Effect of Bioactive Glass-Based Root Canal Sealer on the Incidence of Postoperative Pain after Root Canal Obturation.

The purpose of this study is to evaluate the effect of a bioactive glass-based root canal sealer, Nishika Canal Sealer BG (CS-BG), on the incidence of postoperative pain (PP) after root canal obturation (RCO). Eleven dentists performed pulpectomy or infected root canal treatments for 555 teeth. During RCO, CS-BG was used. After RCO, the rate of PP and the factors affecting PP (pain during RCO and pain immediately after RCO) were analyzed. PP was observed in eight teeth (1.5%), and within 7 days after RCO, there were no teeth with pain. In these teeth with PP, there was a significant difference in the occurrence of pain during RCO, but not in the occurrence of pain immediately after RCO, when compared with pulpectomy and infected root canal treatment. These clinical results show that CS-BG has an excellent biocompatibility, and can suppress the distress of patients during RCO.

Celecoxib inhibits osteoblast differentiation independent of cyclooxygenase activity.

Non-steroidal anti-inflammatory drugs (NSAIDs) exert their effects primarily by inhibiting the activity of cyclooxygenase (COX), thus suppressing prostaglandin synthesis. Some NSAIDs are known to perform functions other than pain control, such as suppressing tumour cell growth, independent of their COX-inhibiting activity. To identify NSAIDs with COX-independent activity, we examined various NSAIDs for their ability to inhibit osteoblastic differentiation using the mouse pre-osteoblast cell line MC3T3-E1. Only celecoxib and valdecoxib strongly inhibited osteoblastic differentiation, and this effect was not correlated with COX-inhibiting activity. Moreover, 2,5-dimethyl (DM)-celecoxib, a celecoxib analogue that does not inhibit COX activity, also inhibited osteoblastic differentiation. Celecoxib and DM-celecoxib inhibited osteoblastic differentiation induced by bone morphogenetic protein (BMP)-2 in C2C12 mouse myoblast cell line. Although celecoxib suppresses the growth of some tumour cells, the viability and proliferation of MC3T3-E1 cells were not affected by celecoxib or DM-celecoxib. Instead, celecoxib and DM-celecoxib suppressed BMP-2-induced phosphorylation of Smad1/5, a major downstream target of BMP receptor. Although it is well known that COX plays important roles in osteoblastic differentiation, these results suggest that some NSAIDs, such as celecoxib, have targets other than COX and regulate phospho-dependent intracellular signalling, thereby modifying bone remodelling.

The effects of chloride ion binding on the photochemical properties of sensory rhodopsin II from Natronomonas pharaonis.

Whether Cl(-) binds to the sensory rhodopsin II from Natronomonas pharaonis (NpSRII) that acts as a negative phototaxis receptor remains controversial. Two previous photoelectrochemical studies using SnO2 transparent electrodes and ATR-FTIR demonstrated that Cl(-) binding affects the photoinduced proton release from Asp193 in phospholipid (PC)-reconstituted NpSRII (Iwamoto et al., 2004; Kitade et al., 2009). In this study, we investigated the effects of Cl(-) on the photochemistry of NpSRII solubilized by detergent (DDM). Even under these conditions, Cl(-) could bind to NpSRII with a Kd of approximately 250 mM; this value is ∼ 10-fold larger than that in the PC membrane. The binding of Cl(-) to NpSRII depended on the pH of the medium. In addition, Cl(-) binding induced the following effects: (1) a small red shift in the absorbance spectrum originating from the partial protonation of Asp75, (2) the formation of an interaction through a hydrogen-bonding network between Asp75 and Asp193, which is a proton-releasing residue, (3) several changes of the kinetic behavior of the photocycle, and (4) a photoinduced initial proton release from Asp193. The pKa values of Asp193 at various Cl(-) concentrations were also estimated. Based on the difference between the pKa values of Asp193 in Cl(-) bound and unbound NpSRII, the distance between the bound Cl(-) and Asp193 was determined to be approximately 6.1 Å, which agrees with the value estimated from the crystal structure presented by Royant et al. (2001). Therefore, the Cl(-) binding site affecting the photochemical properties of NpSRII is identical to the site proposed by Royant et al. (2001). This assignment was also supported by an experiment that introduced a mutation at Arg72.

High-resolution MRI predicts steroid injection response in carpal tunnel syndrome patients.

OBJECTIVES: To correlate median nerve T2 signal and shape at the carpal tunnel with steroid injection (SI) response in carpal tunnel syndrome (CTS) patients. METHODS: One hundred and sixty-three CTS wrists of 92 consecutive patients who were scheduled to undergo SI were prospectively evaluated with 3-T magnetic resonance imaging (MRI) and a nerve conduction study. All patients underwent axial high-resolution T2-weighted MRI (in-plane resolution of 0.25 × 0.25 mm). The CTS wrists were classified into three groups according to the nerve T2 signal and the flattening ratio at the hook of hamate level: group 1, high and oval; group 2, high and flat; group 3, low and flat. Clinical response to SI was evaluated at 6 months after injection. RESULTS: One hundred and thirteen of the 163 wrists (69.3%) responded well to SI. The percentage of improvement was 81.7% (49/60) in group 1, 69.9% (51/73) in group 2, and 43.3% (13/30) in group 3 (P < 0.01). On stepwise logistic regression analysis high-resolution MRI was the only significant independent factor for SI response in CTS patients (P < 0.01). CONCLUSIONS: High-resolution MRI correlates well with SI response in CTS patients and seems useful for predicting SI response. KEY POINTS: • MRI may help determine appropriate care in carpal tunnel syndrome. • MRI helps in therapeutic decision-making whenever steroid injection is considered. • T2 signal decrease of the median nerve correlates with poor outcome. • T2 signal decrease of median nerve may reflect fibrosis and amyloid deposition.

Sole existence of antithrombin antibody in patients with systemic lupus erythematosus showing tendency of its antigenic determinants directing against exosite II (antithrombin/heparin binding site) of thrombin.

We conducted an investigation to determine the antigenic determinants of antithrombin antibody (aThr), which has recently been recognized as a new antiphospholipid antibody mostly co-existing with antiprothrombin antibody, employing patients with systemic lupus erythematosus and antiphospholipid syndrome. Using an enzyme-linked immunosorbent assay we found aThr in 34 of 83 patients (40.9%), and 27 of these 34 patients (79.4%) with aThr were all negative for other antiphospholipid antibodies. An optical density value of six of 30 patients (20.0%) with aThr showed more than a 40% reduction of reactivity to thrombin with the addition of antithrombin in a dose-dependent manner. The inhibition percentage of aThr to thrombin was prominently increased to 11 of 30 (37%) along with its inhibition rate (100% at the highest) by the co-existence of heparin. Seven out of 30 patients with aThr (23.3%) showed a reduction of the optical density value with the addition of hirudin. Our findings suggest that aThr exists solely in patients with systemic lupus erythematosus without other antiphospholipid antibodies, and the antigenic determinants of aThr are directed to exosite I (hirudin binding site) and exosite II (antithrombin/heparin binding site) on the thrombin surface, with exosite II predominance. Accordingly, aThr could be an isolated and additional new marker of thrombosis/hemostasis. Since our patients who were positive only for aThr do not have a past history of antiphospholipid-associated complications at this stage, however, further long-term follow-up and additional studies in these clinical settings are needed to verify our hypothesis in the future.