Stimulation phosphatidylinositol 3-kinase/protein kinase B signaling by Porphyromonas gingivalis lipopolysacch aride mediates interleukin-6 and interleukin-8 mRNA/protein expression in pulpal inflammation.

BACKGROUND/PURPOSE: The signaling mechanisms for Porphyromonas gingivalis lipopolysaccharide (PgLPS)-induced inflammation in human dental pulp cells are not fully clarified. This in vitro study aimed to evaluate the involvement of phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) pathway in PgLPS-induced pulpal inflammation. METHODS: Human dental pulp cells (HDPCs) were challenged with PgLPS with or without pretreatment and coincubation with a PI3K/Akt inhibitor (LY294002). The gene or protein levels of PI3K, Akt, interleukin (IL)-6, IL-8, alkaline phosphatase (ALP), osteocalcin and osteonectin were analyzed by reverse transcription polymerase chain reaction (PCR), real-time PCR, western blotting, and immunofluorescent staining. In addition, an enzyme-linked immunosorbent assay was used to analyze IL-6 and IL-8 levels in culture medium. RESULTS: In response to 5 µg/ml PgLPS, IL-6, IL-8, and PI3K, but not Akt mRNA expression of HDPCs, was upregulated. IL-6, IL-8, PI3K, and p-Akt protein levels were stimulated by 10-50 µg/ml of PgLPS in HDPCs. PgLPS also induced IL-6 and IL-8 secretion at concentrations higher than 5 µg/ml. Pretreatment and co-incubation by LY294002 attenuated PgLPS-induced IL-6 and IL-8 mRNA expression in HDPCs. The mRNA expression of ALP, but not osteocalcin and osteonectin, was inhibited by higher concentrations of PgLPS in HDPCs. CONCLUSION: P. gingivalis contributes to pulpal inflammation in HDPCs by dysregulating PI3K/Akt signaling pathway to stimulate IL-6 and IL-8 mRNA/protein expression and secretion. These results are useful for understanding the pulpal inflammation and possible biomarkers of inflamed pulp diagnosis and treatment.

Effect of butyrate, a bacterial by-product, on the viability and ICAM-1 expression/production of human vascular endothelial cells: Role in infectious pulpal/periapical diseases.

AIM: To investigate the effects of butyric acid (BA), a metabolic product generated by pulp and root canal pathogens, on the viability and intercellular adhesion molecule-1 (ICAM-1) production of endothelial cells, which are crucial to angiogenesis and pulpal/periapical wound healing. METHODOLOGY: Endothelial cells were exposed to butyrate with/without inhibitors. Cell viability, apoptosis and reactive oxygen species (ROS) were evaluated using an MTT assay, PI/annexin V and DCF fluorescence flow cytometry respectively. RNA and protein expression was determined using a polymerase chain reaction assay and Western blotting or immunofluorescent staining. Soluble ICAM-1 (sICAM-1) was measured using an enzyme-linked immunosorbent assay. The quantitative results were expressed as mean ± standard error (SE) of the mean. The data were analysed using a paired Student's t-test where necessary. A p-value ≤0.05 was considered to indicate a statistically significant difference between groups. RESULTS: Butyrate (>4 mM) inhibited cell viability and induced cellular apoptosis and necrosis. It inhibited cyclin B1 but stimulated p21 and p27 expression. Butyrate stimulated ROS production and hemeoxygenase-1 (HO-1) expression as well as activated the Ac-H3, p-ATM, p-ATR, p-Chk1, p-Chk2, p-p38 and p-Akt expression of endothelial cells. Butyrate stimulated ICAM-1 mRNA/protein expression and significant sICAM-1 production (p < .05). Superoxide dismutase, 5z-7oxozeaenol, SB203580 and compound C (p <  .05), but not ZnPP, CGK733, AZD7762 or LY294002, attenuated butyrate cytotoxicity to endothelial cells. Notably, little effect on butyrate-stimulated sICAM-1 secretion was found. Valproic acid, phenylbutyrate and trichostatin (three histone deacetylase inhibitors) significantly induced sICAM-1 production (p < .05). CONCLUSION: Butyric acid inhibited proliferation, induced apoptosis, stimulated ROS and HO-1 production and increased ICAM-1 mRNA expression and protein synthesis in endothelial cells. Cell viability affected by BA was diminished by some inhibitors; however, the increased sICAM-1 secretion by BA was not affected by any of the tested inhibitors. These results facilitate understanding of the pathogenesis, prevention and treatment of pulpal/periapical diseases.

Horizontal root fracture in posterior teeth without dental trauma: A diseased condition with special characteristics.

Horizontal root fractures (HRF) were observed mostly in the anterior teeth of young adults due to dental injury. However, HRFs in posterior teeth (PHRF) without dental trauma cannot be neglected. The etiology and risk factors of PHRF were unclear. Lower premolars and palatal root of maxillary molars were particularly affected, indicating the specificity of this diseased entity. PHRF were mainly reported in Asian population, suggesting possible racial difference. Whereas most PHRF teeth showed symptoms mimicking endodontic and periodontal lesions, some affected teeth were asymptomatic. Periodontal pocket, soft tissue swelling, chronic pain or discomfort during mastication were commonly noted. Diagnosis of PHRF depended on thorough clinical examination, radiographic images or exploratory surgery. Intracanal bleeding and electronic apex locator confirmation during endodontic treatment were also useful for diagnosis. Flexible splinting, endodontic/periodontal treatment or root amputation were treatment strategies to preserve the fractured teeth. The aim of this narrative review is to summarize the demography, tooth and root distribution, diagnostic methods, etiology and possible related factors, clinical features, radiographic characteristics, and the treatment schemes of PHRF without dental trauma. A better understanding and identification of this particular root fracture could be achieved. The diagnostic tools and practical management are useful for clinical guides.

Preparation of Calcium Phosphate Compounds on Zirconia Surfaces for Dental Implant Applications.

Titanium is widely used in medical implants despite the release of heavy metal ions over long-term use. Zirconia is very close to the color of teeth; however, its biological inertness hinders bonding with bone tissue. Alkaline treatment and coatings of calcium phosphate can be used to enhance bone regeneration adjacent to dental implants. This study examined the effects of alkaline treatment, calcium phosphate coatings, and sintering, on the physical properties of implant material. Our analysis confirmed that the calcium phosphate species were octacalcium phosphate (OCP). The sintering of calcium phosphate was shown to create B-type HAP, which is highly conducive toward the differentiation of mesenchymal stem cells (MSCs) into osteoblasts for the facilitation of bone integration. Conclusions: This study demonstrated the room-temperature fabrication of dental implants with superhydrophilic surfaces to enhance biocompatibility.

Magnesium Modified ß-Tricalcium Phosphate Induces Cell Osteogenic Differentiation In Vitro and Bone Regeneration In Vivo.

In vitro, in vivo, and clinical studies have shown how the physicochemical and biological properties of ß-tricalcium phosphate (ß-TCP) work in bone regeneration. This study aimed to improve the properties of ß-TCP by achieving optimum surface and bulk ß-TCP chemical/physical properties through the hydrothermal addition of magnesium (Mg) and to later establish the biocompatibility of ß-TCP/Mg for bone grafting and tissue engineering treatments. Multiple in vitro and in vivo analyses were used to complete ß-TCP/Mg physicochemical and biological characterization. The addition of MgO brought about a modest rise in the number of ß-TCP surface particles, indicating improvements in alkaline phosphatase (ALP) activity on day 21 (p < 0.05) and in the WST-1assay on all days (p < 0.05), with a corresponding increase in the upregulation of ALP and bone sialoprotein. SEM analyses stated that the surfaces of the ß-TCP particles were not altered after the addition of Mg. Micro-CT and histomorphometric analysis from rabbit calvaria critical defects resulted in ß-TCP/Mg managing to reform more new bone than the control defects and ß-TCP control at 2, 6, and 8 weeks (* p ≤ 0.05, ** p ≤ 0.01, *** p ≤ 0.001, and **** p ≤ 0.0001). The hydrothermal addition of MgO to the ß-TCP surfaces ameliorated its biocompatibility without altering its surface roughness resulting from the elemental composition while enhancing cell viability and proliferation, inducing more bone regeneration by osteoconduction in vivo and osteoblastic differentiation in vitro.

Genetic Susceptibility and Protein Expression of Extracellular Matrix Turnover-Related Genes in Oral Submucous Fibrosis.

Betel quid (BQ) chewing increased the risk of oral cancer and oral submucous fibrosis (OSMF), an oral premalignant disorder (OPMD) with malignant transformation potential. BQ components such as areca nut (AN), trauma by coarse AN fiber, catechin, copper, alkaloids, stimulated reactive oxygen species (ROS), inflammation and cytotoxicity are suggested to be the contributing factors. They may induce tissue inflammation, proliferation of fibroblasts and collagen deposition, myofibroblast differentiation and contraction, collagen cross-links and inhibit collagen phagocytosis, finally leading to the development of OSMF and oral cancer. These events are mediated by BQ components-induced changes of extracellular matrix (ECM) turnover via regulation of TGF-ß1, plasminogen activator inhibitor-1 (PAI-1), cystatin, lysyl oxidase (LOX) and tissue inhibitors of metalloproteinases (TIMPs) and metalloproteinases (MMPs). Genetic susceptibility is also involved in these disease processes. Further understanding the molecular mechanisms of BQ-induced OSMF and oral cancer can be helpful for future disease prevention and treatment.

Antiplatelet, antioxidative, and anti-inflammatory effects of hydroquinone.

Platelets play crucial roles in thrombosis and hemostasis through platelet activation and aggregation that are crucial in cardiovascular diseases. Hydroquinone (HQ) and its derivatives are present in many dermatological creams, paints, motor fuels, air, microorganisms, and plant products like wheat bread, fruit, coffee, and red wine. The effect of HQ on humans is not clear. In this study, we found that HQ (>25 µM) inhibited arachidonic acid (AA)-induced platelet aggregation. HQ suppressed AA-induced thromboxane B2 production of platelets. HQ (>10 µM) also attenuated ex vivo platelet-rich plasma aggregation. HQ prevented the interleukin (IL)-1ß-induced 8-isoprostane, and PGE2 production, but not IL-8 production of pulp cells. These results indicate that HQ may have an antiplatelet effect via inhibition of thromboxane production. HQ has antioxidative and anti-inflammatory effects, and possible inhibition of COX. Exposure and consumption of HQ-containing products, food or drugs may have antiplatelet, antioxidative, and anti-inflammatory effects.

IL-1ß-induced ICAM-1 and IL-8 expression/secretion of dental pulp cells is differentially regulated by IRAK and p38.

BACKGROUND/PURPOSE: Interleukin 1 beta (IL-1ß) is a pro-inflammatory cytokine involved in the acute and chronic inflammatory processes of dental pulp. Intercellular adhesion molecule-1 (ICAM-1) and IL-8 are two major inflammatory mediators. However, the role of interleukin-1 receptor-associated kinases (IRAKs) signaling pathways in responsible for the inflammatory effects of IL-1ß on dental pulp cells is not clear. METHODS: Cultured human dental pulp cells were exposed to IL-1ß with/without pretreatment and co-incubation with IRAK1/4 inhibitor or SB203580 (p38 inhibitor). IRAK-1 phosphorylation was evaluated by immunno fluorescent staining. The protein expression of ICAM-1 and IL-8 were tested by western blotting. The secretion of soluble ICAM-1 (sICAM-1) and IL-8 was measured by enzyme-linked immunosorbant assay (ELISA). RESULTS: IL-1ß stimulated IRAK-1 phosphorylation of pulp cells within 120 min of exposure. IRAK1/4 inhibitor attenuated the IL-1ß-induced ICAM-1, but not IL-8 protein expression. IRAK1/4 inhibitor also prevented the IL-1ß-induced sICAM-1, but not IL-8 secretion. SB203580 showed little effect on IL-1ß-induced sICAM-1 secretion, but effectively inhibited its induction of IL-8 secretion in pulp cells. CONCLUSION: The Results reveal the important role of IL-1ß in pulpal inflammatory responses via stimulation of IL-8 and ICAM-1 expression and secretion. Moreover, IL-1ß-induced effects on IL-8 and ICAM-1 are differentially regulated by IRAK1/4 and p38 signaling in dental pulp cells. Blocking of IRAKs and p38 signaling may have potential to control inflammation of dental pulp in the future.

IL-1ß induced IL-8 and uPA expression/production of dental pulp cells: Role of TAK1 and MEK/ERK signaling.

BACKGROUND/PURPOSE: Interleukin 1 beta (IL-1ß) is a pro-inflammatory cytokine involved in the inflammatory processes of dental pulp. IL-8 and urokinase plasminogen activator (uPA) are two inflammatory mediators. However, the role of transforming growth factor beta-activated kinase-1 (TAK1) and mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) signaling pathways in responsible for the effects of IL-1ß on IL-8 and uPA expression/secretion of dental pulp cells are not clear. METHODS: Human dental pulp cells were exposed to IL-1ß with/without pretreatment with 5z-7-oxozeaneaeol (a TAK1 inhibitor) or U0126 (a MEK/ERK inhibitor). TAK1 activation was determined by immunofluorescent staining. The protein expression of IL-8 was tested by western blot. The expression of IL-8 and uPA mRNA was studied by reverse transcriptase-polymerase chain reaction (RT-PCR). The secretion of IL-8 and uPA was measured by enzyme-linked immunosorbent assay. RESULTS: Exposure of dental pulp cells to IL-1ß (0.1-10 ng/ml) stimulated IL-8 and uPA expression. IL-1ß also induced IL-8 and uPA secretion of dental pulp cells. IL-1ß stimulated p-TAK1 activation of pulp cells. Pretreatment and co-incubation of pulp cells by 5z-7oxozeaenol (1 and 2.5 µM) and U0126 (10 and 20 µM) prevented the IL-1ß-induced IL-8 and uPA expression. 5z-7oxozeaenol and U0126 also attenuated the IL-1ß-induced IL-8 and uPA secretion. CONCLUSION: IL-1ß is important in the pathogenesis of pulpal inflammatory diseases and repair via stimulation of IL-8 and uPA expression and secretion. These events are associated with TAK1 and MEK/ERK signaling. Blocking of TAK1 and MEK/ERK signaling has potential to control inflammation of dental pulp.

Butyrate Stimulates Histone H3 Acetylation, 8-Isoprostane Production, RANKL Expression, and Regulated Osteoprotegerin Expression/Secretion in MG-63 Osteoblastic Cells.

Butyric acid as a histone deacetylase (HDAC) inhibitor is produced by a number of periodontal and root canal microorganisms (such as Porphyromonas, Fusobacterium, etc.). Butyric acid may affect the biological activities of periodontal/periapical cells such as osteoblasts, periodontal ligament cells, etc., and thus affect periodontal/periapical tissue destruction and healing. The purposes of this study were to study the toxic effects of butyrate on the matrix and mineralization marker expression in MG-63 osteoblasts. Cell viability was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay. Cellular apoptosis and necrosis were analyzed by propidium iodide/annexin V flow cytometry. The protein and mRNA expression of osteoprotegerin (OPG) and receptor activator of nuclear factor kappa-B ligand (RANKL) were analyzed by Western blotting and reverse transcriptase-polymerase chain reaction (RT-PCR). OPG, soluble RANKL (sRANKL), 8-isoprostane, pro-collagen I, matrix metalloproteinase-2 (MMP-2), osteonectin (SPARC), osteocalcin and osteopontin (OPN) secretion into culture medium were measured by enzyme-linked immunosorbant assay. Alkaline phosphatase (ALP) activity was checked by ALP staining. Histone H3 acetylation levels were evaluated by immunofluorescent staining (IF) and Western blot. We found that butyrate activated the histone H3 acetylation of MG-63 cells. Exposure of MG-63 cells to butyrate partly decreased cell viability with no marked increase in apoptosis and necrosis. Twenty-four hours of exposure to butyrate stimulated RANKL protein expression, whereas it inhibited OPG protein expression. Butyrate also inhibited the secretion of OPG in MG-63 cells, whereas the sRANKL level was below the detection limit. However, 3 days of exposure to butyrate (1 to 8 mM) or other HDAC inhibitors such as phenylbutyrate, valproic acid and trichostatin stimulated OPG secretion. Butyrate stimulated 8-isoprostane, MMP-2 and OPN secretion, but not procollagen I, or osteocalcin in MG-63 cells. Exposure to butyrate (2⁻4 mM) for 3 days markedly stimulated osteonectin secretion and ALP activity. In conclusion, higher concentrations of butyric acid generated by periodontal and root canal microorganisms may potentially induce bone destruction and impair bone repair by the alteration of OPG/RANKL expression/secretion, 8-isoprostane, MMP-2 and OPN secretion, and affect cell viability. However, lower concentrations of butyrate (1⁻4 mM) may stimulate ALP, osteonectin and OPG. These effects are possibly related to increased histone acetylation. These events are important in the pathogenesis and repair of periodontal and periapical destruction.

An analysis of the relevance and proximity between maxillary posterior root apices to the maxillary sinus and the buccal cortical bone plate.

Background/purpose: Understanding the relationship between maxillary sinus and posterior root apices is critical in preventing dental treatment complications. This study aimed to analyze and showcase the relationship between the posterior root apices and the maxillary sinus floor, the distance to the buccal cortical bone, and their correlation with age, gender, and sides. Materials and methods: Cone-beam computed tomography images were collected from 94 patients with a total of 478 maxillary posterior teeth and 997 roots. The shortest distance from root apices to the closest border of maxillary sinus and the outer buccal cortical bone margin were measured and grouped for statistical analysis for the differences (P < 0.05). Results: The root apices of maxillary molars and single-rooted second premolars were located closer to the maxillary sinus compared to first premolars (P < 0.01). The buccal root of two-rooted first premolar had the shortest horizontal distance to the buccal cortical bone among all roots (P < 0.01). The lowest position of the maxillary sinus floor was mostly located at the palatal side (P < 0.01) and between the buccal and palatal root apices (P < 0.01) in the maxillary premolars and molars, respectively. Increasing age would lead to longer distances between the root apices and the maxillary sinus (P < 0.01). Additionally, male patients had thicker buccal cortical bone than female patients (P < 0.01). Conclusion: Different tooth positions, age, and gender significantly impact the relationships between root apices and the maxillary sinus and buccal cortical plates, informing patient-centered and individually tailored approaches for more effective and safer surgical endodontic treatment.

Inducing cyclooxygenase-2 expression, prostaglandin E2 and prostaglandin F2α production of human dental pulp cells by activation of toll-like receptor-3, mitogen-activated protein kinase kinase/extracellular signal-regulated kinase and p38 signaling.

Background/purpose: Bacterial infection was the major etiology for pulpal/root canal infection. This study aimed to investigate the activation of toll-like receptor-3 (TLR) on cyclooxygenase-2 (COX-2) expression and prostaglandin E2 (PGE2) and PGF2α production of human dental pulp cells (HDPCs) and associated signaling. Materials and methods: HDPCs were exposed to different concentrations of Poly (I:C) (a TLR3 activator). Cell viability was determined by 3- (4,5-Dimethylthiazol-2-yl)-2,5- diphenyltetrazolium bromide (MTT) assay and alkaline phosphatase (ALP) activity was evaluated by ALP staining. Activation of extracellular signal-regulated kinase (ERK) and p38 by Poly (I:C) was determined by immunofluorescent staining. The COX-2 protein expression was analyzed by Western blot. PGE2 and PGF2α production was measured by enzyme-linked immunosorbent assay. The mRNA expression was studied by real-time polymerase-chain reaction. Moreover, HDPCs were exposed to Poly(I:C) with/without U0126 or SB203580 treatment and analysis of COX-2 expression and prostanoid production were conducted. Results: Poly (I:C) showed little effect on ALP activity, but decreased viability of HDPCs. It stimulated COX-2 mRNA and protein expression. Poly (I:C) induced PGE2 and PGF2α production of HDPCs. Poly (I:C) activated p-ERK, and p-p38 protein expression. Treatment by U0126 (a mitogen-activated protein kinase kinase (MEK)/ERK inhibitor) and SB203580 (a p38 inhibitor) attenuated Poly (I:C)-induced COX-2 mRNA and protein expression as well as PGE2 and PGF2α production. Conclusion: TLR3 activation is involved in the infection and inflammatory responses of pulp tissues, via MEK/ERK, and p38 signaling to mediate COX-2 expression as well as PGE2 and PGF2α production, contributing to the pathogenesis and progression of pulpal/periapical diseases.

Association between oral health status and occlusal bite force in young adults.

Background/purpose: Oral health is related to general health and a person's overall well-being. The aim of the present study was to explore the association between oral health status and bite force among young adults. Materials and methods: Maximum bite force (MBF) was measured using Dental Prescale II in conjunction with a pressure-sensitive film and bite force analyzer in 40 young adults aged 20 to 40. Supragingival dental plaque was collected and cultured. Plaque weight, pH, and colony counts were assessed. The decayed, missing, and filled teeth index (DMFT) and body mass index (BMI) were recorded. Results: Bite force was negatively correlated with the number of missing teeth and the sum of missing and filled teeth. When the filled-to-remaining-teeth ratio (F/R ratio) was less than 8%, the bite force was significantly higher compared to an F/R ratio of 8-25%. Additionally, the amount of total bacteria was positively correlated with total bite force, and the quantity of Streptococcus mutans (S. mutans) along with total bacteria was positively correlated with bite force in the molar region (∗P < 0.05). The molar region predominantly contributed to bite force. Conclusion: Elevated levels of cariogenic bacteria may increase the risk of tooth loss, subsequently leading to reduced bite force. This reduction in bite force can further impact the efficiency of chewing function and, consequently, the quality of life. An F/R ratio above 8% could be easily calculated clinically and could serve as a guide to identify patients, particularly young adults, at risk of reduced bite force.

Inducing cathepsin L expression/production, lysosomal activation, and autophagy of human dental pulp cells by dentin bonding agents, camphorquinone and BisGMA and the related mechanisms.

Camphorquinone (CQ) and resin monomers are included in dentin bonding agents (DBAs) and composite resin to restore tooth defects due to abrasion, crown fracture, or dental caries. DBAs, CQ, and bisphenol A-glycidyl methacrylate (BisGMA) applications influence the biological activities of the dental pulp. The current investigation aimed to delineate the effect of DBAs, CQ, and BisGMA on cathepsin L production/expression, lysosomal activity, and autophagy induction in human dental pulp cells (HDPCs). HDPCs were exposed to DBAs, CQ, or BisGMA with/without inhibitors for 24 h. Enzyme-linked immunosorbent assay was employed to determine the cathepsin L level in culture medium. The cell layer was utilized to measure cell viability by 3-(4,5-dimethyl-thiazol-2-yl)-2,5-diphenyl -tetrazolium bromide (MTT) assay. Real-time PCR was used to evaluate the mRNA expression. Western blotting or immunofluorescent staining was used to study protein expression. Lysosomal density was evaluated by lysotracker red staining. We found that DBAs, CQ, and BisGMA stimulated cathepsin L mRNA, protein expression, and production in HDPCs. In addition, CQ and BisGMA induced lysosomal activity, Beclin1, ATG12, LC3B, Bax, and p53 expression in HDPCs, indicating the stimulation of autophagy. Glutathione (GSH) prevented CQ- and BisGMA-induced cytotoxicity. Moreover, E64d, cathepsin L inhibitor (two cathepsin inhibitors), and Pifithrin-α (a p53 inhibitor) showed little preventive effect toward CQ- and BisGMA-induced cytotoxicity. Autophagy inhibitors (NH4Cl, Lys05) mildly enhanced the CQ- and BisGMA-induced cytotoxicity. These results indicate that DBAs stimulated cathepsin L, possibly due to their content of CQ and BisGMA that may induce cathepsin L in HDPCs. CQ and BisGMA stimulated lysosomal activity, autophagy, and apoptosis, possibly via induction of Beclin 1, ATG12, LC-3B, Bax, and p53 expression. In addition, CQ and BisGMA cytotoxicity was related to redox change and autophagy. These events are important role in pulpal changes after the restoration of tooth decay using CQ- and BisGMA-containing DBAs and resin composite.

Peri-Implant Marginal Bone Changes around Dental Implants with Platform-Switched and Platform-Matched Abutments: A Retrospective 5-Year Radiographic Evaluation.

Preserving the marginal bone level (MBL) is essential for the long-term success of dental implant therapy, and bone remodeling around dental implants is considered to vary with time. Numerous studies comparing the platform-switching (PS) and platform-matching (PM) dental implants have indicated that PS dental implants showed a lesser reduction for the MBL, and the majority of them had a relatively short period. This study aimed to evaluate vertical and horizontal bone defects by using digital periapical radiographs to examine the changes in MBL around PM and PS dental implants over 5 years after functional loading. The vertical MBL (vMBL) was measured from the implant-abutment junction to the first bone-to-implant contact. The horizontal MBL (hMBL) was measured from the implant-abutment junction to the bone crest. All data were presented as means ± standard errors. Paired and independent t-tests with Welch's correction were used to analyze the data. A total of 61 dental implants in 38 patients after 5 years of functional loading were evaluated. Over time, PS dental implants were more likely to gain bone; by contrast, PM dental implants were more likely to lose bone during the observation time. Changes in vMBL for PS dental implants were significantly less than those for PM dental implants at 1-year (p = 0.045), 3-year (p = 0.021), and 5-year (p = 0.010) loading. Likewise, changes in hMBL for PS dental implants were significantly smaller than in those for PM dental implants at 3-year (p = 0.021) and 5-year (p = 0.006) loading; however, the changes were minimal in both approaches. PS dental implants had a significant increment in the percentage of bone integration, whereas that for PM dental implants dropped over time, with no significance. In PS dental implants that occlude with natural teeth, vertical and horizontal bone gain was observed, and it was significant at 3 years (p = 0.023). A significant horizontal bone gain was observed in the opposing natural teeth at 3-year (p = 0.002) and 5-year loading (p = 0.002). The PS concept appears to preserve more MBL around dental implants by stabilizing the vMBL and hMBL over a 5-year period. A minimal marginal bone change was detected in both concepts. The opposing natural teeth at PS dental implants showed a favorable effect on marginal bone tissues.

bFGF stimulated plasminogen activation factors, but inhibited alkaline phosphatase and SPARC in stem cells from apical Papilla: Involvement of MEK/ERK, TAK1 and p38 signaling.

INTRODUCTION: Basic fibroblast growth factor (bFGF) plays a critical role in odontoblast differentiation and dentin matrix deposition, thereby aiding pulpo-dentin repair and regeneration. OBJECTIVES: The purpose of this study was to clarify the effects of bFGF on plasminogen activation factors, TIMP-1), ALP; and SPARC (osteonectin) expression/production of stem cells from apical papilla (SCAP) in vitro; and the involvement of MEK/ERK, p38, Akt, and TAK1 signaling. METHODS: SCAP were exposed to bFGF with/without pretreatment and co-incubation with various signal transduction inhibitors (U0126, SB203580, LY294002, and 5Z-7-oxozeaenol). The expression of FGF receptors (FGFRs), PAI-1, uPA, p-ERK, p-TAK1, and p-p38 was analyzed via immunofluorescent staining. The gene expression and protein secretion of SCAP were determined via real-time PCR and ELISA. ALP activity was evaluated via ALP staining. RESULTS: SCAP expressed FGFR1, 2, 3, and 4. bFGF stimulated the PAI-1, uPA, uPAR, and TIMP-1 mRNA expression (p < 0.05). bFGF induced PAI-1, uPA, and soluble uPAR production (p < 0.05) but suppressed the ALP activity and SPARC production (p < 0.05) of SCAP. bFGF stimulated ERK, TAK1, and p38 phosphorylation of SCAP. U0126 (a MEK/ERK inhibitor) and 5Z-7-oxozeaenol (a TAK1 inhibitor) attenuated the bFGF-induced PAI-1, uPA, uPAR, and TIMP-1 expression and production of SCAP, but SB203580 (a p38 inhibitor) did not. LY294002, SB203580, and 5Z-7oxozeaenol could not reverse the inhibition of ALP activity caused by bFGF. Interestingly, U0126 and 5Z-7-oxozeaenol prevented the bFGF-induced decline of SPARC production (p < 0.05). CONCLUSION: bFGF may regulate fibrinolysis and matrix turnover via modulation of PAI-1, uPA, uPAR, and TIMP-1, but bFGF inhibited the differentiation (ALP, SPARC) of SCAP. These events are mainly regulated by MEK/ERK, p38, and TAK1. Combined use of bFGF and SCAP may facilitate pulpal/root repair and regeneration via regulation of the plasminogen activation system, migration, matrix turnover, and differentiation of SCAP.

Marginal Bone Level Evaluation of Fixed Partial Dental Prostheses Using Preformed Stock versus CAD/CAM Customized Abutments.

Background: The maintenance of marginal bone levels around dental implants is an important criterion for evaluating the success of implants. Although computer-aided design/computer-aided manufacturing (CAD/CAM) customized abutments (CAs) provide more flexible solutions, compared with the original preformed stock abutments (PAs), there are dimensional tolerances and underlying drawbacks in the production of CAD/CAM CAs, which may change the tightness and seamless connection between fixtures and abutments set by the manufacturer and then affect the long-term stability of the abutments. This study aimed to examine the change in both mesial and distal bone levels using digital periapical radiographs to evaluate the difference between CAD/CAM CAs and original PAs.Material and methods: Radiographs were taken before delivery; after functional loading for 1 month; and after 3, 6, and 12 months; and the vertical marginal bone levels (vMBLs) of both the mesial and distal surrounding implant bones were measured. All data are presented as means ± standard errors and were analyzed using Student's t-test. A p-value < 0.05 was judged to represent a significant difference. Results: A total of 57 implants in 50 patients were divided into 22 CAD/CAM CAs and 35 original stock abutments. The PAs appeared to have a more stable bone level. By contrast, the amount of bone level change in the CAs was higher than that in the PAs. The change in the vMBL of the CAs was significantly more than that of the PAs after functional loading for 1 month (p = 0.006), 3 months (p = 0.013), 6 months (p = 0.014), and 12 months (p = 0.002). In contrast, the distal marginal bone level was lower than the mesial marginal bone level in any period. Nevertheless, the bone levels of the CAs and PAs in any period were comparable with no significant difference. Conclusions: Significant differences were found between the mesial and distal bone levels in the PAs. The CAD/CAM CAs showed a significantly greater bone level change than the original stock abutments after functional loading.

Marginal Bone Loss around Implant-Retaining Overdentures versus Implant-Supported Fixed Prostheses 12-Month Follow-Up: A Retrospective Study.

Few studies have compared marginal bone loss (MBL) around implant-retaining overdentures (IODs) vs. implant-supported fixed prostheses (FPs). This study evaluated the mean MBL and radiographic bone-implant interface contact (r-BIIC) around IODs and implant-supported FPs. We also investigated osseointegration and MBL around non-submerged dental implants. We measured the changes between the MBL in the mesial and distal sites immediately after prosthetic delivery and after one year. The mean MBL and its changes in the IOD group were significantly higher. The mean percentage of r-BIIC was significantly higher in the FP group. MBL and its changes in males were significantly higher in the IOD group. The percentage of r-BIIC was significantly higher in the FP group. MBL in the lower site in the IOD group was significantly higher. Regarding MBL, the location of the implant was the only significant factor in the IOD group, while gender was the only significant predictor in the FP group. Regarding the r-BIIC percentage, gender was a significant factor in the FP group. We concluded that non-submerged dental implants restored with FPs and IODs maintained stable bone remodeling one year after prosthetic delivery.

Equation for Tooth Size Prediction from Mixed Dentition Analysis for Taiwanese Population: A Pilot Study.

BACKGROUND: In mixed dentition analysis, estimation of the mesiodistal width of unerupted permanent canines and premolars is essential for successful diagnosis and treatment planning. The present study aimed to develop a simple linear equation to predict permanent tooth sizes from mixed dentition analysis for Taiwanese people. METHODS: The sample comprised 200 dental casts, derived from Taiwanese patients (100 males and 100 females; age, 12-35 years). Mesial distal tooth widths were measured in dental casts with a digital caliper. A student's t-test was conducted to detect tooth size correlations with gender-specific differences, as well as intra-arch counterparts. Standard linear regression was conducted to develop a simple equation representing predictions of canine-premolar relationships. RESULTS: All teeth were not significantly different between the left and right sides, regardless of gender and upper or lower arches. In terms of types of teeth, males had larger tooth dimensions in both arches than females. New regression equations for estimating the dimensions of the unerupted canines and premolars in the Taiwanese population were developed. CONCLUSIONS: Using a sample of Taiwanese people, new models derived for females and males separately were developed, which should provide highly accurate predictions for unerupted canines and premolars in the Taiwanese population.

Vertical Root Fracture in Non-Endodontically and Endodontically Treated Teeth: Current Understanding and Future Challenge.

A vertical root fracture (VRF) is a complex complication that usually leads to tooth extraction. The aim of this article is to review the prevalence, demography, distribution, diagnostic methods, etiology and predisposing factors, clinical features, radiographic characteristics and treatment strategies of VRFs in non-endodontically treated teeth (VRFNETT) and endodontically treated teeth (VRFETT). Search terms for each subject related to VRFNETT and VRFETT were entered into MEDLINE, PubMed and Google Scholar. Systematic reviews, retrospective cohort studies, demographic research, clinical studies, case reports and case series were reviewed. Most of the VRFs were found in patients older than 40 years old. Older populations were discovered in the non-endodontically treated VRF group when compared to the endodontically treated VRF group. Male patients were found at a greater prevalence than females in the non-endodontically treated VRF group. The initial occurrence of a VRF may accompany radiolucent lines within the root canal, unusual space between the canal wall and intracanal material, a widening of the PDL space along the periradicular surfaces, angular bony destruction, step-like bone defects, V-shaped diffuse bone defects, or root resorptions corresponding to the fracture line before the clear separation of the fractured fragment. The indicative clinical and radiographic signs of VRF included a coronally positioned sinus tract, deep-narrow periodontal defects, the displacement of a fractured fragment, periradicular radiolucent halos and the widening of the root canal space. Interestingly, VRFNETT are more often observed in the Chinese population. Some patients with multiple VRFs were observed, suggesting possible predisposing factors in genetics and tooth development. The management of a VRF usually involves a multidisciplinary approach. The common distribution and features of VRFNETT and VRFETT were elucidated to facilitate recognition and diagnosis. Besides extraction, variable therapeutic schemes, such as the repair of the VRF, root amputation and others reported in earlier literature, are available. A long-term prognosis study of the various therapeutic strategies is needed.