Effect of beverage solutions and toothbrushing on the surface roughness,microhardness, and color stainability of a vitreous CAD-CAM lithium disilicate ceramic

Statement of problem

Computer-aided design and computer-aided manufacturing (CAD-CAM) has enhanced the physicomechanical stability of ceramics. However, various factors in the oral cavity may impair the longevity of restorations by negatively affecting their properties. Appropriate surface treatments such as glaze application or mechanical polishing are necessary to diminish these effects.

Lead alters parathyroid hormone-related peptide and transforming growth factor-beta1 effects and AP-1 and NF-kappaB signaling in chondrocytes.

The skeletal system is an important target for lead toxicity. One of the impacts of lead in the skeleton, the inhibition of axial bone development, is likely due to its effect on the normal progression of chondrocyte maturation that is central to the process of endochondral ossification. Since little is known about the effect of lead on chondrocyte function/maturation, its impact on (1) growth factor-induced proliferation, (2) expression of maturation-specific markers type X collagen and BMP-6, and (3) the activity of AP-1 and NF-kappaB was examined in chick growth plate and sternal chondrocyte models. Exposure to lead alone (1-30 microM) resulted in a dose-dependent inhibition of thymidine incorporation in growth plate chondrocytes. Lead also blunted the stimulation of thymidine incorporation by parathyroid hormone-related peptide (PTHrP) and transforming growth factor-beta1 (TGF-beta1), two critical regulators of chondrocyte maturation. Lead (1 and 10 microM), TGF-beta1 (3 ng/ml) and PTHrP (10(-7) M) all significantly inhibited the expression of type X collagen, a marker of chondrocyte terminal differentiation. However, when in combination, lead completely reversed the inhibition of type X collagen by PTHrP and TGF-beta1. The effect of lead on BMP-6. an inducer of terminal differentiation. was also examined. Independently, lead and TGF-beta1 were without effect on BMP-6 expression, but PTHrP significantly suppressed it. Comparatively, lead did not alter PTHrP-mediated suppression of BMP-6, but in combination with TGF-beta1. BMP-6 expression was increased 3-fold. To determine if lead effects on signaling might play a role in facilitating these events, the impact of lead on NF-kappaB and AP-1 signaling was assessed using luciferase reporter constructs in sternal chondrocytes. Lead had no effect on the AP-1 reporter, but it dose-dependently inhibited the NF-kappaB reporter. PTHrP, which signals through AP-1, did not activate the NF-kappaB reporter and did not affect inhibition of this reporter by lead. In contrast, PTHrP activation of the AP-1 reporter was dose-dependently enhanced by lead. These findings, which establish that chondrocytes are important targets for lead toxicity, suggest that the effects of lead on bone growth are derived from its impact on the modulation of chondrocyte maturation by growth factors and second messenger signaling responses.     

Viral interleukin‐10 gene inhibition of inflammation,osteoclastogenesis, and bone resorption in response to titanium particles

Objective

To evaluate the potential of viral interleukin‐10 (vIL‐10) gene therapy as an approach to prevent wear debris–induced inflammation, osteoclastogenesis, and bone resorption as it relates to periprosthetic osteolysis in patients with total joint replacements.

Methods

Replication‐defective adenovirus vectors expressing vIL‐10 (AdvIL‐10) or LacZ (AdLacZ) target genes were used to transduce fibroblast‐like synoviocytes (FLS) in vitro, and the effects of these cells on wear debris–induced proinflammatory cytokine production and receptor activator of nuclear factor κB ligand + macrophage colony‐stimulating factor splenocyte osteoclastogenesis were assessed by enzyme‐linked immunosorbent assay and tartrate‐resistant acid phosphatase assay. The effects of AdvIL‐10 administration on wear debris–induced osteolysis in vivo were analyzed using the mouse calvaria model, in which AdLacZ was used as the control.

Results

In the presence of AdLacZ‐infected FLS, titanium particle–stimulated macrophages exhibited a marked increase in secretion of tumor necrosis factor α (TNFα) (6.5‐fold), IL‐6 (13‐fold), and IL‐1 (5‐fold). Coculture with AdvIL‐10–transduced FLS suppressed cytokine secretion to basal levels, while addition of an anti–IL‐10 neutralizing antibody completely blocked this effect. The vIL‐10–transduced FLS also inhibited osteoclastogenesis 10‐fold in an anti–IL‐10–sensitive manner. In vivo, titanium implantation resulted in a 2‐fold increase in osteoclasts (P < 0.05) and in a 2‐fold increase in sagittal suture area (P < 0.05). This increase over control levels was completely blocked in mice receiving intraperitoneal injections of AdvIL‐10, all of whom had measurable serum vIL‐10 levels for the duration of the experiment. Immunohistochemistry demonstrated reduced cyclooxygenase 2 and TNFα expression in AdvIL‐10–infected animals.

Conclusion

This study demonstrates that gene delivery of vIL‐10 inhibits 3 processes critically involved in periprosthetic osteolysis: 1) wear debris–induced proinflammatory cytokine production, 2) osteoclastogenesis, and 3) osteolysis.