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BACKGROUND: Motion between a tendon graft and bone tunnel may impair graft incorporation and lead to tunnel widening. HYPOTHESIS: Healing of a tendon graft in a bone tunnel is inhibited by graft-tunnel motion. STUDY DESIGN: Controlled laboratory study. METHODS: Anterior cruciate ligament reconstruction was performed in 5 cadaveric rabbit limbs, and 3-dimensional graft-tunnel motion was measured using micro-computed tomography. The authors then performed bilateral anterior cruciate ligament reconstruction in 15 rabbits and used histomorphometry to compare tendon-to-bone healing between the tunnel aperture, midtunnel, and tunnel exit and between the anterior and posterior aspects of the tunnel. RESULTS: Graft-tunnel motion was greatest at the tunnel apertures and least at the tunnel exit in cadaveric testing. Healing of the graft was slowest at the tunnel apertures. Tendon-bone interface width was greater at the aperture than at the tunnel exit for the femoral tunnel (P = .04). There was an inverse correlation between time zero graft-tunnel motion and healing in the femoral tunnel (P = .005). There was closer apposition of new bone to the tendon graft in the posterior half of the interface (P < .05). Osteoclasts were found at the tunnel apertures. CONCLUSION: Although graft-tunnel motion was only measured in cadaveric animals, results suggest that healing may be affected by the local mechanical environment, as graft healing in the femoral tunnel was inversely proportional to the magnitude of graft-tunnel motion. CLINICAL RELEVANCE: Graft-tunnel motion may impair early graft incorporation and may lead to osteoclast-mediated bone resorption, contributing to tunnel widening. Early, aggressive postoperative rehabilitation may have detrimental effects on graft-to-bone healing. [ABSTRACT FROM AUTHOR]

Background: Non-steroidal anti-inflammatory drugs are commonly used to reduce pain and inflammation in orthopaedic patients. Selective cyclooxygenase-2 (COX-2) inhibitors have been developed to minimize drug-specific side effects. However, they are suspected to impair both bone and tendon healing. The objective of this study is to evaluate the effect of COX-2 inhibitor administration on tendon-to-bone healing and prostaglandin E (PGE2) concentration., Methods: Thirty-two New Zealand white rabbits underwent reconstructions of the anterior cruciate ligaments and were randomized into four groups: Two groups postoperatively received a selective COX-2 inhibitor (Celecoxib) on a daily basis for 3 weeks, the two other groups received no postoperative COX-2 inhibitors at all and were examined after three or 6 weeks. The PGE2 concentration of the synovial fluid, the osseous integration of the tendon graft at tunnel aperture and midtunnel section, as well as the stability of the tendon graft were examined via biomechanic testing., Results: After 3 weeks, the PGE2 content of the synovial fluid in the COX-2 inhibitor recipients was significantly lower than that of the control group (p = 0.018). At the same time, the COX-2 inhibitor recipients had a significantly lower bone density and lower amount of new bone formation than the control group (p = 0.020; p = 0.028) in the tunnel aperture. At the 6-week examination, there was a significant increase in the PGE2 content within synovial fluid of the COX-2 inhibitor recipients (p = 0.022), whose treatment with COX-2 inhibitors had ended 3 weeks earlier; in contrast, the transplant stability decreased and was reduced by 37% compared to the controls., Conclusions: Selective COX-2 inhibitors cause impaired tendon-to-bone healing, weaken mechanical stability and decrease PGE2 content of the synovial fluid. The present study suggests a reluctant use of COX-2 inhibitors when tendon-to-bone healing is intended.

Purpose: The aim of this study was to evaluate a subset of matrix metalloproteinases (MMPs) and proinflammatory cytokines within the synovium, from traumatic knee disorders (TKDs) and nontraumatic osteoarthritis (OA)., Methods: MMP-1, MMP-3, interleukin 1beta, and tumor necrosis factor (TNF) alpha gene expression was quantified by use of TaqMan-based real-time polymerase chain reaction (Applied Biosystems, Foster City, CA) in synovial tissue samples obtained from 12 patients with OA and 32 with TKDs. In addition, the levels of serum inflammatory parameter C-reactive protein (CRP) were recorded. At arthroscopy, the amount of chondral damage was graded based on the Outerbridge classification., Results: Quantitative analysis showed no significant differences in the expression levels of MMPs, interleukin 1beta, or TNF-alpha messenger RNA between the synovial tissues of patients with OA and TKD, but CRP level was significantly increased in the OA group. A significant correlation was also seen regarding the gene expression levels between MMP-1 and -3, as well as between CRP and MMPs tested. Furthermore, significant relations between TNF-alpha and MMP-1 plus MMP-3 were observed in the OA synovial tissue. The level of TNF-alpha in the synovial tissue correlated with the time after injury as well as chondral damage in patients with TKD., Conclusions: This study shows similar changes in the inflammatory patterns of synovial tissue of TKD and OA suggesting a likely disease progression. Moreover, the correlation between CRP and MMP expression levels indicates their essential role in joint degeneration in synovial tissue of primary OA patients., Clinical Relevance: TNF-alpha could provide a factor to quantify individual risk for the development of OA., (2010 Arthroscopy Association of North America. Published by Elsevier Inc. All rights reserved.)

Aim: Improvement of the bony incorporation of a soft-tissue graft after ACL reconstruction by local administration of Osteoprotegerin between the bone and tendon graft., Method: Fifteen New Zealand White rabbits underwent unilateral anterior cruciate ligament (ACL) reconstruction using an autologous semitendinosis tendon graft. We compared the effect of three OPG doses (5 microg, 50 microg, or 100 microg) at the tendon-bone interface to the controls (OPG carrier) and ACL reconstruction only. Specimens were analyzed at 3 weeks using radiology, histology and histomorphometry to investigate the effect of OPG on the bony incorporation of the tendon graft., Results: Animals treated with OPG 100 microg had a significant (p = 0.007) increase in newly-formed bone around the graft compared to the control group (0.16 +/- 0.01 mm(2); 0.06 +/- 0.02 mm(2)). No significant differences were found between the controls and the other groups (tendon graft only, OPG 5 microg, and 50 microg) (p > 0.05). Bone mineral density, measured in image-pixel brightness (IPB; reference range: 0-255), along the edge of the bone tunnel was greater in the OPG 100 microg group (169.5 +/- 5.9 IPB) compared to the control group (150.3 +/- 4.3 IPB) but this was not statistically significant (p = 0.083). There was a significant decrease in the number of osteoclasts per high-power microscopic fields (HPF) lining the bone tunnel in the OPG 100 microg group compared to the control group (4.4 +/- 2.5 cells/HPF; 6.4 +/- 1.8 cells/HPF) (p = 0.022). No significant differences were found between the control group and the other groups in osteoclast numbers (p > 0.05)., Conclusion: Since tendon-bone healing requires new bone formation and bone ingrowth around a tendon graft, OPG may improve biologic graft fixation. A potential implication could be earlier return to function or better conditions in revision surgery.