The bone matrix is composed mostly of collagen, but the initial and continuous presence of fibronectin was found to be crucial for collagen matrix integrity in vitro. It has been assumed that osteoblasts produce the fibronectin required for bone matrix formation. Using transgenic mice, we conditionally deleted fibronectin in the osteoblasts and in the liver using the cre-loxP system. We also used mice with mutated fibronectin and conditionally deleted b 1 -integrin in osteoblasts to identify the receptor involved in fibronectin effects on osteoblasts. Conditional deletion of fibronectin in the differentiating osteoblasts [using the 2.3 kb collagen-a1(I) promoter] failed to show a decrease in fibronectin amount in the bone matrix despite evidence of successful deletion. Using these mice we established that osteoblast-derived fibronectin solely affects osteoblast function. This effect was not mediated by integrins that bind to the RGD motif. Conditional deletion of fibronectin in the liver showed a marked decrease in fibronectin content in the matrix associated with decreased mineral-to-matrix ratio and changed biomechanical properties but had no effect on osteoblasts or osteoclasts. In conclusion, osteoblast fibronectin affects osteoblasts function. This does not seem to be mediated by the RGD motif on fibronectin. In contrast, liver-derived fibronectin affects bone matrix properties without affecting osteoblast or osteoclast function. A novel role for liver-derived circulating fibronectin thus was defined and delineated from that of locally produced fibronectin. ß
Prostaglandin E2 (PGE2), thromboxane A2 (TXA2), and prostacyclin (PGI2) are naturally occurring metabolites of arachidonic acid which have been associated with inflammation. To assess the relative importance of these mediators in periodontal diseases, the levels of all three were measured by radioimmunoassay in human tissues removed during surgery. TXA2 and PGI2 were determined as their stable hydrolysis products thromboxane B2 (TXB2) and 6‐keto‐prostaglandin F1α (6‐K‐PGF1α), respectively. Tissues from periodontal pockets were separated into superficial (n = 8) and deep (n = 22) samples. Noninflamed gingival samples (n = 3) were taken from distal wedges with no clinical evidence of periodontal disease. Most of the samples taken from deep sites (73%) had measurable PGE2 with a mean level of 122 pg/mg. Half of these samples also had measurable TXB2 which correlated positively with levels of PGE2. Half of the superficial gingival samples had detectable levels of PGE2, and none had detectable TXB2. 6‐K‐PGF1α was found in virtually all samples but at somewhat lower levels in noninflamed tissue. Neither PGE2 nor TXB2 were detected in noninflamed samples.
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