Lubricin surface modification improves tendon gliding after tendon repair in a canine model in vitro.

This study investigated the effects of lubricin on the gliding of repaired flexor digitorum profundus (FDP) tendons in vitro. Canine FDP tendons were completely lacerated, repaired with a modified Pennington technique, and treated with one of the following solutions: saline, carbodiimide derivatized gelatin/hyaluronic acid (cd-HA-gelatin), carbodiimide derivatized gelatin to which lubricin was added in a second step (cd-gelatin + lubricin), or carbodiimide derivatized gelatin/HA + lubricin (cd-HA-gelatin + lubricin). After treatment, gliding resistance was measured up to 1,000 cycles of simulated flexion/extension motion. The increase in average and peak gliding resistance in cd-HA-gelatin, cd-gelatin + lubricin, and cd-HA-gelatin + lubricin tendons was less than the control tendons after 1,000 cycles (p < 0.05). The increase in average gliding resistance of cd-HA-gelatin + lubricin treated tendons was also less than that of the cd-HA-gelatin treated tendons (p < 0.05). The surfaces of the repaired tendons and associated pulleys were assessed qualitatively with scanning electron microscopy and appeared smooth after 1,000 cycles of tendon motion for the cd-HA-gelatin, cd-gelatin + lubricin, and cd-HA-gelatin + lubricin treated tendons, while that of the saline control appeared roughened. These results suggest that tendon surface modification can improve tendon gliding ability, with a trend suggesting that lubricin fixed on the repaired tendon may provide additional improvement over that provided by HA and gelatin alone.

Lubricin surface modification improves extrasynovial tendon gliding in a canine model in vitro.

BACKGROUND: Lubricin is the principal lubricant in synovial fluid. Although lubricin has been identified in tendons, especially on the surface of intrasynovial tendons such as the flexor digitorum profundus tendon, its ability to improve tendon gliding is unknown. The purpose of this study was to investigate the effects of exogenously applied lubricin on the gliding of extrasynovial tendons in a canine model in vitro. METHODS: Forty peroneus longus tendons, along with the proximal pulley in the ipsilateral hind paw, were harvested from adult mongrel dogs. After the gliding resistance of the normal tendons was measured, the tendons were treated with one of the following solutions: saline solution, lubricin, carbodiimide derivatized gelatin (cd-gelatin), carbodiimide derivatized gelatin with hyaluronic acid (cd-HA-gelatin), or carbodiimide derivatized gelatin to which lubricin had been added in a second step (cd-gelatin plus lubricin). Tendon gliding resistance was measured for 1000 cycles of simulated flexion-extension motion of the tendon. Transverse sections of the tendons were examined qualitatively at 100x magnification to estimate surface smoothness after 1000 cycles. RESULTS: There was no significant difference in the gliding resistance between the tendons treated with saline solution and those treated with lubricin alone, or between the tendons treated with cd-HA-gelatin and those treated with cd-gelatin plus lubricin; however, the gliding resistance of the tendons treated with cd-gelatin plus lubricin was significantly lower than that of the tendons treated with saline solution, lubricin alone, or cd-gelatin alone (p < 0.05). After 1000 cycles of tendon motion, the gliding resistance of the tendons treated with cd-gelatin plus lubricin decreased 18.7% compared with the resistance before treatment, whereas the gliding resistance of the saline-solution-treated controls increased >400%. The tendon surfaces treated with cd-gelatin plus lubricin or with cd-HA-gelatin appeared smooth even after 1000 cycles of tendon motion, whereas the other surfaces appeared roughened. CONCLUSIONS: While the addition of lubricin alone did not affect friction in this tendon gliding model, the results indicate that lubricin may preferentially adhere to a tendon surface pretreated with cd-gelatin and, when so fixed in place, lubricin does have an important effect on tendon lubrication.

Association between friction and wear in diarthrodial joints lacking lubricin.

OBJECTIVE: The glycoprotein lubricin (encoded by the gene Prg4) is secreted by surface chondrocytes and synovial cells, and has been shown to reduce friction in vitro. In contrast to man-made bearings, mammalian diarthrodial joints must endogenously produce friction-reducing agents. This study was undertaken to investigate whether friction is associated with wear. METHODS: The lubricating ability of synovial fluid (SF) samples from humans with genetic lubricin deficiency was tested in vitro. The coefficient of friction in the knee joints of normal and lubricin-null mice was measured ex vivo; these joints were also studied by light and electron microscopy. Atomic force microscopy was used to image and measure how lubricin reduces friction in vitro. RESULTS: SF lacking lubricin failed to reduce friction in the boundary mode. Joints of lubricin-null mice showed early wear and higher friction than joints from their wild-type counterparts. Lubricin self-organized and reduced the work of adhesion between apposing asperities. CONCLUSION: These data show that friction is coupled with wear at the cartilage surface in vivo. They imply that acquired lubricin degradation occurring in inflammatory joint diseases predisposes the cartilage to damage. Lastly, they suggest that lubricin, or similar biomolecules, will have applications in man-made devices in which reducing friction is essential.

Lubricating ability of aspirated synovial fluid from emergency department patients with knee joint synovitis.

OBJECTIVE: To determine if joint effusions encountered in the emergency department (ED) requiring arthrocentesis possess normal lubricating ability or evidence cartilage degeneration. Chondroprotection of articulating joint surfaces is provided by lubricin, a mucinous glycoprotein that is a product of megakaryocyte-stimulating factor gene (GenBank U70136) expression. Loss of synovial fluid's (SF) lubricating ability has been implicated in the pathogenesis of degenerative joint disease. METHODS: A retrospective ED observational study from May 1, 1999, to October 1, 2000, of adult and pediatric patients presenting with radiographically negative knee joint complaints and clinical evidence of joint effusion. Knee joints were aspirated by the emergency physician and the synovial fluid tested for lubricating ability and collagen type II degeneration. Lubricating ability was assayed in vitro in an arthrotripsometer oscillating latex apposed to polished glass under a load of 0.35 106 N/m2. Results were reported as the coefficient of friction ( micro ) relative to that of a 0.9% NaCl control; negative deltamicro value indicates lubrication. Comparisons of deltamicro were made to normal SF and aspirates from patients with osteoarthritis (OA) and rheumatoid arthritis. Collagen type II fragments were measured by a novel sandwich ELISA. RESULTS: Synovial fluid aliquots (n = 57) lubricated poorly with deltamicro = -0.045 (95% confidence interval = -0.006, -0.083) compared to normal SF with D micro = -0.095 (95% CI = -0.088, -0.101). Only 20.6% of knee joint aspirates possessed normal lubricating ability. An association exists between nucleated cell count and deltamicro described by a logarithmic function. Collagen type II fragments were present in aspirates at a concentration of 0.636 microg/ml (95% CI 0.495-0.777 microg/ml), significantly higher than 0.173 microg/ml (95% CI 0.154-0.193 microg/ml) in the OA comparison group. CONCLUSION: Knee joints with synovitis, commonly encountered in the ED, are frequently nonlubricated bearings and display catabolism of collagen type II. This may play a role in acute cartilage destruction ultimately resulting in posttraumatic OA.