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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