Bioactive glass and arginine dentifrices reduce root sensitivity during daily activities following non-surgical periodontal therapy: A randomized controlled trial.

BACKGROUND: Evidence on the efficacy of calcium sodium phosphosilicate (CSPS) and arginine dentifrices on reducing root sensitivity (RS) following non-surgical periodontal therapy (NSPT) is limited. The aim of this study was to compare the efficacy of these dentifrices in reducing RS during daily activities in patients undergoing NSPT. METHODS: Using a double-blind randomized controlled trial, CSPS, arginine, or control dentifrices were randomly assigned to 45 RS individuals following NSPT. The participants used the dentifrices 2×/day for 8 weeks. A self-reported visual analog scale (VAS) was assessed during daily activities. RESULTS: Self-reported VAS scores were similar among the three groups at each time point. The with-in group analysis revealed that the arginine dentifrice reduced RS from Week 1-8 compared with baseline in response to cold. Similarly, the CSPS dentifrice reduced RS at Week 4 and 8. The CSPS and arginine dentifrices exhibited RS relief resulting from toothbrushing starting at Week 4 and 2, respectively. In response to air, RS relief was observed from Week 4 in the arginine group. The number of patients with VAS > 2 in response to cold declined at Week 2 and 4 in the CSPS and arginine groups, respectively. In response to toothbrushing, only 10% in the test groups still had RS at Week 8. In response to air, the number of RS patients only in the arginine group decreased at Week 4. CONCLUSION: The CSPS and arginine dentifrices provided comparable RS relief during daily activities within 2-4 weeks and remained effective up to 8 weeks.

Bioactive glass and arginine dentifrices immediately relieved dentine hypersensitivity following non-surgical periodontal therapy: A randomized controlled trial.

BACKGROUND: There is no report concerning calcium sodium phosphosilicate (CSPS) and arginine dentifrices in reducing dentine hypersensitivity (DH) in patients undergoing non-surgical periodontal therapy. The aim of the study was to compare the efficacy of a dentifrice containing bioactive glass, 5% CSPS, and 8% arginine dentifrice in relieving DH in patients undergoing non-surgical therapy. METHODS: Using a double-blind randomized controlled trial, 45 volunteers with DH following non-surgical therapy were immediately applied with one of three dentifrices containing: 5% CSPS, 8% arginine, or control on DH teeth. The participants then continued to brush twice daily for 8 weeks. DH was assessed using the Schiff cold air sensitivity scale and tactile tests at baseline, immediately after application, and up to 8 weeks. RESULTS: The Schiff analysis revealed that the CSPS dentifrice significantly reduced DH immediately and declined through week 8. The arginine group demonstrated reduced DH through week 2. In contrast, DH reduction in the control began later at week 1. The visual analog scale analysis demonstrated that only CSPS had a significantly reduced percentage DH at the immediate, 2, 4, and 8 weeks compared with the baseline. The percentage of patients with DH (Schiff score ≥2) in the CSPS and arginine groups reduced to ≈ 50% after the in-office application. The number of DH patients treated with CSPS then decreased to 9% at the 2-week evaluation. CONCLUSION: The CSPS and arginine dentifrices were beneficial in reducing periodontitis patient's discomfort, immediately and in the first 2 weeks following non-surgical periodontal therapy.

Bioactive glass versus Arginine dentifrices on the reduction of dentin permeability and acid tolerance.

OBJECTIVES: To compare the efficacy of calcium sodium phosphosilicate (CSPS) and arginine dentifrices on dentin permeability and acid tolerance. MATERIAL AND METHODS: Sixty dentin discs were randomly assigned into 3 groups, then brushed for 1 min with CSPS, arginine, or fluoride (control) dentifrices. To test acid tolerance, each disc was soaked in 6% citric acid for 1 min. Dentin permeability was measured before, following brushing, and acid challenge. Ten discs per group were similarly treated and evaluated for tubule occlusion following a single dentifrice application, while other five discs per group were employed in an acid tolerance assay. RESULTS: The percentage reduction in dentin permeability was 39.26%, 32.27%, and 21.71% in the arginine, CSPS, and control groups, respectively. The differences in dentin permeability reduction between the arginine and CSPS groups following brushing and acid challenge were not significant (p = 0.398 and p = 0.211, respectively). The arginine dentifrice demonstrated a significant reduction in permeability compared with the control (p = 0.011). In addition, the occlusion exhibited by the arginine and CSPS dentifrices was more resistant to acid challenge compared with that of the control (p < 0.001). From SEM analysis, dentinal tubule occlusion was observed after a single application in all groups. Some open dentinal tubules were detected in the test groups, while almost all of the orifices were open in the fluoride group following acid challenge. CONCLUSIONS: There is no significant difference between arginine and CSPS dentifrices in reducing dentin permeability following a single application and acid challenge. Following acid challenge, the reduced permeability generated by arginine and CSPS was more stable compared with the fluoride dentifrice.

Periodontitis as the risk factor of chronic kidney disease: Mediation analysis.

AIM: To determine sequences and magnitude of causality among periodontitis, diabetes and chronic kidney disease (CKD) by mediation analysis. METHODS: Ten-year-data were retrieved from the Electric Generation Authority of Thailand (EGAT) study. A cohort of 2,635 subjects was identified with no CKD at baseline. The interested outcome was CKD incidence defined as glomerular filtration rate <60 ml/min/1.73 m2 . The percentage of proximal sites with clinical attachment loss ≥5 mm was used to represent periodontitis. Mediation analysis with 1,000-replication bootstrapping was applied to two causal diagrams, diagram A (Periodontitis â†’ Diabetes → CKD) and diagram B (Diabetes â†’ Periodontitis → CKD). RESULTS: The cumulative incidence of CKD was 10.3 cases per 100 persons during 10-year period. In diagram A, each increasing percentage of proximal sites with severe periodontitis increased the adjusted odds ratio of CKD 1.010 (95% CI: 1.005, 1.015) and 1.007 (95% CI: 1.004, 1.013), by direct and indirect effect through diabetes, respectively. In diagram B, diabetes increased the odds of CKD twofold, with 6.5% of this effect mediated via periodontitis. CONCLUSIONS: Periodontitis had significant direct effect, and indirect effect through diabetes, on the incidence of CKD. Awareness about systemic morbidities from periodontitis should be emphasized.

Memory T cell subsets in healthy gingiva and periodontitis tissues.

BACKGROUND: In the gingival sulcus, effective and balanced innate and adaptive immune responses against subgingival plaque microbiome are crucial to maintain immune homeostasis. In this study, we investigated the memory T cell subsets in healthy gingiva and periodontitis tissues. METHODS: Anatomical localization of T cells (CD3+ , CD4+ , and CD8+ ) in healthy gingiva and periodontitis tissues were examined immunohistochemically. Subsets of memory T cells from isolated gingival cells were analyzed by flow cytometry using a cocktail of monoclonal antibodies (anti-CD69, anti-CD103, anti-CD45RA, anti-CCR7, anti-CD28, and anti-CD95). Intracellular cytokine staining of interleukin (IL)-17 and interferon (IFN)-γ expression on memory T cells in periodontitis tissues was also investigated. RESULTS: We found that healthy gingiva contains two memory T cell populations; a CD69- recirculating population and a CD69+ gingiva-resident memory T cell population. CD4+ T cells with transitional memory (TTM ) phenotype (CD45RA- CCR7- CD28+ CD95+ ) constitute the major subset within these two populations. A significant increase in the proportion of CD4+ CD69+ CD103- memory T cells was observed in periodontitis tissues compared with healthy gingiva. CD4+ memory T cells from periodontitis tissues produced either IL-17 or IFN-γ whereas CD8+ memory T cells produced only IFN-γ. CONCLUSIONS: Our findings suggest that recirculating and gingiva-resident memory T cells could represent an important part of the immune surveillance network in the connective tissue, maintaining periodontal homeostasis. Imbalance of subgingival bacterial communities could damage gingival barrier allowing bacterial antigens to get access to the deeper connective tissue where they activate memory T cells leading to deleterious inflammation; a hallmark of periodontitis.

Human Memory B Cells in Healthy Gingiva, Gingivitis, and Periodontitis.

The presence of inflammatory infiltrates with B cells, specifically plasma cells, is the hallmark of periodontitis lesions. The composition of these infiltrates in various stages of homeostasis and disease development is not well documented. Human tissue biopsies from sites with gingival health (n = 29), gingivitis (n = 8), and periodontitis (n = 21) as well as gingival tissue after treated periodontitis (n = 6) were obtained and analyzed for their composition of B cell subsets. Ag specificity, Ig secretion, and expression of receptor activator of NF-κB ligand and granzyme B were performed. Although most of the B cell subsets in healthy gingiva and gingivitis tissues were CD19(+)CD27(+)CD38(-) memory B cells, the major B cell component in periodontitis was CD19(+)CD27(+)CD38(+)CD138(+)HLA-DR(low) plasma cells, not plasmablasts. Plasma cell aggregates were observed at the base of the periodontal pocket and scattered throughout the gingiva, especially apically toward the advancing front of the lesion. High expression of CXCL12, a proliferation-inducing ligand, B cell-activating factor, IL-10, IL-6, and IL-21 molecules involved in local B cell responses was detected in both gingivitis and periodontitis tissues. Periodontitis tissue plasma cells mainly secreted IgG specific to periodontal pathogens and also expressed receptor activator of NF-κB ligand, a bone resorption cytokine. Memory B cells resided in the connective tissue subjacent to the junctional epithelium in healthy gingiva. This suggested a role of memory B cells in maintaining periodontal homeostasis.

Differential inflammasome activation by Porphyromonas gingivalis and cholesterol crystals in human macrophages and coronary artery endothelial cells.

OBJECTIVE: Observational evidence suggests association between periodontitis and atherosclerotic vascular disease (ASVD), however the cause-effect remains unclear. In this study, we investigated the mechanistic link of the two diseases by measuring production of interleukin (IL)-1ß, a potent inflammatory cytokine, induced via inflammasome activation by a key periodontal pathogen--Porphyromonas gingivalis LPS and cholesterol crystals (CC). METHODS: An in vitro model of primary human monocyte-derived macrophages (M1 and M2 macrophages) and coronary artery endothelial cells (HCAEC) was employed as a source of inflammasome product-IL-1ß. Both cell types are essential in initial inflammatory process of ASVD. As inflammasome activation requires 2 signals, P. gingivalis LPS was used as a signal1 and CC as a signal2. RESULTS: We found markedly release of IL-1ß from P. gingivalis LPS-primed M1 and M2 macrophages treated with CC. Unlike macrophages, HCAEC showed no release of IL-1ß in response to P. gingivalis LPS priming and subsequent treatment with either CC or extracellular danger molecule adenosine-5'-triphosphate (signal2). However, HCAEC, which were primed with pro-inflammatory cytokine TNF-α (signal1) and treated with adenosine-5'-triphosphate, consistently secreted minimal IL-1ß. The amount of IL-1ß released from activated HCAEC was much lower than that from M1 or M2 macrophages. CONCLUSIONS: P. gingivalis LPS and CC induced a differential activation of the inflammasome between human macrophages and HCAEC. The mechanistic role of periodontal infection in inflammasome activation as a cause of ASVD requires further investigation.

Calprotectin S100A9 calcium-binding loops I and II are essential for keratinocyte resistance to bacterial invasion.

Epithelial cells expressing calprotectin, a heterodimer of S100A8 and S100A9 proteins, are more resistant to bacterial invasion. To determine structural motifs that affect resistance to bacterial invasion, mutations were constructed in S100A9 targeting the calcium-binding loops I and II (E36Q, E78Q, E36Q,E78Q) and the C terminus (S100A9(1-99) and S100A9(1-112)), which contains putative antimicrobial zinc-binding and phosphorylation sites. The S100A8 and mutated S100A9 encoding plasmids were transfected into calprotectin-negative KB carcinoma cells. All transfected cells (except KB-sham) expressed 27E10-reactive heterodimers. In bacterial invasion assays with Listeria monocytogenes and Salmonella enterica serovar Typhimurium (Salmonella typhimurium), cell lines expressing S100A8 in complex with S100A9E36Q, S100A9E78Q, S100A9(1-99), or S100A9(1-112) mutants or the S100A9(1-114) (full-length) calprotectin resisted bacterial invasion better than KB-sham. When compared with KB-S100A8/A9(1-114), cells expressing truncated S100A9(1-99) or S100A9(1-112) with S100A8 also showed increased resistance to bacterial invasion. In contrast, glutamic acid residues 36 and 78 in calcium-binding loops I and II promote resistance in epithelial cells, because cells expressing S100A9E36Q,E78Q with S100A8 were unable to resist bacterial invasion. Mutations in S100A9 E36Q, E78Q were predicted to cause loss of the calcium-induced positive face in calprotectin, reducing interactions with microtubules and appearing to be crucial for keratinocyte resistance to bacterial invasion.

ANTI-INFECTIVE PROTECTIVE PROPERTIES OF S100 CALGRANULINS.

The calgranulins are a subgroup of proteins in the S100 family (calgranulin A, S100A8; calgranulin B, S100A9 and calgranulin C, S100A12) that provide protective anti-infective and anti-inflammatory functions for the mammalian host. In this review, we discuss the structure-function relationships whereby S100A8 and S100A9, and for comparison, S100A12, provide intra- and extracellular protection during the complex interplay between infection and inflammation and how the calgranulins are regulated to optimally protect the host. Ideally located to support epithelial barrier function, calprotectin, a complex of S100A8/S100A9, is expressed in squamous mucosal keratinocytes and innate immune cells present at mucosal surfaces. The calgranulins are also abundantly produced in neutrophils and monocytes, whereas expression is induced in epidermal keratinocytes, gastrointestinal epithelial cells and fibroblasts during inflammation. The calgranulins show species-specific expression and function. For example, S100A8 is chemotactic in rodents but not in humans. In humans, S100A12 appears to serve as a functional chemotactic homolog to murine S100A8. Transition metal-binding and oxidation sites within calgranulins are able to create structural changes that may orchestrate new protective functions or binding targets. The calgranulins thus appear to adopt a variety of roles to protect the host. In addition to serving as a leukocyte chemoattractant, protective functions include oxidant scavenging, antimicrobial activity, and chemokine-like activities. Each function may reflect the concentration of the calgranulin, post-transcriptional modifications, oligomeric forms, and the proximal intracellular or extracellular environments. Calprotectin and the calgranulins are remarkable as multifunctional proteins dedicated to protecting the intra- and extracellular environments during infection and inflammation.