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*

OBJECTIVES: To investigate the effect of recombinant human fibroblast growth factor 21 (rhFGF21) on the proliferation and mineralization of cementoblasts and its mechanism. METHODS: Hematoxylin eosin, immunohistochemical staining, and immunofluorescence were used to detect the expression and distribution of fibroblast growth factor 21 (FGF21) in rat periodontal tissues and cementoblasts (OCCM-30), separately. Cell Counting Kit-8 was used to detect the proliferation of OCCM-30 under treatment with rhFGF21. Alkaline phosphatase staining and Alizarin Red staining were used to detect the mineralization state of OCCM-30 after 3 and 7 days of mineralization induction. The transcription and protein expression of the osteogenic-related genes Runx2 and Osterix were detected by real-time quantitative polymerase chain reaction (PCR) and Western blot analysis. The expression levels of genes of transforming growth factor β (TGFβ)/bone morphogenetic protein (BMP) signaling pathway in OCCM-30 were detected through PCR array analysis. RESULTS: FGF21 was expressed in rat periodontal tissues and OCCM-30. Although rhFGF21 had no significant effect on the proliferation of OCCM-30, treatment with 50 ng/mL rhFGF21 could promote the mineralization of OCCM-30 cells after 7 days of mineralization induction. The transcriptional levels of Runx2 and Osterix increased significantly at 3 days of mineralization induction and decreased at 5 days of mineralization induction. Western blot analysis showed that the protein expression levels of Runx2 and Osterix increased during mineralization induction. rhFGF21 up-regulated Bmpr1b protein expression in cells. CONCLUSIONS rhFGF21 can promote the mineralization ability of OCCM-30. This effect is related to the activation of the TGFβ/BMP signaling pathway.
Humans ; Rats ; Animals ; Dental Cementum ; Core Binding Factor Alpha 1 Subunit/metabolism* ; Cell Differentiation ; Bone Morphogenetic Proteins/metabolism* ; Transforming Growth Factor beta/pharmacology*

External apical root resorption is among the most common risks of orthodontic treatment, and it cannot be completely avoided and predicted. Risk factors causing orthodontic root resorption can generally be divided into patient- and treatment-related factors. Root resorption that occurs during orthodontic treatment is usually detected by radiographical examination. Mild or moderate root absorption usually does no obvious harm, but close attention is required. When severe root resorption occurs, it is generally recommended to suspend the treatment for 3 months for the cementum to be restored. To unify the risk factors of orthodontic root resorption and its clinical suggestions, we summarized the theoretical knowledge and clinical experience of more than 20 authoritative experts in orthodontics and related fields in China. After discussion and summarization, this consensus was made to provide reference for orthodontic clinical practice.
Humans ; Tooth Movement Techniques/adverse effects* ; Root Resorption/etiology* ; Consensus ; Dental Cementum ; Risk Factors

Dental Cementum ; Humans ; Tooth Fractures

Coffin-Lowry-Syndrome (CLS) is a X-linked mental retardation characterized by skeletal dysplasia and premature tooth loss. We and others have previously demonstrated that the ribosomal S6 kinase RSK2, mutated in CLS, is essential for bone and cementum formation; however, it remains to be established whether RSK2 plays also a role in mechanically induced bone remodeling during orthodontic tooth movement (OTM). We, therefore, performed OTM in wild-type (WT) mice and Rsk2-deficient mice using Nitinol tension springs that were fixed between the upper left molars and the incisors. The untreated contralateral molars served as internal controls. After 12 days of OTM, the jaws were removed and examined by micro-computed tomography (µCT), decalcified histology, and immunohistochemistry. Our analysis of the untreated teeth confirmed that the periodontal phenotype of Rsk2-deficient mice is characterized by alveolar bone loss and hypoplasia of root cementum. Quantification of OTM using µCT revealed that OTM was more than two-fold faster in Rsk2-deficient mice as compared to WT. We also observed that OTM caused alveolar bone loss and root resorptions in WT and Rsk2-deficient mice. However, quantification of these orthodontic side effects revealed no differences between WT and Rsk2-deficient mice. Taken together, Rsk2 loss-of-function accelerates OTM in mice without causing more side effects.
Animals ; Coffin-Lowry Syndrome ; Dental Cementum ; Mice ; Root Resorption ; Tooth Movement Techniques ; X-Ray Microtomography

BACKGROUND: The mandibular third molar (M3) is typically the last permanent tooth to erupt because of insufficient space and thick soft tissues covering its surface. Problems such as alveolar bone loss, development of a periodontal pocket, exposure of cementum, gingival recession, and dental caries can be found in the adjacent second molars (M2) following M3 extraction. The specific aims of the study were to assess the amount and rate of bone regeneration on the distal surface of M2 and to evaluate the aspects of bone regeneration in terms of varying degree of impaction. METHODS: Four series of panoramic radiographic images were obtained from the selected cases, including images from the first visit, immediately after extraction, 6 weeks, and 6 months after extraction. ImageJ software® (NIH, USA) was used to measure linear distance from the region of interest to the distal root of the adjacent M2. Radiographic infrabony defect (RID) values were calculated from the measured radiographic bone height and cementoenamel junction with distortion compensation. Repeated measures of analysis of variance and one-way analysis of variance were conducted to analyze the statistical significant difference between RID and time, and a Spearman correlation test was conducted to assess the relationship between Pederson’s difficulty index (DI) and RID. RESULTS: A large RID (> 6 mm) can be reduced gradually and consistently over time. More than half of the samples recovered nearly to their normal healthy condition (RID ≤ 3 mm) by the 6-month follow-up. DI affected the first 6 weeks of post-extraction period and only showed a significant positive correlation with respect to the difference between baseline and final RID. CONCLUSIONS: Additional treatments on M2 for a minimum of 6 months after an M3 extraction could be recommended. Although DI may affect bone regeneration during the early healing period, further study is required to elucidate any possible factors associated with the healing process. The DI does not cause any long-term adverse effects on bone regeneration after surgical extraction.
Alveolar Bone Loss ; Bone Regeneration ; Compensation and Redress ; Dental Caries ; Dental Cementum ; Follow-Up Studies ; Gingival Recession ; Molar ; Molar, Third ; Periodontal Pocket ; Retrospective Studies ; Tooth ; Tooth Cervix

Inflammatory external root resorption (IERR) refers to the pathological process of dissolving the hard tissue on the outer surface of the tooth root by the body's own immune system under the stimulation of various physical and chemical factors such as infection, stress, trauma and orthodontic treatment. Severe IERR can lead to endodontic and periodontal diseases, and even the loss of teeth. Therefore, understanding the etiology and the pathogenic mechanism of IERR are of importance in its prevention and treatment. This article will review the etiology and the regulation mechanisms of IERR.
Dental Cementum ; Humans ; Root Resorption ; Tooth Root

OBJECTIVE: The purpose of this study is to investigate the potential effects of sclerostin (SOST) on the biological funtions and related mechanisms of cementoblasts under mechanical stress. METHODS: OCCM-30 cells were treated with varying doses of SOST (0, 25, 50, and 100 ng·mL⁻¹) and were loaded with uniaxial compressive stress (2 000 μ strain with a frequency of 0.5 Hz) for six hours. Western blot was utilized to detect the expressions of β-catenin, p-smad1/5/8, and smad1/5/8 proteins. Alkaline phosphatase (ALP) activity was determined, and reverse transcription polymerase chain reaction was used to measure the expressions of runt-related transcription factor 2 (Runx-2), osteocalcin (OCN), bone sialoproteins (BSP), receptor activator of NF-κB ligand (RANKL) and osteoprotegerin (OPG) mRNA. RESULTS: The expression of p-smad
1/5/8 was significantly downregulated with increasing SOST. β-catenin and smad1/5/8 exhibited no difference. ALP activity decreased under mechanical compressive stress with increasing SOST concentrations. Runx-2 expression was reduced with increasing SOST concentrations, and a similar trend was observed for the BSP and OCN expressions. When the SOST concentration was enhanced, RANKL expression gradually increased, whereas the expression of OPG decreased. CONCLUSIONS Under mechanical comprehensive stress, SOST can adjust the bone morphogenetic protein (BMP) /smad signal pathway. Osteosclerosis inhibits the mineralization of cementoblasts under mechanical compressive stress, which may be achieved by inhibiting the expressions of osteogenesis factors (Runx2, OCN, BSP, and others) and by promoting the ratio of cementoclast-related factors (RANKL/OPG) through BMP signal pathways.
Bone Morphogenetic Proteins ; metabolism ; Core Binding Factor Alpha 1 Subunit ; Dental Cementum ; Osteocalcin ; Smad Proteins ; metabolism ; Stress, Mechanical

PURPOSE: To histologically characterize periodontal healing at 8 weeks in surgically created dehiscence defects in beagle dogs that received a collagen matrix with periodontal ligament (PDL) progenitor cells. METHODS: The bilateral maxillary premolars and first molars in 6 animals were used. Standardized experimental dehiscence defects were made on the buccal side of 3 premolars, and primary culturing of PDL progenitor cells was performed on the molars. Collagen matrix was used as a scaffold and a delivery system for PDL progenitor cells. The experimental sites were grafted with collagen matrix (COL), PDL progenitor cells with collagen matrix (COL/CELL), or left without any material (CTL). Histologic and histomorphometric analyses were performed after 8 weeks. RESULTS: The defect height from the cementoenamel junction to the most apical point of cementum removal did not significantly differ across the CTL, COL, and COL/CELL groups, at 4.57±0.28, 4.56±0.41, and 4.64±0.27 mm (mean ± standard deviation), respectively; the corresponding values for epithelial adhesion were 1.41±0.51, 0.85±0.29, and 0.30±0.41 mm (P<0.05), the heights of new bone regeneration were 1.32±0.44, 1.65±0.52, and 1.93±0.61 mm (P<0.05), and the cementum regeneration values were 1.15±0.42, 1.81±0.46, and 2.57±0.56 mm (P<0.05). There was significantly more new bone formation in the COL/CELL group than in the CTL group, and new cementum length was also significantly higher in the COL/CELL group. However, there were no significant differences in the width of new cementum among the groups. CONCLUSIONS: PDL progenitor cells carried by a synthetic collagen matrix may enhance periodontal regeneration, including cementum and new bone formation.
Animals ; Bicuspid ; Bone Regeneration ; Collagen ; Dental Cementum ; Dogs ; Molar ; Osteogenesis ; Periodontal Ligament ; Regeneration ; Stem Cells ; Tooth Cervix ; Transplants

OBJECTIVE: Orthodontic root resorption (ORR) due to orthodontic tooth movement is a difficult treatment-related adverse event. Caspases are important effector molecules for apoptosis. At present, little is known about the mechanisms underlying ORR and apoptosis in the cementum. The aim of the present in vivo study was to investigate the expression of tartrate-resistant acid phosphatase (TRAP), caspase 3, caspase 8, and receptor activator of nuclear factor kappa-B ligand (RANKL) in the cementum in response to a heavy or an optimum orthodontic force. METHODS: The maxillary molars of male Wistar rats were subjected to an orthodontic force of 10 g or 50 g using a closed coil spring. The rats were sacrificed each experimental period on days 1, 3, 5, and 7 after orthodontic force application. And the rats were subjected to histopathological and immunohistochemical analyses. RESULTS: On day 7 for the 50-g group, hematoxylin and eosin staining revealed numerous root resorption lacunae with odontoclasts on the root, while immunohistochemistry showed increased TRAP- and RANKL-positive cells. Caspase 3- and caspase 8-positive cells were increased on the cementum surfaces in the 50-g group on days 3 and 5. Moreover, the number of caspase 3- and caspase 8-positive cells and RANKL-positive cells was significantly higher in the 50-g group than in the 10-g group. CONCLUSIONS: In our rat model, ORR occurred after apoptosis was induced in the cementum by a heavy orthodontic force. These findings suggest that apoptosis of cementoblasts is involved in ORR.
Acid Phosphatase ; Animals ; Apoptosis ; Caspase 3 ; Caspase 8 ; Caspases* ; Dental Cementum ; Eosine Yellowish-(YS) ; Hematoxylin ; Humans ; Immunohistochemistry ; Male ; Models, Animal ; Molar ; Osteoclasts ; Rats ; Rats, Wistar ; Root Resorption* ; Tooth Movement