scholarly journals Cigarette Smoking and Opium Use in Relation to the Oral Microbiota in Iran

Author(s):  
Zeni Wu ◽  
Yongli Han ◽  
J. Gregory Caporaso ◽  
Nicholas Bokulich ◽  
Ashraf Mohamadkhani ◽  
...  

Cigarette smoking and opium use are associated with periodontal disease caused by specific bacteria such as Porphyromonas gingivalis , which suggests a link between cigarette smoking and opium use and the oral microbiota. Alterations of the oral microbiota in cigarette smokers compared to nonsmokers have been reported, but this has not been studied across diverse populations.

2018 ◽  
Vol 200 (11) ◽  
pp. e00790-17 ◽  
Author(s):  
Christopher J. Rocco ◽  
Lauren O. Bakaletz ◽  
Steven D. Goodman

ABSTRACTThe oral cavity is home to a wide variety of bacterial species, both commensal, such as various streptococcal species, and pathogenic, such asPorphyromonas gingivalis, one of the main etiological agents of periodontal disease. Our understanding of how these bacteria ultimately cause disease is highly dependent upon understanding how they coexist and interact with one another in biofilm communities and the mechanisms by which biofilms are formed. Our research has demonstrated that the DNABII family of DNA-binding proteins are important components of the extracellular DNA (eDNA)-dependent matrix of bacterial biofilms and that sequestering these proteins via protein-specific antibodies results in the collapse of the biofilm structure and release of the resident bacteria. While the high degree of similarity among the DNABII family of proteins has allowed antibodies derived against specific DNABII proteins to disrupt biofilms formed by a wide range of bacterial pathogens, the DNABII proteins ofP. gingivalishave proven to be antigenically distinct, allowing us to determine if we can use anti-P. gingivalisHUβ antibodies to specifically target this species for removal from a mixed-species biofilm. Importantly, despite forming homotypic biofilmsin vitro,P. gingivalismust enter preexisting biofilmsin vivoin order to persist within the oral cavity. The data presented here indicate that antibodies derived against theP. gingivalisDNABII protein, HUβ, reduce by half the amount ofP. gingivalisorganisms entering into preexisting biofilm formed by four oral streptococcal species. These results support our efforts to develop methods for preventing and treating periodontal disease.IMPORTANCEPeriodontitis is one of the most prevalent chronic infections, affecting 40 to 50% of the population of the United States. The root cause of periodontitis is the presence of bacterial biofilms within the gingival space, withPorphyromonas gingivalisbeing strongly associated with the development of the disease. Periodontitis also increases the risk of secondary conditions and infections such as atherosclerosis and infective endocarditis caused by oral streptococci. To induce periodontitis,P. gingivalisneeds to incorporate into preformed biofilms, with oral streptococci being important binding partners. Our research demonstrates that targeting DNABII proteins with an antibody disperses oral streptococcus biofilm and preventsP. gingivalisentry into oral streptococcus biofilm. These results suggest potential therapeutic treatments for endocarditis caused by streptococci as well as periodontitis.


Author(s):  
Paul D. Veith ◽  
Mikio Shoji ◽  
Nichollas E. Scott ◽  
Eric C. Reynolds

Porphyromonas gingivalis is an oral pathogen primarily associated with severe periodontal disease and further associated with rheumatoid arthritis, dementia, cardiovascular disease, and certain cancers. Protein glycosylation can be important for a variety of reasons including protein function, solubility, protease resistance, and thermodynamic stability.


2013 ◽  
Vol 40 (10) ◽  
pp. 907-915 ◽  
Author(s):  
David F. Lappin ◽  
Danae Apatzidou ◽  
Anne-Marie Quirke ◽  
Jessica Oliver-Bell ◽  
John P. Butcher ◽  
...  

2017 ◽  
Vol 5 (46) ◽  
Author(s):  
Richard D. Haigh ◽  
Liam A. Crawford ◽  
Joseph D. Ralph ◽  
Joseph J. Wanford ◽  
Sonia R. Vartoukian ◽  
...  

ABSTRACT Periodontal disease comprises mild to severe inflammatory host responses to oral bacteria that can cause destruction of the tooth-supporting tissue. We report genome sequences for 18 clinical isolates of Porphyromonas gingivalis, Prevotella intermedia, and Tannerella forsythia, Gram-negative obligate anaerobes that play a role in the periodontal disease process.


mBio ◽  
2018 ◽  
Vol 9 (2) ◽  
Author(s):  
Maryta N. Sztukowska ◽  
Lindsay C. Dutton ◽  
Christopher Delaney ◽  
Mark Ramsdale ◽  
Gordon Ramage ◽  
...  

ABSTRACT The pleiomorphic yeast Candida albicans is a significant pathogen in immunocompromised individuals. In the oral cavity, C. albicans is an inhabitant of polymicrobial communities, and interspecies interactions promote hyphal formation and biofilm formation. C. albicans colonizes the subgingival area, and the frequency of colonization increases in periodontal disease. In this study, we investigated the interactions between C. albicans and the periodontal pathogen Porphyromonas gingivalis . C. albicans and P. gingivalis were found to coadhere in both the planktonic and sessile phases. Loss of the internalin-family protein InlJ abrogated adhesion of P. gingivalis to C. albicans , and recombinant InlJ protein competitively inhibited interspecies binding. A mutant of C. albicans deficient in expression of major hyphal protein Als3 showed diminished binding to P. gingivalis , and InlJ interacted with Als3 heterologously expressed in Saccharomyces cerevisiae . Transcriptional profiling by RNA sequencing (RNA-Seq) established that 57 genes were uniquely upregulated in an InlJ-dependent manner in P. gingivalis - C. albicans communities, with overrepresentation of those corresponding to 31 gene ontology terms, including those associated with growth and division. Of potential relevance to the disease process, C. albicans induced upregulation of components of the type IX secretion apparatus. Collectively, these findings indicate that InlJ-Als3-dependent binding facilitates interdomain community development between C. albicans and P. gingivalis and that P. gingivalis has the potential for increased virulence within such communities. IMPORTANCE Many diseases involve the concerted actions of microorganisms assembled in polymicrobial communities. Inflammatory periodontal diseases are among the most common infections of humans and result in destruction of gum tissue and, ultimately, in loss of teeth. In periodontal disease, pathogenic communities can include the fungus Candida albicans ; however, the contribution of C. albicans to the synergistic virulence of the community is poorly understood. Here we characterize the interactions between C. albicans and the keystone bacterial pathogen Porphyromonas gingivalis and show that coadhesion mediated by specific proteins results in major changes in gene expression by P. gingivalis , which could serve to increase pathogenic potential. The work provides significant insights into interdomain interactions that can enhance our understanding of diseases involving a multiplicity of microbial pathogens.


2016 ◽  
Vol 23 (4) ◽  
pp. 346-352 ◽  
Author(s):  
Young-Suk Choi ◽  
Ji-Hoi Moon ◽  
Tae-Geum Kim ◽  
Jin-Yong Lee

ABSTRACTFimbrial protein fimbrillin (FimA), a major structural subunit ofPorphyromonas gingivalis, has been suggested as a vaccine candidate to controlP. gingivalis-induced periodontal disease. Previously, cDNAs encoding IgG monoclonal antibodies (MAbs) against purified FimA fromP. gingivalis2561 have been cloned, and the MAbs have been produced in rice cell suspension. Here we examined the biological activities of the plant-produced MAb specific for FimA (anti-FimA plantibody) ofP. gingivalisin vitroandin vivo. The anti-FimA plantibody recognized oligomeric/polymeric forms of native FimA in immunoblot analysis and showed high affinity for native FimA (KD= 0.11 nM). Binding ofP. gingivalis(108cells) to 2 mg of saliva-coated hydroxyapatite beads was reduced by 53.8% in the presence of 1 μg/ml plantibody. Anti-FimA plantibody (10 μg/ml) reduced invasion of periodontal ligament cells byP. gingivalis(multiplicity of infection, 100) by 68.3%. Intracellular killing ofP. gingivalisopsonized with the anti-FimA plantibody by mouse macrophages was significantly increased (77.1%) compared to killing of bacterial cells with irrelevant IgG (36.7%). In a mouse subcutaneous chamber model, the number of recoverableP. gingivaliscells from the chamber fluid was significantly reduced when the numbers of bacterial cells opsonized with anti-FimA plantibody were compared with the numbers of bacterial cells with irrelevant IgG, 66.7% and 37.1%, respectively. Thesein vitroandin vivoeffects of anti-FimA plantibody were comparable to those of the parental MAb. Further studies withP. gingivalisstrains with different types of fimbriae are needed to investigate the usefulness of anti-FimA plantibody for passive immunization to controlP. gingivalis-induced periodontal disease.


2021 ◽  
Vol 73 (1) ◽  
Author(s):  
Mohammad Iqbal Janhangeer ◽  
Ghada Youssef ◽  
Weal El Naggar ◽  
Dalia El Remisy

Abstract Background Chronic heavy cigarette smoking can affect the right ventriclular function. The standard echocardiography may not show early right ventricular functional changes, and a more sensitive measure is needed. The aim of this work was to evaluate the subtle subclinical effects of chronic heavy cigarette smoking on the right ventricular function. The study included 55 healthy asymptomatic chronic heavy cigarette smokers (smoking history of at least 5 pack-years and a daily cigarette consumption of at least 1 pack) and 35 healthy non-smoking control subjects. Patients underwent a full clinical assessment and a conventional as well as a 2D-speckle tracking transthoracic echocardiography of the right ventricle and data was compared between the 2 groups. Results The mean age was 32.9 ± 7.2 years in smokers and 30.9 ± 7.9 years in non-smokers (p = 0.227). The 2 groups showed comparable conventional right ventricular systolic and diastolic functions. Smokers showed a significantly lower (less negative) right ventricular global longitudinal strain (− 19.0 ± 3.2% vs. − 24.5 ± 3.5%, p < 0.001). Patients with a higher daily cigarette consumption showed a poorer right ventricular global longitudinal strain (p = 0.014). Conclusion Chronic heavy cigarette smoking can adversely affect the right ventricular function, a finding that can be easily missed by conventional echocardiography and can be better detected by the right ventricular speckle tracking.


2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 240.2-241
Author(s):  
F. Zekre ◽  
R. Cimaz ◽  
M. Paul ◽  
J. L. Stephan ◽  
S. Paul ◽  
...  

Background:Idiopathic juvenile arthritis (JIA) is a heterogeneous group of pathologies whose origin remains unknown at present (1). They are characterised by a systemic inflammatory and joint disease affecting children under 16 years of age. The current classification groups the different forms of JIA into 7 distinct entities (systemic forms, polyarticular forms with or without rheumatoid factors, oligoarticular forms, inflammatory arthritis associated with enthesopathies (ERA), arthritis associated with psoriasis and unclassifiable arthritis). Exact etiology of JIA is still unknown. To date, the various hypotheses put forward on the occurrence of JIAs integrate the genetic and environmental framework.The link between periodontal disease and rheumatoid arthritis (RA) is largely reported. Recently, Porphyromonas gingivalis (P. gingivalis) infection explained the occurrence of arthritis in rodent and in RA (2). Several studies mention the beneficial effect of P. gingivalis treatment on disease activity.Currently, there are very few studies on the prevalence of P. gingivalis in patients with JIA and the possible involvement of the germ in the development of inflammatory joint diseases in the pediatric population(3)(4).Objectives:The objective of our study is to determine presence of high IgG antibodies against P. gingivalis and Prevotella Intermedia in a cohort of patients with JIA compared to a control population and to determine variation of level according to sub-classes of JIA.Methods:Sera were obtained from 101 patients satisfying the ILAR classification criteria for JIA and in 25 patients with two other dysimmune disorders (type 1 diabetes and juvenile inflammatory bowel disease). Level of IgG antibodies against P. gingivalis and Prevotella Intermedia were obtained by homemade ELISA already used previously (5).Results:In the JIA group, major children were oligarthritis (47.5%), polyarthritis represents 31.7% of JIAs, ERA and systemic forms of JIA are respectively 9 and 11%. For the control group, 10 (40%) children had diabetes and 15 (60%) had IBD.Levels of anti-P. gingivalis anti-Prevotella Intermedia antibodies were higher in AJI group compared at control groups (P<0.01, P<0.05). Theses difference are mainly related to oligoarthritis and ERA subsets for both P. gingivalis and Prevotella Intermedia.Figure 1.Relative titer of antibodies to P. gingivalis and anti Prevotella intermedia. *: P<0.05; **: P<0.01; ***: P<0.001. P. gingivalis (control vs oligoarthritis p= 0.0032. control vs ERA p= 0.0092). Prevotella intermedia (control vs oligoarthritis p= 0.0194. control vs ERA p= 0.0039).Conclusion:We confirmed high level of anti-P. gingivalis and anti-Prevotella intermedia antibodies in JIA compared to other inflammatory disorders. For the first time, we observed that this high level was mainly in oligoarthritis and ERA. Further investigations are required to investigate involvement of oral dysbiosis in AJI pathogenesis. As observed in RA, it could be a new way to integrate in JIA therapy management.References:[1]Thatayatikom A, De Leucio A. Juvenile Idiopathic Arthritis (JIA). StatPearls Publishing; 2020[2]Cheng Z, Meade J, Mankia K, Emery P, Devine DA. Periodontal disease and periodontal bacteria as triggers for rheumatoid arthritis. Best Pract Res Clin Rheumatol. 2017;31(1):19–30.[3]Romero-Sánchez C, Malagón C, Vargas C, Fernanda Torres M, Moreno LC, Rodríguez C, et al. Porphyromonas Gingivalis and IgG1 and IgG2 Subclass Antibodies in Patients with Juvenile Idiopathic Arthritis. J Dent Child Chic Ill. 2017 May 15;84(2):72–9.[4]Lange L, Thiele GM, McCracken C, Wang G, Ponder LA, Angeles-Han ST, et al. Symptoms of periodontitis and antibody responses to Porphyromonas gingivalis in juvenile idiopathic arthritis. Pediatr Rheumatol Online J. 2016 Feb 9[5]Rinaudo-Gaujous M, Blasco-Baque V, Miossec P, Gaudin P, Farge P, Roblin X, et al. Infliximab Induced a Dissociated Response of Severe Periodontal Biomarkers in Rheumatoid Arthritis Patients. J Clin Med. 2019 May 26;8(5).Disclosure of Interests:None declared.


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