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Friction and Lubrication in Synovial Joints

When the bearings fail in a machine, they do so because of friction and wear. The engineer responsible for the design of such machines studies these processes, selects the optimal contact surfaces to minimize wear, and chooses the lubricant that most effectively limits the amount of friction. It is axiomatic, however, that friction and wear can never be eliminated from any working bearing.

Our problem is more complex because the living bearings that concern us can, within limits, repair themselves and are therefore renewable. Thus, the fundamental clinical issue is one of balance. As long as repair keeps pace with wear, the living bearing may function normally. When this balance is lost, the bearing is at risk of failure, and it may be useful to dissect out and quantify the opposing processes of wear and repair in order to select the best target for therapeutic intervention. The wear side of this balance largely depends on how effectively the joint is lubricated.

In this issue of The Journal Greg Jay and his colleagues report on the significant progress they have made toward understanding one important component of the normal lubrication system¹. Their work has focused on lubricin, the boundary layer lubricant that was first isolated from synovial fluid and characterized by David Swann, et al over 20 years ago². Current molecular techniques have now permitted full sequencing of its protein core, recognition of its parent gene, tracing its origin to synovial fibroblasts, and identification of 2 other products, including the SZP (superficial zone protein) of cartilage, that are derived from the same gene. Still to come, one hopes, are a more complete characterization of the "glyco" components of this glycoprotein, specific tools to assess the quantity and quality of lubricin in normal and diseased joints, a more thorough assessment of its possible interactions with hyaluronan and phospholipids, comparative studies in other species (that might culminate in a knock-out mouse lacking the comparable gene and its product), and ultimate clinical strategies that would augment and preserve this biologic protector of normal human bearings.

Boundary layer lubricants, like lubricin, reduce friction and wear by providing a smooth and slippery coating for the

contact surfaces just as a layer of ice coats a winter sidewalk. Complementary to this mechanism is an important additional component of hydrodynamic lubrication. Such a system reduces friction by allowing one bearing surface to ride freely over the other on an interposed film of protecting fluid. The magnificent design of cartilage permits this tissue to utilize this mechanism to provide the largest measure of its own protection. Since its matrix is both fluid-filled and compressible, loaded cartilage expresses fluid from its surface and this expressed fluid separates it from its mate³. As a femoral condyle, for instance, glides over a tibial plateau, it exudes water ahead of its own advancing contact surface, thus "greasing the skids" for low friction service. This process has literally been frozen in time by John Clark and his colleagues in recent experiments of appealing simplicity⁴. His design permits normal rabbit joints to be loaded in vitro, immersed in liquid nitrogen, fixed in situ, sectioned, and then examined by scanning electron microscopy. This work confirms the normal cartilagenous compression under load and shows that this process smooths and enlarges the opposing loaded areas. Most importantly, it reveals a continuous film of fluid, 100 nanometers thick, that separates one surface from the other and thereby prevents direct, abrasive contact.

Where does hyaluronan fit in this picture? This huge molecular constituent confers the most conspicuous characteristic of normal synovial fluid, its striking viscosity. It is intuitively attractive to believe that more viscous fluids will be more slippery and are therefore better lubricants. This is largely untrue, however, of the boundary layer mechanism. Test systems that focus on this aspect, such as the latex-on-glass system of Jay, et al, show that lysis of hyaluronan with hyaluronidase has no significant effect, but friction increases substantially when the bathing synovial fluid is pretreated with proteolytic enzymes and lubricin is destroyed⁵. When the cartilage-on-cartilage bearing of the intact joint is studied, however, hyaluronan does become important^6,7. This observation seems entirely consistent with the hydrodynamic aspect of joint lubrication. Articular motion, of course, is inherently cyclic and the flow of viscous synovial fluid is much slower than that of water. Hyaluronan would seem most valuable in minimizing outflow within the interposed film of fluid during the brief period when any one area of cartilage is under a moving load.

The clinical connotations of these concepts remain confusing. We perceive friction in our patients’ joints mainly thorough crepitus, but this measure is so coarse that most crepitant joints must already be well down the road toward bearing failure. By history, by examination, and in the laboratory we have no current tools that permit us to recognize those less symptomatic joints with increased friction that are likely to wear out soonest. The available evidence suggests, however, that accelerated wear will be most likely in joints affected by inflammatory disease⁸. In symptomatic rheumatoid joints, for instance, metalloprotease activity should limit lubricin effectiveness, while hyaluronan quantity and quality are obviously diminished. Perhaps the "robust rheumatoid" patient who remains physically active but loses more cartilage is an example of a setting in which rheumatologists should be more concerned about articular friction and wear. Experienced clinicians may remember other cases (many of my own being in spondyloarthropathies) where focal cartilage loss came fast, and wonder whether impaired lubrication and enhanced friction may have played a role.

In contrast to inflammatory disease, there is less reason to expect increased friction in osteoarthritic joints, since hyaluronan quantity and quality are relatively preserved and lubricin seems less likely to be attacked by proteolytic enzymes, but this is the setting where most efforts are now made to limit wear. Loss of excess weight and simple off-loading measures both seem to be effective and obviously make sense in any articular disease. What, however, is the appropriate rationale for the serial hyaluronan injections that are now in such widespread usage around the globe? This is the single intervention intended to provide needed lubrication to diseased human joints, but there is a serious flaw in the logic^9,10. The operant concept that such viscosupplementation will "restore rheological homeostasis" seems clearly at variance with the many studies demonstrating relatively rapid efflux and limited articular residence of the injected hyaluronan¹¹.

In the history of any affected knee, each hyaluronan injection would seem to be little more than a very temporary patch in a long, bumpy road. And yet they seem to help many patients¹². Do they indeed induce some abiding effect on the cartilage matrix, the chondrocyte, the synovium, or some other articular component that ultimately leads to less wear of cartilage and a longer bearing life? If so, they will both help our patients and add to our knowledge of how normal joints work and why they fail in disease. The history of our field contains numerous examples of flawed logic (gold injections) or serendipitous observations (chloroquine) that produced clinical benefits we are still trying to understand. Perhaps hyaluronan injections belong on this list. Given our present knowledge of articular lubrication, however, it seems unlikely that transient changes in synovial fluid viscosity will produce an enduring, clinical response.

PETER A. SIMKIN, MD,
Professor of Medicine,
Division of Rheumatology,
Box 356428,
University of Washington,
Seattle, WA 98195, USA.

Address reprint requests to Dr. Simkin.

REFERENCES

1.Jay GD, Britt DE, Cha C-J. Lubricin is a product of megakaryocyte stimulating factor gene expression by human synovial fibroblasts. J Rheumatol 2000;27:594-600.

2.Swann DA, Sotman S, Dixon M, Brooks C. The isolation and partial characterization of the major glycoprotein from the articular lubricating fraction from bovine synovial fluid. Biochem J 1977;161:473-85.

3.Mow VC, Ateshian GA, Spilker RL. Biomechanics of diarthrodial joints: a review of twenty years of progress. J Biomech Eng 1993;115:460-7.

4.Clark JM, Norman AG, Kaab MJ, Notzli HP. The surface contour of articular cartilage in an intact, loaded joint. J Anat 1999; 195:45-56.

5.Linn FC, Radin EL. Lubrication of animal joints. III. The effect of certain alterations of the cartilage and lubricant. Arthritis Rheum 1968;11:674-82.

6.Mabuchi K, Obara T, Ikegami K, Yamaguchi T, Kanayama T. Molecular weight independence of the effect of additive hyaluronic acid on the lubricating characteristics in synovial joints with experimental deterioration. Clin Biomech 1999;14:352-6.

7.Murakami T, Higaki H, Sawae Y, Ohtsuki N, Moriyama S, Nakanishi Y. Adaptive multimode lubrication in natural synovial joints and artificial joints. Proc Inst Mech Eng 1998;212:23-35.

8.Reimann I. Pathological human synovial fluids. Viscosity and boundary lubricating properties. Clin Orthop 1976;119:237-41.

9.Marshall KW. Viscosupplementation for osteoarthritis: current status, unresolved issues, and future directions. J Rheumatol 1998;25:2056-8.

10.Simon LS. Viscosupplementation therapy with intra-articular hyaluronic acid. Fact or fantasy? Rheum Dis Clin North Am 1999;25:345-57.

11.Fraser JR, Laurent TC, Laurent UB. Hyaluronan: its nature, distribution, functions and turnover. J Intern Med 1997;242:27-33.

12.Wobig M. Hylan G-F 20 (Synvisc) for the treatment of osteoarthritis of the knee: Clinical studies and practical considerations. J Clin Rheumatol 1999;5 Suppl 6:12-7.