OBJECTIVES: To evaluate the sensitivity of QLF and OCT in detecting initial dental erosion in vitro.

METHODS: 12 human incisors were embedded in resin except for a window on the buccal surface. Bonding agent was applied to half of the window, creating an exposed and non-exposed area. Baseline measurements were taken with QLF, OCT and surface microhardness. Samples were immersed in orange juice for 60 min and measurements taken stepwise every 10 min. QLF was used to compare the loss of fluorescence between the two areas. The OCT system, OCS1300SS (Thorlabs Ltd.), was used to record the intensity of backscattered light of both areas. Multiple linear regression and paired t test were used to compare the change of the outcome measures.

RESULTS: All 3 instruments demonstrated significant dose responses with the erosive challenge interval (p < 0.05) and a detection threshold of 10 min from baseline. Thereafter, surface microhardness demonstrated significant changes after every 10 min of erosion, QLF at 4 erosive intervals (20, 40, 50 and 60 min) while OCT at only 2 (50 and 60 min).

PURPOSE: The purpose of this clinical study was to evaluate the safe distance in the interforaminal region of the mandible measured from the genial tubercle level for implant osteotomy in a Chinese-Malaysian population.

MATERIAL AND METHODS: A total of 201 Digital Imaging and Communications in Medicine (DICOM) files were selected for the study from the CBCTs of dentate or edentulous Chinese-Malaysian adult patients with ongoing or completed treatments. Measurements were made with implant planning software. The anatomy of the whole mandible was assessed in the coronal cross-sectional, horizontal view and in panoramic view. Measurements were obtained in millimeters on one side by locating and marking a genial tubercle and then marking the mesial margin of the mental foramen and the anterior loop of the inferior alveolar nerve. The corresponding points of these landmarks were identified on the crest of the mandibular ridge to measure the linear distances. All the measurement steps were repeated on the other side. The linear distance of 2 mm was deducted from the total distance between the genial tubercle and the anterior loop separately for left and right side measurements to identify the safe zone. The mixed 2-way analysis of variance (ANOVA) test was used to analyze side and sex-related variations.

METHODS: This is a prospective substudy nested within the CRASH-3 trial, a randomised placebo-controlled trial of TXA (loading dose 1 g over 10 min, then 1 g infusion over 8 hours) in patients with isolated head injury. CRASH-3 trial patients were recruited between July 2012 and January 2019. Participants in the current substudy were a subset of trial patients enrolled at 10 hospitals in the UK and 4 in Malaysia, who had at least one CT head scan performed as part of the routine clinical practice within 28 days of randomisation. The primary outcome was the volume of intraparenchymal haemorrhage (ie, contusion) measured on a CT scan done after randomisation. Secondary outcomes were progressive intracranial haemorrhage (post-randomisation CT shows >25% of volume seen on pre-randomisation CT), new intracranial haemorrhage (any haemorrhage seen on post-randomisation CT but not on pre-randomisation CT), cerebral infarction (any infarction seen on any type of brain scan done post-randomisation, excluding infarction seen pre-randomisation) and intracranial haemorrhage volume (intraparenchymal + intraventricular + subdural + epidural) in those who underwent neurosurgical haemorrhage evacuation. We planned to conduct sensitivity analyses excluding patients who were severely injured at baseline. Dichotomous outcomes were analysed using relative risks (RR) or hazard ratios (HR), and continuous outcomes using a linear mixed model.

RESULTS: 1767 patients were included in this substudy. One-third of the patients had a baseline GCS (Glasgow Coma Score) of 3 (n=579) and 24% had unilateral or bilateral unreactive pupils. 46% of patients were scanned pre-randomisation and post-randomisation (n=812/1767), 19% were scanned only pre-randomisation (n=341/1767) and 35% were scanned only post-randomisation (n=614/1767). In all patients, there was no evidence that TXA prevents intraparenchymal haemorrhage expansion (estimate=1.09, 95% CI 0.81 to 1.45) or intracranial haemorrhage expansion in patients who underwent neurosurgical haemorrhage evacuation (n=363) (estimate=0.79, 95% CI 0.57 to 1.11). In patients scanned pre-randomisation and post-randomisation (n=812), there was no evidence that TXA reduces progressive haemorrhage (adjusted RR=0.91, 95% CI 0.74 to 1.13) and new haemorrhage (adjusted RR=0.85, 95% CI 0.72 to 1.01). When patients with unreactive pupils at baseline were excluded, there was evidence that TXA prevents new haemorrhage (adjusted RR=0.80, 95% CI 0.66 to 0.98). In patients scanned post-randomisation (n=1431), there was no evidence of an increase in infarction with TXA (adjusted HR=1.28, 95% CI 0.93 to 1.76). A larger proportion of patients without (vs with) a post-randomisation scan died from head injury (38% vs 19%: RR=1.97, 95% CI 1.66 to 2.34, p<0.0001).

CONCLUSION: TXA may prevent new haemorrhage in patients with reactive pupils at baseline. This is consistent with the results of the CRASH-3 trial which found that TXA reduced head injury death in patients with at least one reactive pupil at baseline. However, the large number of patients without post-randomisation scans and the possibility that the availability of scan data depends on whether a patient received TXA, challenges the validity of inferences made using routinely collected scan data. This study highlights the limitations of using routinely collected scan data to examine the effects of TBI treatments.