vasoactive-intestinal-peptide and Periodontitis

The aim of the present study was to evaluate the therapeutic efficacy of vasoactive intestinal peptide (VIP), an immunoregulatory molecule, in experimental periodontitis.. Sixty-three male Sprague-Dawley rats were divided into five groups: control; lipopolysaccharide (LPS); LPS + 0.1 nmol VIP; LPS + 1 nmol VIP; and LPS + 10 nmol VIP. Saline was injected into the gingiva of control rats on days 1, 3, and 5, whereas the other groups received injections of Escherichia coli LPS. VIP groups received intraperitoneal injections of relevant dosages on days 2, 4, 6, 8, and 10. The control and LPS groups were given saline instead of VIP in the same manner. On day 11, serum samples were obtained, and rats were sacrificed. Alveolar bone loss; serum levels of tumor necrosis factor-alpha, interleukin (IL)-1beta, -10, and -18, soluble receptor activator of nuclear factor-kappa B ligand (sRANKL), and osteoprotegerin (OPG); and the immune expression of RANKL and OPG were evaluated.. The application of VIP caused a dose-dependent decline in alveolar bone loss compared to the LPS group, but the differences were not significant (P >0.05). A reduction in the histologic findings of inflammation was observed in all VIP groups. The 1- and 10-nmol VIP groups showed significantly lower serum sRANKL and OPG levels compared to the LPS group (P <0.05). The number of positively stained vessels for endothelial OPG was greater in the 1-nmol VIP group than in the LPS group (P <0.05).. When periodontitis was induced by E. coli LPS, VIP downregulated the inflammatory response and inhibited alveolar bone loss, possibly by differentially regulating the tissue levels of RANKL and OPG.

Topics: Alveolar Bone Loss; Animals; Dose-Response Relationship, Drug; Down-Regulation; Endothelium, Vascular; Escherichia coli; Immunologic Factors; Injections, Intraperitoneal; Interleukin-10; Interleukin-18; Interleukin-1beta; Lipopolysaccharides; Male; Osteoprotegerin; Periodontitis; Random Allocation; RANK Ligand; Rats; Rats, Sprague-Dawley; Sodium Chloride; Time Factors; Treatment Outcome; Tumor Necrosis Factor-alpha; Vasoactive Intestinal Peptide

To evaluate the role of the anti-inflammatory neuropeptide vasoactive intestinal peptide (VIP) in periodontal health and disease and to determine the effects of periodontal treatment, resulting in a return to periodontal health, on the levels of VIP in gingival crevicular fluid (GCF).. At baseline, 10 subjects with periodontitis (nine females, one male, mean age 43.0, SD 7.3) started a course of non-surgical periodontal treatment. Clinical indices were measured at one periodontitis and one clinically healthy site at an initial visit and at 8 weeks after the completion of treatment in each subject. A 30-s sample of GCF was collected from each test site using perio paper strips. The volume of GCF was measured and each sample subsequently analysed for VIP by radioimmunoassay. One healthy site was sampled from each member of a control group (10 females, mean age 29.9, SD 8.2 years) with clinically healthy gingiva and no periodontitis.. The clinical condition of all periodontitis sites improved as a result of periodontal treatment. The levels of VIP (pg/30 s sample) in periodontitis-affected sites fell significantly from 302.0 (SD 181.2) at the initial visit to 78.0 (54.4) after treatment, p = 0.007. The reduction in the concentration of VIP (pg/ micro L) in GCF from 524.3 (322.3) to 280.8 (280.2) was not statistically significant. The levels of VIP in clinically healthy sites fell from 115.5.5 (74.3) to 77.8 (32.3), n.s. and the concentration changed little from 883.8 (652.1) to 628.7 (323.3), n.s. There were substantially smaller amounts of VIP (25.8, SD 12.8) pg in healthy sites sampled from control subjects.. VIP is present in GCF in greater quantities in periodontitis-affected than clinically healthy sites. In addition, the reduction in inflammation resulting from effective periodontal treatment is associated with a reduction in the levels of VIP in gingival crevicular fluid.

Topics: Adult; Anti-Inflammatory Agents; Dental Scaling; Female; Follow-Up Studies; Gingiva; Gingival Crevicular Fluid; Gingival Hemorrhage; Humans; Male; Middle Aged; Neuropeptides; Oral Hygiene; Periodontitis; Root Planing; Statistics, Nonparametric; Vasoactive Intestinal Peptide

The histological appearance of the gingiva in children with Down's syndrome (DS) was studied with special reference to inflammatory involvement and innervation. A dense infiltration of inflammatory cells was seen in the propria of most of the DS patients, including a few polymorphonuclear leucocytes. A hyperplasia of the epithelium was also found. The innervation of the gingiva was studied using immunohistochemistry. Nerve fibers as well as nerve bundles immunoreactive to neurofilament (NF) were seen in the propria, while occasionally intraepithelial NF fibers were observed. Calcitonin gene-related peptide (CGRP)-immunoreactive fibers and fiber bundles were also visualized, but they were less abundant than NF fibers. The density of NF and CGRP fibers and fiber bundles was estimated by semiquantitative evaluation. A higher density of NF and CGRP immunoreactive structures was observed in the propria of DS patients compared to the control subjects, while no obvious alteration was seen in their distribution in the propria. In addition, sparsely distributed fibers immunoreactive to peptide histidine isoleucine amide (PHI) and vasoactive intestinal polypeptide (VIP) fibers as well as neuropeptide Y (NPY) and tyrosine hydroxylase (TH) were seen, mainly surrounding blood vessels. A few substance P (SP) fibers were also found, mostly close to the epithelium. No obvious differences of these sparsely distributed fibers were seen in the DS patients compared to controls. Thus, a profound inflammatory involvement of the gingiva of DS patients is seen concomitant with a hyperinnervation of the presumed sensory component of the gingival innervation. In contrast, no alterations were seen in the density of neuronal markers related to autonomic nerve fibers. The sensory hyperinnervation observed is probably not specifically related to DS, but may be due to a sprouting of afferent nerves induced by the inflammatory reaction. However, factors released from the sensory afferents could contribute to the gingival inflammation seen in DS.

Topics: Adolescent; Adult; Calcitonin Gene-Related Peptide; Child; Down Syndrome; Female; Gingiva; Gingivitis; Humans; Immunohistochemistry; Intermediate Filaments; Male; Nerve Fibers; Neuropeptides; Neutrophils; Periodontitis; Vasoactive Intestinal Peptide