ABSTRACT
AIM: To investigate the diagnostic ability of maximum standardised uptake value (SUVmax) at combined single-photon-emission computed tomography/computed tomography (SPECT/CT) for the evaluation of osteonecrosis of the jaw. MATERIALS AND METHODS: Seven patients with mandibular osteonecrosis (three osteoradionecrosis, three medication-related osteonecrosis of the jaw (MRONJ), and one rheumatoid arthritis) underwent SPECT/CT at 4 hours after injection of technetium 99m hydroxymethylene diphosphonate. The SPECT/CT parameters SUVmax were compared for the osteonecrosis with normal mandible. Statistical analyses among the SUVmax of osteonecrosis were performed by one-way repeated measures analysis of variance with Tukey's HSD (honestly significant difference) test. A p-value <0.05 was considered statistically significant. RESULTS: SUVmax for MRONJ and rheumatoid arthritis (23.24±8.63) were significantly higher than those for osteoradionecrosis (9.05±1.39, p=0.005) and normal mandible (3.57±0.46, p=0.000). CONCLUSIONS: SUVmax derived from bone SPECT/CT could be useful for the evaluation of osteonecrosis of the jaw.
Subject(s)
Arthritis, Rheumatoid/diagnostic imaging , Bisphosphonate-Associated Osteonecrosis of the Jaw/diagnostic imaging , Mandibular Diseases/diagnostic imaging , Osteoradionecrosis/diagnostic imaging , Single Photon Emission Computed Tomography Computed Tomography , Aged , Aged, 80 and over , Female , Humans , Male , Middle Aged , Radiopharmaceuticals , Technetium Tc 99m Medronate/analogs & derivatives , Whole Body ImagingABSTRACT
2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD; dioxin), a member of a class of environmental pollutants represented by polychlorinated dibenzo-p-dioxins and dibenzofurans, is one of the most toxic artificial compounds ever developed. In this study, we identified a novel TCDD target gene, DIF-3 (dioxin inducible factor-3), by cDNA representational difference analysis. DIF-3 protein is a nuclear factor and possesses a zinc-finger motif at its N-terminus. High DIF-3 mRNA expression in the testes was demonstrated by Northern blot analysis and abundant DIF-3 protein was detected during spermatogenesis. Thus, these results suggest that DIF-3 may be a target gene mediating the reproductive toxicity induced by TCDD.
Subject(s)
Gene Expression Regulation, Developmental/drug effects , Nuclear Proteins/genetics , Polychlorinated Dibenzodioxins/pharmacology , Spermatogenesis , Animals , Animals, Newborn , Blotting, Northern , Blotting, Western , Cell Line , DNA, Complementary , Expressed Sequence Tags , Fluorescent Antibody Technique, Indirect , Gene Expression Profiling , Male , Mice , Molecular Sequence Data , Molecular Weight , Nuclear Proteins/analysis , Nuclear Proteins/chemistry , Nuclear Proteins/physiology , Oligonucleotide Array Sequence Analysis , RNA, Messenger/genetics , RNA, Messenger/metabolism , Reverse Transcriptase Polymerase Chain Reaction , Stem Cells , Testis/metabolism , Zinc FingersABSTRACT
The compound 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) has been shown recently to be carcinogenic, but little is currently known about the molecular mechanism of TCDD affecting cell proliferation and carcinogenesis. In this report, we demonstrate that TCDD suppresses the expression of the checkpoint protein, Mad2. Suppression of Mad2 was also observed in aryl hydrocarbon receptor-deficient mouse embryonic fibroblasts, suggesting that TCDD suppresses Mad2 by a novel TCDD receptor signaling mechanism. In addition, HeLa cells treated with TCDD failed to arrest in mitosis after nocodazole treatment. The Mad2 protein plays a significant role in accurate chromosome segregation in mitotic cells. Our data suggest that TCDD may increase chromosomal instability through the suppression of Mad2 expression.
