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The control specimens had significantly more osteoclasts (p?mTOR inhibitor was no difference in vessel density at the insertion site. The rhPTH specimens also had significantly better collagen fiber organization (p?IRS1 bone and mineralized fibrocartilage formation in this model, consistent with prior studies5, 7, 18 this did not translate into improved biomechanical properties. In fact, the load to failure was lower in the rhPTH-treated animals at 2 weeks. There are several possible reasons that may explain why the improved tissue formation at the healing tendon�Cbone interface did not translate into improvements in biomechanical properties. Simple formation of both bone and fibrocartilage will not strengthen the attachment if the newly formed tissue is not well integrated with the tendon. The newly formed tissue needs to be integrated at the microstructural www.selleckchem.com/products/jq1.html level, with re-establishment of collage fiber continuity, which was not evaluated here. Other ultrastructural parameters such as collagen cross-linking will also affect biomechanical properties. An alteration in the balance of osteoclastic resorption versus osteoblastic bone formation may have an adverse effect on tissue material properties. The rhPTH group had significantly more osteoblasts and procollagen formation at 7 and 28 days, suggesting a possible imbalance between bone resorption and formation. Although rhPTH resulted in more new bone formation, this newly formed bone needs to undergo remodeling in order to gain strength. Exposure to appropriate mechanical loading signals is likely required to direct optimal remodeling of this newly formed tissue. Longer time points may demonstrate a positive effect of rhPTH via improved bone maturation and remodeling over time. Excessive angiogenesis may also have an adverse effect on material properties.