The long-term effects of orthodontic appliances in the oral environment and the subsequent leaching of metals are relatively unknown. A method for determining the effects of various types of soldering and welding, both of which in turn could lead to leaching of metal ions, on the growth of osteoblasts, fibroblasts, and oral keratinocytes in vitro, is proposed. The effects of cell behaviour of metal wires on osteoblast differentiation, expressed by alkaline phosphatase (ALP) activity; on fibroblast proliferation, assayed by the 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulphophenil)-2H-tetrazolium-phenazine ethosulphate method; and on keratinocyte viability and migration on the wires, observed by scanning electron microscopy (SEM), were tested. Two types of commercially available wires normally used for orthodontic appliances, with a similar chemical composition (iron, carbon, silicon, chromium, molybdenum, phosphorus, sulphur, vanadium, and nitrogen) but differing in nickel and manganese content, were examined, as well as the joints obtained by electrical resistance welding, traditional soldering, and laser welding. Nickel and chromium, known as possible toxic metals, were also examined using pure nickel- and chromium-plated titanium wires. Segments of each wire, cut into different lengths, were added to each well in which the cells were grown to confluence. The high nickel and chromium content of orthodontic wires damaged both osteoblasts and fibroblasts, but did not affect keratinocytes. Chromium strongly affected fibroblast growth. The joint produced by electrical resistance welding was well tolerated by both osteoblasts and fibroblasts, whereas traditional soldering caused a significant (P < 0.05) decrease in both osteoblast ALP activity and fibroblast viability, and prevented the growth of keratinocytes in vitro. Laser welding was the only joining process well tolerated by all tested cells.

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The activity of hypoxanthine-guanine phosphoribosyltransferase (HPRT) is virtually absent in Lesch-Nyhan disease (LND), an X-linked genetic disorder characterized by uric acid accumulation and neurodevelopmental dysfunction. The biochemical basis for the neurological and behavioral abnormalities have not yet been completely explained. Prior studies of cells from affected patients have shown abnormalities of NAD metabolism. In the current studies, NAD metabolism was evaluated in HPRT gene knock-out mice. NAD content and the activities of the enzymes required for synthesis and breakdown of this coenzyme were investigated in blood, brain and liver of HPRT− and control mice. NAD concentration and enzyme activities were found to be significantly increased in liver, but not in brain or blood of the HPRT− mice. These results demonstrate that changes in NAD metabolism occur in response to HPRT deficiency depending on both species and tissue type.

The enzyme poly(ADP-ribose) polymerase (PARP-1, EC 2.4.2.30) is activated by DNA strand breaks caused by several agents and utilizes NAD to form polyADPR, bound to acceptor proteins. The involvement of PARP-1 in autoimmune diseases has been suggested: antiPARP autoantibodies are described in systemic lupus erythematosus (SLE), DNA strand breaks have been evidenced in systemic sclerosis (SSc). We tested poly(ADP-ribosyl)ation activity and NAD concentration in PMC from patients affected by SLE or SSc and from controls. Lower PARP-1 activity and higher NAD concentration were observed in pathological conditions than controls, supporting the role of PARP-1 activation in modulating NAD concentration.

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