Differentiation of radicular cysts and radicular granulomas via texture analysis of multi-slice computed tomography images.

OBJECTIVES: This study aimed to establish a method for differentiating radicular cysts from granulomas via texture analysis (TA) of multi-slice computed tomography (CT) images. METHODS: A total of 222 lesions with multi-slice computed tomography images acquired at our hospital between 2013 and 2022 that were pathologically diagnosed were included in this study. Cases of contrast-enhanced images, severe metallic artefacts, and lesions that were not sufficiently large to be analysed were excluded. The images were chronologically divided into a training group and a validation group. The radiological characteristics were determined. Subsequently, a TA was performed. Pyradiomics software was used for the TA of three-dimensionally segmented volumes extracted from 2 mm slice thickness images with a soft-tissue algorithm. Features that differed significantly between the two lesions in the training group were extracted and used to create machine-learning models. The discriminative ability of these models was evaluated in the validation group using receiver operating characteristic curve analysis. RESULTS: A total of 131 lesions, comprising 28 radicular cysts and 103 granulomas, were analysed. Forty-three texture features that exhibited significant variations were extracted. A support vector machine and decision tree model, with areas under the curves of 0.829 and 0.803, respectively, were created. These models showed high discriminative abilities, even for the validation group, with areas under the curve of 0.727 and 0.701, respectively. Both models showed superior performance compared with that of the models based on radiographic findings. CONCLUSION: Discriminatory models were established for the TA of radicular cysts and granulomas using CT images.

Differential properties of mitosis-associated events following CHK1 and WEE1 inhibitor treatments in human tongue carcinoma cells.

CHK1 and WEE1 play pivotal roles in G2/M checkpoint following exogenous DNA damage and regulation of DNA replication under normal cellular conditions. Here, we monitored and compared the cell cycle kinetics of mitosis-associated events after CHK1 and WEE1 inhibitor treatments in a human tongue cancer cell line (SAS). A fluorescent ubiquitination-based cell cycle indicator (Fucci) that reflects SCFSKP2 and APCCDH1 E3 ligase activities was used to monitor cell cycle progression. Numerous γH2AX-positive cells were observed within the S phase population of cells following CHK1 inhibitor treatment, and polyploid cells exhibiting DNA damage emerged via abortive mitosis (endomitosis) at 24 h post treatment. While WEE1 inhibitor-treated cells exhibited similar polyploidy via endomitosis at later time points, they possessed fewer γH2AX foci during S phase, and polyploid cells exhibiting DNA damage were scarce. Instead, mitosis duration greatly extended and was accompanied by an abnormal emission of Fucci red fluorescence. Kinetic analysis of Fucci fluorescence revealed that abnormal emission occurred at early M phase in a manner independent of green fluorescence degradation as a marker of APCCDH1 activation. When an inhibitor of the essential spindle checkpoint factor MPS1 was co-treated with a WEE1 inhibitor, the elongated mitosis duration and abnormal red fluorescence were abrogated, and WEE1-induced reduction of clonogenic survival was offset. We demonstrate novel differential effects on mitosis-associated events following CHK1 and WEE1 inhibitor treatments.

General rules for clinical and pathological studies on oral cancer (2nd edition): a synopsis.

For doctors and other medical staff treating oral cancer, it is necessary to standardize the basic concepts and rules for oral cancer to achieve progress in its treatment, research, and diagnosis. Oral cancer is an integral part of head and neck cancer and is treated in accordance with the general rules for head and neck cancer. However, detailed rules based on the specific characteristics of oral cancer are essential. The objective of this article was to contribute to the development of the diagnosis, treatment, and research of oral cancer, based on the correct and useful medical information of clinical, surgical, pathological, and imaging findings accumulated from individual patients at various institutions. Our general rules were revised as the UICC was revised for the 8th edition and were published as the Japanese second edition in 2019. In this paper, the English edition of the "Rules" section is primarily presented.

Induction of endomitosis-like event in HeLa cells following CHK1 inhibitor treatment.

The effects of CHK1 inhibitor on cell cycle kinetics have not been fully investigated yet. In this study, we closely analyzed this kinetics using a CHK1 inhibitor (PF00477736) in HeLa cells expressing fluorescent ubiquitination-based cell cycle indicator (Fucci). This system allowed us to visualize cell cycle progression following CHK1 inhibitor treatment in real-time. FACS analysis showed that high levels of DNA damage as determined by γH2AX immunostaining was induced in S phase and that polyploid cells harboring the same levels of DNA damage appeared thereafter. Surprisingly, time-lapse imaging of Fucci fluorescence revealed that many cells entered M phase at once and exhibited prolonged mitosis; eventually progressing to G1 phase not accompanied by cytokinesis; this is an endomitosis-like event. Most of these cells then underwent S/G2 phases at least once, which corroborated the appearance of polyploid cells. However, a small fraction of cells with 2 N DNA content still remained 24 h after the treatment. When co-treated with MAD2 inhibitor, a core factor constituting spindle checkpoint, the 2 N DNA cell fraction disappeared and almost all cells exhibited endomitosis, leading to enhanced sensitivity. Detailed cell cycle analysis revealed that induction of an endomitosis-like event might be associated with CHK1 inhibitor-induced cell death in HeLa cells.

Distribution and metabolism of 14C-sulfoquinovosylacylpropanediol (14C-SQAP) after a single intravenous administration in tumor-bearing mice.

Sulfoquinovosylacylpropanediol (SQAP) is a novel potent radiosensitizer that inhibits angiogenesis in vivo and results in increased oxigenation and reduced tumor volume. We investigated the distribution, metabolism, and excretion of SQAP in male KSN-nude mice transplanted with a human pulmonary carcinoma, Lu65. For the metabolism analysis, a 2 mg (2.98 MBq)/kg of [glucose-U-14C]-SQAP (CP-3839) was intravenously injected. The injected SQAP was decomposed into a stearic acid and a sulfoquinovosylpropanediol (SQP) in the body. The degradation was relatively slow in the carcinoma tissue.1,3-propanediol[1-14C]-SQAP (CP-3635) was administered through intravenous injection of a 1 mg (3.48 MBq)/kg dose followed by whole body autoradiography of the mice. The autoradiography analysis demonstrated that SQAP rapidly distributed throughout the whole body and then quickly decreased within 4 hours except the tumor and excretion organs such as liver, kidney. Retention of SQAP was longer in tumor parts than in other tissues, as indicated by higher levels of radioactivity at 4 hours. The radioactivity around the tumor had also completely disappeared within 72 hours.

Insulin-like growth factor I receptor regulates the radiation-induced G2/M checkpoint in HeLa cells.

Insulin-like growth factor I receptor (IGF-IR) plays pivotal roles in various biological events, including cell growth, transformation, survival, and DNA repair. In this study, we explored its possible involvement in cell cycle checkpoints, using HeLa cells expressing the fluorescent ubiquitination-based cell cycle indicator (Fucci). We found that IGF-IR inhibitor delayed release from radiation-induced G2 arrest, as demonstrated by FACS and pedigree analysis of Fucci fluorescence. Elongated G2 arrest was also induced by inhibitors of phosphatidylinositol-3 kinase (PI3K) and AKT, but not by inhibitor of MEK, which are two major IGF-IR downstream signaling pathways. Double-strand break (DSB) repair kinetics were not affected by IGF-IR inhibitor. CHK1 inhibitor abrogated radiation-induced G2 arrest, whereas radiation-induced phosphorylation of CHK1 at Ser 345 or Ser 296 was decreased by the IGF-IR inhibitor. However, radiation-induced nuclear localization of CHK1 was prolonged in IGF-IR inhibitor-treated cells in comparison with cells that received radiation alone; in the latter, CHK1 returned to the original diffuse distribution in conjunction with release from G2 arrest. We conclude that IGF-IR directly regulates the G2/M checkpoint via the PI3K/AKT pathway without influencing DSB repair, in part by controlling CHK1 localization between the nucleus and cytoplasm.

Radiosensitivity of quiescent and proliferating cells grown as multicellular tumor spheroids.

The multicellular spheroid model partly mimics tumor microenvironments in vivo and has been reported in plenty of studies regarding radiosensitivity. However, clear isolation of quiescent and proliferating cells in live conditions has been quite difficult owing to technical limitations; therefore, comprehensive characterization could not be done thus far. In this study, we succeeded in separately isolating different cell types using a fluorescent ubiquitination-based cell cycle indicator (Fucci) and determining their radiosensitivities. Unexpectedly, proliferating cells were more radioresistant than quiescent cells due to the contact effect when spheroids were disaggregated immediately after irradiation. However, the radiosensitivity of quiescent cells was not influenced by mild hypoxia (hypoxia-inducible factor-1α-positive but pimonidazole-negative), but their radioresistance became similar to that of proliferating cells due to potentially lethal damage repair when disaggregated 24 h after irradiation. The Fucci system further allowed long-term observation of cell kinetics inside of the spheroid following irradiation using real-time confocal fluorescence scanning. Repeated cycles of recruitment from the quiescent to the proliferating phase resulted in cell loss from the outside of the spheroid toward the inside, causing gradual shrinkage. Interestingly, the central region of the spheroid entered a dormant stage approximately 40 days after irradiation and survived for more than 2 months. Using the Fucci system, we were able to comprehensively characterize the radiosensitivity of spheroids for the first time, which highlights the importance of cell cycle kinetics after irradiation in determining the radiosensitivity under tumor microenvironments.

ARID2 modulates DNA damage response in human hepatocellular carcinoma cells.

BACKGROUND & AIMS: Recent genomic studies have identified frequent mutations of AT-rich interactive domain 2 (ARID2) in hepatocellular carcinoma (HCC), but it is not still understood how ARID2 exhibits tumor suppressor activities. METHODS: We established the ARID2 knockout human HCC cell lines by using CRISPR/Cas9 system, and investigated the gene expression profiles and biological functions. RESULTS: Bioinformatic analysis indicated that UV-response genes were negatively regulated in the ARID2 knockout cells, and they were sensitized to UV irradiation. ARID2 depletion attenuated nucleotide excision repair (NER) of DNA damage sites introduced by exposure to UV as well as chemical compounds known as carcinogens for HCC, benzo[a]pyrene and FeCl3, since xeroderma pigmentosum complementation group G (XPG) could not accumulate without ARID2. By using large-scale public data sets, we validated that ARID2 knockout could lead to similar molecular changes between in vitro and in vivo settings. A higher number of somatic mutations in the ARID2-mutated subtypes than that in the ARID2 wild-type across various types of cancers including HCC was observed. CONCLUSIONS: We provide evidence that ARID2 knockout could contribute to disruption of NER process through inhibiting the recruitment of XPG, resulting in susceptibility to carcinogens and potential hypermutation. These findings have implications for therapeutic targets in cancers harboring ARID2 mutations. LAY SUMMARY: Recent genomic studies have identified frequent mutations of ARID2, a component of the SWItch/Sucrose Non-Fermentable (SWI/SNF) complex, in hepatocellular carcinoma, but it is not still understood how ARID2 exhibits tumor suppressor activities. In current study, we provided evidence that ARID2 knockout could contribute to disruption of DNA repair process, resulting in susceptibility to carcinogens and potential hypermutation. These findings have far-reaching implications for therapeutic targets in cancers harboring ARID2 mutations.

Visualizing cell-cycle kinetics after hypoxia/reoxygenation in HeLa cells expressing fluorescent ubiquitination-based cell cycle indicator (Fucci).

Hypoxia induces G1 arrest in many cancer cell types. Tumor cells are often exposed to hypoxia/reoxygenation, especially under acute hypoxic conditions in vivo. In this study, we investigated cell-cycle kinetics and clonogenic survival after hypoxia/reoxygenation in HeLa cells expressing fluorescent ubiquitination-based cell cycle indicator (Fucci). Hypoxic treatment halted cell-cycle progression during mid-S to G2 phase, as determined by the cell cycle-regulated E3 ligase activities of SCF(Skp2) and APC/C(Cdh1), which are regulators of the Fucci probes; however, the DNA content of the arrested cells was equivalent to that in G1 phase. After reoxygenation, time-lapse imaging and DNA content analysis revealed that all cells reached G2 phase, and that Fucci fluorescence was distinctly separated into two fractions 24h after reoxygenation: red cells that released from G2 arrest after repairing DNA double-strand breaks (DSBs) exhibited higher clonogenic survival, whereas most cells that stayed green contained many DSBs and exhibited lower survival. We conclude that hypoxia disrupts coordination of DNA synthesis and E3 ligase activities associated with cell-cycle progression, and that DSB repair could greatly influence cell-cycle kinetics and clonogenic survival after hypoxia/reoxygenation.

Unusual prolongation of radiation-induced G2 arrest in tumor xenografts derived from HeLa cells.

The effect of ionizing radiation on cell cycle kinetics in solid tumors remains largely unknown because of technical limitations and these tumors' complicated structures. In this study, we analyzed intratumoral cell cycle kinetics after X-irradiation of tumor xenografts derived from HeLa cells expressing the fluorescent ubiquitination-based cell cycle indicator (Fucci), a novel system to visualize cell cycle kinetics in vivo. Cell cycle kinetics after X-irradiation was examined by using tumor sections and in vivo real-time imaging system in tumor xenografts derived from HeLa cells expressing Fucci. We found that G2 arrest was remarkably prolonged, up to 5 days after 10-Gy irradiation, in contrast to monolayer cultures where G2 arrest returned within 24 h. Cells isolated from tumors 5 days after irradiation exhibited a higher surviving fraction than those isolated immediately or one day after irradiation. In this study, we clearly demonstrated unusual post-irradiation cell cycle kinetics in tumor xenografts derived from HeLa-Fucci cells. Our findings imply that prolonged G2 arrest occurring in tumor microenvironments following irradiation may function as a radioresistance mechanism.

Sulfoquinovosylacylpropanediol is a novel potent radiosensitizer in prostate cancer.

OBJECTIVES: To examine the effects of combined treatment with sulfoquinovosylacylpropanediol and X-ray irradiation on the remodeling of the prostate cancer microenvironment, including angiogenic and hypoxic characteristics. METHODS: Human prostate cancer cells (DU145 and PC3) were implanted subcutaneously into the right hind legs of athymic nude mice. After the tumor volume reached 100-300mm(3) , 2mg/kg/day sulfoquinovosylacylpropanediol was given intravenously from day0 to day4, and cells were exposed to 4Gy X-ray irradiation on days0 and 3 (for a total of 8Gy). Tumors were fixed and stained for pathological analyses and immunohistochemical evaluations. To analyze vascular normalization, 60mg/kg pimonidazole dissolved in saline was injected intraperitoneally. RESULTS: Combined treatment with sulfoquinovosylacylpropanediol plus X-ray irradiation enhanced growth inhibition in DU145 xenografts. The tumor vessel density in DU145 cells significantly decreased after the combined treatment. Staining for αsmooth muscle actin in vessels was significantly increased. Pimonidazole staining, showing hypoxic lesions, was negative from 72h, but positive at 6 and 24h after the first combined treatment. In contrast, no enhancement of the microenvironment in PC3 xenografts was observed with sulfoquinovosylacylpropanediol plus X-ray irradiation. CONCLUSION: Sulfoquinovosylacylpropanediol could be a novel potent radiosensitizing agent targeting angiogenesis in prostate cancer.

Estimating Impacts of p16 Status on Tumor Radiosensitivity in Head and Neck Cancer using Predictive Models.

The intrinsic radiosensitivity index (RSI) and genomic-adjusted radiation dose (GARD) were reported to be able to predict the surviving fraction at 2 Gy and therapeutic effect when delivering actual treatment doses using the gene expression profiles of clinical cases. Given the impact of p16 status, a surrogate marker of the human papillomavirus (HPV) infection, on radiosensitivity, we attempted to apply the RSI and GARD to estimate p16-associated radiosensitivity in head and neck squamous cell carcinoma (HNSC). For this purpose, The Cancer Genome Atlas (TCGA) dataset was employed. In the GARD calculation, we assumed that p16-positive patients received 60 Gy in 30 fractions, while p16-negative patients received 70 Gy in 35 fractions. p16 positivity was associated with favorable characteristics compared to negative patients. The RSI and GARD analyses demonstrated increased radiosensitivity and high therapeutic effect in p16-positive patients, compared to p16-negative patients. Additionally, tumor microenvironmental conditions predicted by other models were also significantly affected by p16 status. Collectively, the models used in this study could be a promising tool for estimating p16-associated radiosensitivity in HNSC.

In vitro and in silico study of biological effects on cancer cells in the presence of metallic materials during radiotherapy.

X-ray therapy aims to eliminate tumours while minimizing side effects. Intense mucositis is sometimes induced when irradiating the oral cavity with a dental metal crown (DMC). However, the underlying mechanisms of such inducing radiosensitization by DMC remain uncertain. This study explored the radiosensitizing mechanisms around DMCs in an interdisciplinary approach with cell experiments and Monte Carlo simulation with the PHITS code. Clonogenic survival and nuclear 53BP1 foci of a cell line derived from cervical cancer cells (HeLa cells) were measured post-irradiation with therapeutic X-rays near high-Z materials such as Pb or Au plates, and the experimental sensitizer enhancement ratio (SER) was obtained. Meanwhile, the dose enhancement ratio (DER) and relative biological effectiveness for DNA damage yields were calculated using the PHITS code, by considering the corresponding experimental condition. The experiments show the experimental SER values for cell survival and 53BP1 foci near metals are 1.2-1.4, which agrees well with the calculated DER values. These suggest that the radiosensitizing effects near metal are predominantly attributed to the dose increase. In addition, as a preclinical evaluation, the spatial distributions of DER near DMC are calculated using Computed Tomography Digital Imaging and Communications in Medicine (CT-DICOM) data and a simple tooth model. As a result, the DER values evaluated using the CT-DICOM data were lower than those from a simple tooth model. These findings highlight the challenge of evaluating radiosensitizing effects near DMCs using Digital Imaging and Communications in Medicine (DICOM) images due to volume-averaging effects and emphasize the need for a high-resolution (<1 mm) dose assessment method unaffected by these effects.

DNA damage response in a 2D-culture model by diffusing alpha-emitters radiation therapy (Alpha-DaRT).

Diffusing alpha-emitters radiation therapy (Alpha-DaRT) is a unique method, in which interstitial sources carrying 224Ra release a chain of short-lived daughter atoms from their surface. Although DNA damage response (DDR) is crucial to inducing cell death after irradiation, how the DDR occurs during Alpha-DaRT treatment has not yet been explored. In this study, we temporo-spatially characterized DDR such as kinetics of DNA double-strand breaks (DSBs) and cell cycle, in two-dimensional (2D) culture conditions qualitatively mimicking Alpha-DaRT treatments, by employing HeLa cells expressing the Fucci cell cycle-visualizing system. The distribution of the alpha-particle pits detected by a plastic nuclear track detector, CR-39, strongly correlated with γH2AX staining, a marker of DSBs, around the 224Ra source, but the area of G2 arrested cells was more widely spread 24 h from the start of the exposure. Thereafter, close time-lapse observation revealed varying cell cycle kinetics, depending on the distance from the source. A medium containing daughter nuclides prepared from 224Ra sources allowed us to estimate the radiation dose after 24 h of exposure, and determine surviving fractions. The present experimental model revealed for the first time temporo-spatial information of DDR occurring around the source in its early stages.

Clinicopathological analysis of 134 patients with squamous cell carcinoma of the mandibular gingiva.

Objective: The accurate assessment of the involvement of mandibular gingival squamous cell carcinoma (SCC) is essential for determining the extent of resection and is also useful for predicting lymph node metastasis and prognosis. The purpose of this study was to investigate the factors for predicting the prognosis. Study design: We reviewed 134 patients with mandibular gingival SCC treated between 2008 and 2017. The clinical findings, TN stage, relationship between radiographical type and histological pattern, and factors affecting the survival rate were investigated. Results: The moth-eaten radiographic type was significantly associated with histologically infiltrative pattern. For all 134 cases, the 5-year OS was 89.5 %, and 5-year DSS was 93.9 %. The 5-year DSS was 95.0 % for cN0 and/or pN0 cases and 90.3 % for pN (+) cases, with a significant difference. The significant risk factors for lymph node metastasis were teeth extractions by previous physicians and moth-eaten radiographic type. Conclusion: The risk factor for poor prognosis was lymph node metastasis. In addition, teeth extractions by previous physicians and moth-eaten radiographic type were the risk factors for lymph node metastasis. It is recommended that these cases be treated considering the possibility of cervical lymph node metastasis.

Visualizing the effect of tumor microenvironments on radiation-induced cell kinetics in multicellular spheroids consisting of HeLa cells.

In this study, we visualized the effect of tumor microenvironments on radiation-induced tumor cell kinetics. For this purpose, we utilized a multicellular spheroid model, with a diameter of ∼500 µm, consisting of HeLa cells expressing the fluorescent ubiquitination-based cell-cycle indicator (Fucci). In live spheroids, a confocal laser scanning microscope allowed us to clearly monitor cell kinetics at depths of up to 60 µm. Surprisingly, a remarkable prolongation of G2 arrest was observed in the outer region of the spheroid relative to monolayer-cultured cells. Scale, an aqueous reagent that renders tissues optically transparent, allowed visualization deeper inside spheroids. About 16 h after irradiation, a red fluorescent cell fraction, presumably a quiescent G0 cell fraction, became distinct from the outer fraction consisting of proliferating cells, most of which exhibited green fluorescence indicative of G2 arrest. Thereafter, the red cell fraction began to emit green fluorescence and remained in prolonged G2 arrest. Thus, for the first time, we visualized the prolongation of radiation-induced G2 arrest in spheroids and the differences in cell kinetics between the outer and inner fractions.

Visualizing the effect of hypoxia on fluorescence kinetics in living HeLa cells using the fluorescent ubiquitination-based cell cycle indicator (Fucci).

Fluorescent proteins are widely used for the direct visualization of events such as gene expression and subcellular localization in mammalian cells. It is well established that oxygen is required for formation of functional chromophore; however, the effect of hypoxia on fluorescence emission has rarely been studied. For this purpose, under hypoxic conditions, we investigated the kinetics of red and green fluorescence in HeLa cells from two fluorescent proteins, monomeric Kusabira Orange 2 (mKO2) and monomeric Azami Green (mAG), respectively, using the fluorescent ubiquitination-based cell cycle indicator (Fucci). In this system, cells in G1 or other phases emit red or green fluorescence, respectively. We found that hypoxia abrogated both red and green fluorescence about ~10h after the treatment, although their protein levels were almost maintained. The treatment did not significantly affect fluorescence in cells constitutively expressing the same fluorescent proteins lacking the ubiquitin ligase-binding domains. The abrogation of fluorescence resulted from a combination of ubiquitination-dependent degradation of pre-existing functional proteins during specific cell cycle phases, and the expression of newly synthesized non-fluorescent proteins containing non-oxidized chromophore during hypoxic treatment. Indeed, non-fluorescent cells after hypoxic treatment gradually developed fluorescence after reoxygenation in the presence of cycloheximide; kinetics of recovery were much faster for mAG than for mKO2. Using the Fucci system, we could clearly visualize for the first time the effect of hypoxia on the fluorescence kinetics of proteins expressed in living mammalian cells.

Risk factors for posttreatment mastoid cellulitis in patients with oral malignancy.

OBJECTIVES: To investigate the possible risk factors for mastoid cellulitis after treatment in patients with oral cancer. METHODS: Patients with oral cancer who underwent preoperative and postoperative contrast-enhanced computed tomography (CECT) between January 2017 and March 2020 were retrospectively evaluated. Using an image reporting system, cases with reports containing the keyword "mastoid cellulitis" were registered in the mastoid cellulitis group. Fifty patients with oral cancer who did not develop mastoid cellulitis were randomly selected as the control group. Information concerning age, sex, location, and histopathological type of the primary tumor, presence or absence of cervical lymph node metastasis, and treatment methods were obtained from the hospital's electronic medical records to investigate the association between these factors and the occurrence of mastoid cellulitis. RESULTS: Statistically significant differences were observed in the following factors: age (p = 0.004), primary tumor site (p < 0.001), histopathological type (p = 0.032), radiotherapy (p < 0.001), and chemotherapy (p < 0.001). Logistic regression analysis revealed that maxillary tumors (p < 0.001), histopathological type (p = 0.047), and radiotherapy (p = 0.0301) were significantly associated with the occurrence of mastoid cellulitis. CONCLUSIONS: In oral cancer, the risk of postoperative mastoid cellulitis was higher in patients with a maxillary tumor, histopathology other than squamous cell carcinoma, and history of radiotherapy.

Potential of preoperative fluorodeoxyglucose-positron emission tomography/computed tomography to diagnose contralateral lymph node metastases in patients with oral cancer.

OBJECTIVE: To establish a decision tree using preoperative PET/computed tomography (CT) parameters for detecting contralateral lymph node metastasis (CLNM) in oral cancer patients. METHODS: In total, 140 patients with a confirmed histopathological diagnosis of oral carcinoma showed fluorodeoxyglucose accumulation of contralateral lymph nodes in PET images. Of 260 lymph nodes, eight were metastatic. We compared metastatic and non-metastatic nodes using Fisher-Freeman-Halton exact and Fisher's exact and Mann-Whitney U tests. The diagnostic performance was analyzed using receiver operating characteristic curves. We established a decision tree using exhaustive chi-squared automatic interaction detection algorithm. RESULTS: Five PET/CT parameters were significantly different between metastatic and non-metastatic nodes: the longest ( P  = 0.015) and shortest ( P  = 0.023) diameter, and the maximum standardized uptake values (SUVmax) of the contralateral node ( P  = 0.030), primary tumor ( P  < 0.001), and ipsilateral node ( P  < 0.001). The area under the curves of SUVmax of the primary tumor (0.887), ipsilateral node (0.886), and longest diameter (0.752) were the largest and these three parameters were used as predictive criteria in the decision tree. The accuracy of the decision tree was 97.7% with 100% sensitivity and 97.6% specificity. CONCLUSION: Preoperative PET/CT imaging with a decision tree has the potential to diagnose CLNM in patients with oral cancer.

Gumbel distribution-based technique enables quantitative comparison between streak metal artifacts of multidetector row CT and cone-beam CT: a phantom study.

Cone-beam computed tomography (CBCT), derived from multidetector row CT (MDCT), has a high spatial resolution and has recently been applied to various organs. One of the severe limitations common to CBCT and MDCT is metal artifacts. In particular, streak metal artifacts (SMAs) between multiple metal materials often hinder diagnosis. However, no studies have quantitatively compared the strength of SMAs in MDCT and CBCT. Nomura et al. reported an evaluation method specialized in SMAs of CBCT using the Gumbel distribution (GD), which can also be applied to SMAs of MDCT (Oral Surg Oral Med Oral Pathol Oral Radiol 131: 494-502, 2021, https://doi.org/10.1016/J.OOOO.2020.08.031 ). This study aimed to quantitatively compare SMAs occurring between titanium materials on MDCT and CBCT images using the GD-based method. The SMAs were investigated as follows: A hydroxyapatite block was sandwiched between two titanium rods to generate an SMA. They were placed in an acrylic phantom, simulating a human head, and scanned using an MDCT scanner and two CBCT scanners. The obtained images were analyzed using Gumbel plots and location parameters, and the SMA strength was calculated. The results showed that the SMAs on the MDCT images were significantly weaker than those on the CBCT images. In the CBCT scans, a smaller volume CT dose index value caused stronger SMAs. These results indicate that MDCT is more advantageous than CBCT in terms of SMA reduction when bone morphology between titanium materials must be evaluated. The characteristic should be considered in clinical cases.