The effects of hyperglycemia on the biological behavior of human gingival fibroblasts on a titanium surface.

Abstract

It is well known that diabetes mellitus is one of the high-risk factors for periodontitis and also for the failure of implant restorations. Usually, the success of an implant restoration depends on both the good osseointegration and the stable soft tissue interface on the implant neck. A good gingival interface of the implant neck is the barrier that enables implant to resist oral microorganisms and the site of initiation of peri-implantitis. This study sought to investigate the effects of hyperglycemia on the attachment and proliferation of human gingival fibroblasts (HGFs) on pure titanium surfaces. HGFs were cultured in cell culture mediums with different glucose concentrations (i.e., 5.5, 8. 8, 10, and 15 mmol/L) for 7 d and seeded on pure titanium surfaces. The cells that were seeded on the titanium surfaces had been cultured in cell culture mediums with different glucose concentrations for 3 and 7 d. The attached HGFs on the titanium surfaces were counted for all groups using a blood cell counting plate, and the results were statistically analyzed. The morphologies of the attached HGFs on the titanium surfaces were observed for all the groups using a scanning electronic microscope. As the glucose concentrations increased, the number of attached HGFs on the titanium surfaces decreased. The numbers of attached cells in Groups A and B 7 d after being seeded on the titanium surfaces were more than those 3 d after being seeded (P<0.05). The numbers of attached cells in Groups C and D 3 d after being seeded on the titanium were more than those 7 d after being seeded (P<0.05). The scanning electronic microscope showed that the attached cells in Groups A and B proliferated well, and most cells grew one on top of another. Conversely, the attached cells in Groups C and D proliferated sparsely and the cell morphologies were not good. The attachment and proliferation of HGFs on pure titanium surfaces were inhibited by increases in glucose concentrations, and the inhibition was further enhanced by the passage of time.