento-Maxillo-Facial Medicine, University of Bonn, 53111 Bonn, Germany ; Clinical Research Unit 208, University of Bonn, 53111 Bonn, Germany.

Type 2 diabetes and obesity are increasing worldwide and linked to periodontitis, a chronic disease which is characterized by the irreversible destruction of the tooth-supporting tissues, that is, periodontium. The mechanisms underlying the association of diabetes mellitus and obesity with periodontal destruction and compromised periodontal healing are not well understood, but decreased plasma levels of adiponectin, as found in diabetic and obese individuals, might be a critical mechanistic link. The aim of this in vitro study was to examine the effects of adiponectin on periodontal ligament (PDL) cells under normal and regenerative conditions, and to study the regulation of adiponectin and its receptors in these cells. Adiponectin stimulated significantly the expression of growth factors and extracellular matrix, proliferation, and in vitro wound healing, reduced significantly the constitutive tumor necrosis factor-α expression, and caused a significant upregulation of its own expression. The beneficial actions of enamel matrix derivative on a number of PDL cell functions critical for periodontal regeneration were partially enhanced by adiponectin. The periodontopathogen Porphyromonas gingivalis inhibited the adiponectin expression and stimulated the expression of its receptors. In conclusion, reduced levels of adiponectin, as found in type 2 diabetes and obesity, may compromise periodontal health and healing.
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http://dx.doi.org/10.1155/2014/796565DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4120919PMC
April 2015

Biomechanical loading modulates proinflammatory and bone resorptive mediators in bacterial-stimulated PDL cells.

Mediators Inflamm 2014 25;2014:425421. Epub 2014 May 25.

Department of Diagnosis and Surgery, School of Dentistry at Araraquara, Univ Estadual Paulista (UNESP), 14801-903 Araraquara, SP, Brazil.

The present study aimed to evaluate in vitro whether biomechanical loading modulates proinflammatory and bone remodeling mediators production by periodontal ligament (PDL) cells in the presence of bacterial challenge. Cells were seeded on BioFlex culture plates and exposed to Fusobacterium nucleatum ATCC 25586 and/or cyclic tensile strain (CTS) of low (CTSL) and high (CTSH) magnitudes for 1 and 3 days. Synthesis of cyclooxygenase-2 (COX2) and prostaglandin E2 (PGE2) was evaluated by ELISA. Gene expression and protein secretion of osteoprotegerin (OPG) and receptor activator of nuclear factor kappa-B ligand (RANKL) were evaluated by quantitative RT-PCR and ELISA, respectively. F. nucleatum increased the production of COX2 and PGE2, which was further increased by CTS. F. nucleatum-induced increase of PGE2 synthesis was significantly (P < 0.05) increased when CTSH was applied at 1 and 3 days. In addition, CTSH inhibited the F. nucleatum-induced upregulation of OPG at 1 and 3 days, thereby increasing the RANKL/OPG ratio. OPG and RANKL mRNA results correlated with the protein results. In summary, our findings provide original evidence that CTS can enhance bacterial-induced syntheses of molecules associated with inflammation and bone resorption by PDL cells. Therefore, biomechanical, such as orthodontic or occlusal, loading may enhance the bacterial-induced inflammation and destruction in periodontitis.
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http://dx.doi.org/10.1155/2014/425421DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4058179PMC
February 2015

HMGB1 localization during experimental periodontitis.

Mediators Inflamm 2014 20;2014:816320. Epub 2014 Feb 20.

Department of Diagnosis and Surgery, School of Dentistry at Araraquara, Universidade Estadual Paulista (UNESP), Rua Humaitá, 1680, 2° Andar, Centro, 14801-903 Araraquara, SP, Brazil.

Aim: This study sought to investigate the in vitro expression profile of high mobility group box 1 (HMGB1) in murine periodontal ligament fibroblasts (mPDL) stimulated with LPS or IL-1β and in vivo during ligature- or LPS-induced periodontitis in rats.

Material And Methods: For the in vivo study, 36 rats were divided into experimental and control groups, and biopsies were harvested at 7-30 d following disease induction. Bone loss and inflammation were evaluated. HMGB1 expression was assessed by immunohistochemistry, qPCR, and Western blot.

Results: Significant increases in mPDL HMGB1 mRNA occurred at 4, 8, and 12 h with protein expression elevated by 24 h. HMGB1 mRNA expression in gingival tissues was significantly increased at 15 d in the LPS-PD model and at 7 and 15 d in the ligature model. Immunohistochemical staining revealed a significant increase in the number of HMGB1-positive cells during the experimental periods.

Conclusion: The results show that PDL cells produce HMGB1, which is increased and secreted extracellularly after inflammatory stimuli. In conclusion, this study demonstrates that HMGB1 may be associated with the onset and progression of periodontitis, suggesting that further studies should investigate the potential role of HMGB1 on periodontal tissue destruction.
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http://dx.doi.org/10.1155/2014/816320DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3945472PMC
December 2014

SOCS3 expression correlates with severity of inflammation, expression of proinflammatory cytokines, and activation of STAT3 and p38 MAPK in LPS-induced inflammation in vivo.

Mediators Inflamm 2013 2;2013:650812. Epub 2013 Sep 2.

Department of Diagnosis and Surgery, School of Dentistry at Araraquara, Universidade Estadual Paulista, Rua Humaitá, 1680-Centro, 14801-903 Araraquara, SP, Brazil.

SOCS3 is an inducible endogenous negative regulator of JAK/STAT pathway, which is relevant in inflammatory conditions. We used a model of LPS-induced periodontal disease in rats to correlate SOCS3 expression with the inflammatory status. In vitro we used a murine macrophage cell line to assess the physical interaction between SOCS3 and STAT3 by coimmunoprecipitation. 30 ug of LPS from Escherichia coli were injected in the gingival tissues on the palatal aspect of first molars of the animals 3x/week for up to 4 weeks. Control animals were injected with the vehicle (PBS). The rats were sacrificed at 7, 15, and 30 days. Inflammation and gene expression were assessed by stereometric analysis, immunohistochemistry, RT-qPCR, and western blot. LPS injections increased inflammation, paralleled by an upregulation of SOCS3, of the proinflammatory cytokines IL-1 β , IL-6, and TNF- α and increased phosphorylation of STAT3 and p38 MAPK. SOCS3 expression accompanied the severity of inflammation and the expression of proinflammatory cytokines, as well as the activation status of STAT3 and p38 MAPK. LPS stimulation in a macrophage cell line in vitro induced transient STAT3 activation, which was inversely correlated with a dynamic physical interaction with SOCS3, suggesting that this may be a mechanism for SOCS3 regulatory function.
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http://dx.doi.org/10.1155/2013/650812DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3775441PMC
February 2014

Stimulation of MMP-1 and CCL2 by NAMPT in PDL cells.

Mediators Inflamm 2013 22;2013:437123. Epub 2013 Aug 22.

Experimental Dento-Maxillo-Facial Medicine, Center of Dento-Maxillo-Facial Medicine, University of Bonn, 53111 Bonn, Germany.

Periodontitis is an inflammatory disease caused by pathogenic microorganisms and characterized by the destruction of the periodontium. Obese individuals have an increased risk of periodontitis, and elevated circulating levels of adipokines, such as nicotinamide phosphoribosyltransferase (NAMPT), may be a pathomechanistic link between both diseases. The aim of this in vitro study was to examine the regulation of periodontal ligament (PDL) cells by NAMPT and its production under inflammatory and infectious conditions. NAMPT caused a significant upregulation of 9 genes and downregulation of 3 genes, as analyzed by microarray analysis. Eight of these genes could be confirmed by real-time PCR: NAMPT induced a significant upregulation of EGR1, MMP-1, SYT7, ITPKA, CCL2, NTM, IGF2BP3, and NRP1. NAMPT also increased significantly the MMP-1 and CCL2 protein synthesis. NAMPT was significantly induced by interleukin-1 β and the periodontal microorganism P. gingivalis. NAMPT may contribute to periodontitis through upregulation of MMP-1 and CCL2 in PDL cells. Increased NAMPT levels, as found in obesity, may therefore represent a mechanism whereby obesity could confer an increased risk of periodontitis. Furthermore, microbial and inflammatory signals may enhance the NAMPT synthesis in PDL cells and thereby contribute to the increased gingival and serum levels of this adipokine, as found in periodontitis.
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http://dx.doi.org/10.1155/2013/437123DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3766615PMC
February 2014

Forced orthodontic eruption for augmentation of soft and hard tissue prior to implant placement.

Contemp Clin Dent 2013 Apr;4(2):243-7

Department of Diagnosis and Surgery, School of Dentistry at Araraquara, Univ Estadual Paulista - UNESP, Araraquara, São Paulo, Brazil.

Forced orthodontic eruption (FOE) is a non-surgical treatment option that allows modifying the osseous and gingival topography. The aim of this article is to present a clinical case of a FOE, which resulted in an improvement of the amount of available bone and soft-tissues for implant site development. Patient was referred for treatment of mobility and unesthetic appearance of their maxillary incisors. Clinical and radiographic examination revealed inflamed gingival tissue, horizontal and vertical tooth mobility and interproximal angular bone defects. It was chosen a multidisciplinary treatment approach using FOE, tooth extraction, and immediate implant placement to achieve better esthetic results. The use of FOE, in periodontally compromised teeth, promoted the formation of a new bone and soft-tissue in a coronal direction, without additional surgical procedures, enabling an esthetic, and functional implant-supported restoration.
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http://dx.doi.org/10.4103/0976-237X.114876DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3757892PMC
April 2013

Evaluation of the host response in various models of induced periodontal disease in mice.

J Periodontol 2014 Mar 27;85(3):465-77. Epub 2013 Jun 27.

Department of Diagnosis and Surgery, School of Dentistry at Araraquara, Univ Estadual Paulista-UNESP, Araraquara, São Paulo, Brazil.

Background: The aim of this study is to characterize and evaluate the host response caused by three different models of experimental periodontitis in mice.

Methods: C57BL/6 wild-type female mice were distributed into six experimental groups and sacrificed at 7, 15, and 30 days after the induction of periodontal disease: 1) group C: no treatment control group; 2) group L: periodontal disease induced by ligature; 3) group G-Pg: oral gavage with Porphyromonas gingivalis (Pg); 4) group G-PgFn: oral gavage with Fusobacterium nucleatum + Pg; 5) group I-Pg: heat-killed Pg injected into the palatal mucosa between the molars; and 6) group I-V: phosphate-buffered saline injected into the palatal mucosa. The samples were used to analyze the immune-inflammatory process in the gingival tissue via descriptive histologic and real-time polymerase chain reaction analyses. The alveolar bone loss was evaluated using microcomputed tomography. The data were analyzed using the Kruskal-Wallis test, followed by a post hoc Dunn test and analysis of variance, followed by a Tukey test using a 5% significance level.

Results: Only the ligature model displayed significant alveolar bone loss in the initial period (7 days), which was maintained with time. The group injected with heat-killed Pg displayed significant alveolar bone loss starting from day 15, which continued to progress with time (P <0.05). A significant increase (P <0.05) in the gene expression of proinflammatory cytokines (interleukin-6 and -1β) and proteins involved in osteoclastogenesis (receptor activator of nuclear factor-κB ligand and osteoprotegerin) was observed in the ligature group on day 7.

Conclusion: The ligature and injection of heat-killed Pg models were the most representative of periodontal disease in humans, whereas the oral gavage models were not effective at inducing the disease under the experimental conditions.
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http://dx.doi.org/10.1902/jop.2013.130225DOI Listing
March 2014

Regulation of visfatin by microbial and biomechanical signals in PDL cells.

Clin Oral Investig 2014 Jan 13;18(1):171-8. Epub 2013 Feb 13.

Department of Diagnosis and Surgery, School of Dentistry at Araraquara, Univ Estadual Paulista -- UNESP, Araraquara, Brazil.

Objectives: This in vitro study was established to examine whether visfatin thought to be a link between periodontitis and obesity is produced by periodontal ligament (PDL) cells and, if so, whether its synthesis is modulated by microbial and/or biomechanical signals.

Materials And Methods: PDL cells seeded on BioFlex® plates were exposed to the oral pathogen Fusobacterium nucleatum ATCC 25586 and/or subjected to biomechanical strain for up to 3 days. Gene expression of visfatin and toll-like receptors (TLR) 2 and 4 was analyzed by RT-PCR, visfatin protein synthesis by ELISA and immunocytochemistry, and NFκB nuclear translocation by immunofluorescence.

Results: F. nucleatum upregulated the visfatin expression in a dose- and time-dependent fashion. Preincubation with neutralizing antibodies against TLR2 and TLR4 caused a significant inhibition of the F. nucleatum-upregulated visfatin expression at 1 day. F. nucleatum stimulated the NFκB nuclear translocation. Biomechanical loading reduced the stimulatory effects of F. nucleatum on visfatin expression at 1 and 3 days and also abrogated the F. nucleatum-induced NFκB nuclear translocation at 60 min. Biomechanical loading inhibited significantly the expression of TLR2 and TLR4 at 3 days. The regulatory effects of F. nucleatum and/or biomechanical loading on visfatin expression were also observed at protein level.

Conclusions: PDL cells produce visfatin, and this production is enhanced by F. nucleatum. Biomechanical loading seems to be protective against the effects of F. nucleatum on visfatin expression.

Clinical Relevance: Visfatin produced by periodontal tissues could play a major role in the pathogenesis of periodontitis and the interactions with obesity and other systemic diseases.
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http://dx.doi.org/10.1007/s00784-013-0935-1DOI Listing
January 2014

Combination of orthodontic movement and periodontal therapy for full root coverage in a Miller class III recession: a case report with 12 years of follow-up.

Braz Dent J 2012 ;23(6):758-63

Department of Diagnosis and Surgery, Araraquara Dental School, UNESP - Univ Estadual Paulista, Araraquara, SP, Brazil.

One of the main purposes of mucogingival therapy is to obtain full root coverage. Several treatment modalities have been developed, but few techniques can provide complete root coverage in a class III Miller recession. Thus, the aim of this case report is to present a successful clinical case of a Miller class III gingival recession in which complete root coverage was obtained by means of a multidisciplinary approach. A 17-year-old Caucasian female was referred for treatment of a gingival recession on the mandibular left central incisor. The following procedures were planned for root coverage in this case: free gingival graft, orthodontic movement by means of alignment and leveling and coronally advanced flap (CAF). The case has been followed up for 12 years and the patient presents no recession, no abnormal probing depth and no bleeding on probing, with a wide attached gingiva band. A compromised tooth with poor prognosis, which would be indicated for extraction, can be treated by orthodontic movement and periodontal therapy, with possibility of 100% root coverage in some class III recessions.
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http://dx.doi.org/10.1590/s0103-64402012000600022DOI Listing
January 2014

Orthodontic force increases interleukin-1β and tumor necrosis factor-α expression and alveolar bone loss in periodontitis.

J Periodontol 2013 Sep 3;84(9):1319-26. Epub 2012 Dec 3.

Department of Diagnosis and Surgery, School of Dentistry at Araraquara, Univ Estadual Paulista-UNESP, Araraquara, Brazil.

Background: The present study aims to evaluate the effects of orthodontic movement (OM) on the periodontal tissues of rats with ligature-induced periodontal disease.

Methods: Eighty-eight rats were divided into four groups: 1) negative control (sham operated); 2) periodontal disease; 3) OM; and 4) periodontal disease followed by OM (OMP). Rats were sacrificed 3 hours or 1, 3, or 7 days after OM commencement. Bone volume fraction (BVF) and bone mineral density (BMD) were assessed in hemimaxillae by microcomputed tomography analysis. Expression of the proinflammatory cytokines interleukin (IL)-1β and tumor necrosis factor (TNF)-α were evaluated in gingival samples by quantitative polymerase chain reaction and enzyme-linked immunosorbent assay, and in the furcation region by immunohistochemistry analysis (IHC).

Results: The OMP group had lower BVF and BMD levels compared to the other groups at day 7 (P <0.05). Maximum messenger ribonucleic acid expression of both cytokines was observed in the OMP group at day 1 (P <0.05). In the same period, all proteins were expressed in high levels for all test groups compared to the control group. The number of cells positive for IL-1β and TNF-α by IHC was highest in the OMP group at day 1, with progressive reduction thereafter.

Conclusion: The results suggest that OM acts synergistically with periodontal disease in periodontal breakdown through upregulation of proinflammatory cytokines.
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http://dx.doi.org/10.1902/jop.2012.120510DOI Listing
September 2013

Modulation of host cell signaling pathways as a therapeutic approach in periodontal disease.

J Appl Oral Sci 2012 Mar-Apr;20(2):128-38

Department of Diagnosis and Surgery, School of Dentistry, UNESP-Univ. Estadual Paulista, Araraquara, SP, Brazil.

Recently, new treatment approaches have been developed to target the host component of periodontal disease. This review aims at providing updated information on host-modulating therapies, focusing on treatment strategies for inhibiting signal transduction pathways involved in inflammation. Pharmacological inhibitors of MAPK, NFκB and JAK/STAT pathways are being developed to manage rheumatoid arthritis, periodontal disease and other inflammatory diseases. Through these agents, inflammatory mediators can be inhibited at cell signaling level, interfering on transcription factors activation and inflammatory gene expression. Although these drugs offer great potential to modulate host response, their main limitations are lack of specificity and developments of side effects. After overcoming these limitations, adjunctive host modulating drugs will provide new therapeutic strategies for periodontal treatment.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3894752PMC
http://dx.doi.org/10.1590/s1678-77572012000200002DOI Listing
September 2012

Morphometric study of the root anatomy in furcation area of mandibular first molars.

J Appl Oral Sci 2012 Feb;20(1):76-81

Department of Diagnosis and Surgery, Araraquara Dental School, UNESP, Araraquara, SP, Brazil.

Unlabelled: Furcation involvement in periodontal disease has been a challenge for the dentist.

Objective: The aim of this study was to investigate root dimensions in the furcation area of 233 mandibular first molars.

Material And Methods: Digital photomicrographs were used to obtain the following measurements on the buccal and lingual surfaces of each tooth: root trunk height (RT), horizontal interadicular distance obtained 1 mm (D1) and 2 mm (D2) below the fornix and interadicular angle (IA).

Results: Mean ± standard deviation of buccal and lingual furcation measurements were, respectively, 1.37 ± 0.78 mm and 2.04 ± 0.89 mm for RT; 0.86 ± 0.39 mm and 0.71 ± 0.42 mm for D1; 1.50 ± 0.48 mm and 1.38 ± 0.48 mm for D2; 41.68 ± 13.20° and 37.78 ± 13.18° for IA. Statistically significant differences were found between all measured parameters for buccal and lingual sides (p<0.05, paired t test).

Conclusions: In conclusion, the lingual furcation of mandibular first molars presented narrower entrance and longer root trunk than the buccal furcation, suggesting more limitation for instrumentation and worse prognosis to lingual furcation involvements in comparison to buccal lesions.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3928776PMC
http://dx.doi.org/10.1590/s1678-77572012000100014DOI Listing
February 2012

Expression of suppressor of cytokine signaling 1 and 3 in ligature-induced periodontitis in rats.

Arch Oral Biol 2011 Oct 20;56(10):1120-8. Epub 2011 Apr 20.

Department of Diagnosis and Surgery, School of Dentistry at Araraquara, Univ Estadual Paulista - UNESP, Rua Humaita, 1680-Centro, Araraquara, SP, 14801-903, Brazil.

Objective: Evaluate expression of inducible negative regulators of JAK/STAT pathway and their target proteins during the course of ligature-induced experimental periodontal disease in rats.

Design: Rats were sacrificed 07, 15 and 30 days after disease induction for histological evaluation of periodontal inflammation and macroscopic analysis of alveolar bone loss. SOCS expression and the activation status of STAT1 and STAT3 were evaluated in gingival biopsies by real time PCR and Western blot.

Results: Ligature-induced model presented significant progressive bone loss from 7 to 30 days. Inflammation was evident and similar for 07 and 15 days; however, a decrease on severity at the end of the experimental period was observed. There was a significant (p<0.05) increase on SOCS1 and SOCS3 gene expression in PD compared to control group at 15 and 30days. The SOCS1 and SOCS3 protein expression and activation of STAT1 and STAT3 were increased in earlier periods in the ligature model.

Conclusion: This study suggests that SOCS1 and SOCS3 were directly correlated with regulatory mechanism of the inflammatory process responsible for the periodontal disease destruction.
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http://dx.doi.org/10.1016/j.archoralbio.2011.03.022DOI Listing
October 2011
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