Osteoblasts generate an osteogenic microenvironment when grown on surfaces with rough microtopographies

Osteoblasts respond to microarchitectural features of their substrate. On smooth surfaces (tissue culture plastic, tissue culture glass, and titanium), the cells attach and proliferate but they exhibit relatively low expression of differentiation markers in monolayer cultures, even when confluent. When grown on microrough Ti surfaces with an average roughness (Ra) of 4-7 µm, proliferation is reduced but differentiation is enhanced and in some cases, is synergistic with the effects of surface microtopography. In addition, cells on microrough Ti substrates form hydroxyapatite in a manner that is more typical of bone than do cells cultured on smooth surfaces. Osteoblasts also respond to growth factors and cytokines in a surface-dependent manner. On rougher surfaces, the effects of regulatory factors like 1alpha,25(OH)<inf>2</inf>D<inf>3</inf> or 17beta-estradiol are enhanced. The response to the surface is mediated by integrins, which signal to the cell through many of the same mechanisms used by growth factors and hormones. Studies using PEG-modified surfaces indicate that increased differentiation may be related to altered attachment to the surface. When osteoblasts are grown on surfaces with chemistries or microarchitectures that reduce cell attachment and proliferation, and enhance differentiation, the cells tend to increase production of factors like TGF-beta1 that promote osteogenesis while decreasing osteoclastic activity. Thus, on microrough Ti surface, osteoblasts create a microenvironment conducive to new bone formation

Oral biofilm challenge regulates the RANKL-OPG system in periodontal ligament and dental pulp cells

Inflammatory bone destruction triggered by oral bacteria is a hallmark of chronic and apical periodontitis. Receptor activator of NF-κB ligand (RANKL) activates bone resorption, whereas osteoprotegerin (OPG) blocks its action. These are members of the tumor necrosis factor ligand and receptor families, respectively. Although individual oral pathogens are known to regulate RANKL and OPG expression in cells of relevance to the respective diseases, such as periodontal ligament (PDL) and dental pulp (DP) cells, the effect of polymicrobial oral biofilms is not known. This study aimed to investigate the effect of the Zürich in vitro supragingival biofilm model on RANKL and OPG gene expression, in human PDL and DP cell cultures, by quantitative real-time polymerase chain reaction. RANKL expression was more pronouncedly up-regulated in DP than PDL cells (4-fold greater), whereas OPG was up-regulated to a similar extent. The RANKL/OPG ratio was increased only in DP cells, indicating an enhanced capacity for inducing bone resorption. The expression of pro-inflammatory cytokine interleukin-1β was also increased in DP, but not PDL cells. Collectively, the high responsiveness of DP, but not PDL cells to the supragingival biofilm challenge could constitute a putative pathogenic mechanism for apical periodontitis, which may not crucial for chronic periodontitis