To date, attempts to regenerate functional periodontal tissues (including cementum) are largely unsuccessful due to a lack of full understanding about the cellular origin (epithelial or mesenchymal ...cells) essential for root cementum growth. To address this issue, we first identified a rapid cementum growth window from the ages of postnatal day 28 (P28) to P56. Next, we showed that expression patterns of Axin2 and β-catenin within cementum-forming periodontal ligament (PDL) cells are negatively associated with rapid cementum growth. Furthermore, cell lineage tracing studies revealed that the Axin2+-mesenchymal PDL cells and their progeny rapidly expand and directly contribute to postnatal acellular and cellular cementum growth. In contrast, the number of K14+ epithelial cells, which were initially active at early stages of development, was reduced during rapid cementum formation from P28 to P56. The in vivo cell ablation of these Axin2+ cells using Axin2CreERT2/+; R26RDTA/+ mice led to severe cementum hypoplasia, whereas constitutive activation of β-catenin in the Axin2+ cells resulted in an acceleration in cellular cementogenesis plus a transition from acellular cementum to cellular cementum. Thus, we conclude that Axin2+-mesenchymal PDL cells, instead of K14+ epithelial cells, significantly contribute to rapid cementum growth.
Cement-retained restorations are commonly used on dental implants. Residual excess cement after placement of fixed partial dentures has been associated with clinical and radiographic signs of ...peri-implant disease. The purpose of this study was to explore the relationship between excess dental cement and peri-implant disease using the dental endoscope.
Thirty-nine consecutive patients with implants exhibiting clinical and/or radiographic signs of peri-implant disease were studied. Patients were enrolled in the study during a 5-year period in a private periodontal practice. Twelve of these patients had similar implants without signs of inflammation; these implants served as controls. There were 20 controls and 42 test implants. All were evaluated using a dental endoscope initially, and all but one implant was evaluated at a 30-day follow-up. Results from both groups were assessed by two trained operators and recorded.
None of the controls and all 42 of the test implants had clinical signs of peri-implant disease at initial treatment. Excess cement was found in none of the controls and 34 of the test sites. Thirty days after cement removal, 25 of 33 test sites from which the cement was removed had no clinical or endoscopic signs of inflammation.
Excess dental cement was associated with signs of peri-implant disease in the majority (81%) of the cases. Clinical and endoscopic signs of peri-implant disease were absent in 74% of the test implants after the removal of excess cement.
Cementum, which shares common features with bone in terms of biochemical composition, is important for the homeostasis of periodontium during periodontitis and orthodontic treatment. Sirtuin 6 ...(SIRT6), as a member of the sirtuin family, plays key roles in the osteogenic differentiation of bone marrow mesenchymal stem cells. However, the involvement of SIRT6 in cementoblast differentiation and mineralization and the underlying mechanisms remain unknown. In this study, we observed that the expression of SIRT6 increased during cementoblast differentiation initially. Analysis of the gain‐ and loss‐of‐function indicated that overexpressing SIRT6 in OCCM‐30 cells suppresses cementoblast differentiation and mineralization and downregulating SIRT6 promotes cementogenesis. GLUT1, a glucose transporter necessary in cementogenesis, was inhibited by SIRT6. Overexpressing GLUT1 in SIRT6‐overexpressed OCCM‐30 cells rescued the inhibitory effect of SIRT6 on cementoblast differentiation and mineralization. Moreover, AMPK was activated after overexpressing SIRT6 and inhibited cementoblast differentiation and mineralization. Downregulating the expression of SIRT6 inhibited AMPK activity. Meanwhile, GLUT1 overexpression significantly decreased AMPK activity. Overall, on one hand, SIRT6 inhibited cementoblast differentiation and mineralization by suppressing GLUT1. On the other hand, SIRT6 inhibited cementoblast differentiation and mineralization by activating the AMPK pathway. GLUT1 overexpression also rescued the increased AMPK pathway activated by SIRT6.
SIRT6 inhibited cementoblast differentiation and mineralization by suppressing GLUT1. AMPK pathway also participated in SIRT6 regulated cementogenesis.
Abstract Objective An ideal dental adhesive should provide retentive strength, marginal seal, be relatively simple to achieve and demonstrate clinical durability. Future improvements in adhesive ...bonding to tooth structure require in vitro test methods that provide reliable data for materials development and/or evaluation of experimental variables. The objective of this project was to identify a test method that is relatively easy to perform, repeatable and ultimately useful for predicting clinical outcomes. Methods The Academy of Dental Materials initiated a project to develop and distribute guidance documents on laboratory test methods that are useful for the evaluation of dental adhesives and cements, composite resins and ceramics. Results The dental adhesive sub-group has identified the micro-tensile bond strength test, especially after subjecting the specimens to a durability challenge, as currently the best practical surrogate measure of dental composite restoration retention. Conclusion The following μTBS guidance is meant to aid the researcher in conducting the μTBS test. The authors, while recognizing the limitations of a static, strength-based test method, welcome comments and suggestions for improvements of this guidance document in future revisions.
Periodontitis is a prevalent and chronic inflammatory disease that is interrelated with systemic health. Periodontitis can be promoted by tumor necrosis factor α (TNF-α). Cementum, a vital part of ...the periodontium, is a bone-like mineralized tissue that is produced by cementoblasts. Our laboratory previously revealed that TNF-α inhibits cementoblast differentiation and mineralization. However, how TNF-α modulates cementoblast differentiation and mineralization remains largely unknown. MicroRNA-155 (miR-155) is induced and regulates TNF-α-inhibited osteogenic differentiation. In this study, we found that miR-155-3p was increased during TNF-α-stimulated OCCM-30 cells and involved in cementoblast differentiation and mineralization. Overexpression of miR-155-3p suppressed cementoblast mineralization. Bioinformatics analysis revealed that potassium channel tetramerization domain containing 1 (Kctd1) is a candidate target gene of miR-155-3p. Moreover, miR-155-3p overexpression suppressed KCTD1 levels. Meanwhile, its knockdown increased KCTD1 expression. Transfection with miR-155-3p also inhibited the luciferase activity of 3′-untranslated regions in the Kctd1 wild type but not the mutant. These data indicated that Kctd1 is a direct and novel target of miR-155-3p. The Wnt signaling pathway inhibits cementoblast differentiation, and we further demonstrated that miR-155-3p partially modulates cementoblast differentiation through the canonical Wnt signaling pathway. In addition to the gain/loss function assay of miR-155-3p, the luciferase activity assay of canonical Wnt signaling was performed. The assays revealed that miR-155-3p increased β-catenin-mediated transcriptional activation. Overall, our data clarified that miR-155-3p mediated TNF-α-inhibited cementoblast differentiation by targeting Kctd1, at least partially through canonical Wnt signaling pathway. These findings reveal the expanded function of miRNAs in cementoblast differentiation and mineralization.
Display omitted
To answer the PICOS question: “Is the risk of retention loss equal for SEE and SE approach when universal adhesives and composite restorations are indicated for restoring NCCLs?”
Web ...of Science, PubMed, Cochrane Central Register of Controlled Trials, Scopus, Scientific Electronic Library Online, LILACS, Google Scholar™ and OpenGrey were searched. Only randomized controlled clinical trials in which NCCLs were restored with composites and universal adhesives applied in SEE or SE mode were included. The articles were assessed for the risk of bias, after which meta-analyses were run (fixed-effects model was applied; heterogeneity was explored using Cochran Q test and I2 statistics; α = 0.05) and the certainty of evidence was assessed by the GRADE tool.
Fifteen articles were included in qualitative, while 7 articles were included in quantitative analysis. Seven studies were judged as “low” risk of bias, while 8 were considered as “unclear” risk of bias. Statistically significant difference for retention were observed at 6- and 18/24 months (p = 0.05; OR=0.42, 95% CI 0.18, 0.99; very low certainty of evidence and p = 0.007; OR=0.31, 95% CI 0.13, 0.72; low certainty of evidence, respectively), favoring SEE approach. No other significant differences in clinical outcomes were observed between SEE and SE approach (very low certainty of evidence).
When restoring NCCLs, clinicians might consider applying universal adhesives in SEE mode since it could lead to more predictable retention compared to SE approach up to 2 years of follow-up.
The cementation of indirect restoration is one of the most important steps in prosthetic and restorative dentistry. Cementation aims to bond the prosthetic restoration to the prepared enamel or ...enamel and dentine. Successful cementation protocols prevent biofilm formation at the margin between tooth and restoration and minimize mechanical and biological complications. With the advancements in dental cements, they have been modified to be versatile in terms of handling, curing, and bond strengths. This review presents updates on dental cements, focusing on the composition, properties, advantages, limitations, and indications of the various cements available. Currently, dental restorations are made from various biomaterials, and depending on each clinical case, an appropriate luting material will be selected. There is no luting material that can be universally used. Therefore, it is important to distinguish the physical, mechanical, and biological properties of luting materials in order to identify the best options for each case. Nowadays, the most commonly used dental cements are glass-ionomer and resin cement. The type, shade, thickness of resin cement and the shade of the ceramic, all together, have a tangible influence on the final restoration color. Surface treatments of the restoration increase the microtensile bond strength. Hence, the proper surface treatment protocol of both the substrate and restoration surfaces is needed before cementation. Additionally, the manufacturer's instructions for the thin cement-layer thickness are important for the long-term success of the restoration.
Porphyromonas gingivalis is responsible for the destruction of cementum in patients with periodontitis and periapical periodontitis. However, research about the effects of P. gingivalis on ...cementoblast mineralization and the underlying mechanism is still lacking. Casein kinase 2 interacting protein 1 (Ckip-1) is a scaffold protein that interacts with various proteins and signals to regulate different cell functions, such as cell morphology, apoptosis, and differentiation. In this study, we verified the suppressive effects of P. gingivalis and lipopolysaccharide (Pg-LPS) on OCCM-30 mineralization. We also showed that Ckip-1 gradually decreased during OCCM-30 mineralization but increased with the aggravation of Pg-induced inflammation. However, it remained unchanged when cells were stimulated with Pg-LPS, regardless of the concentration and incubation time. Then, more cellular cementum and enhanced Osterix expression were observed in Ckip-1 knockout mice when compared with the wild-type mice. Meanwhile, Ckip-1 silencing significantly enhanced cementoblast mineralization with or without P. gingivalis–associated inflammation. The trend was opposite when Ckip-1 was overexpressed. Finally, we found that the p38, Akt, and Wnt pathways were activated, while the Erk1/2 pathway was inhibited when Ckip-1 was silenced. The opposite results were also observed in the Ckip-1 overexpression group. Furthermore, we proved that cell mineralization was weakened when p38, Akt inhibitors were applied and strengthened when the Erk1/2 pathway was inhibited. In summary, Ckip-1 is upregulated underP. gingivalis–induced inflammation and negatively regulates cementoblast mineralization partially through mitogen-activated protein kinases and Akt signaling pathways, which may contribute to the restoration of cementum destroyed by P. gingivalis.
Bone sialoprotein (gene: Ibsp; protein: BSP) is a multifunctional extracellular matrix protein present in bone, cementum, and dentin. Accumulating evidence supports BSP as a key regulator of ...mineralized tissue formation via evolutionarily conserved functional domains, including a C-terminal integrin-binding Arg-Gly-Asp (RGD) domain implicated in extracellular matrix–cell signaling. Ablation of Ibsp in mice (Ibsp−/−) results in impaired bone growth and mineralization and defective osteoclastogenesis, with effects in the craniofacial region including reduced acellular cementum formation, detachment of the periodontal ligament (PDL), alveolar bone hypomineralization, and severe periodontal breakdown. We hypothesized that BSP-RGD plays an important role in cementum and alveolar bone formation and mineralization, as well as periodontal function. This hypothesis was tested by replacing the RGD motif with a nonfunctional Lys-Ala-Glu (KAE) sequence in (IbspKAE/KAE) mice and OCCM.30 murine (IbspKAE) cementoblasts. The RGD domain was not critical for acellular or cellular cementum formation in IbspKAE/KAE mice. However, PDL volume and thickness were increased, and significantly more tartrate-resistant acid phosphatase–positive osteoclasts were found on alveolar bone surfaces of IbspKAE/KAE mice versus wild type mice. PDL organization was disrupted as indicated by picrosirius red stain, second harmonic generation imaging, dynamic mechanical analysis, and decreased asporin proteoglycan localization. In vitro studies implicated RGD functions in cell migration, adhesion, and mineralization, and this was confirmed by an ossicle implant model where cells lacking BSP-RGD showed substantial defects as compared with controls. In total, the BSP-RGD domain is implicated in periodontal development, though the scale and scope of changes indicated by in vitro studies indicate that other factors may partially compensate for and reduce the phenotypic severity of mice lacking BSP-RGD in vivo.
PDF
