Chronic hyperglycemia has been associated with an increased prevalence of pathological conditions including cardiovascular disease, cancer, or various disorders of the immune system. In some cases, these associations may be traced back to a common underlying cause, but more often, hyperglycemia and the disturbance in metabolic balance directly facilitate pathological changes in the regular cellular functions. One such cellular function crucial for every living organism is cell cycle regulation/mitotic activity. Although metabolic challenges have long been recognized to influence cell proliferation, the direct impact of diabetes on cell cycle regulatory elements is a relatively uncharted territory. Among other “nutrient sensing” mechanisms, protein O-linked β-N-acetylglucosamine (O-GlcNAc) modification emerged in recent years as a major contributor to the deleterious effects of hyperglycemia. An increasing amount of evidence suggest that O-GlcNAc may significantly influence the cell cycle and cellular proliferation. In our present review, we summarize the current data available on the direct impact of metabolic changes caused by hyperglycemia in pathological conditions associated with cell cycle disorders. We also review published experimental evidence supporting the hypothesis that O-GlcNAc modification may be one of the missing links between metabolic regulation and cellular proliferation.

Background: The treatment of transversal maxillary deficiency usually aims at skeletal expansion. The treatment option highly depends on the maturation stage of the midpalatal suture (MPS), which may vary between individuals at the same chronological age. Therefore, the individual determination of the MPS maturation is crucial. Aims: Our aim was to investigate the applicability of fractal analysis for the quantitative evaluation of MPS maturation. Methods: Nine experienced orthodontists were asked to evaluate the MPS maturation on 51 cone beam computed tomography (CBCT) scans according to the Angelieri classification method. Intra- and inter-examiner reliability was measured using Cohen’s Kappa coefficient. The stages were agreed upon according to the results of the examiners with the highest strength of agreement. Fractal analysis was then performed on the CBCTs and the correlation between the fractal dimension values and maturation stages was then evaluated. Optimal fractal dimension cut-off values were determined using a receiver operating characteristic curve. Results: The cut-off point was found at 1.073, at which the use of fractal dimension for predicting MPS maturation showed 100% sensitivity, 93.7% specificity, 9.5% false positive, 0% false negative rate. Conclusion: Our results provided further evidence that fractal analysis is a reliable tool to determine MPS maturation stage.

Our goal is to show that temporomandibular disorder (TMD) patients with orthopaedic instability can be effectively treated by the combination of occlusal splint therapy and molar intrusion. Diagnostic records of 18 patients reporting previous TMD and treated with splint therapy were evaluated. Postsplint anterior open bite was treated by skeletally anchored molar intrusion. Changes in overjet (OJ), overbite (OB) were measured on articulator mounted models: initially in maximal intercuspidation (MI), centric “de jour”, postsplint centric relation (CR) and postintrusion CR. Changes in ANB (A point-Nasion-B point) angle, mandibular plane–palatal plane angle and facial axis angle were assessed on lateral cephalograms. Morphological changes of the condyle were detected on pre-and posttreatment CBCT images. When compared screening mountings to MI models, significant differences were found in OJ and OB. Following splint wear, there was a significant increase in lower facial height and significant decrease in facial axis angle, which in turn increased ANB angle. OB and OJ showed a significant change on the postsplint mountings when compared to MI. After intrusion, mandible exhibited counterclockwise rotation, which decreased lower facial height, increased OB and facial axis angle and decreased ANB and OJ. Posttreatment CBCTs confirmed improved condylar morphology.Occlusal splint therapy followed by orthodontic molar intrusion provides MI-CR harmony, therefore, it seems to be an effective method for treating TMD patients.

Metallic biomaterials are frequently exposed to chemically aggressive environments that may compromise surface integrity and corrosion resistance. Acidic media containing organic acids represent a relevant challenge for metallic systems, as they can destabilize passive oxide layers and promote surface degradation processes. The present in vitro study investigated acid-induced surface alterations in four commercially relevant orthodontic alloys—nickel–titanium (NiTi), copper–nickel–titanium (CuNiTi), titanium–molybdenum alloy (TMA), and stainless steel—as representative metallic biomaterials. Specimens were exposed to two commercially available acidic beverages with distinct pH conditions, followed by analysis of surface morphology, roughness, and elemental composition using atomic force microscopy (AFM), scanning electron microscopy (SEM), and energy-dispersive X-ray spectroscopy (EDS). The results demonstrated pronounced alloy-dependent differences in degradation behavior. Stainless steel and TMAs exhibited significant increases in surface roughness and morphological alterations, whereas NiTi-based alloys showed comparatively stable surface characteristics. Elemental analysis revealed material-specific compositional variations, suggesting selective surface modification processes under acidic exposure. These differences can be attributed to variations in alloy composition, microstructure, and the stability of passive oxide layers, which collectively govern corrosion resistance in metallic systems. The findings provide insight into acid-induced degradation mechanisms in metallic biomaterials and highlight the importance of material-dependent corrosion behavior under chemically aggressive conditions. These observations may have implications for surface-mediated biological responses and long-term functional performance of metallic biomaterials.