Publications by authors named "Roger M Arce"

18 Publications

  • Page 1 of 1

Resin Bonding of a Lithium-Disilicate Crown Using a Ligated Rubber Dam: A 2-Year Case Report.

Compend Contin Educ Dent 2021 Apr;42(4):188-191

Professor, Department of Restorative Sciences, Dental College of Georgia, Augusta University, Augusta, Georgia.

Enduring glass-ceramic restorations greatly depend on the quality of adhesion of the crown to enamel and dentin. Proper isolation is vital to the success of bonded ceramic restorations. The rubber dam has long been considered the primary method of preventing contamination of the operating field, a crucial requisite for adhesion. However, many dentists do not use rubber dam isolation due to its penchant for slowing down procedures. The authors present a case report that describes a technique for the indirect bonding of a ceramic restoration to a maxillary first molar using rubber dam isolation in conjunction with a floss ligature,a method that is aimed at optimizing operator effectiveness and efficiency.
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April 2021

Dendritic cell derived exosomes loaded with immunoregulatory cargo reprogram local immune responses and inhibit degenerative bone disease .

J Extracell Vesicles 2020 Aug 7;9(1):1795362. Epub 2020 Aug 7.

Department of Periodontics, Dental College of Georgia at Augusta University, GA, USA.

Chronic bone degenerative diseases represent a major threat to the health and well-being of the population, particularly those with advanced age. This study isolated exosomes (EXO), natural nano-particles, from dendritic cells, the "directors" of the immune response, to examine the immunobiology of DC EXO in mice, and their ability to reprogram immune cells responsible for experimental alveolar bone loss . Distinct DC EXO subtypes including immune-regulatory (regDC EXO), loaded with TGFB1 and IL10 after purification, along with immune stimulatory (stimDC EXO) and immune "null" immature (iDCs EXO) unmodified after purification, were delivered via I.V. route or locally into the soft tissues overlying the alveolar bone. Locally administrated regDC EXO showed high affinity for inflamed sites, and were taken up by both DCs and T cells . RegDC EXO-encapsulated immunoregulatory cargo (TGFB1 and IL10) was protected from proteolytic degradation. Moreover, maturation of recipient DCs and induction of Th17 effectors was suppressed by regDC EXO, while T-regulatory cell recruitment was promoted, resulting in inhibition of bone resorptive cytokines and reduction in osteoclastic bone loss. This work is the first demonstration of DC exosome-based therapy for a degenerative alveolar bone disease and provides the basis for a novel treatment strategy.
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http://dx.doi.org/10.1080/20013078.2020.1795362DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7480413PMC
August 2020

Systemic Th17 response in the presence of periodontal inflammation.

J Appl Oral Sci 2020 3;28:e20190490. Epub 2020 Apr 3.

Pontificia Universidad Javeriana, Facultad de Odontología, Centro de Investigaciones Odontológicas, Bogotá, Colombia.

Background: The relationship between periodontitis and the pathogenesis of other inflammatory diseases, such as diabetes, rheumatoid arthritis and obesity has been an important topic of study in recent decades. The Th17 pathway plays a significant role in how local inflammation can influence systemic inflammation in the absence of systemic pathology.

Objective: To determine Th17 biased-cells in systemically healthy patients in the presence of generalized chronic periodontitis.

Methodology: A total of 28 patients were recruited without systemic inflammatory pathology, which was determined by clinical history, the Health Assessment Questionnaire (HAQ) and rheumatoid factor detection. Of these patients, 13 were diagnosed as healthy/gingivitis (H/G) and 15 as generalized chronic periodontitis (GCP). Th17 (CD4+CD161+) cells and Th17IL23R+ (CD4+CD161+IL-23R+) cells were quantified by flow cytometry, based on the total cells and on the lymphocyte region, termed the "enriched population" (50,000 events for each).

Results: The percentages of Th17 cells of the H/G and periodontitis groups were similar on total cells and enriched population (19 vs 21.8; p=4.134 and 19.6 vs 21.8; p=0.55). However, Th17IL23R+ cells differ significantly between periodontally healthy patients and generalized chronic periodontitis patients in both total cell (0.22% vs 0.65%; p=0.0004) and enriched populations (0.2% vs 0.75%; p=0.0266).

Conclusions: GCP patients (otherwise systemically healthy) were characterized by increased Th17-proinflammatory cell phenotype positive for the IL-23 receptor in peripheral blood. The proportion of Th17 cells that are negative for the IL-23 receptor in the peripheral blood of systemically healthy patients seemed to be unaffected by the presence or absence of chronic periodontitis.
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http://dx.doi.org/10.1590/1678-7757-2019-0490DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7135952PMC
April 2020

Polymicrobial synergy within oral biofilm promotes invasion of dendritic cells and survival of consortia members.

NPJ Biofilms Microbiomes 2019 03 18;5(1):11. Epub 2019 Mar 18.

Department of Periodontics, The Dental College of Georgia, Augusta University, Augusta, GA, USA.

Years of human microbiome research have confirmed that microbes rarely live or function alone, favoring diverse communities. Yet most experimental host-pathogen studies employ single species models of infection. Here, the influence of three-species oral microbial consortium on growth, virulence, invasion and persistence in dendritic cells (DCs) was examined experimentally in human monocyte-derived dendritic cells (DCs) and in patients with periodontitis (PD). Cooperative biofilm formation by Streptococcus gordonii, Fusobacterium nucleatum and Porphyromonas gingivalis was documented in vitro using growth models and scanning electron microscopy. Analysis of growth rates by species-specific 16s rRNA probes revealed distinct, early advantages to consortium growth for S. gordonii and F. nucleatum with P. gingivalis, while P. gingivalis upregulated its short mfa1 fimbriae, leading to increased invasion of DCs. F. nucleatum was only taken up by DCs when in consortium with P. gingivalis. Mature consortium regressed DC maturation upon uptake, as determined by flow cytometry. Analysis of dental plaques of PD and healthy subjects by 16s rRNA confirmed oral colonization with consortium members, but DC hematogenous spread was limited to P. gingivalis and F. nucleatum. Expression of P. gingivalis mfa1 fimbriae was increased in dental plaques and hematogenous DCs of PD patients. P. gingivalis in the consortium correlated with an adverse clinical response in the gingiva of PD subjects. In conclusion, we have identified polymicrobial synergy in a three-species oral consortium that may have negative consequences for the host, including microbial dissemination and adverse peripheral inflammatory responses.
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http://dx.doi.org/10.1038/s41522-019-0084-7DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6423025PMC
March 2019

Role of dendritic cell-mediated immune response in oral homeostasis: A new mechanism of osteonecrosis of the jaw.

FASEB J 2020 02 9;34(2):2595-2608. Epub 2020 Jan 9.

Department of Oral Biology and Diagnostic Sciences, Dental College of Georgia, Augusta University, Augusta, GA, USA.

Dendritic cells are an important link between innate and adaptive immune response. The role of dendritic cells in bone homeostasis, however, is not understood. Osteoporosis medications that inhibit osteoclasts have been associated with osteonecrosis, a condition limited to the jawbone, thus called medication-related osteonecrosis of the jaw. We propose that disruption of the local immune response renders the oral microenvironment conducive to osteonecrosis. We tested whether zoledronate (Zol) treatment impaired dendritic cell (DC) functions and increased bacterial load in alveolar bone in vivo and whether DC inhibition alone predisposed the animals to osteonecrosis. We also analyzed the role of Zol in impairment of differentiation and function of migratory and tissue-resident DCs, promoting disruption of T-cell activation in vitro. Results demonstrated a Zol induced impairment in DC functions and an increased bacterial load in the oral cavity. DC-deficient mice were predisposed to osteonecrosis following dental extraction. Zol treatment of DCs in vitro caused an impairment in immune functions including differentiation, maturation, migration, antigen presentation, and T-cell activation. We conclude that the mechanism of Zol-induced osteonecrosis of the jaw involves disruption of DC immune functions required to clear bacterial infection and activate T cell effector response.
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http://dx.doi.org/10.1096/fj.201901819RRDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7712496PMC
February 2020

Periodontal inflammation: Integrating genes and dysbiosis.

Periodontol 2000 2020 02;82(1):129-142

Department of Periodontics, Dental College of Georgia, Augusta University, Augusta, Georgia, USA.

Biofilm bacteria co-evolve and reach a symbiosis with the host on the gingival surface. The disruption of the homeostatic relationship between plaque bacteria and the host can initiate and promote periodontal disease progression. Recent advances in sequencing technologies allow researchers to profile disease-associated microbial communities and quantify microbial metabolic activities and host transcriptional responses. In addition to confirming the findings from previous studies, new putative pathogens and novel genes that have not previously been associated with periodontitis, emerge. For example, multiple studies have reported that Synergistetes bacteria are associated with periodontitis. Genes involved in epithelial barrier defense were downregulated in periodontitis, while excessive expression of interleukin-17 was associated with a hyperinflammatory response in periodontitis and with a unique microbial community. Bioinformatics-enabled gene ontology pathway analyses provide a panoramic view of the bacterial and host activities as they shift from periodontal health to disease. Additionally, host innate factors, such as genetic variants identified by either a candidate-gene approach or genome-wide association analyses, have an impact on subgingival bacterial colonization. Transgenic mice carrying candidate genetic variants, or with the deletion of candidate genes mimicking the deleterious loss-of-function variant effect, provide experimental evidence validating the biologic relevance of the novel markers associated with the microbial phenotype identified through a statistical approach. Further refinement in bioinformatics, data management approaches, or statistical tools, are required to gain insight into host-microbe interactions by harmonizing the multidimensional "big" data at the genomic, transcriptional, and proteomic levels.
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http://dx.doi.org/10.1111/prd.12267DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6924568PMC
February 2020

Disruption of Immune Homeostasis in Human Dendritic Cells via Regulation of Autophagy and Apoptosis by .

Front Immunol 2019 24;10:2286. Epub 2019 Sep 24.

Department of Periodontics, Dental College of Georgia at Augusta University, Augusta, GA, United States.

As fundamental processes of immune homeostasis, autophagy, and apoptosis must be maintained to mitigate risk of chronic inflammation and autoimmune diseases. Periodontitis is a chronic inflammatory disease characterized by oral microbial dysbiosis, and dysregulation of dendritic cell (DC) and T cell responses. The aim of this study was to elucidate the underlying mechanisms by which the oral microbe () manipulates dendritic cell signaling to perturb both autophagy and apoptosis. Using a combination of Western blotting, flow cytometry, qRT-PCR and immunofluorescence analysis, we show a pivotal role for the minor (Mfa1) fimbriae of in nuclear/cytoplasmic shuttling of Akt and FOXO1 in human monocyte-derived DCs. Mfa1-induced Akt nuclear localization and activation ultimately induced mTOR. Activation of the Akt/mTOR axis downregulated intracellular LC3II, also known as Atg8, required for autophagosome formation and maturation. Use of allosteric panAkt inhibitor MK2206 and mTOR inhibitor rapamycin confirmed the role of Akt/mTOR signaling in autophagy inhibition by in DCs. Interestingly, this pathway was also linked to induction of the anti-apoptotic protein Bcl2, decreased caspase-3 cleavage and decreased expression of pro-apoptotic proteins Bax and Bim, thus promoting longevity of host DCs. Addition of ABT-199 peptide to disrupt the interaction of antiapoptotic Bcl2 and its proapoptotic partners BAK/BAX restored apoptotic death to infected DC cells. In summary, we have identified the underlying mechanism by which promotes its own survival and that of its host DCs.
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http://dx.doi.org/10.3389/fimmu.2019.02286DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6769118PMC
November 2020

Systemic Antibiotic Therapy Reduces Circulating Inflammatory Dendritic Cells and Treg-Th17 Plasticity in Periodontitis.

J Immunol 2019 05 3;202(9):2690-2699. Epub 2019 Apr 3.

Department of Periodontics, Dental College of Georgia at Augusta University, Augusta, GA 30912;

Periodontitis (PD) is a common dysbiotic inflammatory disease that leads to local bone deterioration and tooth loss. PD patients experience low-grade bacteremias with oral microbes implicated in the risk of heart disease, cancer, and kidney failure. Although Th17 effectors are vital to fighting infection, functional imbalance of Th17 effectors and regulatory T cells (Tregs) promote inflammatory diseases. In this study, we investigated, in a small pilot randomized clinical trial, whether expansion of inflammatory blood myeloid dendritic cells (DCs) and conversion of Tregs to Th17 cells could be modulated with antibiotics (AB) as part of initial therapy in PD patients. PD patients were randomly assigned to either 7 d of peroral metronidazole/amoxicillin AB treatment or no AB, along with standard care debridement and chlorhexidine mouthwash. 16s ribosomal RNA analysis of keystone pathogen and its consortium members and confirmed the presence of all three species in the reservoirs (subgingival pockets and blood DCs) of PD patients before treatment. Of the three species, was reduced in both reservoirs 4-6 wk after therapy. Further, the frequency of CD1CCCR6 myeloid DCs and IL-1R1 expression on IL-17AFOXP3CD4 T cells in PD patients were reduced to healthy control levels. The latter led to decreased IL-1β-stimulated Treg plasticity in PD patients and improvement in clinical measures of PD. Overall, we identified an important, albeit short-term, beneficial role of AB therapy in reducing inflammatory DCs and Treg-Th17 plasticity in humans with PD.
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http://dx.doi.org/10.4049/jimmunol.1900046DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6857811PMC
May 2019

The influence of vitamin D supplementation on local and systemic inflammatory markers in periodontitis patients: A pilot study.

Oral Dis 2019 Jul 21;25(5):1403-1413. Epub 2019 Apr 21.

Department of Periodontics, The Dental College of Georgia at Augusta University, Augusta, Georgia.

Objectives: Vitamin D deficiency/insufficiency is a worldwide public health issue that has been linked to numerous inflammatory disorders, including periodontitis. There is increasing support for a role for adequate vitamin D levels in overall health. Populations with darker skin color have a higher prevalence of vitamin D deficiency/insufficiency and periodontitis. The purpose of this small pilot study was to investigate the influence of 12 weeks of 25(OH)D vitamin D supplementation (VDS) on mediators of systemic inflammation in dark-skinned, periodontitis patients.

Materials And Methods: A total of 23 patients with moderate to severe periodontitis were randomly assigned to the vitamin D group or placebo group and received intensive single visit scaling and root planning to elicit a systemic inflammatory response.

Results: Vitamin D supplementation increased serum 25(OH)D levels approximately 2-fold over baseline levels; moreover, VDS group had reduced peripheral blood CD3 and CD3+CD8+ cytotoxic T lymphocyte (CTLs) counts and reduced pro-inflammatory salivary cytokines. In contrast, VDS group had higher levels of the autophagy-related proteins and other proteins crucial for anti-microbial autophagy in whole blood PBMCs.

Conclusion: In conclusion, VDS has multiple benefits for reducing systemic inflammation and promoting induction of autophagy-related proteins related to anti-microbial functions.
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http://dx.doi.org/10.1111/odi.13097DOI Listing
July 2019

Oral Pathobiont Activates Anti-Apoptotic Pathway, Promoting both Immune Suppression and Oncogenic Cell Proliferation.

Sci Rep 2018 11 9;8(1):16607. Epub 2018 Nov 9.

Department of Periodontics, Dental College of Georgia, Augusta University, Augusta, Georgia, United States of America.

Chronic periodontitis (CP) is a microbial dysbiotic disease linked to increased risk of oral squamous cell carcinomas (OSCCs). To address the underlying mechanisms, mouse and human cell infection models and human biopsy samples were employed. We show that the 'keystone' pathogen Porphyromonas gingivalis, disrupts immune surveillance by generating myeloid-derived dendritic suppressor cells (MDDSCs) from monocytes. MDDSCs inhibit CTLs and induce FOXP3 + T through an anti-apoptotic pathway. This pathway, involving pAKT1, pFOXO1, FOXP3, IDO1 and BIM, is activated in humans with CP and in mice orally infected with Mfa1 expressing P. gingivalis strains. Mechanistically, activation of this pathway, demonstrating FOXP3 as a direct FOXO1-target gene, was demonstrated by ChIP-assay in human CP gingiva. Expression of oncogenic but not tumor suppressor markers is consistent with tumor cell proliferation demonstrated in OSCC-P. gingivalis cocultures. Importantly, FimA + P. gingivalis strain MFI invades OSCCs, inducing inflammatory/angiogenic/oncogenic proteins stimulating OSCCs proliferation through CXCR4. Inhibition of CXCR4 abolished Pg-MFI-induced OSCCs proliferation and reduced expression of oncogenic proteins SDF-1/CXCR4, plus pAKT1-pFOXO1. Conclusively, P. gingivalis, through Mfa1 and FimA fimbriae, promotes immunosuppression and oncogenic cell proliferation, respectively, through a two-hit receptor-ligand process involving DC-SIGN/CXCR4, activating a pAKTpFOXO1BIMFOXP3 and IDO- driven pathway, likely to impact the prognosis of oral cancers in patients with periodontitis.
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http://dx.doi.org/10.1038/s41598-018-35126-8DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6226501PMC
November 2018

Long-term sustainable dendritic cell-specific depletion murine model for periodontitis research.

J Immunol Methods 2017 10 21;449:7-14. Epub 2017 Jun 21.

Department of Periodontics, The Dental College of Georgia at Augusta University, 1120 15th Street, Augusta, GA 30912, USA. Electronic address:

Dendritic cells (DCs) are specialized antigen-presenting cells that play a pivotal role in the pathogenesis of periodontitis. The use of animal models to study the role of DCs in periodontitis has been limited by lack of a method for sustained depletion of DCs. Hence, the objectives of this study were to validate the zDC-DTR knockin mouse model of conventional DCs (cDCs) depletion, as well as to investigate whether this depletion could be sustained long enough to induce alveolar bone loss in this model. zDC-DTR mice were treated with different dose regimens of diphtheria toxin (DT) to determine survival rate. A loading DT dose of 20ng/bw, followed and maintained with doses of 10ng/bm every 3days for up to 4weeks demonstrated 80% survival. Animals were weighed weekly and peripheral blood was obtained to confirm normal neutrophil counts. Five animals per group were euthanized at baseline, 24h, 1 and 4weeks. Bone marrow (BM), spleen (SP) and gingival tissue (GT) were harvested, and cells were isolated, separated and stained for Pre-DCs precursors (CD45RMHCIICD11cFlt3CD172a) in BM, cDCs (CD11cMHCIICD209) in spleen, and DCs in GT (CD45RMHCIICD11c DC-SIGN/CD209). Pre-DCs in BM were significantly depleted at 24h and depletion maintained for up to 4weeks, as compared to blank (PBS) controls. Circulating cDCs in spleen demonstrated a non-significant trend to deplete in 1week with high variability among mice. GT also showed a similar non-significant trend to deplete in 24h. The zDC-DTR model seems to be viable for evaluating the role of DCs immune homeostasis disruption and alveolar bone loss pathogenesis in response to long-term oral infection.
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http://dx.doi.org/10.1016/j.jim.2017.06.007DOI Listing
October 2017

Gingival crevicular fluid levels of cytokines/chemokines in chronic periodontitis: a meta-analysis.

J Clin Periodontol 2016 09 23;43(9):727-45. Epub 2016 Jun 23.

Department of Periodontics, Dental College of Georgia, Augusta University, Augusta, GA, USA.

Aims: To compare gingival crevicular fluid (GCF) cytokines/chemokines levels between periodontally healthy subjects and subjects diagnosed with chronic periodontitis (ChP), before and after non-surgical periodontal treatment, and to establish their predictive value for periodontal disease progression.

Methods: Studies indexed in MEDLINE and EMBASE published in English, Portuguese and Spanish were eligible for this review. Database searches up to December 2015, and manual search of the reference list from reviews and selected articles was performed. Only studies providing data on GCF cytokines/chemokines levels in subjects diagnosed with ChP and periodontally healthy controls were included. Cross-sectional, case series, single-arm clinical studies, randomized controlled trials and prospective/retrospective cohort studies were included. Meta-analyses were conducted for those cytokines/chemokines with at least three available studies.

Results: GCF levels of IL-1β, IL-6, IFN-γ and MCP-1/CCL2 were significantly higher in subjects diagnosed with ChP than periodontally healthy subjects. A significant decrease in GCF levels of IL-1β and IL-17 was observed after non-surgical periodontal treatment, whereas a significant increase was observed for IL-4.

Conclusion: Evidence for significant differences between periodontal health and ChP was observed for a few cytokines and one chemokine. No conclusions could be drawn with regards to increased risk of disease progression.
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http://dx.doi.org/10.1111/jcpe.12557DOI Listing
September 2016

Dendritic cells: microbial clearance via autophagy and potential immunobiological consequences for periodontal disease.

Periodontol 2000 2015 Oct;69(1):160-80

Dendritic cells are potent antigen-capture and antigen-presenting cells that play a key role in the initiation and regulation of the adaptive immune response. This process of immune homeostasis, as maintained by dendritic cells, is susceptible to dysregulation by certain pathogens during chronic infections. Such dysregulation may lead to disease perpetuation with potentially severe systemic consequences. Here we discuss in detail how intracellular pathogens exploit dendritic cells and escape degradation by altering or evading autophagy. This novel mechanism explains, in part, the chronic, persistent nature observed in several immuno-inflammatory diseases, including periodontal disease. We also propose a hypothetical model of the plausible role of autophagy in the context of periodontal disease. Promotion of autophagy may open new therapeutic strategies in the search of a 'cure' for periodontal disease in humans.
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http://dx.doi.org/10.1111/prd.12096DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4530502PMC
October 2015

Porphyromonas gingivalis evasion of autophagy and intracellular killing by human myeloid dendritic cells involves DC-SIGN-TLR2 crosstalk.

PLoS Pathog 2015 Feb 13;10(2):e1004647. Epub 2015 Feb 13.

Department of Periodontics, Georgia Regents University, Augusta, Georgia, United States of America.

Signaling via pattern recognition receptors (PRRs) expressed on professional antigen presenting cells, such as dendritic cells (DCs), is crucial to the fate of engulfed microbes. Among the many PRRs expressed by DCs are Toll-like receptors (TLRs) and C-type lectins such as DC-SIGN. DC-SIGN is targeted by several major human pathogens for immune-evasion, although its role in intracellular routing of pathogens to autophagosomes is poorly understood. Here we examined the role of DC-SIGN and TLRs in evasion of autophagy and survival of Porphyromonas gingivalis in human monocyte-derived DCs (MoDCs). We employed a panel of P. gingivalis isogenic fimbriae deficient strains with defined defects in Mfa-1 fimbriae, a DC-SIGN ligand, and FimA fimbriae, a TLR2 agonist. Our results show that DC-SIGN dependent uptake of Mfa1+P. gingivalis strains by MoDCs resulted in lower intracellular killing and higher intracellular content of P. gingivalis. Moreover, Mfa1+P. gingivalis was mostly contained within single membrane vesicles, where it survived intracellularly. Survival was decreased by activation of TLR2 and/or autophagy. Mfa1+P. gingivalis strain did not induce significant levels of Rab5, LC3-II, and LAMP1. In contrast, P. gingivalis uptake through a DC-SIGN independent manner was associated with early endosomal routing through Rab5, increased LC3-II and LAMP-1, as well as the formation of double membrane intracellular phagophores, a characteristic feature of autophagy. These results suggest that selective engagement of DC-SIGN by Mfa-1+P. gingivalis promotes evasion of antibacterial autophagy and lysosome fusion, resulting in intracellular persistence in myeloid DCs; however TLR2 activation can overcome autophagy evasion and pathogen persistence in DCs.
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http://dx.doi.org/10.1371/journal.ppat.1004647DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4352937PMC
February 2015

Retrospective study on idiopathic bone cavity and its association with cementoosseous dysplasia.

Oral Surg Oral Med Oral Pathol Oral Radiol 2015 Apr 13;119(4):e246-51. Epub 2014 Oct 13.

Department of Oral and Maxillofacial Pathology, Georgia Regents University, Augusta, Georgia.

Objective: The goal of this study was to reveal clinical and pathologic findings on idiopathic bone cavity lesions (IBC).

Study Design: A retrospective analysis of 20 IBC cases diagnosed from 2004 to 2014 from a university-based maxillofacial pathology service was performed and included all pertinent clinical, histologic, and radiographic findings.

Results: Eleven women (age = 36 ± 12.7) and 9 men (age = 23 ± 17.9) diagnosed with IBC were selected for analysis. There was a higher African-American female predilection (40%). Thirty percent of the cases were associated with florid cementoosseous dysplasia (COD) (all middle-aged African-American women). The location of the lesions was mandibular in 85% of the patients. All symptomatic patients (25%) had concomitant COD. Only 1 patient reported previous trauma, and only 1 patient had prior orthodontic treatment. Follow-up period ranged from 1 to 8 years, with only 1 recurrence 3 years after surgery.

Conclusions: The results suggest that IBC concurrent with COD may not be as rare as the literature implies. Clinicians must be attentive to this possible relationship to ensure accurate diagnosis and appropriate treatment.
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http://dx.doi.org/10.1016/j.oooo.2014.09.032DOI Listing
April 2015

Software tools and surgical guides in dental-implant-guided surgery.

Dent Clin North Am 2014 Jul;58(3):597-626

Department of Periodontics, Georgia Regents University, Augusta, GA 30912, USA.

Cone beam computed tomography has become an essential tool in the diagnosis and planning for implant dentistry. New hardware and software developments have emerged to help implant surgeons to successfully adopt and use different systems in patients requiring prosthetically driven implant dentistry. However, there is the need to develop an adequate planning protocol that includes appropriate acquisition/data manipulation, appropriate use of software tools for interpretation, and appropriate application of such systems during implant surgery. This article examines essential characteristics of the entire implant-guided surgery planning process and points out potential sources of error that could affect clinical accuracy outcomes.
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http://dx.doi.org/10.1016/j.cden.2014.04.001DOI Listing
July 2014

Periodontal treatment effects on endothelial function and cardiovascular disease biomarkers in subjects with chronic periodontitis: protocol for a randomized clinical trial.

Trials 2011 Feb 16;12:46. Epub 2011 Feb 16.

Periodontal Medicine Research Group, Department of Periodontology, School of Dentistry, Universidad del Valle, Calle 4B 36-00, Cali, Colombia.

Background: Periodontal disease (PD) is an infectious clinical entity characterized by the destruction of supporting tissues of the teeth as the result of a chronic inflammatory response in a susceptible host. It has been proposed that PD as subclinical infection may contribute to the etiology and to the pathogenesis of several systemic diseases including Atherosclerosis. A number of epidemiological studies link periodontal disease/edentulism as independent risk factor for acute myocardial infarction, peripheral vascular disease, and cerebrovascular disease. Moreover, new randomized controlled clinical trials have shown an improvement on cardiovascular surrogate markers (endothelial function, sICAM, hsPCR level, fibrinogen) after periodontal treatment. Nonetheless, such trials are still limited in terms of external validity, periodontal treatment strategies, CONSORT-based design and results consistency/extrapolation. The current study is designed to evaluate if periodontal treatment with scaling and root planning plus local delivered chlorhexidine improves endothelial function and other biomarkers of cardiovascular disease in subjects with moderate to severe periodontitis.

Methods/design: This randomized, single-blind clinical trial will be performed at two health centers and will include two periodontal treatment strategies. After medical/periodontal screening, a baseline endothelium-dependent brachial artery flow-mediated dilatation (FMD) and other systemic surrogate markers will be obtained from all recruited subjects. Patients then will be randomized to receive either supragingival/subgingival plaque cleaning and calculus removal plus chlorhexidine (treatment group) or supragingival plaque removal only (control group). A second and third FMD will be obtained after 24 hours and 12 weeks in both treatment arms. Each group will consist of 49 patients (n = 98) and all patients will be followed-up for secondary outcomes and will be monitored through a coordinating center. The primary outcomes are FMD differences baseline, 24 hours and 3 months after treatment. The secondary outcomes are differences in C-reactive protein (hs-CRP), glucose serum levels, blood lipid profile, and HOMA index.

Discussion: This RCT is expected to provide more evidence on the effects of different periodontal treatment modalities on FMD values, as well as to correlate such findings with different surrogate markers of systemic inflammation with cardiovascular effects.

Trial Registration Number: ClinicalTrials.gov Identifier: NCT00681564.
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http://dx.doi.org/10.1186/1745-6215-12-46DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3049125PMC
February 2011

Periodontal disease severity is related to high levels of C-reactive protein in pre-eclampsia.

J Hypertens 2007 Jul;25(7):1459-64

Department of Family Medicine, School of Medicine, Universidad del Valle, Cali, Colombia.

Objective: Recent studies have shown that pre-eclamptic women present a high prevalence of periodontitis, suggesting that active periodontal disease may play a role in the pathogenesis of pre-eclampsia. The present study analysed the effect of periodontal disease in the concentrations of serum high-sensitivity C-reactive protein (hs-CRP), and its association with pre-eclampsia.

Methods: A case-control study was carried out in Cali-Colombia, comprised of 398 pregnant women (145 cases and 253 controls) who were believed to have periodontal disease, between 28 and 36 weeks of gestational age. Pre-eclampsia cases were defined as blood pressure > or = 140/90 mmHg and proteinuria > or = 0.3 g/24 h. Controls were pregnant women with normal blood pressure, without proteinuria, matched by maternal age, gestational age and body mass index. Sociodemographic data, obstetric risk factors, periodontal state, subgingival microbial composition and hs-CRP levels were determined in both groups.

Results: The case and control groups were comparable for sociodemographic characteristics. In women with pre-eclampsia and confirmed periodontal disease (n = 138), hs-CRP levels increased according to the severity of the disease (gingivitis median 4.14 mg/dl; mild periodontitis median 4.70 mg/dl; moderate/severe periodontitis median 8.8 mg/dl; P = 0.01). A similar tendency was observed in controls with periodontal disease (n = 251), but it did not reach statistical significance (gingivitis median 5.10 mg/dl; mild periodontitis median 5.12 mg/dl; moderate/severe periodontitis median 6.90 mg/dl; P = 0.07). A significant difference in hs-CRP levels was observed in pre-eclamptic women with moderate/severe periodontitis compared to controls (P = 0.01).

Conclusion: These findings suggest that chronic periodontitis may increase hs-CRP levels in pregnant women and lead to complications such as pre-eclampsia.
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http://dx.doi.org/10.1097/HJH.0b013e3281139ea9DOI Listing
July 2007