Digital intraoral scanning is a hot topic in the field of oral digital technology. In recent years, digital intraoral scanning has gradually become the mainstream technology in orthodontics, prosthodontics, and implant dentistry. The precision of digital intraoral scanning and the accuracy and stitching of data collection are the keys to the success of the impression. However, the operators are less familiar with the intraoral scanning characteristics, imaging processing, operator scanning method, oral tissue specificity of the scanned object, and restoration design. Thus far, no unified standard and consensus on digital intraoral scanning technology has been achieved at home or abroad. To deal with the problems encountered in oral scanning and improve the quality of digital scanning, we collected common expert opinions and sought to expound the causes of scanning errors and countermeasures by summarizing the existing evidence. We also describe the scanning strategies under different oral impression requirements. The expert consensus is that due to various factors affecting the accuracy of digital intraoral scanning and the reproducibility of scanned images, adopting the correct scanning trajectory can shorten clinical operation time and improve scanning accuracy. The scanning trajectories mainly include the E-shaped, segmented, and S-shaped methods. When performing fixed denture restoration, it is recommended to first scan the abutment and adjacent teeth. When performing fixed denture restoration, it is recommended to scan the abutment and adjacent teeth first. Then the cavity in the abutment area is excavated. Lastly, the cavity gap was scanned after completing the abutment preparation. This method not only meets clinical needs but also achieves the most reliable accuracy. When performing full denture restoration in edentulous jaws, setting markers on the mucosal tissue at the bottom of the alveolar ridge, simultaneously capturing images of the vestibular area, using different types of scanning paths such as Z-shaped, S-shaped, buccal-palatal and palatal-buccal pathways, segmented scanning of dental arches, and other strategies can reduce scanning errors and improve image stitching and overlap. For implant restoration, when a single crown restoration is supported by implants and a small span upper structure restoration, it is recommended to first pre-scan the required dental arch. Then the cavity in the abutment area is excavated. Lastly, scanning the cavity gap after installing the implant scanning rod. When repairing a bone level implant crown, an improved indirect scanning method can be used. The scanning process includes three steps: First, the temporary restoration, adjacent teeth, and gingival tissue in the mouth are scanned; second, the entire dental arch is scanned after installing a standard scanning rod on the implant; and third, the temporary restoration outside the mouth is scanned to obtain the three-dimensional shape of the gingival contour of the implant neck, thereby increasing the stability of soft tissue scanning around the implant and improving scanning restoration. For dental implant fixed bridge repair with missing teeth, the mobility of the mucosa increases the difficulty of scanning, making it difficult for scanners to distinguish scanning rods of the same shape and size, which can easily cause image stacking errors. Higher accuracy of digital implant impressions can be achieved by changing the geometric shape of the scanning rods to change the optical curvature radius. The consensus confirms that as the range of scanned dental arches and the number of data concatenations increases, the scanning accuracy decreases accordingly, especially when performing full mouth implant restoration impressions. The difficulty of image stitching processing can easily be increased by the presence of unstable and uneven mucosal morphology inside the mouth and the lack of relatively obvious and fixed reference objects, which results in insufficient accuracy. When designing restorations of this type, it is advisable to carefully choose digital intraoral scanning methods to obtain model data. It is not recommended to use digital impressions when there are more than five missing teeth.

Objective To explore the potential role of alpinumisoflavone (AIF) in the treatment of temporomandibular joint osteoarthritis (TMJOA) cell model through network pharmacology and molecular docking and to provide a research basis for AIF in the treatment of TMJOA. Methods GeneCards, OMIM, DisGeNET, and PharmGKB databases were used to screen TMJOA disease targets, and PharmMapper and HERB were used to retrieve AIF-related targets. The intersection targets of the compounds and diseases were uploaded to the STRING database to obtain the key targets for GO and KEGG enrichment analysis, while the key targets in related signaling pathways were evaluated through molecular docking. Approval was obtained from the Ethics Committee to extract condylar chondrocytes from 3-week-old SD rats. The CCK-8 assay was used to detect AIF cytotoxicity on condylar chondrocytes. Condylar chondrocytes were induced with 10 ng/mL interleukin 1β (IL-1β) for 24 h to construct a TMJOA cell model. The experiment was divided into three groups: control group, comprising condylar chondrocytes cultured in DMEM for 48 h; IL-1β group, comprising condylar chondrocytes pre-cultured in DMEM for 24 h, after which IL-1β was added to the original culture medium to obtain a medium concentration of 10 ng/mL and allowed to culture for 24 h; and the IL-1β+10 μmol/L AIF group, comprising condylar chondrocytes pre-cultured in DMEM medium containing 10 μmol/L AIF for 24 h, after which IL-1β was added to the original culture medium to obtain a medium concentration of 10 ng/mL and allowed to culture for 24 h. The effect of AIF on condylar chondrocyte apoptosis in the TMJOA cell model was detected by flow cytometry. The experiment was divided into four groups: control group, IL-1β group, IL-1β+10 μmol/L AIF group, and IL-1β+30 μmol/L AIF group. The IL-1β+30 μmol/L AIF group was pre-cultured in DMEM containing 30 μmol/L AIF for 24 h, after which IL-1β was added to the original culture medium to obtain a medium concentration of 10 ng/mL and allowed to culture for 24 h. The remaining three groups were cultured in the same manner as before. The mRNA and protein expression of apoptosis-associated B-cell leukemia/lymphoma-2 (Bcl2), cysteinyl aspartate specific protease 3 (caspase-3), matrix degradation-associated a disintegrin and metalloproteinase with thrombospondin motifs 4 (ADAMTS4), matrix metalloproteinase 3 (MMP3), and matrix metalloproteinase 13 (MMP13) were detected by qPCR and western blot, by AIF in the TMJOA cell model. Results The PharmMapper and HERB database search yielded 300 AIF compound targets. The GeneCards, OMIM, DisGeNET, and PharmGKB databases yielded 378 TMJOA disease targets. Thirty-three potential common targets were obtained by intersecting compounds with disease targets. The common targets were uploaded into the STRING database to obtain 31 key targets that were mainly associated with apoptosis and extracellular matrix degradation. This process may be associated with the MAPK, estrogen, and TNF signaling pathways. The molecular docking results showed that AIF has good binding activity with extracellular signal-regulated kinase 1/2 (ERK1/2) and estrogen receptor gene 1/2 (ESR1/2), which are key targets in the MAPK and estrogen signaling pathways. The CCK-8 assay showed that AIF had no obvious cytotoxicity to condylar chondrocytes. The cell experiments showed that AIF inhibited apoptosis in the IL-1β+10 μmol/L AIF group compared to the IL-1β group. Compared to the IL-1β group in the IL-1β+10 μmol/L AIF group and the IL-1β+30 μmol/L AIF group, AIF upregulated Bcl2 and downregulated caspase-3 mRNA and protein expression and inhibited ADAMTS4, MMP3, and MMP13 mRNA and protein expression. Conclusion AIF inhibited apoptosis in the TMJOA cell model by upregulating Bcl2 and downregulating caspase-3 mRNA and protein expression, and inhibited extracellular matrix degradation induced by IL-1β, thereby delaying TMJOA progression.

Objective To evaluate the impact of ultra-high-molecular-weight polyethylene (UHMWPE)-Ribbond fibers, when combined with different restorative materials, on fracture resistance and marginal adaptation of isolated primary molar defects, to provide a reference for clinical practice. Methods This study was approved by the Ethics Review Committee. A total of 72 extracted primary molars with complete crowns were collected, and 66 primary molars were randomly assigned as experimental groups for the fracture resistance and microleakage tests. The molars were divided into six groups (n = 11) based on the type of restorative materials and the application of Ribbond fibers: Group A1, 3M Filtek Z250 + Ribbond; Group A2, 3M Filtek Z250; Group B1, Beautifil II LS + Ribbond; Group B2, Beautifil II LS; Group C1, 3M Filtek Bulk Fill + Ribbond; and Group C2, 3M Filtek Bulk Fill. Groups A1, B1 and C1 received the fiber-reinforcing technique, whereas Groups A2, B2 and C2 received the direct restorative technique; the remainings were in Group D (blank control group), which did not receive treatment for the fracture resistance test. The fracture resistance test was divided into six experimental groups and one blank control group (n = 6). Primary molar teeth in each experimental group were prepared with Class II cavities and filled. The fracture load of all samples was detected, and the fracture mode was analyzed after thermal cycling. The microleakage test was divided into six experimental groups, with five in each group. Class I cavities with a diameter of 3 mm and depth of 2.5 mm were prepared within the mesial and distal marginal ridges on the occlusal surface and filled for primary molars in each group. Marginal microleakage was assessed after thermal cycling. Results The fracture resistance test results showed that the fracture resistance in groups that received the fiber-reinforcing technique was greater than that in groups that received the direct restorative technique: Group A1>Group A2, Group B1>Group B2, Group C1>Group C2 (P<0.05). The application of Ribbond fibers increased fracture resistance to all tested restorative materials by 37.08% to 39.34%. The proportion of tooth frac-ture decreased significantly in groups A1, C1 compared with A2, C2, with a significant increase in the occurrence rate of “Repairable” (P<0.05). The fracture resistance in Group A1 was significantly greater than that in Group B1 and Group C1 (P<0.05). The marginal microleakage test results showed that the microleakage depth in groups that received the fiber-reinforcing technique was smaller than that in groups that received the direct restorative technique: Group A1<Group A2, Group B1<Group B2, Group C1<Group C2 (P<0.05). The microleakage depth in groups that received the fiber-reinforcing technique decreased by 53.90% to 66.96% compared to that in groups that received the direct restorative technique. The microleakage depth in Group B1 was significantly less than that in Group A1 and Group C1. Conclusion The application of Ribbond fibers combined with various restorative materials could enhance fracture resistance and diminish the microleakage depth to improve marginal adaptation.

Objective To summarize the clinical registration data of endodontic diseases registered in ClinicalTrials.gov in the United States and Chinese Clinical Trial Registry (ChiCTR), and analyze the registration characteristics at home and abroad. Methods We searched the clinical studies related to endodontic disease registered in the two databases from January 1, 2000, to August 20, 2023. We extracted and analyzed the information from clinical studies related to endodontic diseases. The extracted content included information on the registration region, registration year, trial title, research direction, sample size, trial progress, study type, trial design, blinding method, clinical trial phase, and participating institutions. Results The two databases contained a total of 536 191 registered items, of which 634 were endodontic diseases. Clinical trials in the registry of endodontic diseases involved 43 countries, of which the top three were Egypt (188 items), China (130 items), and the America (46 items). In addition, the number of registrations of clinical trials on endodontic diseases has significantly increased since 2015. The research directions were mainly pulposis (434 items), caries (106 items), and periapical diseases (77 items), which mostly involved etiology, drug intervention, surgical intervention, new technology, and new materials. Moreover, there were 430 clinical trials (67.82%) with a sample size < 100 and 185 (29.18%) with a sample size of 100-999. The progress status at the time of registration showed the largest number of completed trials, accounting for 286 items (45.11%), followed by unknown (125 items), recruiting (110 items), and not yet recruiting (81 items). The main research types were intervention studies (546 items, 86.12%), and the main design model was randomized parallel controlled trials (473 items, 74.61%). Additionally, 423 items (66.72%) were marked using the blind method, mainly double-blind trials (195 items), followed by other/unmarked (123 items, 19.40%) and open study (88 items, 13.88%). Furthermore, the largest number of items in the study phase were marked other/unlabeled (388 items), followed by phaseⅡ study (69 items) and preliminary study (62 items). Additionally, 611 items (96.37%) were clinical trials with a number of participating institutions < 3, and 23 items (3.63%) had a number of participating institutions ≥ 3. Conclusion The number of clinical trials registered for endodontic diseases is generally on the rise, but it is still relatively small. The quality of the study design needs to be enhanced, and the registration information in the study phase needs to be improved. Moreover, the number of multicenter trials is small. In the future, we should fully mobilize the talent advantages of well-known stomatology majors in China, take the lead in conducting high-quality, multi-center clinical research, and realize the transformation of results.

Objective To explore the bidirectional causal relationships between periodontitis and asthma using the two-sample Mendelian randomization (MR) method to provide a basis for exploring the etiology and formulating preventive and therapeutic measures of periodontitis and asthma. Methods We performed two-sample bidirectional Mendelian randomization analysis using publicly released European genome-wide association studies (GWAS) statistics for periodontitis (n = 34 615) and asthma (n = 408 422). The inverse variance weighted (IVW) method was employed as the main approach to estimate the bidirectional causal relationships between periodontitis and asthma. In addition, weighted median (WM), MR-Egger regression, maximum likelihood, and Mendelian randomization robust adjusted profile score (MR-RAPS) were used as supplementary analyses. Sensitivity analyses were conducted using Cochran's Q test, Mendelian randomization pleiotropy residual sum and outlier (MR-PRESSO), and leave-one-out analysis. Results A total of 12 and 43 single-nucleotide polymorphisms (SNPs) were included as instrumental variables for periodontitis and asthma, respectively. The results of IVW, WM, MR-Egger regression, maximum likelihood, and MR-RAPS showed that periodontitis was not causally related to the risk of asthma (IVW: OR: 1.003, 95% CI: 0.973-1.035, P = 0.828, WM: OR: 0.990, 95% CI: 0.951-1.031, P = 0.641; MR-Egger regression: OR: 0.988, 95% CI: 0.960-1.028, P = 0.573; maximum likelihood: OR: 1.003, 95% CI: 0.972-1.035, P = 0.834; MR-RAPS: OR: 1.002, 95% CI: 0.970-1.036, P = 0.890) among the European population, and no causal effect of asthma on periodontitis was found (IVW: OR: 1.021, 95% CI: 0.938-1.111, P = 0.633, WM: OR: 1.011, 95% CI: 0.894-1.142, P = 0.866; MR-Egger regression: OR: 1.042, 95% CI: 0.824-1.319, P = 0.731; maximum likelihood: OR: 1.021, 95% CI: 0.938-1.112, P = 0.631; MR-RAPS: OR: 1.017, 95% CI: 0.931-1.110, P = 0.713) among the European population. Cochran's Q test showed no heterogeneity among the included instrumental variables, MR-PRESSO test found no horizontal pleiotropy, and the leave-one-out method did not identify outlier SNPs. Conclusion The results of this study, based on European genetic data, do not support a bidirectional causal association between periodontitis and asthma in the European population.

Objective To investigate the application of mycophenolate mofetil (MMF) in oral mucosal pemphigoid and provide a clinical reference. Methods One case of glucocorticoids combined with MMF in the treatment of oral mucosal pemphigoid was reported, and the clinical application of MMF in oral mucosa-related bullous diseases was discussed. Results One patient with a clinical diagnosis of “oral mucosal pemphigoid” was treated with methylprednisolone (36 mg, qd, morning dose) or combined hydroxychloroquine sulfate (0.1 g/time, bid) and thalidomide capsules (50 mg, qd, bedtime) and other drugs. The patient’s disease was slowly controlled but prone to recurrence. The treatment regimen was immediately adjusted, i.e., methylprednisolone (36 mg, qd, morning dose) was combined with MMF (0.5 g/time, bid) for 2 weeks, which resulted in ideal lesion healing control. After 8 weeks of methylprednisolone combined with MMF, the dose of methylprednisolone was gradually reduced to 12 mg, qd, and MMF was reduced to 0.5 g, qd, the patient’s symptoms improved significantly, and no obvious lesions were found in the mouth. The dose was then reduced and maintained according to the principle of pemphigoid treatment. Methylprednisolone (8 mg, qd, morning dose) and MMF (0.5 g, qd) have been used for 6 months of maintenance treatment, and they are still being followed up. As yet, the patient’s condition is stable without obvious lesions and new blisters, and no obvious side effects have been observed. A review of the literature shows that MMF is widely used in the field of dermatology to treat a variety of immune diseases, such as connective tissue diseases and autoimmune blistering diseases. According to the reports of adverse reactions to MMF, digestive system reactions are the most common adverse reactions; therefore, patients with active gastrointestinal diseases should be treated with caution, followed by bone marrow suppression, and it is recommended to monitor liver function and blood routine in patients using MMF. The safety and efficacy of MMF for treating pemphigoid involving the skin have been reported in the literature, but oral mucosal doctors still lack experience for treating mucous membrane pemphigoid. Conclusions As a new immunosuppressant, MMF has high safety and no obvious side effects and can be considered as a combination adjuvant drug for patients with severe clinical disease and refractory oral mucosal pemphigoid.

Objective To explore the oral mucosal manifestations of Sweet’s syndrome and provide a reference for its early detection and correct diagnosis. Methods The oral mucosal manifestations of a 60-year-old female patient with Sweet’s syndrome are described in detail, followed by a discussion of the related literature. Results The patient had skin erythema of both lower extremities, which was accompanied by oral mucosal ulceration and pain for 3 days. The patient presented with mild cutaneous lesions and diffuse large-scale erosion in the oral mucosa with obvious pain. During the onset of the disease, the patient was accompanied by fever with a temperature of 38.5°C. After visiting the Department of Stomatology, laboratory tests showed an increase in C-reactive protein (35.2 mg/L) and an accelerated erythrocyte sedimentation rate (77.00 mm/h). Scattered red plaques and mild tenderness were observed in the knees and lower limbs. Histopathological examination of the skin lesions revealed scattered infiltration of immature neutrophils across the entire dermis. The patient responded well to glucocorticoid therapy. According to the clinical signs and laboratory examination, combined with the lesion histopathological results, a diagnosis of Sweet’s syndrome was given. The patient was administered 1 mL compound Betamethasone injection only once intramuscularly. In the meantime, the patient was asked to gargle with compound chlorhexidine solution and topically apply recombinant bovine basic fibroblast growth factor solution to the damaged mucosa three times a day for 1 week. After 4 days of medication, the patient’s body temperature had returned to normal and the oral lesions were significantly reduced. After 2 weeks, the erythema in the leg and knee had almost all subsided, and the oral mucosal lesions had disappeared. The patient was followed up 6 months after treatment, with no recurrence of skin lesions. After 2 years of follow-up, the disease was stable with no recurrence. A review of the relevant literature shows that Sweet’s syndrome is a rare inflammatory reactive dermatosis with unknown etiology, which can be divided into three clinical types: specific, tumor-related, and drug-induced. The male/female prevalence ratio is 1:4. The salient clinical manifestations are abrupt onset of painful erythematous plaques or nodules most commonly involving the extremities, often accompanied by pyrexia, elevated neutrophil count, elevation of the erythrocyte sedimentation rate, and positive C-reactive protein. The use of glucocorticoids is the most common treatment for this disease, and most patients see a rapid improvement in skin lesions; however, some may experience infection or recurrence after withdrawal. Some patients with Sweet’s syndrome are accompanied by oral lesions, but cases of oral mucosal damage have been rarely reported, and this condition is easily misdiagnosed. Conclusion Oral mucosal lesions may be extraterritorial manifestations of Sweet’s syndrome, and the patient’s systemic condition should be comprehensively considered. Skin biopsy should be completed as soon as possible to make a clear diagnosis, so as not to delay the disease.

Oral health is an integral component of overall well-being, with the oral cavity serving as a channel for external communication and expression of emotions such as stress and pessimism. Oral diseases can intensify feelings of depression, whereas depression can worsen oral health conditions. As a crucial part of the human microbiome, an imbalance in oral microbiota can release oral pathogenic microbes, which, through pathways including the circulation, nervous, and immune systems, can reach the brain and significantly affect the central nervous system. This can lead to dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis, further intensifying the development of depression. Similarly, an imbalance in oral microbiota in individuals with depression can intensify the occurrence of oral diseases. The relationship between depression and oral diseases is not isolated but rather a complex interplay in which they mutually influence and act as causative factors. To elucidate the causal relationship between oral diseases and depression and devise strategies for the prevention and treatment of both conditions, we explore the interaction mechanisms between oral diseases and depression from the perspective of oral microbiota. The occurrence of dental caries, periapical periodontitis, and periodontal diseases is closely associated with the excessive proliferation of specific bacteria in the oral cavity, such as Streptococcus mutans, Porphyromonas gingivalis, and Fusobacterium nucleatum. These bacteria can directly invade the brain through the compromised blood-brain barrier, activating pro-inflammatory cytokines and worsening depressive symptoms. Inflammatory conditions and ulcers in the oral mucosa are caused by various factors, including infection and immune abnormalities. Because of compromised immune function in individuals with depression, these inflammatory responses are often more severe and difficult to control. Malocclusion, trigeminal neuralgia, and temporomandibular joint disorders increase the risk of depression because of psychological stress and changes in the immune system. We also outline the diagnostic and therapeutic considerations for oral diseases in patients with depression, emphasizing the importance of early intervention for disease management. Future research will explore the therapeutic potential of oral microbiota in individuals with depression, with the aim to improve symptoms and treatment outcomes by adjusting oral microbiota, thus providing novel avenues for the prevention and treatment of depression.

Enterococcus faecalis is the main pathogen causing refractory apical periodontitis (RAP). This bacterium can tolerate harsh environments and trigger periapical immune inflammatory responses that result in persistent infection inside and outside the root canal. Adhesion to the dentin wall of root canals and the subsequent formation of biofilms significantly enhances the drug resistance and anti-erosion ability of Enterococcus faecalis, which is the key factor mediating its pathogenesis. The adhesion of Enterococcus faecalis to dentin involves non-specific adhesion and specific adhesion, and the latter is mediated by adhesion-related virulence factors, mainly including the adhesin of collagen from enterococci (Ace), extracellular surface protein (Esp), gelatinase (GelE), serine protease (SprE), endocarditis and biofilm associated pilus (Ebp) and aggregation substance (AS), which is regulated by multiple two-component systems. The two-component system Fsr can promote the expression of gelE and sprE when the cell population density increases. GelE can further reduce Ace, while the two-component system GrvRS directly downregulates ace expression in response to the serum environment. The two-component systems CroRS and WalRK may also promote and inhibit the expression of various virulence factors, including ace and gelE, thus affecting the adhesion of Enterococcus faecalis. In addition, the mechanochemical preparation and the internal environment of the root canal can also influence the adhesion of Enterococcus faecalis to dentin. Avoiding the introduction of Enterococcus faecalis and using adhesion-interfering medications during root canal treatment can effectively prevent the adhesion of Enterococcus faecalis, and a variety of activated irrigation protocols can also be effective at increasing the clearance of Enterococcus faecalis from the root canal. The design of rational drugs targeting key factors involved in and regulators of the adhesion of Enterococcus faecalis to dentin is expected to provide new ideas and strategies for root canal infection control. The present paper reviews the adhesion of Enterococcus faecalis to dentin and its influencing factors.

Enamel hypoplasia is a disease that results in enamel formation and mineralization abnormalities due to the effects of hereditary or environmental variables during tooth development. Affected teeth may appear to have an aberrant color and structural flaws. Patients often display clinical signs such as tooth defects, tooth sensitivity, and tooth discoloration. The disease can cause patients to feel physically and mentally uncomfortable and negatively impact their ability to chew, swallow, speak, and smile. In this review, the pathophysiology of enamel hypoplasia, which is caused by anomalies in gene regulation and changes in environmental variables, is summarized, along with a list of clinical diagnostic indicators based on the most commonly used disease classifications. The main points are as follows: ① enamel hypoplasia changes only the color and transparency of the affected teeth; ② lesions often occur symmetrically in groups; ③ the age at which systemic diseases or nutritional disorders occur during tooth development can be predicted based on the patient's impaired teeth; and ④ banded or pitted brown depression on the enamel surface can easily be confused with dental fluorosis. It also elaborates on the comprehensive application of tooth bleaching, desensitization, direct or indirect restoration and other treatment modalities according to unique chief complaints by different patients and suggests the use of multidisciplinary cooperative sequential treatment for critical infants and young children. The goal of this review is to provide professionals with the most recent information and advice about enamel hypoplasis. Current literature on this condition is primarily case reports. To further standardize the diagnostic and management approaches for this disease, additional high-quality clinical research and systematic reviews are required.

Vertical root fracture is a type of longitudinal crack originating from the roots of teeth that can occur in vital teeth and teeth after root canal treatment. It is a hard tissue disease of teeth with a complex etiology and poor prognosis. The vertical root fracture that occurs in teeth after pulp treatment is called secondary vertical root fracture (SVRF). A comprehensive judgment should be made based on clinical signs such as pain, swelling, tooth looseness, sinus located near the gum edge, and deep and narrow isolated periodontal pockets, as well as apical films such as periodontal membrane widening, vertical and root bone loss, and “halo” or “J” shaped transmission shadows around the root. For teeth suspected of longitudinal root fractures, three-dimensional imaging such as cone beam computed tomography (CBCT) should be used to assist in the diagnosis. If CBCT shows a defect in the buccal or lingual bone plate, it can increase the possibility of diagnosing SVRF. The setting of CBCT parameters should be optimized by using small field CBCT, enhancing dye-assisted applications, and metal artifact reduction (MAR) tools to reduce the impact of artifacts and improve the accuracy of CBCT diagnosis of SVRF. Magnetic resonance imaging (MRI), digital subtraction radiography (DSR), optical coherence tomography (OCT), and other imaging techniques can detect cracks of different widths, and artificial intelligence (AI) diagnostic technology and predictive models provide further auxiliary means for SVRF diagnosis. SVRF cannot be determined through noninvasive methods, and the final diagnostic method is to detect the presence of SVRF through direct observation within the root canal and during flap surgery.