Background and Objectives: The surface condition of the materials that are used for temporary prostheses influences their microbial colonization, with a direct impact on the oral tissues. This study aims at a comparative analysis of three types of resins for temporary bridges using conventional and digital technologies. The attention was focused on the analysis of the surface characteristics and mechanical strength of these materials. Materials and Methods: The surface condition was assessed for three distinct materials both before and after polishing- heat-curing resin Superpont C + B (SpofaDental, Jicin, Czech Republic) used unconventional technology, Zotion dental milling polymethyl methacrylate (PMMA) block (Zotion, Chongqing, China) for provisional crowns/bridges used in digital subtractive technologies and Freeprint Temp (Detax GmbH & Co. KG, Ettlingen, Germany) resin for temporary crowns and bridges that are used in 3D printing technologies. The two-way ANOVA analysis indicated that polishing leads to a statistically significant increase in roughness coefficients for all the three resins that were tested (p < 0.001). While the highest roughness coefficients were displayed in the 3D cured sample, the largest decrease was reported by the milled sample Results: The results revealed that surface roughness was significantly influenced by both the type of resin that was used (p < 0.001) and the treatment that was induced by finishing and polishing (p < 0.001). Similar p-values were obtained for each of the three resins. Conclusions: The results demonstrated a significant optimization of the surfaces after finishing and polishing and statistically significant differences between the surface parameters and the mechanical properties of the samples. The low values of the roughness and the acceptable values of the mechanical resistance for the conventional samples indicate these materials for the long-term temporary bridge’s realization, allowing the correct restoration of the functions and the rehabilitation at the oral level.

Periodontal diseases generally correspond to a disturbance in the balance between the host’s defense and the micro-organisms colonizing the periodontal environment. The exact mechanisms underlying the destruction of the periodontium remain to be fully elucidated. Our study aims to quantify the main bacteria pool involved in periodontal pathology and associate it with other factors involved in the onset of periodontal disease so that an accurate diagnosis with profound implications for the therapeutic algorithm can be developed. Micro-Ident tests, based on the polymerase chain reaction (PCR) technique, were used for the study group, chosen for their high specificity in identifying periodontopathogenic bacteria and determining their relative numbers. The results of our study indicate an increased concentration of 4.50 (number of strains) for Capnocytophaga, followed by Tannerella forsythia, in a concentration of 3.50; the next highest concentration percentages are for Treponemei denticola, and Prevotela intermedia, low concentrations were found for Fusobacterium nucleatum and Porphyromonas. The concentration of each type of bacteria is reflected in the clinical picture and constitutes the starting point for a targeted antibiotic therapy. Following the effects of antibiotic-targeted therapy obtained from the evaluation of the micro-IDent B test results on the periodontium of the supporting teeth, we observed that the values of the periodontal indices change slightly at 3-month intervals with a predominance of plaque, bleeding, and gingival indices, and less in the indices concerning the depth of the probing pocket and the loss of attachment on the buccal and oral surfaces. In conclusion, our study emphasizes a direct relationship between the subgingival tartar presence and the patients age, gingival recession, presence of periodontal pockets, dental mobility, as well as the periodontal indexes: plaque index, bleeding index, and gingival index. The correlation of negative values of periodontal indices with the nature of the involved bacteria materializes in relevant starting points in the elaboration of the periodontal diagnosis of the therapeutic plan and predictability of the prognosis of oral rehabilitation.

Perioperative management of antithrombotic therapy in oral surgery represents an evolving paradigm. This critical review evaluates the contemporary scientific evidence that challenges the conventional practice of routinely discontinuing anticoagulants and/or antiplatelet agents to prevent postoperative bleeding. The traditional strategy carries an unacceptable risk of iatrogenic, sometimes severe, thromboembolic events. The aim of this systematic narrative review is to synthesize the current evidence (2015–2025) and to outline a new, patient-centered clinical framework that dynamically balances thromboembolic and hemorrhagic risks. Materials and methods: A systematic search of major databases (PubMed/MEDLINE, Scopus, Web of Science) identified relevant studies, structured according to the PICO framework. The search strategy prioritized high-level evidence, including clinical guidelines, systematic reviews, meta-analyses, randomized controlled trials, and prospective cohort studies published between January 2015 and November 2025. Results: The results reinforce an emerging consensus: the basis of safe management is the rigorous application of advanced local hemostasis techniques (e.g., prioritizing resorbable materials, sutures, topical hemostatic agents, and antifibrinolytics) and the use of perioperative decision-making algorithms. These measures allow, in most routine dental surgical procedures, the safe continuation of antithrombotic therapy, thus minimizing the thromboembolic risk without significantly increasing the risk of clinically significant bleeding. In the future, research should focus on optimizing materials science (novel biomaterials and controlled-release systems) and on standardizing and validating protocols in specific populations (e.g., patients on combination therapy or at extreme cardiovascular risk). This review argues that the adoption of this evidence-based model, with local hemostasis as a critical pillar, is essential for modern, ethical, and safe dental practice.

Residual cardiovascular risk arises from dysregulated expression of genes encoding apolipoprotein(a) (LPA), apolipoprotein C-III (APOC3), angiopoietin-like gene 3 (ANGPTL3), and proprotein convertase subtilisin/kexin type 9 (PCSK9). RNA-based therapies, small interfering RNAs (siRNAs), and antisense oligonucleotides (ASOs) modulate these targets at the post-transcriptional level through RNA interference and RNase H-mediated degradation, respectively. This scoping review maps the molecular mechanisms, target involvement, and pharmacodynamic outcomes of RNA therapies for managing residual cardiovascular risk, with contextual comparison to traditional lipid-lowering agents. A systematic search of PubMed, Embase, Web of Science, and Scopus was performed from 2020 to February 2026. Of the 1088 records identified, 30 studies met the inclusion criteria. RNA therapies have demonstrated potential for engagement, with 80–98% reductions in Lp(a) (pelacarsen, olpasiran, zerlasiran, lepodisiran), 50–80% reductions in triglycerides (olezarsen, plozasiran, volanesorsen), and 36–44% reductions in low-density lipoprotein cholesterol (LDL-C). Mechanistically, siRNAs achieve gene silencing through RISC-mediated mRNA cleavage, with sustained pharmacodynamic effects (3–6 months) because of Argonaute-2 stability, while gapmer ASOs recruit RNase H1 for mRNA degradation. Conjugation with GalNAc allows for hepatocyte-specific delivery with a subcutaneous bioavailability of 70–85%. Safety profiles were favorable, with injection site reactions (4–12%) being the most common adverse event. This analysis maps the emerging molecular landscape of RNA therapies, highlighting their substantial precision for targeting residual cardiovascular risk pathways that cannot be addressed by traditional agents.

The efficacy of enzyme therapy is limited by their poor stability under physiological conditions. Thermostable enzymes, derived from extremophilic organisms or generated by advanced protein engineering, offer a revolutionary solution to this long-standing challenge. They are widely used in industrial biocatalysis. Their therapeutic applications are poorly investigated and spread across diverse disciplines. While most applications are in the preclinical stages, emerging evidence from animal models demonstrates proof-of-concept for thermostable antioxidant enzymes in cardiovascular, neurodegenerative, and inflammatory diseases. This review critically assesses the translational landscape, distinguishing between established therapeutic enzymes (e.g., asparaginase, PEGylated SOD) and emerging experimental candidates. This narrative review consolidates existing knowledge about thermostable enzyme engineering and their emerging functions as molecular therapies, particularly in oxidative stress-related diseases. This review synthesizes recent advances in structural biology, computational protein design, biomaterials engineering, and translational antioxidant strategies, highlighting how breaking down disciplinary barriers is accelerating the development of sustainable and self-regenerating antioxidant platforms. By integrating molecular precision with systems-level therapeutic design, engineered thermostable antioxidant enzymes exemplify the future of biological development, where multidisciplinary collaboration drives innovation against oxidative stress-driven pathologies. Engineered thermostable enzymes provide a versatile basis for next-generation therapeutics, with the potential to address medical needs through improved stability, targeted activity, and multifunctional design.

Background/Objectives: Mucopolysaccharidosis type III (MPS III, Sanfilippo syndrome) is an autosomal recessive lysosomal storage disorder caused by deficiencies in enzymes required for heparan sulfate degradation. While primarily recognized for its devastating neurodegenerative course, the systemic extent of glycosaminoglycan (GAG) accumulation remains under-characterized. This study aims to provide a detailed multisystemic pathological mapping of MPS III to challenge the traditional "brain-only" disease paradigm and highlight the clinical relevance of extracerebral involvement. Methods: We present a comprehensive clinicopathological analysis of a 15-year-old female patient with a history of profound neuropsychomotor delay, refractory epilepsy, and spastic tetraplegia. Following her death due to terminal bronchopneumonia during palliative care, a complete forensic and pathological autopsy was conducted. Tissue samples from all major organ systems were processed using routine Hematoxylin-Eosin (HE) staining alongside specialized histochemical stains to identify intracellular storage products. Results: Macroscopic evaluation revealed significant diffuse cerebral atrophy, meningoencephalic edema, cardiac valvulopathy with compensatory myocardial remodeling, and hepatosplenomegaly. Furthermore, erosive gastrointestinal lesions and degenerative renal changes were identified. Histopathological examination confirmed widespread cytoplasmic vacuolization across diverse cell populations, including neurons, hepatocytes, renal tubular cells, and the reticuloendothelial system. These findings demonstrate that GAG deposition is a generalized process affecting nearly every parenchymal structure. Conclusions: Although neurological decline dominates the clinical phenotype, our findings underscore that MPS III is a true systemic storage disorder. Significant involvement of the cardiovascular and visceral systems contributes to the disease's complexity and mortality. This case reinforces the critical diagnostic value of a comprehensive autopsy in delineating the full morphological spectrum of Sanfilippo syndrome, providing essential insights for multidisciplinary management.