An analysis of selected secretion systems of Pseudomonas species

Direct secretion systems which deliver molecules from one cell to another have huge significance in shaping bacterial communities or in determining the outcome of bacterial associations with eukaryotic organisms. This work examines the roles of the Type III Secretion System (T3SS) and the Type VI Secretion System (T6SS) systems of Pseudomonas, a widespread genus including clinical pathogens and biocontrol strains. Bioinformatic analysis of T6SS phylogeny and associated gene content within Pseudomonas identified several T6SS phylogenetic groups, and linked T6SS components VgrG and Hcp encoded outside of T6SS gene loci with their cognate T6SS phylogenetic groups. Remarkably, such “orphan” vgrG and hcp genes were found to occur in diverse, horizontally transferred, operons often containing putative T6SS accessory components and effectors. The prevalence of a widespread superfamily of T6SS lipase effectors (Tle) was assessed in metagenomes from various environments. The abundance of the Tle superfamily and individual families varied between niches, suggesting there is niche specific selection and specialisation of Tle. Experimental work also discovered that P. fluorescens F113 uses the SPI-1 T3SS to avoid amoeboid grazing in mixed populations. This finding may represent a significant aspect of F113 rhizocompetence, and the rhizocompetence of other Rhizobacteria.

Long-term statin therapy in patients with systolic heart failure and normal cholesterol:effects on elevated serum markers of collagen turnover, inflammation, and B-type natriuretic peptide

BACKGROUND: The role of statin therapy in heart failure (HF) is unclear. The amino-terminal propeptide of procollagen type III (PIIINP) predicts outcome in HF, and yet there are conflicting reports of statin therapy effects on PIIINP.

OBJECTIVES: This study determined whether there was an increase in serum markers of inflammation, fibrosis (including PIIINP), and B-type natriuretic peptide (BNP) in patients with systolic HF and normal total cholesterol and determined the effects of long-term treatment with atorvastatin on these markers.

METHODS: Fifty-six white patients with systolic HF and normal cholesterol levels (age 72 [13] years; 68% male; body mass index 27.0 [7.3] kg/m(2); ejection fraction 35 [13]%; 46% with history of smoking) were randomly allocated to atorvastatin treatment for 6 months, titrated to 40 mg/d (A group) or not (C group). Age- and/or sex-matched subjects without HF (N group) were also recruited. Biomarkers were measured at baseline (all groups) and 6 months (A and C groups).

RESULTS: Serum markers of collagen turnover, inflammation, and BNP were significantly elevated in HF patients compared with normal participants (all P < 0.05). There were correlations between these markers in HF patients but not in normal subjects. Atorvastatin treatment for 6 months caused a significant reduction in the following biomarkers compared with baseline: BNP, from median (interquartile range) 268 (190-441) pg/mL to 185 (144-344) pg/mL; high-sensitivity C-reactive protein (hs-CRP), from 5.26 (1.95 -9.29) mg/L to 3.70 (2.34-6.81) mg/L; and PIIINP, from 4.65 (1.86) to 4.09 (1.25) pg/mL (all P < 0.05 baseline vs 6 months). Between-group differences were significant for PIIINP only (P = 0.027). There was a positive interaction between atorvastatin effects and baseline hs-CRP and PIIINP (P < 0.01).

CONCLUSIONS: Long-term statin therapy reduced PIIINP in this small, selected HF population with elevated baseline levels. Further evaluation of statin therapy in the management of HF patients with elevated PIIINP is warranted.

Hypoxia-induced DNA hypermethylation in human pulmonary fibroblasts is associated with Thy-1 promoter methylation and the development of a pro-fibrotic phenotype

BACKGROUND: Pulmonary fibrosis is a debilitating and lethal disease with no effective treatment options. Understanding the pathological processes at play will direct the application of novel therapeutic avenues. Hypoxia has been implicated in the pathogenesis of pulmonary fibrosis yet the precise mechanism by which it contributes to disease progression remains to be fully elucidated. It has been shown that chronic hypoxia can alter DNA methylation patterns in tumour-derived cell lines. This epigenetic alteration can induce changes in cellular phenotype with promoter methylation being associated with gene silencing. Of particular relevance to idiopathic pulmonary fibrosis (IPF) is the observation that Thy-1 promoter methylation is associated with a myofibroblast phenotype where loss of Thy-1 occurs alongside increased alpha smooth muscle actin (α-SMA) expression. The initial aim of this study was to determine whether hypoxia regulates DNA methylation in normal human lung fibroblasts (CCD19Lu). As it has been reported that hypoxia suppresses Thy-1 expression during lung development we also studied the effect of hypoxia on Thy-1 promoter methylation and gene expression.

METHODS: CCD19Lu were grown for up to 8 days in hypoxia and assessed for global changes in DNA methylation using flow cytometry. Real-time PCR was used to quantify expression of Thy-1, α-SMA, collagen I and III. Genomic DNA was bisulphite treated and methylation specific PCR (MSPCR) was used to examine the methylation status of the Thy-1 promoter.

RESULTS: Significant global hypermethylation was detected in hypoxic fibroblasts relative to normoxic controls and was accompanied by increased expression of myofibroblast markers. Thy-1 mRNA expression was suppressed in hypoxic cells, which was restored with the demethylating agent 5-aza-2'-deoxycytidine. MSPCR revealed that Thy-1 became methylated following fibroblast exposure to 1% O2.

CONCLUSION: These data suggest that global and gene-specific changes in DNA methylation may play an important role in fibroblast function in hypoxia.

The enteropathogenic Escherichia coli effector NleH inhibits apoptosis induced by Clostridium difficile toxin B

Clostridium difficile is a leading cause of nosocomial infections, causing a spectrum of diseases ranging from diarrhoea to pseudomembranous colitis triggered by a range of virulence factors including C. difficile toxins A (TcdA) and B (TcdB). TcdA and TcdB are monoglucosyltransferases that irreversibly glycosylate small Rho GTPases, inhibiting their ability to interact with their effectors, guanine nucleotide exchange factors, and membrane partners, leading to disruption of downstream signalling pathways and cell death. In addition, TcdB targets the mitochondria, inducing the intrinsic apoptotic pathway resulting in TcdB-mediated apoptosis. Modulation of apoptosis is a common strategy used by infectious agents. Recently, we have shown that the enteropathogenic Escherichia coli (EPEC) type III secretion system effector NleH has a broad-range anti-apoptotic activity. In this study we examined the effects of NleH on cells challenged with TcdB. During infection with wild-type EPEC, NleH inhibited TcdB-induced apoptosis at both low and high toxin concentrations. Transfected nleH1 alone was sufficient to block TcdB-induced cell rounding, nuclear condensation, mitochondrial swelling and lysis, and activation of caspase-3. These results show that NleH acts via a global anti-apoptotic pathway.

NleH effectors interact with Bax inhibitor-1 to block apoptosis during enteropathogenic Escherichia coli infection

The human pathogens enteropathogenic (EPEC) and enterohemorrhagic Escherichia coli and the related mouse pathogen Citrobacter rodentium subvert a variety of host cell signaling pathways via their plethora of type III secreted effectors, including triggering of an early apoptotic response. EPEC-infected cells do not develop late apoptotic symptoms, however. In this study we demonstrate that the NleH family effectors, homologs of the Shigella effector kinase OspG, blocks apoptosis. During EPEC infection, NleH effectors inhibit elevation of cytosolic Ca(2+) concentrations, nuclear condensation, caspase-3 activation, and membrane blebbing and promote cell survival. NleH1 alone is sufficient to prevent procaspase-3 cleavage induced by the proapoptotic compounds staurosporine, brefeldin A, and tunicamycin. Using C. rodentium, we found that NleH inhibits procaspase-3 cleavage at the bacterial attachment sites in vivo. A yeast two-hybrid screen identified the endoplasmic reticulum six-transmembrane protein Bax inhibitor-1 (BI-1) as an NleH-interacting partner. We mapped the NleH-binding site to the N-terminal 40 amino acids of BI-1. Knockdown of BI-1 resulted in the loss of NleH's antiapoptotic activity. These results indicate that NleH effectors are inhibitors of apoptosis that may act through BI-1 to carry out their cytoprotective function.

Cortactin recruitment by enterohemorrhagic Escherichia coli O157:H7 during infection in vitro and ex vivo

Enterohemorrhagic Escherichia coli (EHEC) O157:H7 is an important human pathogen that colonizes the gut mucosa via attaching and effacing (A/E) lesions; A/E lesion formation in vivo and ex vivo is dependent on the type III secretion system (T3SS) effector Tir. Infection of cultured cells by EHEC leads to induction of localized actin polymerization, which is dependent on Tir and a second T3SS effector protein, TccP, also known as EspF(U). Recently, cortactin was shown to bind both the N terminus of Tir and TccP via its SH3 domain and to play a role in EHEC-triggered actin polymerization in vitro. In this study, we investigated the recruitment of cortactin to the site of EHEC adhesion during infection of in vitro-cultured cells and mucosal surfaces ex vivo (using human terminal ileal in vitro organ cultures [IVOC]). We have shown that cortactin is recruited to the site of EHEC adhesion in vitro downstream of TccP and N-WASP. Deletion of the entire N terminus of Tir or replacing the N-terminal polyproline region with alanines did not abrogate actin polymerization or cortactin recruitment. In contrast, recruitment of cortactin to the site of EHEC adhesion in IVOC is TccP independent. These results imply that cortactin is recruited to the site of EHEC adhesion in vitro and ex vivo by different mechanisms and suggest that cortactin might have a role during EHEC infection of mucosal surfaces.

Assessment of turbulence model predictions for a centrifugal compressor simulation

Steady-state computational fluid dynamics (CFD) simulations are an essential tool in the design process of centrifugal compressors. Whilst global parameters, such as pressure ratio and efficiency, can be predicted with reasonable accuracy, the accurate prediction of detailed compressor flow fields is a much more significant challenge. Much of the inaccuracy is associated with the incorrect selection of turbulence model. The need for a quick turnaround in simulations during the design optimisation process, also demands that the turbulence model selected be robust and numerically stable with short simulation times.
In order to assess the accuracy of a number of turbulence model predictions, the current study used an exemplar open CFD test case, the centrifugal compressor ‘Radiver’, to compare the results of three eddy viscosity models and two Reynolds stress type models. The turbulence models investigated in this study were (i) Spalart-Allmaras (SA) model, (ii) the Shear Stress Transport (SST) model, (iii) a modification to the SST model denoted the SST-curvature correction (SST-CC), (iv) Reynolds stress model of Speziale, Sarkar and Gatski (RSM-SSG), and (v) the turbulence frequency formulated Reynolds stress model (RSM-ω). Each was found to be in good agreement with the experiments (below 2% discrepancy), with respect to total-to-total parameters at three different operating conditions. However, for the off-design conditions, local flow field differences were observed between the models, with the SA model showing particularly poor prediction of local flow structures. The SST-CC showed better prediction of curved rotating flows in the impeller. The RSM-ω was better for the wake and separated flow in the diffuser. The SST model showed reasonably stable, robust and time efficient capability to predict global and local flow features.

Desenvolvimento de um relatório de suporte à declaração ambiental de produto: perfis de alumínio

A Avaliação do Ciclo de Vida (ACV) considera todo o ciclo de vida do produto, desde a extração e obtenção da matérias-primas, passando pela produção e fabrico de materiais e energia, até ao tratamento de fim de vida e destino final do produto. As Declarações Ambientais de Produto (DAP) são declarações ambientais Tipo III que apresentam um conjunto de informação quantificada e fidedigna, que funciona como uma excelente ferramenta de comunicação relativa ao desempenho ambiental do produto ao longo do seu ciclo de vida. Este relatório de estágio visa, por um lado, analisar os impactes ambientais no decurso do processo de produção do perfil de alumínio sujeito ao tratamento acetinado 20 natural (AC20NA) e, por outro, elaborar um relatório de suporte, que servirá de base para o desenvolvimento da DAP do perfil de alumínio AC20NA a submeter ao sistema DAPHabitat. O relatório foi elaborado tendo por base a norma EN 15804 e inclui as fases obrigatórias (A1-A3). Desta forma, utilizou-se ao software SimaPro para a análise dos impactes ambientais das várias fases do processo de fabrico do perfil de alumínio em estudo. As fases consideradas foram a extrusão, a anodização (tratamento de superfície), a Estação de Tratamento de águas Residuais Industriais (ETARI) e a embalagem. A fase que mais contribui para as diferentes categorias de impacte é a extrusão, uma vez que é nesta fase que é utilizada a matéria-prima para a produção dos perfis de aluminío.

A bacterial acetyltransferase targets the protein kinase ZIP1, a positive regulator of plant immunity

Pseudomonas syringae is a model bacterial pathogen that penetrates the leaf to reach the plant apoplast, where it replicates causing disease. In order to do that, the pathogen must interfere and suppress a two-tiered plant defense response: PTI (PAMP-Triggered Immunity, or basal resistance) and ETI (Effector-Triggered Immunity). P. syringae uses a type III secretion system to directly deliver effector proteins inside the plant cell cytosol, many of which are known to suppress PTI, some of which are known to trigger ETI, and a handful of which are known to suppress ETI. Bacterial infection can also trigger a systemic plant defense response that protects the plant against additional pathogen attacks known as SAR (Systemic Acquired Resistance). We are particularly interested in the molecular and cellular mechanisms involved in effector-mediated defense evasion by P. syringae, in particular those involved in the suppression of ETI and SAR, and/or mediation of hormone signaling. Here we present data describing effector-mediated interference with plant immunity, by means of acetylation of a key positive regulator of local and systemic responses. Our work identifies a novel plant target for effector function, and characterizes its function. This work illustrates how analyzing the means by which a given effector interferes with its target can provide novel information regarding eukaryotic molecular mechanisms.

Broad-scale mapping of seafloor habitats in the north-east Atlantic using existing environmental data

If marine management policies and actions are to achieve long-term sustainable use and management of the marine environment and its resources, they need to be informed by data giving the spatial distribution of seafloor habitats over large areas. Broad-scale seafloor habitat mapping is an approachwhich has the benefit of producing maps covering large extents at a reasonable cost. This approach was first investigated by Roff et al. (2003), who, acknowledging that benthic communities are strongly influenced by the physical characteristics of the seafloor, proposed overlaying mapped physical variables using a geographic information system (GIS) to produce an integrated map of the physical characteristics of the seafloor. In Europe the method was adapted to the marine section of the EUNIS (European Nature Information System) classification of habitat types under the MESH project, andwas applied at an operational level in 2011 under the EUSeaMap project. The present study compiled GIS layers for fundamental physical parameters in the northeast Atlantic, including (i) bathymetry, (ii) substrate type, (iii) light penetration depth and (iv) exposure to near-seafloor currents andwave action. Based on analyses of biological occurrences, significant thresholds were fine-tuned for each of the abiotic layers and later used in multi-criteria raster algebra for the integration of the layers into a seafloor habitat map. The final result was a harmonised broad-scale seafloor habitat map with a 250 m pixel size covering four extensive areas, i.e. Ireland, the Bay of Biscay, the Iberian Peninsula and the Azores. The map provided the first comprehensive perception of habitat spatial distribution for the Iberian Peninsula and the Azores, and fed into the initiative for a pan- European map initiated by the EUSeaMap project for Baltic, North, Celtic and Mediterranean seas.

New prophylactic and therapeutic treatments to combat pathogenic Enterohaemorrhagic Escherichia coli

Bacterial diarrhoeal diseases have significant influence on global human health, and are a leading cause of preventable death in the developing world. Enterohaemorrhagic Escherichia coli (EHEC), pathogenic strains of E. coli that carry potent toxins, have been associated with a high number of large-scale outbreaks caused by contaminated food and water sources. This pathotype produces diarrhoea and haemorrhagic colitis in infected humans, and in some patients leads to the development of haemolytic uremic syndrome (HUS), which can result in mortality and chronic kidney disease. A major obstacle to the treatment of EHEC infections is the increased risk of HUS development that is associated with antibiotic treatment, and rehydration and renal support are often the only options available. New treatments designed to prevent or clear E. coli infections and reduce symptoms of illness would therefore have large public health and economic impacts. The three main aims of this thesis were: to explore mouse models for pre-clinical evaluation in vivo of small compounds that inhibit a major EHEC colonisation factor, to assess the production and role of two proteins considered promising candidates for a broad-spectrum vaccine against pathogenic E. coli, and to investigate a novel compound that has recently been identified as a potential inhibitor of EHEC toxin production. As EHEC cannot be safely tested in humans due to the risk of HUS development, appropriate small animal models are required for in vivo testing of new drugs. A number of different mouse models have been developed to replicate different features of EHEC pathogenesis, several of which we investigated with a focus on colonisation mediated by the Type III Secretion System (T3SS), a needle-like structure that translocates bacterial proteins into host cells, resulting in a tight, intimate attachment between pathogen and host, aiding colonisation of the gastrointestinal tract. As E. coli models were found not to depend significantly on the T3SS for colonisation, the Citrobacter rodentium model, a natural mouse pathogen closely related to E. coli, was deemed the most suitable mouse model currently available for in vivo testing of T3SS-targeting compounds. Two bacterial proteins, EaeH (an outer membrane adhesin) and YghJ (a putative secreted lipoprotein), highly conserved surface-associated proteins recently identified as III protective antigens against E. coli infection of mice, were explored in order to determine their suitability as candidates for a human vaccine against pathogenic E. coli. We focused on the expression and function of these proteins in the EHEC O157:H7 EDL933 strain and the adherent-invasive E. coli (AIEC) LF82 strain. Although expression of EaeH by other E. coli pathotypes has recently been shown to be upregulated upon contact with host intestinal cells, no evidence of this upregulation could be demonstrated in our strains. Additionally, while YghJ was produced by the AIEC strain, it was not secreted by bacteria under conditions that other YghJ-expressing E. coli pathotypes do, despite the AIEC strain carrying all the genes required to encode the secretion system it is associated with. While our findings indicate that a vaccine that raises antibodies against EaeH and YghJ may have limited effect on the EHEC and AIEC strains we used, recent studies into these proteins in different E. coli pathogens have suggested they are still excellent candidates for a broadly effective vaccine against E. coli. Finally, we characterised a small lead compound, identified by high-throughput screening as a possible inhibitor of Shiga toxin expression. Shiga toxin production causes both the symptoms of illness and development of HUS, and thus reduction of toxin production, release, or binding to host receptors could therefore be an effective way to treat infections and decrease the risk of HUS. Inhibition of Shiga toxin production by this compound was confirmed, and was shown to be caused by an inhibitory effect on activation of the bacterial SOS response rather than on the Shiga toxin genes themselves. The bacterial target of this compound was identified as RecA, a major regulator of the SOS response, and we hypothesise that the compound binds covalently to its target, preventing oligomerisation of RecA into an activated filament. Altogether, the results presented here provide an improved understanding of these different approaches to combating EHEC infection, which will aid the development of safe and effective vaccines and anti-virulence treatments against EHEC.

Reduced Plasma Angiotensin Ii Levels Are Reversed By Hydroxyurea Treatment In Mice With Sickle Cell Disease.

Sickle cell disease (SCD) pathogenesis leads to recurrent vaso-occlusive and hemolytic processes, causing numerous clinical complications including renal damage. As vasoconstrictive mechanisms may be enhanced in SCD, due to endothelial dysfunction and vasoactive protein production, we aimed to determine whether the expression of proteins of the renin-angiotensin system (RAS) may be altered in an animal model of SCD. Plasma angiotensin II (Ang II) was measured in C57BL/6 (WT) mice and mice with SCD by ELISA, while quantitative PCR was used to compare the expressions of the genes encoding the angiotensin-II-receptors 1 and 2 (AT1R and AT2R) and the angiotensin-converting enzymes (ACE1 and ACE2) in the kidneys, hearts, livers and brains of mice. The effects of hydroxyurea (HU; 50-75mg/kg/day, 4weeks) treatment on these parameters were also determined. Plasma Ang II was significantly diminished in SCD mice, compared with WT mice, in association with decreased AT1R and ACE1 expressions in SCD mice kidneys. Treatment of SCD mice with HU reduced leukocyte and platelet counts and increased plasma Ang II to levels similar to those of WT mice. HU also increased AT1R and ACE2 gene expression in the kidney and heart. Results indicate an imbalanced RAS in an SCD mouse model; HU therapy may be able to restore some RAS parameters in these mice. Further investigations regarding Ang II production and the RAS in human SCD may be warranted, as such changes may reflect or contribute to renal damage and alterations in blood pressure.

Antitumor Activity Of Irradiated Riboflavin On Human Renal Carcinoma Cell Line 786-o.

Riboflavin (vitamin B2) is a precursor for coenzymes involved in energy production, biosynthesis, detoxification, and electron scavenging. Previously, we demonstrated that irradiated riboflavin (IR) has potential antitumoral effects against human leukemia cells (HL60), human prostate cancer cells (PC3), and mouse melanoma cells (B16F10) through a common mechanism that leads to apoptosis. Hence, we here investigated the effect of IR on 786-O cells, a known model cell line for clear cell renal cell carcinoma (CCRCC), which is characterized by high-risk metastasis and chemotherapy resistance. IR also induced cell death in 786-O cells by apoptosis, which was not prevented by antioxidant agents. IR treatment was characterized by downregulation of Fas ligand (TNF superfamily, member 6)/Fas (TNF receptor superfamily member 6) (FasL/Fas) and tumor necrosis factor receptor superfamily, member 1a (TNFR1)/TNFRSF1A-associated via death domain (TRADD)/TNF receptor-associated factor 2 (TRAF) signaling pathways (the extrinsic apoptosis pathway), while the intrinsic apoptotic pathway was upregulated, as observed by an elevated Bcl-2 associated x protein/B-cell CLL/lymphoma 2 (Bax/Bcl-2) ratio, reduced cellular inhibitor of apoptosis 1 (c-IAP1) expression, and increased expression of apoptosis-inducing factor (AIF). The observed cell death was caspase-dependent as proven by caspase 3 activation and poly(ADP-ribose) polymerase-1 (PARP) cleavage. IR-induced cell death was also associated with downregulation of v-src sarcoma (Schmidt-Ruppin A-2) viral oncogene homologue (avian)/protein serine/threonine kinase B/extracellular signal-regulated protein kinase 1/2 (Src/AKT/ERK1/2) pathway and activation of p38 MAP kinase (p38) and Jun-amino-terminal kinase (JNK). Interestingly, IR treatment leads to inhibition of matrix metalloproteinase-2 (MMP-2) activity and reduced expression of renal cancer aggressiveness markers caveolin-1, low molecular weight phosphotyrosine protein phosphatase (LMWPTP), and kinase insert domain receptor (a type III receptor tyrosine kinase) (VEGFR-2). Together, these results show the potential of IR for treating cancer.

Biochemical And Morphological Alterations In The Achilles Tendon Of Mdx Mice.

Dystrophin-deficient muscles have repeated cycles of necrosis and regeneration, being susceptible to injury induced by muscle contractions. Some studies have demonstrated that tendons are also affected in mdx mice, based especially on the changes in biomechanical properties arising from the respective linked muscles. However, most studies have focused only on alterations in the myotendinous junction. Thus, the purpose of this work was to study biochemical and morphological alterations in the Achilles tendons of 60-day-old mdx mice. Hydroxyproline quantification, showed higher collagen concentration in the mdx mice as compared with the control. No difference between the tendons of both groups was found in the noncollagenous proteins dosage, and in the amount of collagen type III detected in the western blotting analysis. The zymography for gelatinases detection showed higher amounts of metaloproteinase-2 (active isoform) and of metalloproteinase-9 (latent isoform) in the mdx mice. Measurements of birefringence, using polarization microscopy, showed higher molecular organization of the collagen fibers in the tendons of mdx mice in comparison to the control group, with presence of larger areas of crimp. Ponceau SS-stained tendon sections showed stronger staining of the extracellular matrix in the mdx groups. Toluidine blue-stained sections showed more intense basophilia in tendons of the control group. In morphometry, a higher number of inflammatory cells was detected in the epitendon of mdx group. In conclusion, the Achilles tendon of 60-day-old mdx mice presents higher collagen concentration and organization of the collagen fibers, enhanced metalloproteinase-2 activity, as well as prominent presence of inflammatory cells and lesser proteoglycans.

Periodontal outcomes and social, racial and gender inequalities in Brazil: a systematic review of the literature between 1999 and 2008

The objective of this study was to review the Brazilian epidemiologic literature on periodontal outcomes and socio-demographic factors, assessing bibliographic and methodological characteristics of this scientific production, as well as the consistency and statistical significance of the examined associations. A systematic review was carried out in six bibliographic sources. The review was limited to the period between 1999 and 2008, without any other type of restriction. Among the 410 papers identified, 29 were included in the review. An increasing number of articles, specifically in the last four years of study, was observed. However, there is a concentration of studies in the South and Southeast regions of Brazil, and many of them are not closely connected to theoretical formulations in the field. In spite of these shortcomings, the review findings corroborate the idea that poor socioeconomic conditions are associated with periodontal outcomes, as demonstrated primarily by income and schooling indicators.