Joints.

Last updated Wednesday, January 19, 2005

Joint stability

Factors of stability

A number of factors interact to confer stability, while permitting motion in active human joints. First among these is the shape of the component parts. In the hips, for example, weight bearing drives the femoral head into a relatively deep socket, the acetabulum. The articular members are configured and positioned so that normal loading enhances the closeness of their fit.

Ligaments provide a second major stabilizing influence as they guide and align normal joints through their range of motion. An excellent example is the collateral and cruciate ligaments of the knee. These strong, relatively inelastic structures limit articular motion to flexion and extension.

Within the axes of motion, however, more flexible constraints are required. This need is met by muscles and tendons. Muscular stabilization is perhaps most obvious in the shoulder, which is the quintessential polyaxial joint. The rotator cuff muscles approximate and stabilize the articular surfaces of the shoulder as larger muscles with better leverage provide the power for effective shoulder motion.

Movies

• Hip stability (0.11 MB)
• Knee stability (0.22 MB)
• Shoulder stability (0.50 MB)

Synovial fluid

Synovial fluid contributes significant stabilizing effects as an adhesive seal that freely permits sliding motion between cartilaginous surfaces while effectively resisting distracting forces. This property is most easily demonstrated in small articulations such as the metacarpophalangeal joints. The common phenomenon of "knuckle cracking" reflects the fracture of this adhesive bond. Secondary cavitation within the joint space causes a radiologically obvious bubble of gas that requires up to 30 minutes to dissolve before the bond can be reestablished and the joint can be "cracked" again. This adhesive property depends on the normally thin film of synovial fluid between all intraarticular structures. When this film enlarges as a pathologic effusion, the stabilizing properties are lost.

In normal human joints, a thin film of synovial fluid covers the surfaces of synovium and cartilage within the joint space. The volume of this fluid increases when disease is present to provide an effusion that is clinically apparent and may be easily aspirated for study. For this reason, most knowledge of human synovial fluid comes from patients with joint disease. Because of the clinical frequency, volume, and accessibility of knee effusions, our knowledge is largely limited to findings in that joint.

In the synovium, as in all tissues, essential nutrients are delivered and metabolic by-products are cleared by the bloodstream perfusing the local vasculature. Synovial microvessels contain fenestrations that facilitate diffusion-based exchange between plasma and the surrounding interstitium. Free diffusion provides full equilibration of small solutes between plasma and the immediate interstitial space. Further diffusion extends this equilibration process to include all other intracapsular spaces including the synovial fluid and the interstitial fluid of cartilage. Synovial plasma flow and the narrow diffusion path between synovial lining cells provide the principal limitations on exchange rates between plasma and synovial fluid.

This process is clinically relevant to the transport of therapeutic agents in inflamed synovial joints. Many investigators have made serial observations of drug concentrations in plasma and synovial fluid after oral or intravenous administration. Predictably, plasma levels exceed those in synovial fluid during the early phases of absorption and distribution. This gradient reverses during the subsequent period of elimination when intrasynovial levels exceed those of plasma. These patterns reflect passive diffusion alone, and no therapeutic agent is known to be transported into or selectively retained within the joint space.

Metabolic evidence of ischemia provides a second instance when the delivery and removal of small solutes becomes clinically relevant. In normal joints and in most pathologic effusions, essentially full equilibration exists between plasma and synovial fluid. The gradients that drive net delivery of nutrients (glucose and oxygen) or removal of wastes (lactate and carbon dioxide) are too small to be detected. In some cases, however, the synovial microvascular supply is unable to meet local metabolic demand, and significant gradients develop. In these joints, the synovial fluid reveals a low oxygen pressure (PO2), low glucose, low pH, high lactate, and high carbon dioxide pressure (PCO2). Such fluids are found regularly in septic arthritis, often in rheumatoid disease, and infrequently in other kinds of synovitis. Such findings presumably reflect both the increased metabolic demand of hyperplastic tissue and impaired microvascular supply.

Consistent with this interpretation is the finding that ischemic rheumatoid joints are colder than joints containing synovial fluid in full equilibration with plasma. Like other peripheral tissues, joints normally have temperatures lower than that of the body's core. The knee, for instance, has a normal intraarticular temperature of 32?C. With acute local inflammation, articular blood flow increases and the temperature approaches 37?C. As rheumatoid synovitis persists, however, microcirculatory compromise may cause the temperature to fall as the tissues become ischemic.

The clinical implications of local ischemia remain under investigation. Decreased synovial fluid pH, for instance, was found to correlate strongly with radiographic evidence of joint damage in rheumatoid knees. Other work has shown that either joint flexion or quadriceps contraction may increase intrasynovial pressure and thereby exert a tamponade effect on the synovial vasculature. This finding suggests that normal use of swollen joints may create a cycle of ischemia and reperfusion that leads to tissue damage by toxic oxygen radicals.

Normal articular cartilage has no microvascular supply of its own and, therefore, is at risk in ischemic joints. In this tissue, the normal process of diffusion is supplemented by the convection induced by cyclic compression and release during joint usage. In immature joints, the same pumping process promotes exchange of small molecules with the interstitial fluid of underlying trabecular bone. In adults, however, this potential route of supply is considered unlikely, and all exchange of solutes may occur through synovial fluid. This means that normal chondrocytes are farther from their supporting microvasculature than are any other cells in the body. The vulnerability of this extended supply line is clearly shown in synovial ischemia.

The normal proteins of plasma also enter synovial fluid by passive diffusion. In contrast to small molecules, however, protein concentrations remain substantially less in synovial fluid than in plasma. In aspirates from normal knees, the total protein was only 1.3 g/dL, a value roughly 20% of that in normal plasma. Moreover, the distribution of intrasynovial proteins differs from that found in plasma. Large proteins such as IgM and cr2-macroglobulin are underrepresented, whereas smaller proteins are present in relatively higher concentrations. The mechanism determining this pattern is reasonably well understood. The microvascular endothelium provides the major barrier limiting the escape of plasma proteins into the surrounding synovial interstitium. The protein path across the endothelium is not yet clear; conflicting experimental evidence supports the fenestrae, intercellular junctions, and cytoplasmic vesicles as the predominant sites of plasma protein escape. What does seem clear is that the process follows diffusion kinetics. This means that smaller proteins, which have fast diffusion coefficients, will enter the joint space at rates proportionately faster than those of large proteins with relatively slow diffusion coefficients.

In contrast, proteins leave synovial fluid through Iymphatic vessels, a process that is not size-selective. Protein clearance may vary with joint disease. In particular, joints affected by rheumatoid arthritis (RA) experience significantly more rapid removal of proteins than do those of patients with osteoarthritis. Thus, in all joints, there is a continuing, passive transport of plasma proteins involving synovial delivery in the microvasculature, diffusion across the endothelium, and ultimate Iymphatic return to plasma.

The intrasynovial concentration of any protein represents the net contributions of plasma concentration, synovial blood flow, microvascular permeability, and Iymphatic removal. Specific proteins may be produced or consumed within the joint space. Thus, lubricin is normally synthesized within synovial cells and released into synovial fluid where it facilitates boundary layer lubrication of the cartilage-on-cartilage bearing. In disease, additional proteins may be synthesized, such as IgG rheumatoid factor in RA, or released by inflammatory cells, such as Iysosomal enzymes. In contrast, intraarticular proteins may be depleted by local consumption, as are complement components in rheumatoid disease.

Synovial fluid protein concentrations vary little between highly inflamed rheumatoid joints and modestly involved osteoarthritic articulations. Microvascular permeability to protein, however, is more than twice as great in RA as in osteoarthritis. This marked difference in permeability leads to only a minimal increase in protein concentration, because the enhanced ingress of proteins is largely offset by a comparable rise in Iymphatic egress. These findings illustrate that synovial microvascular permeability cannot be evaluated from protein concentrations unless the kinetics of delivery or removal are concurrently assessed.

Intraarticular pressure

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