Titanium Substratum Roughness as a Determinant of Human Gingival Fibroblast Fibronectin and α-Smooth Muscle Actin Expression

The most appropriate surface treatment to enhance gingival connective tissue formation on the abutment of dental implants remains undefined, with healing associated with a scar-like response. We have previously shown that topographies with an arithmetic average of the absolute profile height deviations (R-a) = 4.0 induces an anti-fibrotic phenotype in human gingival fibroblasts (HGFs) by causing nascent adhesion formation. With bacterial colonization considerations, we hypothesized that a lower R-a could be identified that would alter adhesion stability and promote a matrix remodeling phenotype. Focal adhesions (FAs) area decreased with increasing roughness, although no differences in cell attachment or proliferation were observed. Alpha smooth muscle actin (alpha-SMA) protein levels were significantly reduced on R-a = 3.0 and 4.0 vs. 0.1 (p < 0.05), with incorporation of alpha-SMA into stress fibers most prominent on R-a = 0.1. Fibronectin protein levels were reduced on 3.0 and 4.0 vs. 0.1 (p < 0.05), and R-a = 1.5 and deeper significantly altered fibronectin deposition. Addition of exogenous TGF-beta 3 increased HGF adhesion size on 0.1 surfaces, but not on any other topography. We conclude that R-a = 1.5 is sufficient to reduce adhesion size and inhibit alpha-SMA incorporation into stress fibers in HGFs, but 3.0 is required in the presence of exogenous TGF-beta 3. Our findings have implications for inhibiting fibrotic tissue formation surrounding percutaneous devices such as dental implants.

Automated summary

The study suggests that specific surface treatments on dental implant abutments can impact the anti-fibrotic phenotype in human gingival fibroblasts, leading to decreased adhesion size and inhibition of fibrotic tissue formation.