Peri-implant soft tissue integration of immediately loaded implants in posterior macaque mandible: a histomorphometric study

Background: Today, one critical goal in implant placement is the achievement of optimal soft tissue integration. Reports thus far have demonstrated successful soft tissue preservation in delayed loaded implants placed in anterior jaws. The aim of this study was to histomorphometrically examine the soft tissues around immediately loaded implants placed in the macaque posterior mandible. Methods: Splinted crowns on screw-shaped titanium implants (8 mm length, 3.5 mm diameter) were utilized. Three implants each were placed in the premolar-molar edientulous mandibular segments of 6 adult monkeys (Macaca fascicularis); one side served as the control (delayed loading) and the other as the test sites (immediate loading). The animals were sacrificed after 3 months of loading. Histomorphometry of 6 soft tissue indices including the sulcus depth (SD), junctional epithelium (JE), connective tissue contact (CTC), biologic width (BW = SD + JE + CTC), DIM (distance between the implant top and coronal gingiva), and DIB (distance between the implant top and first implant-to-bone contact) was performed on non-decalcified sections. Results: No significant differences in the mean soft tissue scores (mm) between the test (SD = 0.68 +/- 0.63; JE = 1.71 +/- 1.04; CTC = 1.51 +/- 1.14; DIM = 2.27 +/- 1.18; DIB = 1.32 +/- 1.21; BW 3.9) and control (SD = 0.88 + 0.57; JE = 1.66 + 0.77; CTC 1.24 +/- 0.92; DIM = 2.38 +/- 0.81; DIB = 1.19 +/- 0.91; BW 3.78) groups were observed (P>0.01). Conclusion: These findings suggest that the dimensions of the peri-implant soft tissues were within the biologic range and were not influenced by immediate functional loading or posterior location of the implants in the macaque mandible

HIV Alters Plasma and M. tuberculosis-induced Cytokine Production in Patients with Tuberculosis

To test the hypothesis that HIV infection brings about an alteration in the immune response to tuberculosis (TB), mycobacterial antigen-induced production and plasma levels of the inflammatory cytokine interferon-g (IFN-g) and its regulatory cytokines interleukin-12 (IL-12), IL-18, and IL-10 were determined in patients infected dually with HIV and TB and compared with individuals with either disease and with healthy controls. Peripheral blood mononuclear cells (PBMCs) of TB patients with HIV infection produced lesser amounts of IFN-g and IL-12 compared with TB patients without HIV infection after in vitro stimulation with mycobacterial antigens. There was no difference in antigen-induced IL-18 production in TB patients with or without HIV infection. The in vivo cytokine pattern did not correlate with that seen in vitro. Higher levels of IFN-g, IL-12, and IL-18 were detected in the plasma of TB patients infected with HIV compared with TB patients without HIV infection. The presence of significantly higher plasma levels of proinflammatory cytokines suggests a greater degree of immune activation in individuals with HIV and TB, particularly those with low CD4 counts. In vitro IL-10 production by HIV-positive TB patients was similar to that of the HIV-negative TB group and higher than in HIV-positive individuals without TB, but the plasma levels were similar. HIV infection downregulates the in vitro Th1 cytokine response to TB and simultaneously increases systemic levels of these cytokines