Cemental tear is a rare and indetectable condition unless obvious clinical signs present with the involvement of surrounding periodontal and periapical tissues. Due to its clinical manifestations similar to common dental issues, such as vertical root fracture, primary endodontic diseases, and periodontal diseases, as well as the low awareness of cemental tear for clinicians, misdiagnosis often occurs. The critical principle for cemental tear treatment is to remove torn fragments, and overlooking fragments leads to futile therapy, which could deteriorate the conditions of the affected teeth. Therefore, accurate diagnosis and subsequent appropriate interventions are vital for managing cemental tear. Novel diagnostic tools, including cone-beam computed tomography (CBCT), microscopes, and enamel matrix derivatives, have improved early detection and management, enhancing tooth retention. The implementation of standardized diagnostic criteria and treatment protocols, combined with improved clinical awareness among dental professionals, serves to mitigate risks of diagnostic errors and suboptimal therapeutic interventions. This expert consensus reviewed the epidemiology, pathogenesis, potential predisposing factors, clinical manifestations, diagnosis, differential diagnosis, treatment, and prognosis of cemental tear, aiming to provide a clinical guideline and facilitate clinicians to have a better understanding of cemental tear.
Humans ; Dental Cementum/injuries* ; Consensus ; Diagnosis, Differential ; Cone-Beam Computed Tomography ; Tooth Fractures/therapy*

Objective To investigate the role of CISD1 in gefitinib-resistant non-small cell lung cancer(NSCLC),so as to provide a potential therapeutic target for the treatment of gefitinib-resistant NSCLC.Methods Bioinformatics online platforms TIMER2.0 and HPA were used to analyze the expression level of CISD1 in lung cancer.TIMER2.0 and GEPIA2.0 were used to analyze the correlation between the expression levels of CISD1 and SLC7A11 in lung cancer.The correlation between CISD1 and overall survival rate of lung cancer patients was analyzed using KMPLOT.Human lung carcinoma cell line PC9 and gefitinib-resistant cell line PC9/GR were treated with gefitinib,and cell viability was detected using the CCK8 method.shCISD1 lentivirus infection was used to knockdown CISD1 in PC9/GR cells.Western blotting was employed to detect the protein expression levels of CISD1 and SLC7A11.PC9/GR cells were divided into shNC+DMSO group,shNC+gefitinib group,shCISD1 group,shCISD1+ferrostatin-1 group,and shCISD1+gefitinib group.Plate clone formation assay was used to detect cell proliferation capacity.FerroOrange fluorescent probe and C11-BODIPY fluorescent probe were used to detect intracellular free Fe2+content and intracellular lipid peroxide level,respectively.Results CISD1 was significantly overexpressed in lung carcinoma(P＜0.001).The expression level of CISD1 was negatively correlated with the overall survival rate of lung cancer patients and negatively correlated with the expression level of SLC7A11.Compared with the DMSO control group,gefitinib treatment significantly reduced clone formation and CISD1 protein expression levels in both PC9 and PC9/GR cells(P＜0.05),but the reduction was less pronounced in PC9/GR cells.shCISD1 infection significantly inhibited the protein expression levels of CISD1 and SLC7A11 in PC9/GR cells(P＜0.05)and enhanced the sensitivity of PC9/GR cells to gefitinib.Compared with the shNC+DMSO group,both the shNC+gefitinib group and the shCISD1 group showed significantly reduced clone formation ability(P＜0.05),but increased Fe2+and lipid peroxidation levels(P＜0.05).Compared with the shCISD1 group,the shCISD1+ferrostatin-1 group showed significantly increased clone formation ability(P＜0.05),but decreased Fe2+and lipid peroxidation levels(P＜0.05).Compared with the shNC+gefitinib group,the shCISD1+gefitinib group showed significantly reduced clone formation ability(P＜0.05),but increased Fe2+and lipid peroxidation levels(P＜0.05).Conclusion Knockdown of CISD1 promotes the sensitivity of NSCLC to gefitinib by inducing ferroptosis,which provides a new potential therapeutic target for the treatment of gefitinib-resistant NSCLC.

Objective To investigate the role of CISD1 in gefitinib-resistant non-small cell lung cancer(NSCLC),so as to provide a potential therapeutic target for the treatment of gefitinib-resistant NSCLC.Methods Bioinformatics online platforms TIMER2.0 and HPA were used to analyze the expression level of CISD1 in lung cancer.TIMER2.0 and GEPIA2.0 were used to analyze the correlation between the expression levels of CISD1 and SLC7A11 in lung cancer.The correlation between CISD1 and overall survival rate of lung cancer patients was analyzed using KMPLOT.Human lung carcinoma cell line PC9 and gefitinib-resistant cell line PC9/GR were treated with gefitinib,and cell viability was detected using the CCK8 method.shCISD1 lentivirus infection was used to knockdown CISD1 in PC9/GR cells.Western blotting was employed to detect the protein expression levels of CISD1 and SLC7A11.PC9/GR cells were divided into shNC+DMSO group,shNC+gefitinib group,shCISD1 group,shCISD1+ferrostatin-1 group,and shCISD1+gefitinib group.Plate clone formation assay was used to detect cell proliferation capacity.FerroOrange fluorescent probe and C11-BODIPY fluorescent probe were used to detect intracellular free Fe2+content and intracellular lipid peroxide level,respectively.Results CISD1 was significantly overexpressed in lung carcinoma(P＜0.001).The expression level of CISD1 was negatively correlated with the overall survival rate of lung cancer patients and negatively correlated with the expression level of SLC7A11.Compared with the DMSO control group,gefitinib treatment significantly reduced clone formation and CISD1 protein expression levels in both PC9 and PC9/GR cells(P＜0.05),but the reduction was less pronounced in PC9/GR cells.shCISD1 infection significantly inhibited the protein expression levels of CISD1 and SLC7A11 in PC9/GR cells(P＜0.05)and enhanced the sensitivity of PC9/GR cells to gefitinib.Compared with the shNC+DMSO group,both the shNC+gefitinib group and the shCISD1 group showed significantly reduced clone formation ability(P＜0.05),but increased Fe2+and lipid peroxidation levels(P＜0.05).Compared with the shCISD1 group,the shCISD1+ferrostatin-1 group showed significantly increased clone formation ability(P＜0.05),but decreased Fe2+and lipid peroxidation levels(P＜0.05).Compared with the shNC+gefitinib group,the shCISD1+gefitinib group showed significantly reduced clone formation ability(P＜0.05),but increased Fe2+and lipid peroxidation levels(P＜0.05).Conclusion Knockdown of CISD1 promotes the sensitivity of NSCLC to gefitinib by inducing ferroptosis,which provides a new potential therapeutic target for the treatment of gefitinib-resistant NSCLC.

Objective:To assess the mechanism of exacerbation of colonic damage in rat colitis model induced by trinitrobenzene sulfonic acid(TNBS)treated wi th celecoxib(a selective COX-2 inhibitor).Methods:The rats w ere randomized in to four groups.Group 1 and Group 2 were study groups.Group 3 and Group 4 were control groups.Colitis was induced by intracolonic administration of TNBS(25 g /L)in a vehicle of 50% ethanol(0.25 mL)of study groups.The rats of study gro ups were treated orally,beginning 3 h before induction of colitis and continuin g twice per day thereafter for up to 7 d,with celecoxib(1.25 mg/kg,Group 1)a nd distilled water(1 mL/0.3 kg,Group 2)respectively.In control experiments,the rats of Group 4 were treated orally with celecoxib(1.25 mg/kg)twice per da y for up to 7 d.Group 3 rats were healthy control rats.All the rats that survi ved until the end of the experiment(d 7)were killed and the severity of coloni c inflammation was assessed.The COX-2 protein expression in colon tissues was e xamined by immunohistochemistry.Results:The colonic damage of Group 1 was exac erbated as compared with Group 2.The inflammatory index of colon tissues of Gro up 1(8.5?2.5)was significantly reduced,as compared with Group 2(13.5?1.9,P

Objective: To investigate the chemopreventive effects of pioglitazone (exogenous PPAR? ligand) on rat colon aberrant crypt foci, a rat carcinogenesis model induced by dimethylhydrazine (DMH),and to compare pioglitazone with sulindac (a NSAID). Methods: Thirty two, 8 week old, female Sprague Dawley rats were randomly divided into four groups ( n =8 each). Group 1 rats were injected with DMH alone (120 mg?kg -1 , single subcutaneous injection). Group 2 rats were injected with saline alone. Group 3 rats were pre treated with sulindac (320 mg?kg -1 ) for 7 days before DMH initiation. Group 4 rats were treated with pioglitazone (100 mg?kg -1 ). The animals were killed at the end of the experiment (week 5) and the colons were stained with methylene blue. The aberrant crypt foci (ACF) of the colonic mucosa were assessed. Results: In Group 1 rats (DMH only), the average numbers of ACF/colon and AC/colon were (182?93) and (263?198), respectively. In Group 2 (saline group) rats, no ACF were found. In Group 3 (sulindac group) rats, the average numbers of ACF/colon and AC/colon were (91?49) and (140?69), respectively. Both of them were decreased significantly compared with the values in Group 1 ( P