SILICONE GEL ENHANCES THE DEVELOPMENT OF AUTOIMMUNE-DISEASE IN NEW-ZEALAND BLACK MICE BUT FAILS TO INDUCE IT IN BALB CANPT MICE/

Anecdotal evidence links silicone gel breast implants with the develop ment of autoimmune connective tissue disease in women. To investigate whether silicone gel is capable of directly inducing and/or enhancing the development of autoimmune disease, female BALB/cAnPt (BALB/c) and New Zealand Black (NZB) mice were injected subcutaneously with silicon e gel, pristane, a nonmetabolizable substance that can cause plasmacyt omas in BALB/c and NZB mice, or saline and monitored for the developme nt of glomerulonephritis and autoantibody production. NZB, but not BAL B/c, mice spontaneously develop autoantibodies and an autoimmune hemol ytic anemia by 12 months of age. Over a period of 10 months, biweekly screening for proteinuria revealed increases in urinary protein in NZB mice that received multiple injections of either silicone gel or pris tane. In contrast, urinary protein was unaffected in identically treat ed BALB/c mice. Although, silicone gel had no effect on serum titers o f antierythrocyte antibodies in NZB mice, the hematocrits were signifi cantly decreased. Moreover, silicone gel both increased the concentrat ion of IgM anti-type I collagen antibodies and skewed the immunofluore scent staining pattern of serum autoantibodies on HEp-2 cells. In cont rast, silicone gel failed to induce the production of anti-erythrocyte or antinuclear antibodies in BALB/c mice and induced only slight incr eases in IgG anti-type I collagen antibodies. These results suggest th at silicone gel can exacerbate the development of autoimmune disease i n autoimmune NZB mice, but fails to induce disease in normal BALB/c mi ce. This is consistent with several epidemiological studies failing to demonstrate an increase in the incidence of autoimmune disease in wom en with breast implants. However, because silicone gel was able to exa cerbate autoimmune disease in NZB mice, it may play a similar role in the development of autoimmune disease in a small percentage of women w ho are genetically susceptible to such diseases. (C) 1998 Academic Pre ss.