RESUMEN
Background: Scientific literature lacks strong support for using narrow diameter implants (NDI) in high masticatory force areas, especially in molars. Implant splinting in cases of multiple missing teeth reduces lateral forces, improves force distribution, and minimizes stress on implants. However, no studies have evaluated the fatigue load resistance of unitary or splinted implants. Methods: This in vitro study compares five groups of new metal alloy implants, including unitary and splinted implants with varying diameters. Mechanical characterization was assessed using a BIONIX 370 testing machine (MTS, Minneapolis, MN, USA) according to ISO 14801. For each of the five study sample groups, (n = 5) specimens underwent monotonic uniaxial compression at break testing and (n = 15) cyclic loading to determine the maximum force (Fmax) and the fatigue life (LF) values. Scanning electron microscopy (SEM) was employed for the fractographic analysis of the fractured samples. Results: The Fmax values for unitary samples ranged from 196 N to 246 N, whereas the two-splinted samples displayed significantly higher values, ranging from 2439 N to 3796 N. Similarly, the LF values for unitary samples ranged from 118 N to 230 N, while the two-splinted samples exhibited notably higher values, ranging from 488 N to 759 N. Conclusions: The observed resistance difference between sample groups in terms of Fmax and LF may be due to variations in effective cross-sectional area, determined by implant diameter and number. Additionally, this disparity may indicate a potential stiffening effect resulting from the splinting process. These findings have significant implications for dental clinical practice, suggesting the potential use of splinted sets of small-sized NDI as replacements for posterior dentition (premolars and molars) in cases of alveolar bone ridge deficiencies.
RESUMEN
OBJECTIVE: To characterize extracellular vesicles (EVs) in gingival crevicular fluid (GCF) and saliva samples from healthy/gingivitis and periodontitis patients and correlate them with clinical inflammatory periodontal parameters. MATERIAL AND METHOD: An exploratory study, including 86 subjects, was conducted. Clinical and periodontal data were recorded, and oral fluid samples were obtained. EVs were precipitated by ExoQuick-TC™ and characterized by nanoparticle tracking (NanoSight™), Western blot (WB), transmission electron microscopy (TEM), and ELISA analysis. RESULTS: TEM showed nanoparticles morphologically compatible with EVs, and WB analysis revealed bands of specific EV markers (CD9, TSG101, and Alix) in both oral fluids of periodontitis and healthy/gingivitis subjects. The total concentration of EVs in GCF was increased in periodontitis patients compared to healthy/gingivitis subjects (p = .017). However, we did not observe differences in the EV concentration of saliva samples (p = .190). The size of GCF-EVs was 144.2 nm in periodontitis and 160.35 nm in healthy/gingivitis patients (p = .038). The CD63 exosome marker was increased in GCF of periodontitis patients (p = .00001). The total concentration of EVs in GCF was correlated with bleeding on probing (rho = 0.63, p = .002), periodontal probing depth (rho = 0.56, p = .009), and clinical attachment level (rho = 0.48, p = .030). CONCLUSION: Periodontitis patients have an increased concentration of EVs in GCF, and their role in periodontitis should be clarified.
RESUMEN
La enfermedad periodontal agresiva suele producirse en pacientes jóvenes, sistémicamente sanos, en los que se observa una agregación familiar y la pérdida de inserción y ósea son rápidas. Este tipo de enfermedad puede estar causada por un componente bacteriano, genético y ambiental. El tratamiento periodontal puede ser igual de efectivo en esta forma de la enfermedad. Sin embargo, debido a la importante susceptibilidad de estos pacientes, es esencial la motivación en el cuidado de la higiene oral y en el cumplimiento delos mantenimientos periodontales (AU)
Aggressive Periodontitis is usually seen in young patients, systemically healthy, with a familial aggregation and a rapid rate of attachment and bone loss. It may be caused by a bacterial, genetic and environmental component. Periodontal treatment is as effective as in other periodontal pathologies. However, oral hygiene compliance and periodontal recallsare important due to the high susceptibility of these patients (AU)
