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Repopulation of Dentin Surfaces by Periodontal Ligament Cells and Endothelial Cells
Author(s) -
Terranova Victor P.,
Odziemiec Christine,
Tweden Katherine S.,
Spadone Donald P.
Publication year - 1989
Publication title -
journal of periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.036
H-Index - 156
eISSN - 1943-3670
pISSN - 0022-3492
DOI - 10.1902/jop.1989.60.6.293
Subject(s) - periodontal fiber , chemistry , dentin , fibroblast growth factor , regeneration (biology) , microbiology and biotechnology , fibronectin , growth factor , cell growth , adhesion , cell , biochemistry , dentistry , biology , medicine , receptor , organic chemistry
T he 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 125 I–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. 125 I–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 chemoattractant than b–FGF alone for PDL cells. The data indicate that b–FGF can stimulate PDL and human endothelial cell migration and human endothelial cell proliferation. BasicFGF binding is increased by the exposure of type I collagen in dentin.