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BACKGROUND:

The main objectives of this study were to describe and compare the microbiota of 1) deep dentinal lesions of deciduous teeth of children affected with severe early childhood caries (S-ECC) and 2) the unstimulated saliva of these children and 3) the unstimulated saliva of caries-free children, and to compare microbiota compositional differences and diversity of taxa in these sampled sites.

METHODS:

Children with S-ECC and without S-ECC were recruited. The saliva of all children with and without S-ECC was sampled along with the deep dentinal microbiota from children affected by S-ECC. The salivary microbiota of children affected by S-ECC (n = 68) was compared to that of caries-free children (n = 70), by Illumina MiSeq sequencing of 16S rRNA amplicons. Finally, the caries microbiota of deep dentinal lesions of those children with S-ECC was investigated.

RESULTS:

Using two beta diversity metrics (Bray Curtis dissimilarity and UniFrac distance), the caries microbiota was found to be distinct from that of either of the saliva groups (caries-free & caries-active) when bacterial abundance was taken into account. However, when the comparison was made by measuring only presence and absence of bacterial taxa, all three microbiota types separated. While the alpha diversity of the caries microbiota was lowest, the diversity difference between the caries samples and saliva samples was statistically significant (p < 0.001). The major phyla of the caries active dentinal microbiota were Firmicutes (median abundance value 33.5%) and Bacteroidetes (23.2%), with Neisseria (10.3%) being the most abundant genus, followed by Prevotella (10%). The caries-active salivary microbiota was dominated by Proteobacteria (median abundance value 38.2%) and Bacteroidetes (27.8%) with the most abundant genus being Neisseria (16.3%), followed by Porphyromonas (9.5%). Caries microbiota samples were characterized by high relative abundance of Streptococcus mutans, Prevotella spp., Bifidobacterium and Scardovia spp.

CONCLUSIONS:

Distinct differences between the caries microbiota and saliva microbiota were identified, with separation of both salivary groups (caries-active and caries-free) whereby rare taxa were highlighted. While the caries microbiota was less diverse than the salivary microbiota, the presence of these rare taxa could be the difference between health and disease in these children.

INTRODUCTION:
Apical periodontitis (AP) and cardiovascular diseases (CVDs) are chronic conditions triggered by an inflammatory process and sharing similar pathogeneses and molecular players. Previous studies have suggested that AP may perpetuate a systemic inflammation state and, in turn, contribute to CVD. In this study, we investigated the potential association between endodontic pathology and CVD using epidemiological and genetic approaches.

METHODS:
Epidemiologic analysis was performed by querying the medical and dental records of >2 million patients. We retrieved information on positive/negative history for endodontic pathologies and CVDs using diagnostic and treatment codes from a dental school-based and a hospital-based patient electronic health record system. A case-control genetic association study was also performed; 10 single nucleotide polymorphisms in genes identified as strongly associated with CVDs were genotyped in 195 cases with AP and 189 control individuals without AP. Data analyses were performed using the chi-square and Fisher exact tests. P ≤.05 indicates significant difference between groups.

RESULTS:
Significant associations were found between the presence of endodontic pathology and a history of hypertension, myocardial infarction, cerebrovascular accident, pacemaker, congestive heart failure, heart block, deep vein thrombosis, and cardiac surgery (0.0001 ≤ P ≤ .008). A modest association was found for heart murmur and atrial fibrillation (P = .04). A trend toward positive association (P = .05) was also found between AP and a single nucleotide polymorphism in KCNK3, a gene known to be involved in increased susceptibility to hypertension.

CONCLUSIONS:
Significant associations were found between endodontic pathology and various CVDs and CVD-related risk factors, particularly hypertension. A trend toward a positive association was also found between AP and KCNK3, suggesting that common genetic variations may underlie different diseases. Additional studies with larger sample sizes have the potential to elucidate common mechanisms underlying AP and CVD.

BACKGROUND:

In recent years, several state dental programs, researchers and the Dental Quality Alliance (DQA) have sought to develop baseline quality measures for dentistry as a way to improve health outcomes, reduce costs and enhance patient experiences. Some of these measures have been tested and validated for various population groups. However, there are some unintended consequences and challenges with quality measurement in dentistry as observed from our previous work on refining and transforming dental quality measures into e-measures.

MAIN BODY:

Some examples of the unintended consequences and challenges associated with implementing dental quality measures include: a de-emphasis on patient-centeredness with process-based quality measures, an incentivization of unethical behavior due to fee-for-service reimbursement systems, the risk of compromising patient and provider autonomy with plan-level measures, a disproportionate benefits of dental quality measurement going toward payers, and the risk of alienating smaller dental offices due to the resource-intensive nature of quality measurement.

CONCLUSION:

As our medical counterparts have embraced quality measurement for improved health outcomes, so too must the dental profession. Our ultimate goal is to ensure the delivery of high quality, patient-centered dental care and effective quality measurement is the first step. By continuously monitoring the performance of dental quality measures and their continued refinement when unintended consequences are observed, we can improve patient and population health outcomes.

INTRODUCTION:
The aim of this study was to assess whether apical lesions are associated with inflammatory serum markers of cardiovascular risk, especially high-sensitivity C-reactive protein (hsCRP), in young adults.

METHODS:
In this cross-sectional study, otherwise healthy individuals with apical lesions of endodontic origin (ALEOs) and a clinical diagnosis of asymptomatic apical periodontitis and controls aged between 18 and 40 years were included. Patients’ sociodemographic characteristics, medical history, and classic cardiovascular risk factors were recorded, and the pathobiological determinants of atherosclerosis in youth score was calculated. Oral clinical and radiographic examinations were performed. Blood samples were collected to determine the lipid profile, glycated hemoglobin, hsCRP, immunoglobulin G, interleukin (IL)-6, IL-10, IL-12p70, matrix metalloproteinase 8, soluble vascular cellular adhesion molecule-1, soluble intercellular adhesion molecule-1, and soluble E-selectin. Bivariate and multivariate analyses adjusting for oral and classic cardiovascular risk factors were performed.

RESULTS:
hsCRP levels were significantly higher in ALEO patients versus controls (median = 2.54 vs 0.78), whereas the pathobiological determinants of atherosclerosis in youth score was comparable among the groups. Also, the levels of IL-6, matrix metalloproteinase 8, and soluble E-selectin were significantly higher in ALEO patients. hsCRP, IL-6, and IL-12 correlated with soluble adhesion molecules. Bivariate analysis based on hsCRP serum concentrations ≥1 mg/L showed an odds ratio (OR) = 6.8, and the risk increased 3.3 times for an additional ALEO. In multivariate analysis, ALEO was significantly associated with hsCRP levels ≥1 mg/L (OR = 5.1-12.8) independently of the adjustment model. ALEO also associated with CRP levels >3 mg/L, which was significant after the adjustment for covariates (OR = 4.0).

CONCLUSIONS:
ALEO is associated with the systemic inflammatory burden and cardiovascular risk determined by hsCRP, supporting a mechanistic link for cardiovascular diseases in young adults.

Cannabis use is an emergent risk factor for periodontitis, a chronic bacterial-induced disease of the supporting structures of the teeth. However, the mechanisms by which marijuana exposure predisposes to periodontal tissue destruction have yet to be elucidated. Therefore, we examined the influence of physiologically relevant doses of major marijuana-derived phytocannabinoid subtypes (cannabidiol [CBD]; cannabinol [CBN]; and tetrahydrocannabinol [THC], 1.0 μg/ml) on the interactions of three ultrastructurally variant oral pathogens, Porphyromonas gingivalis, Filifactor alocis, and Treponema denticola with the immune system. CBD, CBN, and THC each suppressed P. gingivalis-induced IL-12 p40, IL-6, IL-8, and TNF release while enhancing the anti-inflammatory cytokine, IL-10, from human innate cells. Similar phenomena were observed in F. alocis- and T. denticola-exposed human monocytes and human gingival keratinocytes. Higher phytocannabinoid doses (≥5.0 μg/ml) compromised innate cell viability and inhibited the growth of P. gingivalis and F. alocis, relative to unexposed bacteria. T. denticola, however, was resistant to all cannabinoid doses tested (up to 10.0 μg/ml). Pharmaceutical inhibition and efficient gene silencing indicated that a common CB2/PI3K axis of immune suppression is triggered by phytocannabinoids in vitro. This pathway does not appear to perpetuate through the canonical GSK3β-dependent cholinergic anti-inflammatory pathway, the predominant endogenous inflammatory control system. In a repetitive, transient oral infection model, CBD also suppressed P. gingivalis-induced innate immune markers in wild-type mice, but not in CB2-/- mice. If such phenomena occur in humans in situ, environmental cannabinoids may enhance periodontitis via direct toxic effects on specific oral bacteria; by compromising innate cell vitality; and/or through a suppressed innate response to periodontal pathogens involving a CB2/PI3K signaling lineage.

This review of literature paper was done in order to conduct a review of the literature and an assessment of the effects of titanium implant corrosion on peri-implant health and success in the oral environment. This paper evaluates and critically reviews the findings of the multiple in-depth in vivo and in vitro studies that are related to corrosion aspects of the titanium and its alloys. A literature survey was conducted by electronic search in Medline and studies that were published between 1940 and August 2018 were selected. The search terms used were types of corrosion, corrosion of titanium implants, titanium corrosion, metal ion release from the titanium implants, fretting and pitting corrosion, implant corrosion, peri implantitis, and corrosion. Both in vivo and in vitro studies were also included in the review. The search and selection resulted in 64 articles. These articles were divided on the basis of their context to different kinds of corrosion related to titanium dental implants. It is evident that metal ions are released from titanium and titanium alloy dental implants as a result of corrosion. Corrosion of implants is multifactorial, including electrical, chemical, and mechanical factors, which have an effect on the peri-implant tissues and microbiota. The literature surveyed showed that corrosion related to titanium and its alloys has an effect on the health of peri-implant soft and hard tissue and the long term survival of metal dental implants. It can be concluded that presence of the long-term corrosion reaction along with continuous corrosion leads to the release of ions into the peri-implant tissue but also to a disintegration of the implant that contribute to material fatigue and even fracture of the abutments and implant body or both. This combined impact of the corrosion, bacterial activity, chemical reactions, and functional stresses are to be looked at as important factors of implant failure. The findings can be used to explore the possible strategies of research to investigate the biological impact of implant materials.