Each part of a joint has one or more specific functions that are essential for the overall performance of the joint.
Therefore, anything that affects one part of a joint will disrupt the total function of the joint. Likewise, anything that affects joint motion will affect all the structures that constitute that joint. This relationship between form and function is essential for therapists to remember during rehabilitation after injury. For example, when a bone is broken, the fracture may be the main injury that dictates subsequent treatment, but lack of motion and decreased loading also will affect cartilage, ligaments, joint capsule, tendons, and muscles. The ideal rehabilitation protocol considers the behavior of all the affected structures and in- cludes interventions tailored to induce adaptations in each structure. This means understanding the time course and nature of the adaptation of each tissue to altered loading conditions.
Complex joints are more likely to be affected by injury, disease, or aging than are simple joints. Complex joints have more parts and are subject to more wear and tear than are stability joints. The function of the complex joints depends on a number of interrelated factors. For example, the capsule must produce synovial fluid, which must be of the appropriate composition and of sufficient quantity to lubricate and nourish the joint. The hyaline cartilage must be smooth enough that the joint surfaces can move easily, yet permeable enough to receive nourish- ment from the joint fluid. The cartilage must undergo periodic compressive loading and unloading to facilitate movement of the fluid, and the collagen network must be intact to contain the fluid attracted to the PGs. The ligaments and capsules must be strong enough to provide sufficient support for stability and yet be flexible enough to permit normal joint motion. Tendons must be able to withstand the forces generated by muscles as they produce movement.
Disease
The general effects of disease, injury, immobilization, and overuse may be illustrated by using the normal function of a joint structure as a basis for analysis. For example, when the synovial membrane of a joint is affected by a disease like rheumatoid arthritis, the production, and perhaps the composition, of the synovial fluid changes. Lubrication of the joint is also affected. The disease process and the Joint motions commonly include a combination of slid-
ing, spinning, and rolling. Although we typically use anatomical landmarks to represent the axis of rotation for various joints, the combination of sliding and spinning or rolling produces curvilinear motion and a moving axis of motion. An axis that moves during rolling or sliding mo- tions forms a series of successive points (or axis locations).
The axis of rotation at any particular point in the joint motion is called the instantaneous axis of rotation (IAR).
Moving axes of rotation occur most notably when opposing articular surfaces are of unequal size. In some joints, such as the shoulder, the articulating surface of the moving bone (humerus) is larger than the surface of the stabilized compo- nent (glenoid fossa of the scapula). In other joints, such as the metacarpophalangeal and interphalangeal joints of the fingers, the articulating surface of the moving bone is smaller than the surface of the stabilized component. When the articulating surface of a moving component is larger than the stabilized component, a pure motion such as rolling would result in the larger moving component’s rolling off the smaller articulating surface before the motion is completed. Therefore, combination motions, in which a moving component rolls in one direction and slides in the opposite direction, help to increase the ROM available to the joint and keep opposing joint surfaces in contact with each other. The rolling and sliding arthrokinematic move- ments of the articular surfaces are not usually visible and thus have not been described in the traditional classification system of joint movement. However, these arthrokinematics motions are considered in the six degrees of freedom model described by White and Panjabi.27These authors have sug- gested that motion at the intervertebral symphysis joints between the bodies of the vertebrae in the vertebral column occurs in six planes, around three axes. The implication is that motion at the joints of the body might be more thor- oughly described by using a six-degrees-of-freedom model, as is done to describe available motions in Chapter 1 and at many of the joints covered in this text.
All synovial joints have a close-packed position in which the joint surfaces are maximally congruent and the ligaments and capsule are maximally taut. The close- packed position is usually at the extreme end of a ROM.
In the close-packed position, a joint possesses its greatest stability and is resistant to tensile forces that tend to cause distraction (separation) of the joint surfaces. Little or no joint play is possible. The position of full extension is the close-packed position for the humeroulnar, knee, and in- terphalangeal joints.6,29In the loose-packed position of a joint, the articular surfaces are relatively free to move in relation to one another. The loose-packed position of a joint is any position other than the close-packed position, although the term is most commonly used to refer to the position at which the joint structures are most lax and the joint cavity has a greater volume than in other positions.
In the loose-packed position, the joint has a maximum amount of joint play (accessory movements). An exter- nally applied force, such as that applied by a therapist or physician, can produce movement of one articular surface
structures. Immobilization is particularly detrimental to joint structure and function. Immobilization may be exter- nally imposed by a cast, bedrest, weightlessness, or denerva- tion or may be self-imposed as a reaction to pain and inflam- mation. An injured joint subjected to inflammation and swelling will assume a loose-packed position to accommo- date the increased volume of fluid within the joint space.
This position may be referred to as the position of comfort because pain is decreased in this position. Each joint has a position of minimum pressure and maximum volume. For the knee and hip joints, the position of comfort is between 30° and 45° of flexion; for the ankle joint, the position is at 15° of plantar flexion.29If the joint is immobilized for a few weeks in the position of comfort, the joint capsule will adapt (shorten), and contractures108will develop in the surround- ing soft tissues. Consequently, resumption of a normal range of joint motion will be difficult.
Effects on Ligament and Tendon
Ligaments and tendons adapt to decreased load by decreas- ing their collagen content and reducing cross-linking among collagen molecules, although their overall size may remain the same. The tissue thus weakens, and the resump- tion of previously normal loading may cause increased stress and strain.16,17The musculotendinous junction of tendons loses its interdigitating structure when not loaded, which makes it weaker.89The time course of these adaptations is fairly rapid. Ligaments and tendons show a 50% decrease in tensile strength and stiffness after 8 weeks of immobiliza- tion.16,17It is assumed that ligaments and tendons eventually recover their mechanical properties, but the time course of this recovery appears to be slow, and the total time for recovery is unknown. In general, the time course for the loss of mechanical properties occurs over weeks, whereas recovery can take 12 to 18 months or more.21Gradual re- loading is necessary to restore tendon and ligament strength.
Effects on Articular Surfaces and Bone
The effects of immobilization are not confined to the surrounding soft tissues but may also affect the articular surfaces of the joint and the underlying bone. Biochemical and morphological changes may include: proliferation of fibrofatty connective tissue within the joint space, adhe- sions between the folds of the synovium, atrophy of carti- lage, regional osteoporosis, weakening of ligaments at their insertion sites as a result of osteoclastic resorption of bone and Sharpey’s fibers, a decrease in the PG content, and in- crease in the water content of articular cartilage.32,109,110 Thinning and softening of the articular cartilage occur, and deformation under compressive test load increases up to 42%. As a result of changes in joint structures brought about by immobilization, decreases may be evident in the ROM available to the joint, the time between loading and failure, and the energy-absorbing capacity of the bone- ligament complex. Swelling or immobilization of a joint also inhibits and weakens the muscles surrounding the changes in joint structure that occur in rheumatoid arthri-
tis involve far more than just synovial fluid alteration, but the disease does change the composition and the quantity of the synovial fluid. In another type of arthritis, os- teoarthritis, which may be genetic and/or mechanical in origin, the cartilage is the focus of the disease process.
Erosion and splitting of the cartilage occur. As a result, friction is increased between the joint surfaces, thus fur- ther increasing the erosion process.
Injury
Joint support is decreased after injury to one or more of its components. If a table has an unstable joint between a leg and the table top, damage and disruption of function may occur as a result of instability. If a heavy load is placed on the damaged table joint, the joint surfaces will separate under the compressive load and the leg may be angled. The once- stable joint now allows mobility, and the leg may wobble back and forth. This motion may cause screws to loosen or nails to bend and ultimately to be torn out of one of the wooden components.
Complete failure of the table joint may result in splin- tering of the wooden components, especially if the already weakened joint is subjected to excessive, sudden, or pro- longed loads. The effects of decreased support in a human joint are similar to those in the table joint. Separation of the bony surfaces occurs and may result in wobbling or a deviation from the normal alignment of the bony compo- nents. Changes in alignment create abnormal joint open- ing on the side where a ligament is torn. Other ligaments, tendons, and the joint capsule may be subjected to in- creased loading, leading them to become excessively stretched and unable to provide protection. The intact side of the joint may be subjected to abnormal compression during weight-bearing or motion. In canine experiments in which an unstable knee joint is produced as a result of transection of the anterior cruciate ligament of the knee, morphologic, biochemical, biomechanical, and metabolic changes occur in the articular cartilage shortly after the transection.106 Later, articular cartilage becomes thicker and shows fibrillation, and osteophytes develop. The car- tilage shows much higher water content than in the oppo- site knee, and the synovial fluid content of the knee is increased. In addition, a sharp increase in bone turnover occurs, as does a thickening of the subchondral bone.106 According to Van Osch and colleagues, joint instability is a well-known cause of secondary osteoarthritis involving the knee joint.107The recognition that joint injuries, es- pecially ligament injuries, lead to osteoarthritis suggests greater efforts are required to prevent and treat sport injuries in young people.
Immobilization (Stress Deprivation)
Any process or event that disturbs the normal function of a specific joint structure will start a chain of events that eventually affects every part of a joint and its surrounding
joint.111–114Therefore, the joint is unable to function nor- mally and is at high risk of additional injury.115A summary of the possible effects of prolonged immobilization is pre- sented in Table 2–8.
surgery, (2) reduction in the duration of casting periods after fractures and sprains, (3) development of dynamic splinting devices to allow joint motion while preventing un- wanted motion that may damage healing structures, (4) use of graded loading after immobilization, and (5) extension of the recovery period to months rather than days or weeks.
The continuous passive motion device can move joints passively and repeatedly through a specified portion of the physiological ROM. The speed of the movement and the ROM can be controlled. Continuous passive motion de- vices produce joint motion under low loading conditions, which in turn produces medium-frequency alternating compression, which may stimulate cartilage formation. It is easier to control loading with these devices than with active movements and therefore easier to avoid the potentially deleterious compressive-tensile stresses and strains produced by active muscle contractions. Continuous passive motion was shown to prevent some of the tendon weakening that occurs during immobilization, though not enough to main- tain normal tissue strength.116
Recognition of the adverse effects of immobilization has led to the development of several strategies to help minimize the consequences of immobilization: (1) use of continuous passive motion (CPM) devices after joint
Table 2–8 Effects of Increased and Decreased Load on Connective Tissues
TISSUE DECREASED LOAD INCREASED LOAD
Tendon and ligament Decreased collagen concentration Increased cross-sectional area
Decreased cross-linking Increased collagen concentration
Decreased tensile strength Increased cross-linking
Increased tensile strength Increased stiffness
Menisci Decreased PGs Increased PGs
Bone Decreased collagen synthesis Denser bone
Decreased bone formation Increased synthesis of collagen and bone Increased bone resorption
Cartilage Thinning of cartilage Increased PG synthesis
Advancing of subchondral bone Increased volume?
Decreased PG synthesis Fewer PG aggregates
Joint capsule Disordered collagen fibrils Not specifically examined
Abnormal cross-linking
Synovium Adhesion formation Not specifically examined
Fibrofatty tissue proliferation into joint space
PG, proteoglycan.
CASE APPLICATION
Deleterious Effects of
Immobilization case 2–11
Mr. Chen’s joints and surrounding structures will undergo striking changes during immobilization:
• Bone: weakened, decreased collagen and mineral content (osteopenia)
• Capsule: shrinking, increased resistance to movement (stiffer)
• Ligament: decreased cross-links, decreased tensile strength (weaker)
• Tendon: decreased cross-links, disorganization of collagen fibrils, decreased tensile strength (weaker)
• Muscle: loss of sarcomeres in series, decreased contractile proteins (shorter, less force production)
• Cartilage: swelling, decreased PG concentration (softer, weaker)
These changes occur within 8 weeks, but recovery may take 18 months or longer.
ConceptCornerstone 2-10
Effects of Altered Loading on Connective Tissue
• Connective tissues become weaker and lose their nor- mal structure if they are not loaded.
• Changes with decreased load occur rapidly.
• Recovery of normal structure and function requires gradual progressive loading.
• Loads should be tailored to the connective tissue.
Cartilage Response to Exercise
The response of cartilage to immobilization has been described,124but its response to increased physiological loading is largely unknown. The health of articular car- tilage depends on the application and removal of com- pressive loads. Chondrocytes are directly connected to their microenvironment through attachments between cell membrane proteins (integrins) and collagen fibrils, and mechanical forces are transduced into intracellular synthetic activity. The mechanisms of this transduction and the magnitude and frequency of the loading that will optimize cartilage structure are not yet known.
This is an area of active research, as cartilage injuries heal very poorly, and the use of transplanted material to repair cartilage defects is being explored. Since Salter’s work,125 it is well known that motion enhances tissue formation in cartilage defects, but the tissue formed is fibrocartilage, not hyaline articular cartilage. Unlike fibroblasts in bone, ligament, and tendon, chondrocytes do not readily migrate and repair areas that have been injured. Defects that extend to subchondral bone are thought to have better healing potential because of the presence of pluripotential mesenchymal cells (from bone marrow) that can differentiate into chondroblasts under the right loading conditions—hence the use of drilling to treat osteochondral defects.124 There are no quantitative data available about changes in human artic- ular cartilage after immobilization or exercise, although MRI shows promise in this regard. It appears that cyclic low-magnitude, low-frequency (less than 1-Hz) com- pressive loads may be best for inducing or maintaining cartilage structure.
Tendon Response to Exercise
Tendons respond to increased tensile loads by increasing their collagen concentration, collagen cross-linking, tensile strength, and stiffness. Woo et al. showed that after 12 months of physical training, the extensor digitorum ten- dons of swine increased their weight, strength, collagen content, and stiffness to match the normally stronger flexor digitorum longus, which did not change in response to the same program.95 Biochemical changes occurred in chicken Achilles tendons after strenuous intermittent running, with increased collagen synthesis, cross-linking, tensile strength, and stiffness, although tendon size and weight did not change.126,127Chronic increased loading causes tendon hy- pertrophy and increased cross-linking.127–129 In other words, both structural and material changes can take place.
Interestingly, exercise also appears to offset some of the changes that occur in connective tissue with age.130Progres- sive tensile loading has been used successfully to treat chronic tendon disorders, under the assumption that the tendon adapts to the increased loads.77,78,97–99
Ligament Response to Exercise
The effects of exercise in preventing negative changes in healing ligaments and the positive effects of activity on
Exercise
All tissues appear to respond favorably to gradual progres- sive loading by adapting to meet increased mechanical demands. Exercise influences cell shape and physiological functions and can have a direct effect on matrix alignment.
The response to exercise varies among tissues and depends on the nature of the stimulus, including the amount, type, and frequency of loading. The mechanism of connective tissue response to exercise appears to involve cells’ detect- ing tissue strain and then modifying the type and amount of tissue they produce. The amount, type, and frequency of deformation are important. Low-frequency compressive loading will increase cartilage formation, whereas higher frequencies can enhance bone synthesis. Higher magnitude or sustained loading will induce fibrocartilage formation, whereas tensile loads induce tissue formation resembling that found in tendon or ligament. According to Mueller and Maluf’s Physical Stress Theory,80maintaining the nor- mal mechanical state of connective tissues appears to re- quire repetitive loading beyond a threshold level. Below this threshold, the immobilization changes previously de- scribed rapidly occur.
Bone Response to Exercise
Bone deposition is increased with weight-bearing exercise and in areas of bone subjected to increased muscle force.117,118This response of bone form to function, Wolff’s law, has been known for over 100 years, and exercise is now used as a therapeutic intervention to prevent bone loss.119A systematic review showed that in 11 of 16 studies, post- menopausal women showed improvements in bone density with either exercise or exercise plus calcium or estrogen.118 The use of interventions to prevent bone loss and resulting osteoporosis during space flight is an area of active research.
Bone formation appears very sensitive to strains as well as (or perhaps instead of) the magnitude of the applied load.
Very low magnitude high-frequency vibration has been shown to increase trabecular bone formation by 34%.120 This suggests that even very low loads, well below the threshold for physical damage, may increase bone density.
Rubin et al. proposed that these far smaller high-frequency (10- to 30-Hz) mechanical signals that continually barrage the skeleton during longer term activities, such as standing and walking, are what regulate skeletal architecture.120–122 Even short durations of loading are effective, and just 10 minutes of low-load, high-frequency stimulation has been shown to prevent bone loss induced by disuse.120 Lanyon suggested that the asymmetrical strains during normal load-bearing activities create an ever-changing strain distribution, that it is the novelty of the strain that induces bone adaptation, and that the osteogenic response saturates rapidly.123 He further suggested that exercise regimens designed to control bone architecture can use- fully capitalize on this feature of the adaptive (re-)model- ing response. Each exercise session should include as many novel strain distributions as possible, preferably involving high peak strains and strain rates.