Incidence and factors related to flare-ups in a graduate endodontic programme

Aim  To investigate the incidence and factors related to endodontic flare-ups in nonsurgical root canal treatment (NSRCT) cases completed by graduate endodontic residents at University of Pennsylvania, USA.
Methodology  Residents at University of Pennsylvania enter all clinical patient records into an electronic database called PennEndo database. Analysis of records of 6580 patients treated from September 2000 to July 2005 revealed a total of 26 patients with flare-ups (0.39%). Patients were categorized to have undergone flare-up when they attended for an unscheduled visit and active treatment, and when they suffered from severe pain and or swelling after initiation or continuation of NSRCT. SAS software was used to develop a logistic regression model with flare-up as a dependent variable. Independent variables included in the model were: history of previous pain, one vs. two visit NSRCT, periapical diagnosis, tooth type, rotary versus hand instrumentation, and lateral versus vertical compaction of gutta-percha.
Results  The odds for developing a flare-up in teeth with a periapical radiolucency were 9.64 times greater than teeth without a periapical radiolucency ( P  = 0.0090). There was no statistically significant difference in flare-ups between one and two visits NSRCT. The odds of developing a flare-up increased 40 fold when NSRCT was completed in three or more visits. However, this result may have been confounded by addition of an unscheduled visit in patients suffering from flare-ups. Other independent variables did not have any statistically significant correlations.
Conclusions  A low percentage of patients experienced flare-ups during NSRCT procedures. The presence of a periapical lesion was the single most important predictor of flare-ups during NSRCT.     

Lack of association between ACE and bradykinin B2 receptor gene polymorphisms and ACE inhibitor-induced coughing in hypertensive Koreans

Background & Objective:  Angiotensin converting enzyme (ACE) inhibitors are used widely in therapy for hypertension, congestive heart failure and myocardial infarction. However, coughing, one of their major adverse effects limits their use. It is documented that Asians are more liable to coughing than Europeans. The aim of this study was to investigate genetic polymorphism involved in ACE inhibitor-induced coughing.
Methods:  We monitored hypertensive subjects ( n  = 110) treated with ACE inhibitors, and tested for any associations between ACE inhibitor-induced coughing and polymorphisms in the genes for ACE and the bradykinin B2 receptor, which are suspected to be related to coughing.
Results & Discussion:  We found no significant differences between the groups with coughing and without coughing in the frequency of ACE I/D (Insertion/Deletion) polymorphisms. One single nucleotide polymorphism was discovered in the promoter (−58T/C) and, one in intron-exon junction upsteam of exon 2 (−59C/A), of the bradykinin B2 receptor gene. However, no significant correlation was found between those genotypes or allele distributions and ACE inhibitor-induced coughing.
Conclusion:  We found no significant links between polymorphisms of the ACE gene or bradykinin B2 receptor gene with ACE inhibitor-induced coughing in hypertensive Koreans. But, the topic remains controversial and requires more study.     

Mandibular canal variant: a case report

The mandibular canal transmits the inferior alveolar artery, vein and the inferior alveolar nerve. From an embryological perspective, there might be three inferior dental nerves innervating three groups of mandibular teeth. During rapid prenatal growth and remodeling in the ramus region there is spread of intramembranous ossification that eventually forms the mandibular canal. Occurrence of bifid/trifid mandibular canals in some patients is secondary to incomplete fusion of these three nerves. Various types of bifid mandibular canals have been classified according to anatomical location and configuration. This case report highlights an unusual variant of the mandibular canal.     

Chloroquine-induced autophagic vacuole accumulation and cell death in glioma cells is p53 independent

Glioblastoma (GBM) is a high-grade central nervous system malignancy and despite aggressive treatment strategies, GBM patients have a median survival time of just 1 year. Chloroquine (CQ), an antimalarial lysosomotropic agent, has been identified as a potential adjuvant in the treatment regimen of GBMs. However, the mechanism of CQ-induced tumor cell death is poorly defined. We and others have shown that CQ-mediated cell death may be p53-dependent and at least in part due to the intrinsic apoptotic death pathway. Here, we investigated the effects of CQ on 5 established human GBM lines, differing in their p53 gene status. CQ was found to induce a concentration-dependent death in each of these cell lines. Although CQ treatment increased caspase-3–like enzymatic activity in all 5 cell lines, a broad-spectrum caspase inhibitor did not significantly attenuate death. Moreover, CQ caused an accumulation of autophagic vacuoles in all cell lines and was found to affect the levels and subcellular distribution of cathepsin D, suggesting that altered lysosomal function may also play a role in CQ-induced cell death. Thus, CQ can induce p53-independent death in gliomas that do not require caspase-mediated apoptosis. To potentially identify more potent chemotherapeutics, various CQ derivatives and lysosomotropic compounds were tested on the GBM cells. Quinacrine and mefloquine were found to be more potent than CQ in killing GBM cells in vitro and given their superior blood–brain barrier penetration compared with CQ may prove more efficacious as chemotherapeutic agents for GBM patients.     

Advanced prostate cancer activates coagulation: a controlled study of activation markers of coagulation in ambulatory patients with localized and advanced prostate cancer.

Cancer and increased age are risk factors for coagulation activation. Patients with advanced prostate cancer, which usually presents in the seventh to eighth decade of life, are likely to be at increased risk for thrombosis. We report results of a controlled study of changes in specific and sensitive markers of coagulation activation in patients with prostate cancer. Complete blood count, prothrombin time, partial thromboplastin time, prothrombin fragment 1 + 2 (F1 + 2), thrombin-antithrombin complex (TAT) and quantitative D-dimers (DD) were measured in 30 patients of advanced prostate cancer (androgen ablated), in 30 newly diagnosed localized prostate cancer patients, in 30 healthy age-matched volunteers, and in 20 healthy young volunteers. Plasma F1 + 2 (P < 0.05) and DD (P < 0.05), but not TAT, were significantly elevated in healthy elderly males (mean age, 77 years) when compared with healthy young volunteers (mean age, 35 years). F1 + 2, TAT and DD were significantly elevated in advanced prostate cancer when compared with healthy age-matched controls (P < 0.001). In conclusion, advanced prostate cancer patients have significantly increased levels of sensitive markers of coagulation activation compared with healthy age-matched controls. This data can be used to plan studies to determine the risk of clinically significant coagulopathy and the role of primary prophylaxis in patients with advanced prostate cancer.