Browsing by Subject "X-Ray Microtomography"

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    Ability of Caries Detection Methods to Determine Caries Lesion Activity
    (2019-12) Aldawood, Fatma; Ando, Masatoshi; Hara, Anderson T.; Diefenderfer, Kim E.
    Background: Non-cavitated caries lesions form due to acid diffusion and demineralization of enamel subsurface with an intact surface layer (SL). Caries lesions progress when the outcome of demineralization and remineralization processes over time is net mineral loss. Lesions that continue to demineralize are called active, while those that display no evidence of further demineralization are called inactive. Micro-computed-tomography (µCT) analysis provides objective non-destructive measurements of the thickness of the surface layer (SL) and severity of caries lesions. Aims: 1) To investigate if visual/tactile suspected active non-cavitated early white spot lesions present a thinner surface layer than inactive ones; 2) To investigate if there is an association between the thickness of the surface layer (SLT) and caries activity, as determined by QLF during dehydration (△QD); 3) To determine lesion severity by comparing lesion volume and maximum depth correlation with △Q value at 15 s from QLF during dehydration. Materials and Methods: Thirty extracted human premolars exhibiting non-cavitated approximal white spot early lesions stored in 0.1.-percent thymol/4C and treated with 5.0-percent NaOCl/30 min were included in the study. Fifteen active and 15 inactive lesions were determined by visual/tactile examinations by consensus of two experienced examiners. Roughness measurements (Ra) were acquired using non-contact optical profilometry. Two-dimensional minimum (2D-min), maximum (2D-max), average (2D-avg) SL and three-dimensional (3D) analyses, volume and depth of lesions were determined from µCT image analysis. A series of fluorescence images were acquired at baseline (hydrated), at 1 s, at 5 s, at 10 s and at 15 s by QLF. During image acquisition, surfaces were dehydrated with continuous-compressed-air. △Q and △Q/s (△QD) were calculated. Data were analyzed using two-sample t-tests and Pearson correlation coefficients (p < 0.05). Results: Surface roughness of active and inactive lesions was not significantly different (p > 0.08). Overall lesion volume and depth in dentin were significantly larger in active lesions (p = 0.022, p = 0.009). SL thickness of active and inactive lesions was not significantly different (2D = 0.121, 3D = 0.080, 2D-avg = 0.446, 2D-min = 0.197, 2D-max = 0.122). △QD at 1s was significantly larger for active lesions (p = 0.046). ΔQ at 15 s of dehydration had a moderate positive association with lesion volume (r = 0.56). △QD had a weak negative association with SL thickness (2D-avg) and (2D-min). Conclusions: 1) Active and inactive non-cavitated lesions show no difference in SL thickness; 2) QLF during dehydration (△QD) does not correlate well with SL thickness; 3) ΔQ at 15 s of dehydration correlates moderately well with lesion volume and is consistent with caries activity assessed by visual/tactile examination.
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    Effects of a checkpoint kinase inhibitor, AZD7762, on tumor suppression and bone remodeling
    (Spandidos Publications, 2018-09) Wang, Luqi; Wang, Yue; Chen, Andy; Jalali, Aydin; Liu, Shengzhi; Guo, Yunxia; Na, Sungsoo; Nakshatri, Harikrishna; Li, Bai-Yan; Yokota, Hiroki; Biomedical Engineering, School of Engineering and Technology
    Chemotherapy for suppressing tumor growth and metastasis tends to induce various effects on other organs. Using AZD7762, an inhibitor of checkpoint kinase (Chk) 1 and 2, the present study examined its effect on mammary tumor cells in addition to bone cells (osteoclasts, osteoblasts and osteocytes), using monolayer cell cultures and three-dimensional (3D) cell spheroids. The results revealed that AZD7762 blocked the proliferation of 4T1.2 mammary tumor cells and suppressed the development of RAW264.7 pre-osteoclast cells by downregulating nuclear factor of activated T cells cytoplasmic 1. AZD7762 also promoted the mineralization of MC3T3 osteoblast-like cells and 3D bio-printed bone constructs of MLO-A5 osteocyte spheroids. While a Chk1 inhibitor, PD407824, suppressed the proliferation of tumor cells and the differentiation of pre-osteoclasts, its effect on gene expression in osteoblasts was markedly different compared with AZD7762. Western blotting indicated that the stimulating effect of AZD7762 on osteoblast development was associated with the inhibition of Chk2 and the downregulation of cellular tumor antigen p53. The results of the present study indicated that in addition to acting as a tumor suppressor, AZD7762 may prevent bone loss by inhibiting osteoclastogenesis and stimulating osteoblast mineralization.