Health and wellbeing of under-five year olds in New Zealand 2017

Dental caries has been identified by the New Zealand (NZ) Ministry of Health (MoH) as the country’s most prevalent chronic disease.1 Dental diseases of the oral cavity include, but are not limited to, dental caries, developmental defects of enamel and/or dentine, dental erosion and periodontal disease.2 Dental caries and periodontal disease are largely preventable and are currently considered significant global health burdens.2,3 Dental caries involves the pathological destruction of tooth tissue by acids produced by cariogenic bacteria, and the progression of this disease can lead to pain, difficulty with eating, sleeping, and concentrating.2 Dental caries is multifactorial, with contributing factors including not only the presence and number of cariogenic pathogens or dental anomalies, but also modifiable factors such as diet, poor oral hygiene, and drug and alcohol abuse. Periodontal diseases affect the gingival tissues (gums) and surrounding tooth-supporting structures, and are a major cause of tooth loss. Periodontal pathogens are primarily responsible for the presence of this disease, with a number of modifiable factors shown to contribute to its severity and progression.2,4 Many of the modifiable risk factors for both dental caries and periodontal disease are also implicated in other chronic diseases such as diabetes, heart disease, and obesity, and they are also inextricably linked to socio-economic deprivation.5-7 Children are born without the bacteria that cause tooth decay; these are likely to be acquired from direct transfer via the saliva of their primary caregiver. If a primary caregiver has high amounts of untreated dental caries, then there is a much greater risk of cariogenic bacteria being passed to their child’s oral cavity, therefore placing them at greater risk of developing dental caries from an earlier age.8,9 Horizontal transmission of cariogenic bacteria between kindergarten children has also been demonstrated, and although the transmission rates are low, measures to disrupt this chain of infection from child to child are needed.10 Poor oral health impacts directly on many aspects of life, including nutrition, education, mental and physical well-being, and it has been directly linked to poor general health.2,3,11,12 Untreated dental caries can result in pain, acute and chronic infection. The appearance of untreated dental caries or lost teeth due to caries can be unsightly, resulting in stigmatisation, embarrassment, and low self-esteem. Both dental caries and periodontal disease cause halitosis (bad breath), impacting negatively on social and personal interactions, and potentially hindering employment opportunities.2 In 2016, the FDI World Dental Federation re-defined oral health as… “… multi-faceted and includes the ability to speak, smile, smell, taste, touch, chew, swallow and convey a range of emotions through facial expressions with confidence and without pain, discomfort and disease of the craniofacial complex. Further attributes include that it is a fundamental component of health and physical and mental wellbeing. It exists along a continuum influenced by the values and attitudes of individuals and communities; [it] reflects the physiologic, social, and psychological attributes that are essential to quality of life; [it] is influenced by the individual’s changing experiences, perceptions, expectations and ability to adapt to circumstances”.7 This new definition was designed to reflect a move away from the traditional bio-medical model of oral health towards embracing a broader bio-psychosocial model that considers both the impact of oral health on quality of life, and wider social determinants of health.

Basic science232. Certolizumab pegol prevents pro-inflammatory alterations in endothelial cell function

Background: Cardiovascular disease is a major comorbidity of rheumatoid arthritis (RA) and a leading cause of death. Chronic systemic inflammation involving tumour necrosis factor alpha (TNF) could contribute to endothelial activation and atherogenesis. A number of anti-TNF therapies are in current use for the treatment of RA, including certolizumab pegol (CZP), (Cimzia ®; UCB, Belgium). Anti-TNF therapy has been associated with reduced clinical cardiovascular disease risk and ameliorated vascular function in RA patients. However, the specific effects of TNF inhibitors on endothelial cell function are largely unknown. Our aim was to investigate the mechanisms underpinning CZP effects on TNF-activated human endothelial cells. Methods: Human aortic endothelial cells (HAoECs) were cultured in vitro and exposed to a) TNF alone, b) TNF plus CZP, or c) neither agent. Microarray analysis was used to examine the transcriptional profile of cells treated for 6 hrs and quantitative polymerase chain reaction (qPCR) analysed gene expression at 1, 3, 6 and 24 hrs. NF-κB localization and IκB degradation were investigated using immunocytochemistry, high content analysis and western blotting. Flow cytometry was conducted to detect microparticle release from HAoECs. Results: Transcriptional profiling revealed that while TNF alone had strong effects on endothelial gene expression, TNF and CZP in combination produced a global gene expression pattern similar to untreated control. The two most highly up-regulated genes in response to TNF treatment were adhesion molecules E-selectin and VCAM-1 (q 0.2 compared to control; p > 0.05 compared to TNF alone). The NF-κB pathway was confirmed as a downstream target of TNF-induced HAoEC activation, via nuclear translocation of NF-κB and degradation of IκB, effects which were abolished by treatment with CZP. In addition, flow cytometry detected an increased production of endothelial microparticles in TNF-activated HAoECs, which was prevented by treatment with CZP. Conclusions: We have found at a cellular level that a clinically available TNF inhibitor, CZP reduces the expression of adhesion molecule expression, and prevents TNF-induced activation of the NF-κB pathway. Furthermore, CZP prevents the production of microparticles by activated endothelial cells. This could be central to the prevention of inflammatory environments underlying these conditions and measurement of microparticles has potential as a novel prognostic marker for future cardiovascular events in this patient group. Disclosure statement: Y.A. received a research grant from UCB. I.B. received a research grant from UCB. S.H. received a research grant from UCB. All other authors have declared no conflicts of interes

Host Association of Campylobacter Genotypes Transcends Geographic Variation ▿ †

Genetic attribution of bacterial genotypes has become a major tool in the investigation of the epidemiology of campylobacteriosis and has implicated retail chicken meat as the major source of human infection in several countries. To investigate the robustness of this approach to the provenance of the reference data sets used, a collection of 742 Campylobacter jejuni and 261 Campylobacter coli isolates obtained from United Kingdom-sourced chicken meat was established and typed by multilocus sequence typing. Comparative analyses of the data with those from other isolates sourced from a variety of host animals and countries were undertaken by genetic attribution, genealogical, and population genetic approaches. The genotypes from the United Kingdom data set were highly diverse, yet structured into sequence types, clonal complexes, and genealogical groups very similar to those seen in chicken isolates from the Netherlands, the United States, and Senegal, but more distinct from isolates obtained from ruminant, swine, and wild bird sources. Assignment analyses consistently grouped isolates from different host animal sources regardless of geographical source; these associations were more robust than geographic associations across isolates from three continents. We conclude that, notwithstanding the high diversity of these pathogens, there is a strong signal of association of multilocus genotypes with particular hosts, which is greater than the geographic signal. These findings are consistent with local and international transmission of host-associated lineages among food animal species and provide a foundation for further improvements in genetic attribution