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).
CONCLUSION: It can be concluded that OCT and QLF were able to detect demineralization after 10 min of erosive challenge and could be used to monitor the progression of demineralization of initial enamel erosion in vitro.
MATERIALS AND METHODS: The OncoCarta(™) panel v1.0 assay was used to characterize oncogenic mutations. In addition, exons 4-11 of the TP53 gene were sequenced. Statistical analyses were conducted to identify associations between mutations and selected clinico-pathological characteristics and risk habits.
RESULTS: Oncogenic mutations were detected in PIK3CA (5.7%) and HRAS (2.4%). Mutations in TP53 were observed in 27.7% (31/112) of the OSCC specimens. Oncogenic mutations were found more frequently in non-smokers (p = 0.049) and TP53 truncating mutations were more common in patients with no risk habits (p = 0.019). Patients with mutations had worse overall survival compared to those with absence of mutations; and patients who harbored DNA binding domain (DBD) and L2/L3/LSH mutations showed a worse survival probability compared to those patients with wild type TP53. The majority of the oncogenic and TP53 mutations were G:C > A:T and A:T > G:C base transitions, regardless of the different risk habits.
CONCLUSION: Hotspot oncogenic mutations which are frequently present in common solid tumors are exceedingly rare in OSCC. Despite differences in risk habit exposure, the mutation frequency of PIK3CA and HRAS in Asian OSCC were similar to that reported in OSCC among Caucasians, whereas TP53 mutations rates were significantly lower. The lack of actionable hotspot mutations argue strongly for the need to comprehensively characterize gene mutations associated with OSCC for the development of new diagnostic and therapeutic tools.