Nickel-containing alloys commonly are used in medical and dental applications that place them into long-term contact with soft tissues. The release of Ni ions from these alloys is disturbing because of the toxic, immunologic, and carcinogenic effects that have been documented for some Ni compounds. In particular, Ni ions in solution recently have been shown to cause expression of inflammatory mediators, such as interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha), and intercellular adhesion molecules (ICAMs) from keratinocytes, monocytes, and endothelial cells. However, the ability of the solid alloys themselves to induce these inflammatory effects has not been demonstrated. An in vitro system was used to determine if Ni-containing biomedical alloys could cause secretion of either IL-1beta or TNF-alpha from monocytes or expression of ICAMs on endothelial cells. Pure nickel, titanium, and three biomedical alloys-18-8 stainless steel, NiTi, and Rexillium III-were evaluated. First, it was determined whether or not the alloys or pure metals could cause cytotoxicity to THP-1 human monocytes or human microvascular endothelial cells (HMVECs) by measuring the succinic dehydrogenase (SDH) activity of the cells. Then, using identical conditions of exposure, the secretion of IL-1beta or TNF-alpha from monocytes or ICAM-1 expression on the HMVECs was determined. Only pure nickel suppressed (by 48% compared to Teflon controls) the SDH activity of the HMVECs or THP-1 monocytes. No alloy or metal caused the HMVECs to express ICAM-1, but the NiTi alloy caused a significant (ANOVA/Tukey) secretion of IL-1beta from the THP-1 monocytes. Secretion of TNF-alpha induced by NiTi was detectable but not statistically significant. The levels of IL-1beta secretion from monocytes were sufficient to induce ICAM-1 expression on HMVECs. The release of Ni from the NiTi was a logical suspect in causing the IL-1beta secretion by monocytes, but its role was not confirmed since other alloys, such as Rexillium III, released the same quantities of Ni yet did not activate the THP-1 monocytes. Within the limitations of in vitro conditions, our results indicate that NiTi alloys pose a risk of promoting an inflammatory response in soft tissues by activating monocytes. Further study is needed to substantiate this finding in vivo.

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Dental amalgam fillings interact in a complex way with the environment in the oral cavity as they are subjected to chemical, biological, mechanical, and thermal forces. These forces change the restoration's appearance and properties, while metal ions, amalgam debris, non-metallic corrosion products, and mercury vapor are released into the oral cavity. The phenomena and conditions that affect the amalgam/environment interaction include the chemistry and biochemistry of the environment, formation of biofilms on the amalgam surfaces, existence of localized corrosion cells, galvanic contacts with other metallic restorations, abrasion during mastication, and synergistic effects of the different forces. Corrosion processes result in a degradation of the functional amalgam properties, while tarnishing reactions cause discoloration. Corrosion degradation of amalgam fillings is due mainly to localized corrosion cells in pores and crevices. Corrosion on occlusal surfaces is accelerated by abrasion during mastication, which removes the protective surface films. The average total amounts of metal species, including mercury, released per day in vivo from a restoration have not been determined. Much of the reported indirect evidence for high mercury release rates is either unreliable or controversial. A more detailed investigation is needed and will require the development of more sophisticated techniques of sampling in vivo, as well as both experimental and theoretical modeling in vitro.

Cathodic stripping is used to determine the oxide thickness on copper. For copper oxidized at elevated temperatures the potential-time curve at constant cathodic current density features two distinct regions, corresponding to the reduction of two different oxides. The sequence in which the oxides are reduced at constant current density has been examined here using potential-time measurements and electron spectroscopy for chemical analysis. The results show that the top layer of cupric oxide, if continuous, is cathodically reduced first at a higher potential, followed by reduction of the inner layer of cuprous oxide at a lower potential. This conclusion is at variance with a reduction model used in measurements of the oxide thickness in the industry and accepted as part of a standard specification.

Dissolution of mercury from dental amalgam has been shown to be diminished by the formation of a tin oxide film on the surface of the mercury-rich gamma 1 phase (Marek, 1990b). Since tin oxides dissolve at low pH values (Deltombe et al., 1974), acidic conditions in the oral cavity may cause an increase in the mercury release. The purpose of this study was to determine the effect of acidity in the range of pH 1 to pH 8 on the rate of mercury dissolution in synthetic saliva from tin-free and tin-containing gamma 1 phase and two commercial dental amalgams. The tested hypothesis was that pH affects mercury dissolution only when a protective oxide film dissolves in an acidic environment. After exposures of the specimens for 2 hr or 24 hr in sealed glass bottles, the solutions were analyzed by flameless atomic absorption spectrophotometry for mercury and silver. The results have shown pH-independent mercury dissolution in the range of pH 3 to 8, and a much faster dissolution at pH 1. At all pH values, more mercury dissolved from the tin-free phase than from the tin-containing phase, and the rate of dissolution was lowest for the dental amalgams. The results were affected by the length of the test exposure. The pH independence in a wide range of pH values has been attributed to the atomic mechanism of mercury dissolution. The low rate of mercury dissolution from specimens containing tin has been explained by the formation of a barrier tin oxide film, which dissolved only at the lowest pH. Dissolution of silver at low pH values is believed to have accelerated dissolution of mercury from the tin-free gamma 1 phase. Variation of the dissolution rate with concentration of the dissolved species and kinetics of oxide film dissolution caused the effect of the exposure period.

Behavior of implant alloys exposed simultaneously to tensile stresses and corrosion environments has been examined. In the in vivo studies, a stainless steel and a titanium alloy exhibited cracklike features when loaded to the yield stress sigma y and implanted for 16 weeks. A cobalt-chromium alloy stressed beyond sigma y exhibited them in plastically deformed areas. A cobalt-chromium-nickel-molybdenum alloy appeared to be immune. In vitro samples loaded to various stress levels were immersed in Ringer's solution at 37 degrees C. Half of them were subjected to applied anodic potentials; the remaining control group was not. The applied potentials were dc potentials of magnitude similar to those generated by bioelectric effects. No attempt was made to duplicate time dependence or wave forms. Cracklike features were observed in the stainless steel and in the titanium alloy loaded to or beyond sigma y and polarized for 38 weeks. None were observed below sigma y. For the controls, no cracklike features were observed at any stress level after 53 1/2 weeks. Polarization measurements and potential versus time measurements were performed to study possible mechanisms for crack propagation. These investigations suggest that the in vivo corrosion environment is more severe than a 37 degrees C Ringer's solution because of the influence of both bioelectric effects and organic constituents. The implications of these studies for the performance of prosthetic devices is discussed.

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