What Are the Contributing Factors for Postsurgical Relapse After Two-Jaw Surgery in Patients With Cleft Lip and Palate.

The purpose of this study was to investigate the amount and pattern of postsurgical relapse after 2-jaw surgery in cleft lip and palate patients in terms of the sagittal and vertical aspects. The samples consisted of 21 adult patients who had the similar initial skeletodental pattern before surgery and underwent 2-jaw surgery. They were divided into high relapse (n = 11) and low relapse groups (n = 10) (criteria, 30% forward relapse of the B point). After the cephalometric variables of cephalograms taken at 1 month before surgery (T0), immediately after surgery (T1), and at least 1 year after surgery (T2) were measured, the Wilcoxon test, Mann-Whitney U test, and Pearson correlation test were performed for statistical analysis. When compared with the low relapse group, the high relapse group exhibited significant counterclockwise rotation of the distal segment of the mandible resulting in more forward movement of the mandible and significant labioversion of the maxillary incisors during T1-T2. The amount of postsurgical relapse of the mandible had a positive relationship with the amounts of setback and clockwise rotation of the mandible with surgery. In addition, the more decrease in overbite through surgery occurred, the more relapse (forward movement of the mandible) produced. Therefore, for the prevention of significant postsurgical relapse of the mandible in cleft patients, it is necessary to reduce unnecessary clockwise rotation of the mandible and to increase the vertical stability of maxilla during orthognathic surgery.

Repression of TNF-alpha-induced IL-8 expression by the glucocorticoid receptor-beta involves inhibition of histone H4 acetylation.

Increased expression of a number of proinflammatory genes, including IL-8, is associated with inflammatory conditions such as asthma. Glucocorticoid receptor (GR)beta, one of the GR isoforms, has been suggested to be upregulated in asthma associated with glucocorticoid insensitivity and to work as a dominant negative inhibitor of wild type GRalpha. However, recent data suggest that GRbeta is not a dominant negative inhibitor of GRalpha in the transrepressive process and has its own functional role. We investigated the functional role of GRbeta expression in the suppressive effect of glucocorticoids on tumor necrosis factor (TNF)-alpha-induced IL-8 release in an airway epithelial cell line. GRbeta expression was induced by treatment of epithelial cells with either dexamethasone or TNF-alpha. GRbeta was able to inhibit glucocorticoid-induced transcriptional activation mediated by binding to glucocorticoid response elements (GREs). The suppressive effect of dexamethasone on TNF-alpha-induced IL-8 transcription was not affected by GRbeta overexpression, rather GRbeta had its own weak suppressive activity on TNF-alpha-induced IL-8 expression. Overall histone deacetylase activity and histone acetyltransferase activity were not changed by GRbeta overexpression, but TNF-alpha-induced histone H4 acetylation at the IL-8 promoter was decreased with GRbeta overexpression. This study suggests that GRbeta overexpression does not affect glucocorticoid-induced suppression of IL-8 expression in airway epithelial cells and GRbeta induces its own histone deacetylase activity around IL-8 promoter site.