BACKGROUND: Rapid expansion of the dental arch is an effective way to rapidly expanse the jaw. Compared with rapid expansion, the slow expansion has higher stability and less recurrence, but the reports on the long-term stability of quad helix expansion are rare. OBJECTIVE: To retrospectively analyze the clinical effect of quad helix expansion in orthodontics. METHODS: Twenty-two subjects with dental arch stenosis in mixed dentition and early permanent dentition who experienced an expansion of at least 3 mm with quad helix appliance were selected for this study. Plaster dental casts and posteroanterior radiographs were evaluated at the beginning of the treatment (T1), at the completion of phase I quad helix expansion or ful treatment (T2), and approximately 2 years fol owing the completion of treatment (T3). The distance between two first molars was measured on the model. J point was drawn on the posteroanterior radiograph in order to measure the distance between the bilateral base bones and the molar inclination, as wel as to evaluate the corrective and orthopedic effects of dental arch expansion. RESULTS AND CONCLUSION: Compared with that before expansion, the first permanent molar inclination and the distance between base bones on two sides were significant increased after quad helix expansion; there were no significant differences in the distance between two first permanent molars, first permanent molar inclination and the distance between bilateral base bones on two sides when compared after quad helix expansion and after 2-year fol ow-up (P > 0.05). The results indicate that the long-term effect of quad helix expansion is stable with orthopedic effect.

砄bjective: To determine the effects of interleukin 1 receptor antagonist( IL lra) on the production of IL 6 induced by IL 1? in human gingival fibroblasts(HGFs). Methods:HGFs at passage 5 were exposed to various concentrations of IL 1? with or without IL 1r? . IL 6 in the culture medium was measured with a sandwish ELISA assay. Results:IL 6(?g/L) produced by HGFs exposed to IL 1? at the concentrations (?g/L) of 0.1, 1.0, 10 and 100 were 207?40.29, 235?80.78, 370?40.62, 570?68.17 and 737.5?83.47 respectively. While that by HGFs exposed to IL 1? at 10 ?g/L with IL 1r?(?g/L) at 1, 10, 100 and 1 000 were 387.5?49.69, 312.5?26.81, 242.5?25.86 and 217.5?21.65 respectively. Conclusion: IL lra can inhibite the IL 1? induced IL 6 production in HGFs.

Periodontitis is a common chronic inflammatory disease. Recent studies have shown that chronic stress (CS) might modulate periodontal disease, but there are few models of CS-induced periodontitis, and the underlying mechanisms are unclear. The present study established a rat model of periodontitis associated with CS induced by nylon thread ligatures. The severity of periodontitis was evaluated in this model by radiographic and pathological examination. The inflammatory reaction indicated by the elevated serum levels of interleukin (IL)-1β, IL-6 and IL-8 was assessed by enzyme-linked immunosorbent assay. Toll-like receptor-4 (TLR4) and glucocorticoid receptor-α (GR-α) expressions were detected by reverse transcriptase-PCR and western blotting. Open-field tests and serum corticosterone were used to evaluate CS. The results showed that CS induced behavioral changes and increased corticosterone levels of the animals with periodontitis. CS stimulation markedly increased alveolar bone loss, periodontal pocket depth and the number of plaques. It also enhanced the inflammatory reaction. These results suggest that CS accelerated the ligature-induced pathological changes associated with periodontitis. Further analysis of the mechanisms involved showed that GR-α expression was significantly downregulated in periodontal tissues of the animals undergoing CS. Blocking GR-α signaling in lipopolysaccharide and corticosteroid-treated human periodontal ligament fibroblast cells in vitro significantly upregulated the expression of p-Akt (protein kinase B) and TLR4, promoted nuclear factor-κB activity and increased levels of IL-1β, IL-6 and IL-8. This research suggests that CS might accelerate the pathological progression of periodontitis by a GR-α signaling-mediated inflammatory response and that this may be a potential therapeutic target for the treatment of periodontal disease, particularly in patients with CS.
Alveolar Bone Loss ; Animals ; Blotting, Western ; Corticosterone ; Enzyme-Linked Immunosorbent Assay ; Fibroblasts ; Humans ; In Vitro Techniques ; Interleukin-6 ; Interleukin-8 ; Interleukins ; Ligation ; Models, Animal ; Nylons ; Periodontal Diseases ; Periodontal Ligament ; Periodontal Pocket ; Periodontitis* ; Phosphotransferases

This study assessed the roles of chronic stress (CS) in the stimulation of the sympathetic nervous system and explored the underlying mechanisms of periodontitis. Using an animal model of periodontitis and CS, the expression of tyrosine hydroxylase (TH) and the protein levels of the alpha1-adrenergic receptor (alpha1-AR) and beta2-adrenergic receptor (beta2-AR) were assessed. Furthermore, human periodontal ligament fibroblasts (HPDLFs) were stimulated with lipopolysaccharide (LPS) to mimic the process of inflammation. The proliferation of the HPDLFs and the expression of alpha1-AR and beta2-AR were assessed. The inflammatory-related cytokines interleukin (IL)-1beta, IL-6 and IL-8 were detected after pretreatment with the alpha1/beta2-AR blockers phentolamine/propranolol, both in vitro and in vivo. Results show that periodontitis under CS conditions enhanced the expression of TH, alpha1-AR and beta2-AR. Phentolamine significantly reduced the inflammatory cytokine levels. Furthermore, we observed a marked decrease in HPDLF proliferation and the increased expression of alpha1-ARfollowing LPS pretreatment. Pretreatment with phentolamine dramatically ameliorated LPS-inhibited cell proliferation. In addition, the blocking of alpha1-ARsignaling also hindered the upregulation of the inflammatory-related cytokines IL-1beta, IL-6 and IL-8. These results suggest that CS can significantly enhance the pathological progression of periodontitis by an alpha1-adrenergic signaling-mediated inflammatory response. We have identified a potential therapeutic target for the treatment of periodontal disease, particularly in those patients suffering from concurrent CS.
Adrenergic alpha-1 Receptor Antagonists/*therapeutic use ; Animals ; Cells, Cultured ; Cytokines/immunology ; Fibroblasts/immunology/pathology ; Humans ; Lipopolysaccharides/administration & dosage/immunology ; Male ; Periodontal Ligament/cytology/immunology/pathology ; Periodontitis/*drug therapy/*etiology/immunology/pathology ; Phentolamine/*therapeutic use ; Rats ; Rats, Wistar ; Receptors, Adrenergic, alpha-1/analysis/*immunology ; Signal Transduction/drug effects ; *Stress, Physiological/drug effects ; Tyrosine 3-Monooxygenase/analysis/immunology