107 WHOLE BLOOD LEAD (Pb) LEVELS AND PUTATIVE OSTEOARTHRITIS BIOMARKERS IN AFRICAN AMERICAN AND CAUCASIAN MEN: THE JOHNSTON COUNTY OSTEOARTHRITIS PROJECT

Abstract

formation), TRACP (osteoclast number), and GAG release (cartilage turnover). Overall cell viability was monitored using the dye Alamar Blue. Passive release from metabolically inactive femur heads was measured as background. Results: Stimulation of the femur heads with RANKL, PTH, Il-1a and OSM + TNF-a led to an increase in CTX-I release. Adding GM6001 to OSM + TNF-a abrogated the release of CTX-I. Femur heads stimulated with Il-1a, OSM + TNF-a and OSM + TNF-a + GM6001 induced an increase in sGAG release. CTX-II release was increased by RANKL, PTH, Il-1a, OSM + TNF-a and IGF-I. CTX-II release from the OSM + TNFa condition was abrogated when treated with GM6001. The osteoclast marker TRACP increased when stimulated by RANKL, PTH, Il-1a, OSM + TNF-a, OSM + TNF-a + GM6001. PIINP release was reduced when stimulating with Il-1a, OSM + TNF-a, OSM + TNF-a + GM6001, whereas PTH and IGF-I increased PIINP release. Conclusions: We have established a whole tissue model for osteoarthritis consisting of both cartilage and bone, and which is highly responsive to both catabolic and anabolic stimulation. This is useful for testing potential treatments for OA interfering with more than one aspect of the pathological situation. Further it allows for investigating interactions between cartilage and bone cell types. Hopefully, future treatments for OA may be better identified after the establishment of such a system for drug screening.