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INTRODUCTION:

Chronic infections of endodontic origin might predispose to the onset of cardiovascular disease (CVD). The studies depicting the link between apical periodontitis (AP) and CVD are few, and the association is very controversial; also, the markers used are expensive, which makes them difficult to use in general practice. The purpose of this study was to investigate whether an association exists between AP and CVD using noninvasive methods (ie, flow-mediated dilatation [FMD] and carotid intima-media thickness [c-IMT]).

METHODS:

This cross-sectional study included 120 men between 20 and 40 years old free from periodontal disease, CVD, and traditional cardiovascular risk factors; 60 subjects had AP, and 60 acted as controls. All subjects underwent complete physical and dental examination, echocardiography, ultrasound assessment of FMD of the right brachial artery, and c-IMT. Data were analyzed using the Mann-Whitney U test and the Spearman rank correlation (rs) test.

RESULTS:

FMD was found to be significantly impaired in patients with AP (mean = 4.9% ± 2.05%) compared with healthy controls (mean = 9.74% ± 2.59%, P = .000). The study also depicts statistically significant differences between c-IMT of the AP (mean = 0.64 ± 0.12 mm) and control (mean = 0.54 ± 0.08 mm) groups (P = .000). A significant inverse correlation between c-IMT and FMD was observed (rs = -0.381, P = .000).

CONCLUSIONS:

Impaired FMD and greater c-IMT in subjects with AP suggests a potential association between endodontic infection and CVD.

Background:

Systemic lupus erythematosus (SLE) is a potentially fatal complex autoimmune disease, that is characterized by widespread inflammation manifesting tissue damage and comorbidities across the human body including heart, blood vessels, joints, skin, liver, kidneys, and periodontal tissues. The etiology of SLE is partially attributed to a deregulated inflammatory response to microbial dysbiosis and environmental changes. In the mouth, periodontal environment provides an optimal niche for local and systemic inflammation. Our aim was to evaluate the reciprocal impact of periodontal subgingival microbiome on SLE systemic inflammation.

Methods:

Ninety-one female subjects were recruited, including healthy (n = 31), SLE-inactive (n = 29), and SLE-active (n = 31). Patients were screened for probing depth, bleeding on probing, clinical attachment level, and classified according to CDC/AAP criteria with or without periodontal dysbiosis. Serum inflammatory cytokines were measured by human cytokine panel and a targeted pathogenic subgingival biofilm panel was examined by DNA-DNA checkerboard from subgingival plaque samples.

Results:

The results showed significant upregulation of serum proinflammatory cytokines in individuals with SLE when compared to controls. Stratification of subject’s into SLE-inactive (I) and SLE-active (A) phenotypes or periodontitis and non-periodontitis groups provided new insights into SLE pathophysiology. Ten proinflammatory cytokines were upregulated in serum of SLE-I only and one in SLE-A only. Four molecules overlapped in SLE-A and SLE-I. Anti-inflammatory cytokines included IL-4 IL-10, which were upregulated in SLE-I sera (but not SLE-A), controlling clinical phenotypes. Out of 24 significant differential oral microbial abundances found in SLE, 14 unique subgingival bacteria profiles were found to be elevated in SLE. The most severe oral pathogens (Treponema denticola and Tannerella forsythia) showed increase abundances on SLE-A periodontal sites when compared to SLE-I and healthy controls. Inflammation as measured by cytokine-microbial correlations showed that periodontal pathogens dominating the environment increased proinflammatory cytokines systemically.

Conclusions:

Altogether, low-grade systemic inflammation that influenced SLE disease activity and severity was correlated to dysbiotic changes of the oral microbiota present in periodontal diseases.

Richard Watt first became aware of the social roots of oral health inequalities more than 30 years ago when he was a dentist at Greaves Hall psychiatric hospital in Merseyside, UK. There, he witnessed “appalling” levels of oral disease. “The mouth really is a marker of people’s social position and future disease risk”, he says, “and oral diseases are a canary in the coal mine for inequality”. Today, Watt is Professor andChair of Dental Public Health at University College London (UCL) in the Department of Epidemiology and Public Health. Being housed in this department rather than the dental school might seem unusual, but Watt says it allows him to pursue “opportunities for broader integrated research and teaching” and fits his view that oral health is inextricably linked to other chronic diseases: “A lot of my work cuts across different areas of public health and recognises that
rather than look at a single disease in a silo, many chronic conditions share common pathways and causes.” Watt uses this position to be an advocate “influencing policy, challenging injustice, and promoting social equity”, he says.

Platelet-rich fibrin (PRF) therapy has been widely applied in regenerative dentistry, and PRF preparation has been optimized to efficiently form fibrin clots using plain glass tubes. Currently, a shortage of commercially available glass tubes has forced PRF users to utilize silica-coated plastic tubes. However, most plastic tubes are approved by regulatory authorities only for diagnostic use and remain to be approved for PRF therapy. To clarify this issue, we quantified silica microparticles incorporated into the PRF matrix. Blood samples were collected into three different brands of silica-containing plastic tubes and were immediately centrifuged following the protocol for advanced-PRF (A-PRF). Advanced-PRF-like matrices were examined using a scanning electron microscope (SEM), and silica microparticles were quantified using a spectrophotometer. Each brand used silica microparticles of specific size and appearance. Regardless of tube brands and individual donors, significant, but not accidental, levels of silica microparticles were found to be incorporated into the A-PRF-like matrix, which will be consequently incorporated into the implantation sites. Presently, from the increasing data for cytotoxicity of amorphous silica, we cannot exclude the possibility that such A-PRF-like matrices negatively influence tissue regeneration through induction of inflammation. Further investigation should be performed to clarify such potential risks.

INTRODUCTION:

This report includes outcomes for a group of patients with significant periapical lesions who were treated and evaluated in two single-arm, multicenter, prospective, nonsignificant risk clinical studies.

METHODS:

Forty-five teeth were from 45 patients who met the inclusion criteria and consented for the clinical studies and were diagnosed with periapical lesions with periapical index score ≥3. Patients were treated with a standardized treatment protocol including instrumentation to an apical diameter of #20 without orifice enlargement, the GentleWave Procedure, and warm vertical obturation. Clinical signs and radiographic assessments were evaluated at 12 months to assess healing. Success was classified as healing or healed and accounted for the cumulative success rate of healing. Statistical analyses were performed by using Fisher exact test, Pearson correlation, and multivariate logistic regression analyses.

RESULTS:

At 12 months, 44 of 45 teeth (97.8%) were evaluated. The cumulative success rate for the GentleWave Procedure was 97.7%. Forty-three of 44 teeth were completely functional; all teeth had complete resolution for measured indices of mobility, soft tissue lesions, sinus tract, and furcation involvement. No patients experienced moderate or severe pain at 2, 7, and 14 days after procedure. Although only 1 patient was unsuccessful and the presence of clinical symptoms and type of periradicular diagnosis at 12 months were correlated with an unsuccessful outcome, the analyses were limited by the sample size.

CONCLUSIONS:

In this case series analysis, treatment of sizable periapical lesions with the GentleWave Procedure resulted in a success rate of 97.7% at 12-month re-evaluation

OBJECTIVES:
During the treatment of chronic apical periodontitis and pulp necrosis the main role is to irrigate the root canal.

AIM:
The aim of this in vivo study was to irrigate with 0.9% NaCl (Natrium Chloride), 2.5 % NaOCl (Sodium Hypochlorite Solution, Sigma Aldrich – Germany) and 2% CHX (Chlorhexidine Digluconate Solution, Sigma Aldrich – Spain) combined with Gaseous Ozone (Prozone WH, Austria).

MATERIAL AND METHODS:
This study was realised in the University Dentistry Clinical Centre of Kosovo (UDCCK), respectively in the Department of Endodontic and Dental Pathology, Dental Branch, Faculty of Medicine, Prishtina, Kosovo. The 40 subjects involved in this study belonged to both genders, in age between 15 -65 years. The sample selection was randomised. The retroalveolar radiography for each patient was taken in the suspected tooth. As a therapeutic plan the authors decided to disinfect the root canal with the irrigants, as follows: 2.5 % NaOCl, 2 % CHX and gaseous ozone.

RESULTS:
The statistical analyses were based on Kruskal – Vallis test, X – test, DF = 3, r < 0.01. In the isolated average number of the aerobe and anaerobe bacteria colonies, when gaseous ozone was used, there was the significant statistical difference.

CONCLUSIONS:
When gaseous ozone was combined with irrigants 0.9%, 2.5 % NaOCl and 2% CHX, it was concluded that the number of colonies of aerobic and anaerobic bacteria was reduced.

OBJECTIVES:
Collaborative and/or integrative care between oral health and primary care providers can increase access to care to a more expansive population, helping to mitigate oral health related disease. The objective of this review was to present and evaluate different types of care models that exist between oral health and primary care providers in pediatric settings.

METHODS:
A literature search was conducted using five databases: MEDLINE/PubMed, ISI Web of Science, Dentistry and Oral Sciences Source, Cochrane Database, and EMBASE, to identify literature from January 1990 to January 2016. Combinations of controlled terms were utilized. Eligible sources targeted pediatric populations ages 1-17 and provided descriptions of existing collaborative and/or integrative models.

RESULTS:
Data related to the practice model, oral care provided, level of integration/collaboration and workflow were extracted. Sixteen articles were included that discussed 24 models of collaboration. These models provided ranges of services, but each offered a minimum of oral health risk assessment, oral health instruction, topical fluoride application and assessment for further treatment. These models included different levels of collaboration based off a ranking system created by the authors with 16.6 percent (4) classified as low, 54.2 percent (13) as medium and 29.2 percent (7) as high.

CONCLUSIONS:
Existing care models offered varying services and levels of integration and/or collaboration, but each offered a baseline of oral care. Most of these collaborations were based within Federally Qualified Health Centers and aimed to ease access to care issues.

INTRODUCTION:
This case uniquely reports a connection between endodontically infected teeth and systemic disease, and additionally presents ozone therapy as a unique therapy and immune system modulator. It is the world’s first such reported case and the treatment holds invaluable lessons in assessing the “unknown” causes of autoimmunity and inflammation. Additionally, it presents ozone therapy as a most needed unique, non-toxic and powerful anti-infective agent, anti-inflammatory and immune modulator.

CASE PRESENTATION:
The patient was a Mexican male field laborer, age 48 years, in inflammatory crisis with a confirmed case of dermatomyositis. He had received massive prednisone, and powerful immune suppressing drugs just to function, while disease still raged. I encountered him in the field in June 2012 with severe muscle pain, weakness, and diffuse generalized skin rash, essentially unable to do his work. Creatine kinase peaked at 9293 U/L. History and physical examination findings caused suspicion of subclinical infections in endodontically treated teeth. This impression was confirmed in subsequent dental evaluation. He fully recovered after dental infections were confirmed and surgically removed, while receiving ozone therapy until all symptoms and laboratory abnormalities normalized.

CONCLUSION:
Dental focus of occult infection may be a prime cause/trigger of autoimmune disorders and inflammatory disorders, requiring surgical intervention to remove. Ozone therapy, little known in conventional medicine, has been shown in the literature and in this case to be a powerful and safe immune modulator and anti-infective agent. This case has significant relevance across the entire spectrum of both medical and dental practice. It also emphasizes the need for individualized assessment and treatment rather than symptomatic pharmacological approaches treating a “disease” rather than the patient. Subclinical dental infection and ozone therapy are reviewed.

In 1965, the Sugar Research Foundation (SRF) secretly funded a review in the New England Journal of Medicine that discounted evidence linking sucrose consumption to blood lipid levels and hence coronary heart disease (CHD). SRF subsequently funded animal research to evaluate sucrose’s CHD risks. The objective of this study was to examine the planning, funding, and internal evaluation of an SRF-funded research project titled “Project 259: Dietary Carbohydrate and Blood Lipids in Germ-Free Rats,” led by Dr. W.F.R. Pover at the University of Birmingham, Birmingham, United Kingdom, between 1967 and 1971.

Conclusions: Minor increases in inflammation were associated with corresponding increases in features of depression, and these associations occurred in the absence of any physical symptoms. The influenza vaccine could be used to probe causal relationships with a high degree of ecological validity, even in high-risk and vulnerable populations, to better understand the role of inflammation in the pathogenesis of depression.