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Concerns exist over the potential release of elevated levels of metal ions such as Ni and Be from Ni-Cr dental casting alloys, due to their susceptibility to accelerated corrosion. In this investigation, we evaluated the release of metal ions from four commercial Ni-Cr alloys, representing a range of compositions, in three-day cell culture tests. Metal ion release, as measured by atomic absorption spectroscopy, was correlated to changes in cellular morphology, viability, and proliferation. The results showed that the test alloys and their corrosion products did not affect cellular morphology or viabilities, but did decrease cellular proliferation. The types and amounts of metal ions released, which corresponded to the alloys' reported surface and corrosion properties, also correlated to observed decreases in cellular proliferation after 72 h. Neptune, which caused the smallest decrease in cellular proliferation as compared with control cells, released the lowest amount of corrosion products, due to its corrosion-resistant, high-Cr-Mo-containing, homogeneous surface oxide. The other test alloys, which were susceptible to accelerated corrosion processes, released higher levels of metal ions that correlated to larger decreases in thymidine incorporation. Metal ion levels increased with test time for all alloys but were not proportional to bulk alloy compositions. Ni ions were released at slightly higher than bulk alloy compositions, while Be was released at from four to six times that of bulk alloy compositions. The elevated release of Be ions was associated with reduced cellular proliferation.(ABSTRACT TRUNCATED AT 250 WORDS)

Metallic materials utilized for the construction of intra-oral and implant dental restorations include a wide range of relatively pure metals and multicomponent alloys. Basic corrosion and biodegradation properties of these alloys have been studied by both in vitro and in vivo techniques. These property characteristics have been shown to be dependent on composition and metallurgical state, combinations within a construct, surface conditions, mechanical aspects of function, and the local and systemic host environment. The susceptibility of these metallic materials to various forms of biodegradation will be presented, with emphasis on corrosion.

The widespread success of clinical implantology stems from bone's ability to form rigid, load-bearing connections to titanium and certain bioactive coatings. Adhesive biomolecules in the extracellular matrix are presumably responsible for much of the strength and stability of these junctures. Histochemical and spectroscopic analyses of retrievals have been supplemented by studies of osteoblastic cells cultured on implant materials and of the adsorption of biomolecules to titanium powder. These data have often been interpreted to suggest that proteoglycans permeate a thin, collagen-free zone at the most intimate contact points with implant surfaces. This conclusion has important implications for the development of surface modifications to enhance osseointegration. The evidence for proteoglycans at the interface, however, is somewhat less than compelling due to the lack of specificity of certain histochemical techniques and to possible sectioning artifacts. With this caveat in mind, we have devised a working model to explain certain observations of implant interfaces in light of the known physical and biological properties of bone proteoglycans. This model proposes that titanium surfaces accelerate osseointegration by causing the rapid degradation of a hyaluronan meshwork formed as part of the wound-healing response. It further suggests that the adhesive strength of the thin, collagen-free zone is provided by a bilayer of decorin proteoglycans held in tight association by their overlapping glycosaminoglycan chains.