One objective of periodontal therapy after resolution of the infectious process is to facilitate a new connective tissue attachment to the root dentin surface. Here we report that a selective advantage for attachment and growth can be conferred on human gingival fibroblasts by biochemical manipulation of the dentin surface. Tetracycline HCL treatment of the dentin surface increases binding of fibronectin. The adsorbed fibronectin stimulates fibroblast attachment and growth, while suppressing epithelial cell attachment and growth. This biochemical manipulation may provide a useful approach for the treatment of periodontally involved teeth.
This study examines the effects of root surface demineralization and topical fibronectin as adjuncts to reconstructive periodontal surgery. In 14 beagle dogs, horizontal periodontal defects were surgically induced around the mandibular premolars followed by a 6-week period without plaque control. Reconstructive surgery of the defects was subsequently carried out. The root surfaces were debrided and superficially demineralized with citric acid or tetracycline hydrochloride, with or without subsequent application of fibronectin. Mucoperiosteal flaps were raised to cover most of the crowns and sutured. The animals were sacrificed 12 weeks after surgery and block sections of the teeth and surrounding tissues were processed for histology. Analysis included incidence of furcation defects presenting with an epithelial lining, quantification of connective tissue repair relative to the furcation circumference, and regeneration of alveolar bone relative to the furcation defect height. The incidence of root resorption and ankylosis was also analyzed. Within the limitations of this study it was concluded that: (1) citric acid conditioning of the root surface frequently resulted in complete connective tissue repair of the furcation defect; (2) root resorption and ankylosis were prevalent features of the healing response; (3) citric acid and tetracycline treatment had similar potential to induce connective tissue repair and resulted in corresponding incidences of root resorption and ankylosis; (4) application of fibronectin to demineralized root surfaces did not enhance the amount of connective tissue repair and did not alter the pattern of root resorption and ankylosis.
Recent investigations on regeneration of the periodontium have attempted to define factors involved in the formation of a new connective tissue attachment. One essential biological event involved in tissue regeneration is directed cell migration (chemotaxis). Extracellular matrix proteins have been shown to influence chemotaxis, cell proliferation and differentiation. Recently, the extracellular matrix proteins, fibronectin (FN) and laminin (LM), and the polypeptide, endothelial cell growth factor (ECGF), have been shown to stimulate a variety of biological processes. Current assay systems which attempt to define cell migration are the Boyden chamber assay and a random cell migration assay. Neither assay system adequately defines in vivo cell migration. Here we present a new in vitro assay system that tests the capacity of several biological response modifiers applied on dentin to stimulate a chemotactic and proliferative response from various cell types. The assay system consists of two types of assays. Assay I measures the chemotactic activity of test substances bound to dentin. In this assay cells must actively move through a filter (Nuclepore) towards a factor bound to dentin. Assay II examines the ability of dentin-bound biological response modifiers to stimulate directed movement and proliferation of cells on dentin surfaces. We report that periodontal ligament (PDL) cells migrate towards FN and ECGF; that PDL cell migration is enhanced when dentin is preconditioned with tetracycline HCl; that PDL cells have an increased proliferative response when dentin is conditioned with both FN and ECGF; that gingival epithelial cells have increased migratory and proliferative responses when LM is used to condition dentin; and that there is a reciprocal utilization of biological response modifiers by gingival epithelial cells and PDL cells.
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