Predisposal of Interferon Regulatory Factor 1 Deficiency to Accumulate DNA Damage and Promote Osteoarthritis Development in Cartilage.

OBJECTIVE: Interferon regulatory factor 1 (IRF1) is a transcriptional regulator conventionally associated with immunomodulation. Recent molecular analyses mapping DNA binding sites of IRF1 have suggested its potential function in DNA repair. However, the physiologic significance of this noncanonical function remains unexplored. Here, we investigated the role of IRF1 in osteoarthritis (OA), a condition marked by senescence and chronic joint inflammation. METHODS: OA progression was examined in wild-type and Irf1-/- mice using histologic assessments and microcomputed tomography analysis of whole-joint OA manifestations and behavioral assessments of joint pain. An integrated analysis of assay for transposase-accessible chromatin with sequencing and whole transcriptome data was conducted for the functional assessment of IRF1 in chondrocytes. The role of IRF1 in DNA repair and senescence was investigated by assaying γ-H2AX foci and senescence-associated beta-galactosidase activity. RESULTS: Our genome-wide investigation of IRF1 footprinting in chondrocytes revealed its primary occupancies in the promoters of DNA repair genes without noticeable footprint patterns in those of interferon-responsive genes. Chondrocytes lacking IRF1 accumulated irreversible DNA damage under oxidative stress, facilitating their entry into cellular senescence. IRF1 was down-regulated in the cartilage of human and mouse OA. Although IRF1 overexpression did not elicit an inflammatory response in joints or affect OA development, genetic deletion of Irf1 caused enhanced chondrocyte senescence and exacerbated post-traumatic OA in mice. CONCLUSION: IRF1 offers DNA damage surveillance in chondrocytes, protecting them from oxidative stress associated with OA risk factors. Our study provides a crucial and cautionary perspective that compromising IRF1 activity renders chondrocytes vulnerable to cellular senescence and promotes OA development.

Disease-modifying therapeutic strategies in osteoarthritis: current status and future directions.

Osteoarthritis (OA) is the most common form of arthritis. It is characterized by progressive destruction of articular cartilage and the development of chronic pain and constitutes a considerable socioeconomic burden. Currently, pharmacological treatments mostly aim to relieve the OA symptoms associated with inflammation and pain. However, with increasing understanding of OA pathology, several potential therapeutic targets have been identified, enabling the development of disease-modifying OA drugs (DMOADs). By targeting inflammatory cytokines, matrix-degrading enzymes, the Wnt pathway, and OA-associated pain, DMOADs successfully modulate the degenerative changes in osteoarthritic cartilage. Moreover, regenerative approaches aim to counterbalance the loss of cartilage matrix by stimulating chondrogenesis in endogenous stem cells and matrix anabolism in chondrocytes. Emerging strategies include the development of senolytic drugs or RNA therapeutics to eliminate the cellular or molecular sources of factors driving OA. This review describes the current developmental status of DMOADs and the corresponding results from preclinical and clinical trials and discusses the potential of emerging therapeutic approaches to treat OA.

CTRP3 exacerbates tendinopathy by dysregulating tendon stem cell differentiation and altering extracellular matrix composition.

Tendinopathy, the most common disorder affecting tendons, is characterized by chronic disorganization of the tendon matrix, which leads to tendon tear and rupture. The goal was to identify a rational molecular target whose blockade can serve as a potential therapeutic intervention for tendinopathy. We identified C1q/TNF-related protein-3 (CTRP3) as a markedly up-regulated cytokine in human and rodent tendinopathy. Overexpression of CTRP3 enhanced the progression of tendinopathy by accumulating cartilaginous proteoglycans and degenerating collagenous fibers in the mouse tendon, whereas CTRP3 knockdown suppressed the tendinopathy pathogenesis. Functional blockade of CTRP3 using a neutralizing antibody ameliorated overuse-induced tendinopathy of the Achilles and rotator cuff tendons. Mechanistically, CTRP3 elicited a transcriptomic pattern that stimulates abnormal differentiation of tendon stem/progenitor cells and ectopic chondrification as an effect linked to activation of Akt signaling. Collectively, we reveal an essential role for CTRP3 in tendinopathy and propose a potential therapeutic strategy for the treatment of tendinopathy.

Comparison of Root Filling Quality of Two Types of Single Cone-Based Canal Filling Methods in Complex Root Canal Anatomies: The Ultrasonic Vibration and Thermo-Hydrodynamic Obturation versus Single-Cone Technique.

This study aimed to assess the effectiveness of ultrasonic vibration and thermo-hydrodynamic obturation (VibraTHO) using two types of root canal sealers, in comparison to the single-cone (SC) technique and a calcium silicate-based root canal sealer in complex root canal anatomies. Thirty single-rooted human maxillary premolars with two canals that had a complex root canal anatomy of transverse anastomoses or ramifications were prepared and assigned to the following three experimental groups, according to the filling method: SE group, SC technique with Endoseal TCS; VE group, VibraTHO with Endoseal TCS; and VG group, VibraTHO with GuttaFlow 2. Each tooth was scanned using micro-computed tomography, and the volume percentages of the filling material were calculated. The analysis of variance was used to analyze the statistical differences between the three groups (p < 0.05). The mean volume of the filling material was higher in the VG and VE groups than that in the SE group (p < 0.05) along the apical to middle-to-coronal thirds, and significant differences were observed between each root canal area (p < 0.05), with the only exception being at the apical thirds between the VE and SE groups. The VibraTHO technique using GuttaFlow 2 can be a more effective root canal filling method for anatomically complex root canal systems than the SC technique with Endoseal TCS. On the other hand, the VibraTHO technique using Endoseal TCS has a limited effect on improving the quality of the root filling at the apical portion of anatomically complex root canal systems, compared to the SC technique with Endoseal TCS.

Suppression of Osteoarthritis progression by post-natal Induction of Nkx3.2.

Osteoarthritis (OA) is an incurable joint disease affecting 240 million elderly population, and major unmet medical needs exist for better therapeutic options for OA. During skeletal development, Nkx3.2 has been shown to promote chondrocyte differentiation and survival, but to suppress cartilage hypertrophy and blood vessel invasion. Here we show that Nkx3.2 plays a key role in osteoarthritis (OA) pathogenesis. Marked reduction of Nkx3.2 expression was observed in three different murine OA models. Consistent with these findings, analyses of surgery-induced and age-driven OA models revealed that cartilage-specific post-natal induction of Nkx3.2 can suppress OA progression in mice. These results suggest that Nkx3.2 may serve as a promising target for OA drug development.

Ultrasonic vibration and thermo-hydrodynamic technique for filling root canals: Technical overview and a case series.

AIM: To present a novel root canal filling technique: Ultrasonic Vibration & Thermo-Hydrodynamic Obturation (VibraTHO), and its rationale with a series of cases. SUMMARY: The VibraTHO technique was used to fill the root canals of three clinically challenging cases: A C-shaped mandibular molar with complex anatomy, a C-shaped mandibular molar with an infected root canal system and a periapical lesion that required retreatment, and apically bifurcating mesiobuccal canals with a common orifice in a maxillary second molar. The cases were followed up for 15, 7 and 37 months, respectively. After follow-up, normal periapical status was observed without any noticeable radiographic change in the root canal fillings in each case. Periapical radiographs revealed complete healing of the periapical area in cases with pre-operative periapical lesions.

A system-level approach identifies HIF-2α as a critical regulator of chondrosarcoma progression.

Chondrosarcomas, malignant cartilaginous neoplasms, are capable of transitioning to highly aggressive, metastatic, and treatment-refractory states, resulting in significant patient mortality. Here, we aim to uncover the transcriptional program directing such tumor progression in chondrosarcomas. We conduct weighted correlation network analysis to extract a characteristic gene module underlying chondrosarcoma malignancy. Hypoxia-inducible factor-2α (HIF-2α, encoded by EPAS1) is identified as an upstream regulator that governs the malignancy gene module. HIF-2α is upregulated in high-grade chondrosarcoma biopsies and EPAS1 gene amplification is associated with poor prognosis in chondrosarcoma patients. Using tumor xenograft mouse models, we demonstrate that HIF-2α confers chondrosarcomas the capacities required for tumor growth, local invasion, and metastasis. Meanwhile, pharmacological inhibition of HIF-2α, in conjunction with the chemotherapy agents, synergistically enhances chondrosarcoma cell apoptosis and abolishes malignant signatures of chondrosarcoma in mice. We expect that our insights into the pathogenesis of chondrosarcoma will provide guidelines for the development of molecular targeted therapeutics for chondrosarcoma.

Tankyrase inhibition preserves osteoarthritic cartilage by coordinating cartilage matrix anabolism via effects on SOX9 PARylation.

Osteoarthritis (OA) is a prevalent degenerative disease, which involves progressive and irreversible destruction of cartilage matrix. Despite efforts to reconstruct cartilage matrix in osteoarthritic joints, it has been a difficult task as adult cartilage exhibits marginal repair capacity. Here we report the identification of tankyrase as a regulator of the cartilage anabolism axis based on systems-level factor analysis of mouse reference populations. Tankyrase inhibition drives the expression of a cartilage-signature matrisome and elicits a transcriptomic pattern that is inversely correlated with OA progression. Furthermore, tankyrase inhibitors ameliorate surgically induced OA in mice, and stem cell transplantation coupled with tankyrase knockdown results in superior regeneration of cartilage lesions. Mechanistically, the pro-regenerative features of tankyrase inhibition are mainly triggered by uncoupling SOX9 from a poly(ADP-ribosyl)ation (PARylation)-dependent protein degradation pathway. Our findings provide insights into the development of future OA therapies aimed at reconstruction of articular cartilage.

Stress-activated miR-204 governs senescent phenotypes of chondrocytes to promote osteoarthritis development.

A progressive loss of cartilage matrix leads to the development of osteoarthritis (OA). Matrix homeostasis is disturbed in OA cartilage as the result of reduced production of cartilage-specific matrix and increased secretion of catabolic mediators by chondrocytes. Chondrocyte senescence is a crucial cellular event contributing to such imbalance in matrix metabolism during OA development. Here, we identify miR-204 as a markedly up-regulated microRNA in OA cartilage. miR-204 is induced by transcription factors GATA4 and NF-κB in response to senescence signals. Up-regulated miR-204 simultaneously targets multiple components of the sulfated proteoglycan (PG) biosynthesis pathway, effectively shutting down PG anabolism. Ectopic expression of miR-204 in joints triggers spontaneous cartilage loss and OA development, whereas miR-204 inhibition ameliorates experimental OA, with concomitant recovery of PG synthesis and suppression of inflammatory senescence-associated secretory phenotype (SASP) factors in cartilage. Collectively, we unravel a stress-activated senescence pathway that underlies disrupted matrix homeostasis in OA cartilage.

Complete Healing of a Large Cystic Lesion Following Root Canal Treatment with Concurrent Surgical Drainage: A Case Report with 14-Year Follow-Up.

We describe complete healing of an extensive cystic lesion by using a conservative approach: root canal treatment with concurrent surgical drainage. A silicone Foley catheter drain was modified into a surgical drainage stent, which was then used for 4 weeks. Disinfection of the root canal was achieved by the use of hand files and irrigation with 5.25% NaOCl for a minimum of 30 minutes. The irrigant changes were performed at 5-minute intervals, and no intracanal dressing was used. At subsequent follow-up examinations, cone-beam computed tomography and periapical radiographs confirmed that complete healing had occurred around the periapical and lateral areas of affected teeth. This case report indicates the potential for healing of large cystic lesions by nonsurgical root canal treatment.

Pleiotropic roles of metallothioneins as regulators of chondrocyte apoptosis and catabolic and anabolic pathways during osteoarthritis pathogenesis.

OBJECTIVE: The zinc-ZIP8-MTF1 axis induces metallothionein (MT) expression and is a catabolic regulator of experimental osteoarthritis (OA) in mice. The main aim of the current study was to explore the roles and underlying molecular mechanisms of MTs in OA pathogenesis. METHODS: Experimental OA in mice was induced by destabilisation of the medial meniscus or intra-articular injection of adenovirus carrying a target gene (Ad-Zip8, Ad-Mtf1, Ad-Epas1, Ad-Nampt, Ad-Mt1 or Ad-Mt2) into wild type, Zip8fl/fl; Col2a1-Cre, Mtf1fl/fl; Col2a1-Cre and Mt1/Mt2 double knockout mice. Primary cultured mouse chondrocytes were infected with Ad-Mt1 or Ad-Mt2, and gene expression profiles analysed via microarray and reverse transcription-PCR. Proteins in human and mouse OA cartilage were identified via immunostaining. Chondrocyte apoptosis in OA cartilage was determined using terminal deoxynucleotidyl transferase (TdT)-mediated deoxyuridine triphosphate (dUTP) nick end labelling (TUNEL). RESULTS: MTs were highly expressed in human and mouse OA cartilage. Hypoxia-inducible factor 2α, nicotinamide phosphoribosyltransferase and several proinflammatory cytokine pathways, as well as the zinc-ZIP8-MTF1 axis were identified as upstream regulators of MT expression. Genetic deletion of Mt1 and Mt2 enhanced cartilage destruction through increasing chondrocyte apoptosis. Unexpectedly, aberrant overexpression of MT2, but not MT1, induced upregulation of matrix-degrading enzymes and downregulation of matrix molecules through nuclear factor-kappa B (NF-κB) and activator protein-1 (AP-1) activation, ultimately leading to OA. CONCLUSIONS: MTs play an antiapoptotic role in post-traumatic OA. However, aberrant and chronic upregulation of MT2 triggers an imbalance between chondrocyte anabolism and catabolism, consequently accelerating OA development. Our findings collectively highlight pleiotropic roles of MTs as regulators of chondrocyte apoptosis as well as catabolic and anabolic pathways during OA pathogenesis.

Epigenetic Regulation of Chondrocyte Catabolism and Anabolism in Osteoarthritis.

Osteoarthritis (OA) is one of the most prevalent forms of joint disorder, associated with a tremendous socioeconomic burden worldwide. Various non-genetic and lifestyle-related factors such as aging and obesity have been recognized as major risk factors for OA, underscoring the potential role for epigenetic regulation in the pathogenesis of the disease. OA-associated epigenetic aberrations have been noted at the level of DNA methylation and histone modification in chondrocytes. These epigenetic regulations are implicated in driving an imbalance between the expression of catabolic and anabolic factors, leading eventually to osteoarthritic cartilage destruction. Cellular senescence and metabolic abnormalities driven by OA-associated risk factors appear to accompany epigenetic drifts in chondrocytes. Notably, molecular events associated with metabolic disorders influence epigenetic regulation in chondrocytes, supporting the notion that OA is a metabolic disease. Here, we review accumulating evidence supporting a role for epigenetics in the regulation of cartilage homeostasis and OA pathogenesis.

Numerical study on tsunami hazard mitigation using a submerged breakwater.

Most coastal structures have been built in surf zones to protect coastal areas. In general, the transformation of waves in the surf zone is quite complicated and numerous hazards to coastal communities may be associated with such phenomena. Therefore, the behavior of waves in the surf zone should be carefully analyzed and predicted. Furthermore, an accurate analysis of deformed waves around coastal structures is directly related to the construction of economically sound and safe coastal structures because wave height plays an important role in determining the weight and shape of a levee body or armoring material. In this study, a numerical model using a large eddy simulation is employed to predict the runup heights of nonlinear waves that passed a submerged structure in the surf zone. Reduced runup heights are also predicted, and their characteristics in terms of wave reflection, transmission, and dissipation coefficients are investigated.

Improvement of water quality at Dongbin Harbor with construction of an inland canal, Korea.

The behaviors of the water body of Dongbin Harbor located at Pohang City, Gyongpook Province, in Korea were numerically simulated in this study. A canal was planned to connect the harbor and the Hyeongsan River to improve water quality inside the harbor. The current system was first simulated by using a commercial program RMA2, with respect to both tidal currents and river flow. The progress inside the harbor from a supply of fresh water from the Hyeongsan River was then predicted by using RMA4. Both the present and future conditions (before and after construction of an inland canal) were taken into consideration in numerical simulations. It is concluded that the water quality inside the harbor can be improved considerably after construction of the canal.

Leafy vegetable mix supplementation improves lipid profiles and antioxidant status in C57BL/6J mice fed a high fat and high cholesterol diet.

Daily consumption of an antioxidant-rich leafy vegetable mix (LVM) was assessed for beneficial effects on plasma lipid profiles, tissue lipid peroxidation, and oxidative DNA damage in C57BL/6J mice fed a high fat and high cholesterol diet (20% fat and 1% cholesterol, wt/wt) for 4 weeks. The LVM contained beet leaf, angelica, red leaf lettuce, dandelion, green cos lettuce, lollo rosso, romaine lettuce (12.5%, respectively), scotch kale, and red kale (6.25%, respectively). The mice (n = 16) were randomly divided into either the control (high fat and cholesterol diet without LVM) or the LVM (high fat and cholesterol diet with 8% LVM supplement) groups after a 1-week acclimation. Lipid peroxidation as measured by thiobarbituric acid-reactive substances in the plasma, liver, heart, and kidney was significantly lower. Antioxidants (glutathione and beta-carotene) and antioxidant enzyme activities (glutathione peroxidase, glutathione reductase, and superoxide dismutase) were improved in mice fed LVM diet. In the comet assay, tail extent moment, olive tail moment, and tail length were significantly less in the hepatocyte and lymphocyte DNA of the LVM group, indicating the beneficial effect of LVM on the resistance of hepatocytes and lymphocytes DNA to oxidative damage. Findings from the present study suggest that dietary supplementation with LVM may be useful for protecting cells from lipid peroxidation and oxidative DNA damage.

The linear shrinkage and microhardness of packable composites polymerized by QTH or PAC unit.

This study evaluated the effectiveness of a plasma arc curing (PAC) unit for packable resin composite curing. The amount and speed of polymerization shrinkage and the microhardness of packable composites were evaluated in order to compare the PAC unit's effectiveness with a quartz tungsten halogen (QTH) unit. Sure Fil (Dentsply Caulk), Pyramid (BISCO Inc) and Synergy Compact (Colténe/Whaledent) were used as the packable composites. In the case of curing with the PAC unit, the composites were light cured with Apollo 95E (DMD System Inc) for 1 second (Group 1), 2 seconds (Group 2), 3 seconds (Group 3), 6 seconds (Group 4) and 12 seconds (Group 5). For light curing with the QTH unit, the composites were light cured for 60 seconds using XL3000 (Group 6). The linear polymerization shrinkage of each composite was measured using a custom made linometer, and the data was stored in a computer every 0.5 to 0.55 seconds for a total of 60 seconds. For each composite, the amount of polymerization was compared using one-way ANOVA with Tukey at the 95% confidence level. In order to compare the speed of polymerization, the peak time (PT), showing the highest speed of polymerization and maximum speed of polymerization (Smax), were determined from the data and compared using one-way ANOVA with Tukey at the 95% confidence level for each material. Based on the statistical analysis among the PAC-cure groups (Groups 1 through 5), the group that was not statistically different from the QTH-cure group (Group 6) in the amount of linear polymerization shrinkage was determined for each material, and the corresponding curing time of the group was defined as the tentative minimum PAC-curing time (TMPT). For microhardness measurements, the samples were placed in a 2-mm thick Teflon plate. Twenty specimens, randomly divided into the PAC-cure group (Group 1) or the QTH-cure group (Group 2), were prepared for each material. In Group 1, each composite was light cured for TMPT with the PAC unit. In Group 2, each composite was light cured for 60 seconds with the QTH unit. Microhardness was measured on the upper and lower surface. For each material, the microhardness of the upper and lower surface of Groups 1 and 2 was analyzed using two-way ANOVA with Tukey at the 95% confidence level. The amount of polymerization was Group 1

Comparison of linear polymerization shrinkage and microhardness between QTH-cured & LED-cured composites.

This study evaluated the effectiveness of second generation light emitting diode (2ndLED) units in composite curing. In order to compare their effectiveness with that of conventional quartz tungsten halogen light curing units (QTH) and first generation LEDs (1stLED), the amount of linear polymerization shrinkage, polymerization speed and microhardness were measured. Linear polymerization shrinkage was measured every 0.5-0.55 seconds for 60 seconds when composite specimens (Z250, 3M ESPE Dental Products, St Paul, MN, USA) were light cured with five different light sources: XL 3000 (QTH, 3M ESPE Dental Products), Elipar FreeLight 2 (2ndLED, 3M ESPE Dental Products), Ultra-Lume LED2 (2ndLED, Ultradent Products, South Jordan, UT, USA), Elipar FreeLight (1stLED, 3M ESPE Dental Products) and experimental product X (1stLED, Biomedisys, Seoul, Korea). The amount of linear polymerization shrinkage in 60 seconds and the speed of polymerization shrinkage in the first 15 seconds were measured for the different lighting units. The amount of polymerization was compared with one-way ANOVA using Tukey at the 95% confidence level. In order to compare the speed of polymerization, the peak time (PT) showing the highest speed of polymerization and maximum speed of polymerization (Smax) were determined from the data and compared using one-way ANOVA with Tukey at the 95% confidence level for each material. For microhardness measurements, the microhardness of 2-mm composites, Z250, which had been light cured by XL 3000 (G1), FreeLight 2 (G2), Ultra-Lume LED2 (G3), FreeLight (G4) or experimental product X (G5) were compared on the upper and lower surface. The microhardness of each surface was compared between groups using two-way ANOVA with Tukey test at 95% levels of confidence. The amount of polymerization shrinkage at 60 seconds was G1, G2, G3> G4, G5 (p<0.05). PT was G1, G3 G3 >G4, G5 (p<0.05). On the upper composite surface, there was no difference in microhardness between groups (p<0.05). On the lower surface, the microhardness was G1, G2> G3> G4, G5 (p<0.05). There was no difference in microhardness between the upper and lower surface in G1 and G2; whereas, microhardness of the lower surface was lower in G3, G4 and G5. It was concluded that 2ndLEDs and the conventional QTH unit cu red composites moreeffectively than 1stLEDs.

Curing units' ability to cure restorative composites and dual-cured composite cements under composite overlay.

This study compared the efficacy of using conventional low-power density QTH (LQTH) units, high-power density QTH (HQTH) units, argon (Ar) laser and Plasma arc curing (PAC) units for curing dual-cured resin cements and restorative resin composites under a pre-cured resin composite overlay. The microhardness of the two types of restorative resins (Z100 and Tetric Ceram) and a dual-cured resin cement (Variolink II) were measured after they were light cured for 60 seconds in a 2 mm Teflon mold. The recorded microhardness was determined to be the optimum microhard-ness (OM). Either one of the two types of restorative resins (Z100, Tetric Ceram) or the dual cured resin cement (Variolink II) were placed under a 1.5-mm thick and 8 mm diameter pre-cured Targis (Vivadent/Ivoclar AG, Schaan, Liechtenstein) overlay. The specimens that were prepared for each material were divided into four groups depending upon the curing units used (HQTH, PAC, Laser or LQTH) and were further subdi-vided into subgroups according to light curing time. The curing times used were 30, 60, 90 and 120 seconds for HQTH; 12, 24, 36 and 48 seconds for the PAC unit; 15, 30, 45 and 60 for the Laser and 60, 120 or 180 seconds for the LQTH unit. Fifteen specimens were assigned to each sub- group. The microhardness of the upper and and lower composite surfaces under the Targis overlay were measured using an Optidur Vickers hardness-measuring instrument (Göttfert Feinwerktechnik GmbH, Buchen, Germany). In each material, for each group, a three-way ANOVA with Tukey was used at the 0.05 level of significance to compare the microhardnesses of the upper and lower composite surfaces and the previously measured OM of the material. From the OM of each material, 80% OM was calculated and the time required for the microhardness of the upper and lower surface of the specimen to reach 100% and 80% of OM was determined. In Z100 and Tetric Ceram, when the composites were light cured for 120 seconds using the HQTH lamp, microhardnesses of the upper and lower surfaces reached OM. When they were cured with the PAC unit, only 48 seconds was needed for the upper and lower surfaces to reach OM. When they were cured using the laser, the lower surface did not reach OM in any of the groups. When the specimens were cured using the LQTH lamp, 180 seconds of curing was needed for Z100 to reach OM, whereas Tetric Ceram did not reach OM. In Z100, 60, 12, 30 and 60 seconds were needed in HQTH, PAC, Laser and LQTH, respectively, for the specimens to reach 80% OM. Tetric Ceram was needed 60,24,45 and 180 seconds to reach 80% OM. In the Variolink II specimen, microhardness of the upper and lower surfaces did not reach OM even though they were light cured with the HQTH lamp for 120 seconds. When they were cured with the PAC unit, 48 seconds was insufficient for them to reach OM. When they were cured with laser for 45 and 60 seconds, microhardness reached OM on the upper surface but not on the lower surface. However, when they were cured using the LQTH lamp, microhardness did not reach OM on the upper and lower surfaces even though the curing time was extended to three minutes. In Variolink II, 120, 36, 45 and >180 seconds were needed in HQTH, PAC, Laser and LQTH, respectively, for the specimens to reach 80% OM. In conclusion, the PAC system is the most effective curing system to cure the restorative composite and dual cured resin cement under the 1.5 mm Targis overlay, followed by the laser, HQTH and LQTH units. In addition, the restorative composites cured more efficiently than the dual-cured resin cements.

Computed tomography as a diagnostic aid for extracanal invasive resorption.

A case of multiple extracanal invasive resorption is reported. The patient had a history of hypothyroidism for approximately 1 yr before the dental visit. Utilization of computed tomography and a rapid prototyping tooth model in diagnosing the exact location and the size of the resorption area are discussed.