The regeneration of connective tissue attachment is a major goal of clinical periodontics. Recent investigations on biochemically mediated periodontal regeneration have attempted to define the various biological response modifiers which may provide a mechanism for periodontal regeneration. Fibronectin and endothelial cell growth factor have been shown to selectively enhance periodontal ligament (PDL) cell adhesion, migration, and proliferation. In addition, dentin preconditioned with tetracycline HCl (TTC) or citric acid (CA) supports PDL cell adhesion, presumably by exposing collagen fibers. We have now extended these studies to include basic fibroblast growth factor (b-FGF) as a potential meditor of periodontal regeneration. Using AFSCM (assays for specific cell migration), b-FGF in concentrations as low as 10 ng per dentin block significantly stimulated PDL cell chemotaxis, while the antibody against b-FGF inhibited both the chemotactic and proliferative characteristics of the mitogen. We also found that 5 ng and above of b-FGF per dentin block significantly stimulated human endothelial cell migration and proliferation. Using 125I-b-FGF, we demonstrated that the factor binds to native dentin. This binding was increased when the dentin blocks were preconditioned by TTC or CA and reduced when the dentin was subsequently treated with collagenase. 125I-b-FGF also bound with moderate affinity to a type I collagen affinity column whereas the binding to a hydroxylapatite affinity column was negligible. The combination of FN and b-FGF was a marginally more potent chemo-attractant than b-FGF alone for PDL cells.(ABSTRACT TRUNCATED AT 250 WORDS)

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The present study was conducted to evaluate the response of adenoidal T cells and B cells in the production of immunoglobulins. There appears to be a consistent inability of adenoidal T cells to turn on B cells to mature into immunoglobulin-secreting plasma cells. This phenomenon did not appear to be due to suppressor activity of adenoidal T cells because T cells from other sources appeared to effectively result in adenoidal B cell maturation, even in the presence of adenoidal T cells. Both tonsils and adenoids appear to have defective IL-2 production, in response to both mitogens and specific antigens. It is hypothesized that a cytokine(s) may be released in adenoids that downregulate IL-2 production and result in immune suppression in the adenoids of children with recurrent otitis media and chronic sinusitis.

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