ABSTRACT Aim To determine the radiographic detection rate of suspected cemental tear on periapical radiographs and to evaluate its association with localised radiographic periodontal breakdown and initial diagnostic pathways. Materials and Methods We retrospectively screened 370,061 periapical radiographs from 203,286 patients (2022–2024) for features suggestive of cemental tear. Three calibrated examiners independently assessed the radiographs and linked their findings to clinical records. Relative radiographic bone loss (rRBL%) was measured at suspected sites and compared with within‐patient reference sites. Results Cemental tear was radiographically suspected in 1573 teeth (tooth‐level detection rate, 0.43%) from 1509 patients (patient‐level detection rate, 0.74%). The detection rate increased with age (OR 1.46 per decade; p < 0.001). The suspected sites showed greater localised radiographic periodontal breakdown than the reference sites ( p < 0.001), and age and sex remained associated with ΔrRBL% after adjustment. Cemental tear was documented as the initial diagnosis in 17 of 1466 tooth‐level records (1.16%). Most of the reviewed records initially documented periodontal or endodontic diagnoses. Conclusions Radiographically suspected cemental tear is associated with greater localised radiographic periodontal breakdown, whereas an initial diagnosis of cemental tear was infrequently documented. Combined clinical‐radiographic evaluation and prospective validation are warranted.
ABSTRACT Aim To develop and externally validate an interpretable machine learning model using routine laboratory data to distinguish current Stage III–IV from Stage I–II periodontitis among adults with established periodontitis. Materials and Methods This two‐centre retrospective study included 1321 patients for development and 584 for external validation at two hospitals of the Zhejiang University School of Medicine. The stacking model used age, sex, smoking status and 13 blood‐derived predictors and was frozen before external validation. Performance was assessed by discrimination, calibration, classification measures, decision‐curve analysis and comparison with simpler models. SHAP and restricted cubic spline analyses were exploratory. Results The stacking model had an out‐of‐fold AUC of 0.827 (95% CI: 0.802–0.851) in development and an external AUC of 0.774 (95% CI: 0.730–0.818). External calibration was less favourable (intercept 0.785, slope 0.822). External AUC was 0.745 for age, sex and smoking status and 0.763 after adding the 13 blood‐derived predictors. Conclusions Among adults with established periodontitis and sufficiently complete predictor data, the model showed moderate external discrimination but less favourable calibration. Blood‐derived predictors added modest discrimination beyond age, sex and smoking status. The model does not replace periodontal examination. Further multi‐centre validation and calibration are needed before clinical use.
Aim To investigate how human palatal fibroblasts (HPFs) from anterior (A) or posterior (P) subepithelial connective tissue grafts (CTGs) regulate oral epithelial cell behaviour, focusing on epidermal growth factor (EGF) and heparin-binding EGF-like growth factor (HB-EGF).Materials and Methods Oral epithelial cells were cocultured with either A-HPFs or P-HPFs under indirect and direct conditions. Proliferation and differentiation were assessed by BrdU, qRT-PCR and immunofluorescence. Growth factor signalling was analysed by ELISA, inhibition/neutralisation experiments, siRNA knockdown and immunoblotting.Results A-HPFs promoted epithelial proliferation but not differentiation under indirect conditions. In contrast, direct contact triggered epithelial differentiation and AP-1 gene induction. EGF mediated proliferation via the EGF receptor (EGFR), whereas HB-EGF induced differentiation via the ErbB4 receptor. HB-EGF knockdown selectively impaired expression of differentiation-associated and AP-1 genes without affecting proliferation. Distinct intracellular signalling was observed, with Erk1/2 activation predominating in indirect coculture and Akt and Stat5 activation in direct coculture.Conclusion This mechanistic in vitro study supports a model in which A-CTG-derived fibroblasts regulate epithelial responses through a transition from paracrine EGF-EGFR to juxtacrine HB-EGF-ErbB4 signalling during wound healing. These findings provide a biological basis for personalised strategies to optimise graft selection and biomaterial functionalisation in periodontal and peri-implant therapy.
