Fracture Characteristics of Commercial PEEK Dental Crowns: Combining the Effects of Aging Time and TiO2 Content.

Polyetheretherketone (PEEK) is an emerging thermoplastic polymer with good mechanical properties and an elastic modulus similar to that of alveolar bone. PEEK dental prostheses for computer-aided design/computer-aided manufacturing (CAD/CAM) systems on the market often have additives of titanium dioxide (TiO2) to strengthen their mechanical properties. However, the effects of combining aging, simulating a long-term intraoral environment, and TiO2 content on the fracture characteristics of PEEK dental prostheses have rarely been investigated. In this study, two types of commercially available PEEK blocks, containing 20% and 30% TiO2, were used to fabricate dental crowns by CAD/CAM systems and were aged for 5 and 10 h based on the ISO 13356 specifications. The compressive fracture load values of PEEK dental crowns were measured using a universal test machine. The morphology and crystallinity of the fracture surface were analyzed by scanning electron microscopy and an X-ray diffractometer, respectively. Statistical analysis was performed using the paired t-test (α = 0.05). Results showed no significant difference in the fracture load value of the test PEEK crowns with 20% and 30% TiO2 after 5 or 10 h of aging treatment; all test PEEK crowns have satisfactory fracture properties for clinical applications. Fracture surface analysis revealed that all test crowns fractured from the lingual side of the occlusal surface, with the fracture extending along the lingual sulcus to the lingual edge, showing a feather shape at the middle part of the fracture extension path and a coral shape at the end of the fracture. Crystalline analysis showed that PEEK crowns, regardless of aging time and TiO2 content, remained predominantly PEEK matrix and rutile phase TiO2. We would conclude that adding 20% or 30% TiO2 to PEEK crowns may have been sufficient to improve the fracture properties of PEEK crowns after 5 or 10 h of aging. Aging times below 10 h may still be safe for reducing the fracture properties of TiO2-containing PEEK crowns.

Influence of Aging on the Fracture Characteristics of Polyetheretherketone Dental Crowns: A Preliminary Study.

Although polyetheretherketone (PEEK) is becoming more widely used in dentistry applications, little is known about how aging will affect this material. Therefore, this study aimed to investigate the influence of an aging treatment on fracture characteristics of PEEK dental crowns. Additionally, the impact of the addition of titanium dioxide (TiO2) into PEEK was examined. Two types of commercial PEEK discs were used in this study, including TiO2-free and 20% TiO2-containing PEEK. The PEEK dental crowns were fabricated and aging-treated at 134 °C and 0.2 MPa for 5 h in accordance with the ISO 13356 specification before being cemented on artificial tooth abutments. The fracture loads of all crown samples were measured under compression tests. Results demonstrated that adding TiO2 enhanced the fracture load of PEEK crowns compared to TiO2-free PEEK crowns before the aging treatment. However, the aging treatment decreased the fracture load of TiO2-containing PEEK crowns while increasing the fracture load of TiO2-free PEEK crowns. The fracture morphology of TiO2-containing PEEK crowns revealed finer feather shapes than that of the TiO2-free PEEK crowns. We concluded that adding TiO2 increased the fracture load of PEEK crowns without aging treatment. Still, the aging treatment influenced the fracture load and microscopic fracture morphology of PEEK crowns, depending on the addition of TiO2.

Natural ingredients from Chinese materia medica for pulmonary hypertension.

Pulmonary hypertension (PH) is a severe pathophysiological condition characterized by pulmonary artery remodeling and continuous increases in pulmonary artery pressure, which may eventually develop to right heart failure and death. Although newly discovered and incredible treatment strategies in recent years have improved the prognosis of PH, limited types of effective and economical drugs for PH still makes it as a life-threatening disease. Some drugs from Chinese materia medica (CMM) have been traditionally applied in the treatment of lung diseases. Accumulating evidence suggests active pharmaceutical ingredients (APIs) derived from those medicines brings promising future for the prevention and treatment of PH. In this review, we summarized the pharmacological effects of APIs derived from CMM which are potent in treating PH, so as to provide new thoughts for initial drug discovery and identification of potential therapeutic strategies in alternative medicine for PH.

Circulating Neutrophil Counts Decrease in Response to Mitigated Air Quality in Stable COPD Patients.

This three-year study, based on the Guangzhou Institute of Respiratory Disease (GRID), chronic obstructive pulmonary disease (COPD) Biobank, was conducted in 36 COPD patients to estimate whether changes in levels of leukocytes, erythrocytes, hemoglobin, and platelets were related to changes in air pollutant concentration. Daily NO2 levels exhibited significant differences between baseline years and the 2010 Asian Game period. We observed significant reductions in leukocyte and neutrophils counts levels, by 15.51% and 23.01%, from pre-Asian Games to during-Asian Games, respectively. In the post-Asian Game period, most pollutants approximated pre-Asian Game period levels, and similar effects were demonstrated in leukocyte and neutrophil counts. For both items, we identified significant increases resulting from elevated NO2 at lag days 0-2/5-6. We concluded that reductions in pollutants during the intervention period were associated with inactivation of hematological events in COPD.

[Cigarette smoke exposure induced pulmonary artery pressure increase through inhibiting Kv1.5 and Kv2.1 mRNA expression in rat pulmonary artery smooth muscles].

OBJECTIVE: To investigate the effect of cigarette smoke exposure on Kv1.5 and Kv2.1 mRNA expression in rat pulmonary arterial smooth muscle cells (PASMCs), and further to clarify the possible mechanism of cigarette smoking induced pulmonary arterial hypertension. METHODS: Primary cell culture and animal experiments were used in this study. Rat distal PASMCs were isolated and cultured by collagenase digestion. PASMCs were treated by nicotine 100 nmol/L. After 48 h, Kv1.5 and Kv2.1 mRNA expression were detected by real-time quantitative PCR and compared with the control group. Rat model of chronic exposure to cigarette smoke was established. Thirty-six male SD rats were randomly divided equally into 6 groups: (1) 1 month control group; (2) 1 month cigarette exposure group; (3) 3 month control group; (4) 3 month cigarette exposure group; (5) 6 month control group; (6) 6 month cigarette exposure group. Direct right heart manometry, HE staining and real-time quantitative PCR were used to detect the effect of smoke exposure on rat right ventricular systolic pressure (RVSP), mean pressure (mPAP), right ventricular hypertrophy index [RV/(LV + S)] as well as Kv1.5 and Kv2.1 mRNA expression on pulmonary artery smooth muscle at different time points (1 month, 3 months and 6 months). RESULTS: The mPAP and RVSP in cigarette smoke exposure 6 month group were (13.08 ± 0.64) mm Hg and (29.73 ± 0.83) mm Hg, slightly higher than those in the control 6 month group [(10.16 ± 0.44) mm Hg and (22.56 ± 0.64) mm Hg] (P < 0.01). The ratio of Kv1.5 mRNA expression in distal pulmonary arteries in 1 month, 3 month, 6 month cigarette exposure group to that in control groups was (52 ± 11)%, (64 ± 19)% and (75 ± 11)% (P < 0.05). The ratio of Kv2.1 mRNA expression in distal pulmonary arteries in 1 month, 3 month, 6 month cigarette exposure groups to that in control groups was (51.0 ± 18.6)%, (78.7 ± 10.1)% and (71.4 ± 2.3)% (P < 0.01); Chronic exposure to cigarette smoke significantly decreased Kv1.5 and Kv2.1 mRNA expression in rat pulmonary arterial smooth muscle at each time point. The ratio of Kv1.5 and Kv2.1 mRNA expression in rat distal PASMCs treated with nicotine (100 nmol/L, 48 h) to control group were (62 ± 14)% (P < 0.05) and (72 ± 15)% (P < 0.01), respectively. Nicotine inhibited Kv1.5 and Kv2.1 mRNA expression in rat distal PASMCs. CONCLUSION: Cigarette smoke exposure may be involved in pulmonary hypertension by downregulating potassium channels Kv1.5 and Kv2.1 mRNA expression in rat pulmonary artery smooth muscles.