CHAPTER SYNOPSIS:
Articular cartilage is uniquely designed to distribute forces across the joint surface. When degenerated or damaged, the normal homeostasis of the cartilage microenvironment is disrupted, resulting in progressive destruction that leads to arthritis, pain, and stiffness. The diagnosis and evaluation of wrist arthritis is based on combining information from presenting complaints, physical examination, and imaging studies. Conservative treatments generally consist of use of nonsteroidal anti-inflammatory drugs (NSAIDs), immobilization, and steroid injections.
INTRODUCTION
Any deviation from normal wrist kinematics can lead to altered joint loading, premature cartilage degeneration, and eventually osteoarthritis (OA). Many disease processes, including traumatic, neuromuscular, metabolic, and inflammatory etiologies, alter the kinematics of the wrist joint and have the potential to create this degenerative environment. The instigating event differs; however, the final common pathway is cartilage destruction, stiffness, and pain.
Articular Cartilage
Articular cartilage is a unique connective tissue consisting of extracellular matrix, water, and a small population of chondrocytes ( Fig. 1-1 ). This tissue is avascular, alymphatic, and aneural; however, it is able to absorb and dissipate high amounts of force and act as a frictionless plane on which our joints glide. The geometry and topographic thickness varies depending on the type and location of the joint. On a cellular level, the chondrocyte plays the key role in cartilage homeostasis, which, if disrupted, leads to osteoarthritis.
Articular cartilage is made up of four unique layers: the superficial, the transitional, the deep, and the calcified cartilage layer. The unique layers differ in proteoglycans (amount and type), cellularity (size, shape, and amount), water content, and collagen concentration. In the superficial layer, collagen is oriented parallel to the joint surface, which gives the articular surface both tensile stiffness and compressive resistance. This sheet of fibrils is also thought to provide a barrier between the cartilage and immune system. Therefore, loss of this layer may result in an autoimmune response to the exposed underlying proteins in addition to the disruption of mechanical defenses. The transitional zone demonstrates increased cellularity and increased proteoglycan concentrations but lower concentrations of water and collagen. The deep layer of articular cartilage is distinguished by perpendicular collagen fibers apparently resisting sheer stresses. This layer has the highest concentration of proteoglycans and the lowest concentration of water. The calcified cartilage layer is the transition point between the articular cartilage and bone.
The chondrocyte is the sole cell in cartilage yet represents only 2% of the total composition of articular cartilage. Chondrocytes vary in morphology and metabolic activity depending on the joint and their location in the cartilaginous structure. In contrast to other cells in the body, they are relatively inactive metabolically because of the avascularity of the tissue. However, the main function of the chondrocyte is to produce and replace appropriate amounts of extracellular matrix and, as such, have all the organelles necessary to create and excrete the matrix. Chondrocytes are able to sense changes in the matrix composition and the mechanical demands of the joint and respond to those stresses by increasing or decreasing the amount of extracellular matrix in the cartilage.
The matrix is composed of fluid and structural molecules. Of articular cartilage’s weight, 80% is water , which freely moves into and out of the tissue with movement, thus creating a lubrication system that also infuses nutrients and dissipates waste. In fact, the mechanical properties of cartilage are determined by water and its interaction with the structural macromolecules (aggregating proteoglycans) of the matrix ( Fig. 1-2 ). Structural molecules such as collagen, proteoglycans, and noncollagenous proteins contribute to the other 20% of the cartilaginous weight. Collagen comprises 60%, proteoglycans 30%, and other proteins 10% of the dry weight of cartilage. Collagen gives the matrix its form and tensile strength, whereas the proteoglycans help fill the framework with water. The other proteins help stabilize the framework and help the chondrocytes bind with the matrix.
Type II collagen is the most abundant collagen subtype in articular cartilage; however, types VI, IX, X, and XI also contribute. Type II collagen forms the cross-banded fibrils that give tensile strength and help maintain cartilage form. Type IX links Type II collagen to the matrix, whereas Type XI binds Type II collagen to itself. Type VI surrounds the chondrocytes and aids chondrocyte attachments to the extracellular matrix. Type X predominately resides near the calcified cartilage zone and the hypertrophic zone of the growth plate and is felt to aid in cartilage mineralization.
The basic unit of an aggregating proteoglycan is the glycosaminoglycan (GAG). A GAG is a repeating disaccharide unit attached to an amino acid. Differing disaccharide units and lengths of the units determine the type and function of the GAG. Concentrations and types of GAGs vary with respect to differing sites of articular cartilage, age of the patient, cartilage injury, and disease. A proteoglycan is one or more GAGs attached to a protein core.
Aggrecans are large proteoglycans that tend to aggregate or amass. Usually, these proteoglycans are made up of GAGs of chondroitin and keratin sulfate. Multiple aggrecans bind to hyaluronic acid via link proteins thus creating a protein aggregate. These large aggregates prevent proteoglycan displacement, help retain water, and create the viscoelastic property of the articular cartilage. The proteoglycan half-life is approximately 3 to 24 years.
Other noncollagenous proteins exist in the matrix. Anchorin CII helps anchor chondrocytes to the matrix collagen fibrils. Cartilage oligomeric protein (COMP) is only found around the chondrocyte and is believed to aid in the binding of the chondrocyte to the matrix.
Chondrocytes and the surrounding matrix work together to prevent arthritic changes and to maintain joint homeostasis. The matrix provides a structural barrier shielding the chondrocytes from joint forces. The chondrocytes, in turn, degrade and synthesize the matrix. Certain cytokines, such as interleukin-1 (IL-1), will stimulate chondrocyte and matrix degradation, whereas others, such as insulin-like growth factor-1 (IGF-1) and transforming growth factor-β (TGF-β), stimulate an anabolic chondrocyte reaction. Chondrocytes are also stimulated to produce matrix by cyclically applied compressive strain. High compressive forces, however, will inhibit matrix formation. Articular cartilage matrix, like bone matrix, degrades with disuse.
Osteoarthritis
Idiopathic osteoarthritis occurs when homeostasis between synthesis and degradation of the extracellular matrix fails. Once again, the chondrocyte is the cell responsible for these changes. Early osteoarthritis appears as fibrillation of the superficial layer of the articular cartilage. As the disease progresses, the fibrillation deepens to become clefts, which eventually reach the subchondral bone ( Fig. 1-3 ). These defects eventually tear, releasing articular cartilage from the subchondral bone and creating full-thickness cartilage defects. The fibrillation and cleft formation also correlate with increasing degradation enzyme (matrix metalloproteinases, or MMPs) activity.
Fibrillation is a visual change, but it signifies a breach of the superficial collagen layer. This breach allows an inflow of water into the articular cartilage, which subsequently decreases proteoglycan concentration. Chondrocytes detect these joint changes and release mediators that stimulate a repair response that may last for years. Anabolic cytokines, such as TGF-β, IGF-1, and bone morphogenetic protein 2 (BMP-2), are expressed, which stimulates the chondrocytes to synthesize matrix molecules and Type II collagen and to proliferate. Matrix molecules are also synthesized to help counteract the catabolic properties of the matrix metalloproteinases.
If the repair response is not strong enough, then a poorly understood and complex metamorphosis occurs as normal “anabolic” chondrocytes switch into a “catabolic” mode. Cytokines, such as IL-1 and TNF-α, initiate and maintain hyaline cartilage destruction by stimulating chondrocytes to produce nitric oxide, MMPs, and aggrecanases. MMPs, in turn, degrade matrix and collagen, and aggrecanases deplete the proteoglycans. As these important stabilizing structures are lost, the breach into the cartilage progresses, more matrix is destroyed, and the chondrocytes die.
Damaged and diminished articular cartilage is unable to dissipate joint forces, which are now absorbed by the subchondral bone. As predicted by Wolf’s law, which states that form follows function, existing trabeculae are thickened and strengthened. This increase in bone density near the articular surface is usually the first radiographic change to occur. Osteophytes may be a similar response to this increased bone stress. Fissures may occur in the subchondral bone. Synovial fluid egresses into the subchondral metaphyseal space, forming subchondral cysts.
With further catabolic activity collagen and aggregates continue to degrade, the matrix fails, and chondrocytes are no longer able to withstand the high loads and subsequently die. End-stage OA consists of denuded bone articulating with denuded bone. With destruction of the articular cartilage, the synovium, ligaments, and capsules are affected. Catabolic cytokines cause these structures to become attenuated, muscles become weak and contracted as a result of joint disuse, and inflammation within the joint continues to cause pain and stiffness.
Posttraumatic Osteoarthritis
Injuries causing capsular or ligamentous damage, direct or indirect chondral impact, and intraarticular fractures can all change normal joint biomechanics and initiate early arthritis. This posttraumatic arthritis is particularly challenging because it often presents in the young population prone to accidents that produce these types of injuries. The specific biologic events leading to posttraumatic arthritis have not been discovered; thus, much of the emphasis is on prevention, restoration of joint congruity, alignment, and stability.
Three different types of articular damage can occur depending on the force applied to the joint surface: Damage to the matrix and cells without visual changes to the joint surface, fissuring and chondral fractures, and intraarticular fractures
As previously outlined, normal articular cartilage can withstand significant loads. Because of unique viscoelastic properties, higher loads can be withstood if the loading process occurs over time. Normal joint loading causes synovial fluid to be pushed into the cartilaginous matrix. This fluid helps to dissipate the joint pressure throughout the articular surface. Subchondral bone also provides support to withstand the forces acting on the joint. A rapidly applied force, however, can fracture the matrix molecules, destroy chondrocytes, and damage subchondral bone. Loads greater than 25 N/mm 2 , in fact, have been shown to cause fissuring and chondrocyte death. A similar load can even fracture the subchondral bone and result in joint incongruity. Increasing loads will subsequently cause more damage to the articular cartilage framework and increased cell death. Impact loading itself has been shown to increase collagen degradation and to decrease production of aggrecans. Articular cartilage deficient of collagen and aggrecans will behave similarly to idiopathic osteoarthritis. Water perfusion will increase and the stiffness of the articular cartilage will decrease. Further loading of the articular surface, whether normal or impacting, subsequently leads to increased mechanical and metabolic stress on chondrocytes. These stresses decrease the chondrocyte’s ability to mount a repair response.
Initially, chondral fractures stimulate a repair response. Proliferating chondrocytes synthesize matrix molecules, although this effort is often short lived. Because of the avascularity of the hyline cartilage, undifferentiated cells cannot migrate to the zone of injury to aid in repair and, often, a void remains. If the defect is large enough and involves a weightbearing portion of the articular surface the normal biomechanics and stresses of the joint are altered and degeneration can occur.
Intraarticular fractures differ in that they damage the tidemark allowing hemorrhage into the joint, a fibrin clot to form, and an inflammatory reaction to take place. Mesenchymal stem cells are able to invade and proliferate and creating new chondral and osseous tissues. However, because of the initial traumatic force, the matrix and chondrocytes also are often severely damaged. Anatomic reduction probably decreases some of the stress on these fragile and much-needed chondrocytes.
Animal studies have augmented our understanding of the joint surfaces’ response to trauma. Anatomic reduction with compression of the fracture fragments in rabbits has been shown to heal with normal hyaline cartilage as viewed by light and electromicroscopy. Compression of the cartilage surface perhaps creates an environment that prevents the ingrowth of fibrocartilage from the subchondral bone.
Displaced and noncompressed fractures, however, heal with fibrocartilage. When drill holes are placed in the articular surface of rabbits, thus simulating a fracture through the tidemark, blood escapes from the subchondral bone and forms a fibrin clot that binds to the collagen. Growth factors such as TGF-β and IGF-1 and 2 are released, angiogenesis occurs, and the migration of undifferentiated cells commences. In the articular portion of the fracture the mesenchymal cells differentiate and some become chondrocytes. These chondrocytes start to produce matrix molecules such as Type II collagen, proteoglycan aggregates, and even some Type I collagen. Eight weeks after injury the fractured articular surface has a blend of hyaline and fibrous cartilage. The collagen fibrils do not follow the normal design of hyaline cartilage thus creating cartilage that is less stiff and more permeable to synovial fluid. The repaired tissue does not integrate with the normal tissue and is unable to dissipate stress and loads through fluid shifting. These areas are prone to fissuring even with physiologic loads.
Intraarticular stepoffs also cause areas of increased stress. Brown has shown that stepoffs will increase the peak pressure at the fracture fragment. With increased stress and decreased strength as a result of injury to the collagen meshwork, articular damage can progress and arthritis ensues. Brown also found that higher peak pressure occurred with decreased cartilage thickness thus resulting in more force being transmitted over a smaller surface area. The answer to how much stepoff or displacement can be tolerated is less clear. Lefkoe and colleagues have shown that 3 mm of displacement and 2 mm of stepoff can be remodeled after 20 weeks in the femurs of rabbits. Using a sheep model, however, Trumble has shown that only a 1-mm or less intraarticular osteotomy site could remodel ( Fig. 1-4 ). Histologic examination revealed decreased articular cartilage on the high side, whereas the low side showed increased chondrocyte cellularity and hypertrophy. It was also noted that the collagen fibrils were attempting to form an overlapping shelf in an effort to restore normal anatomy.
Clinical data are also difficult to interpret. Knirk and Jupiter, after reviewing 40 distal radius fractures, concluded that reduction of the articular surface to within 1 or 2 mm of anatomic alignment was a more important predictor of outcome than the severity of articular surface injury. However, it should be noted that functional outcome after distal radius fracture fixation does not necessarily correlate with radiographic findings. Despite the identification of radiographic OA in 76% of the patients, in another study, all patients had good or excellent functional outcomes. Long-term studies are needed to determine if these good outcomes will be maintained.
Other risk factors for developing posttraumatic arthritis include joint instability, as can be seen in scapholunate instability, lunotriquitral instability, radiocarpal fracture dislocations, and other carpal instabilities. Increasing patient age is a factor, as demonstrated by clinical studies in which patients older than 50 years have a twofold to fourfold greater risk of OA after intraarticular fractures of the knee when compared with younger patients. This may be partially explained by the fact that anabolic cytokine stimulation of chondrocytes to produce matrix molecules seems to decrease with age. Finally, individuals differ in cartilage thickness, modulus, and contract stress. These differences would most likely affect repair and remodeling potentials of the articular surface.
ASSESSMENT
Osteoarthritis and posttraumatic arthritis should be included in the differential diagnoses for any patient presenting with the primary complaint of wrist pain and stiffness. Other etiologies produce similar complaints, and these may have to be excluded even in the presence of definitive radiographic changes. Some of these symptoms, such as de Quervain’s tenosynovitis, can coexist even with the diagnosis of osteoarthritis. It is the identification of exact pain generators and the extent of intraarticular damage that determine definitive treatment options. Conservative treatment often involves a more “shotgun” approach, and the same treatment modality may be able to treat several different potential diagnoses. Other more invasive yet nonoperative options, including intraarticular injections, not only offer a useful, at least temporizing, treatment, but also add valuable diagnostic information.
Some key elements to the patient’s presenting complaints can help establish definitive diagnosis of either posttraumatic arthritis or osteoarthritis. First, of course, is the nature of the pain. In general, arthritic pain may be difficult for the patient to characterize. Presenting complaints may consist of “it just hurts,” “it hurts all over,” or “it hurts deep inside my wrist.” The degree of synovitis, the location of the articular joint involved, and the extent of the bony changes may have profound effects on the presenting symptomatology. This makes definitive diagnosis more challenging than just picking up on a single key phrase complaint. Subsequently, it may be easier to describe patient presentation in terms of mild, moderate, or severe arthritic symptoms. “Symptoms” are specifically used here because radiographic images do not always correlate.
Mild arthritic complaints generally include intermittent pain and stiffness. At the time of presentation these patients may be without any significant symptoms. Questioning may reveal a relatively common symptom pattern consisting of morning stiffness, improvement with activity, and worsening discomfort by the end of the day. Overactivity or moderate stress may exacerbate this discomfort, and this can lead to a “flareup.” For example, a patient with relatively pain-free basilar thumb joint arthritis reports not being able to hold a pencil without pain the week following a weekend of raking. Swelling is not usually a large component of the presentation, although a “sensation of swelling” may be reported. Patients have often already realized that their discomfort can be alleviated with over-the-counter NSAIDs or acetaminophen, and on presentation to the doctor they often report that “they just wanted to make sure there was nothing really wrong.”
Patients with moderate arthritis symptoms tend to have a low level of discomfort at all times. The discomfort is definitely worse with activities, and the patient can often name several activities that clearly exacerbate their discomfort. Turning the car key or opening a tight jar might exacerbate moderate thumb basilar joint arthritis; lifting a carton of milk might exacerbate STT (scaphotrapeziotrapezoidal) or radial carpal arthritis; and playing a round of golf might exacerbate distal radioulnar joint (DRUJ) arthritis. These patients tend to partially respond to over-the-counter antiinflammatory agents and often have educated themselves to certain types of activity modification. It is not uncommon to find a patient like this who has learned how to avoid painful activities, such as racquet sports, but presents to you specifically because he or she wants to get back to these activities. Often these patients have temporarily responded to a steroid injection given by a previous practitioner or have already tried formal splinting regimens.
The last group of patients are made up of those presenting with severe arthritis and constant severe pain. Any activity seems to cause a definite worsening of symptoms. These patients are often protective of the involved extremity and may not want to allow you to fully examine it. They are usually already taking a prescription dose of NSAIDs or narcotic medications as prescribed by a primary provider and often seem to be debilitated by their symptoms. Swelling, crepitation, and pain exacerbated with certain motions are common complaints.
In addition to presenting complaints, the relevant history can be useful in further establishing the diagnosis, particularly in differentiating osteoarthritis and posttraumatic arthritis. A previous wrist fracture would raise the suspicion of radiocarpal or DRUJ arthritis. In particularly severe intraarticular injuries where perfect joint restoration is impossible, posttraumatic arthritis may develop relatively quickly and is not surprising to the treating physician. Other patients, however, who clearly have posttraumatic arthritis once the workup is complete do not even recall having any significant trauma. These cases may represent a “wrist sprain” treated symptomatically with rest, ice, and NSAIDs and after a few weeks forgotten about until several years later when radiographs reveal the presence of SLAC (scapholunate advance collapse) wrist arthritis. Other times, especially in older patients, the “posttraumatic” arthritis is a result of ligament attenuation. No specific injury can be blamed, yet the arthritic pattern is indistinguishable from an SLAC wrist secondary to a scapholunate ligament rupture. Although severe posttraumatic radial carpal arthritis may present as a progressively painful and disabling condition, most osteoarthritic and posttraumatic conditions in the wrist tend to have a cyclic pattern of symptoms. Levels of discomfort, swelling, and stiffness wax and wane with time, although as the years go on the “good months” tend to get a little bit shorter and the “bad months” tend to get not only a little bit longer, but also a little bit more painful. Those patients with severe arthritic symptoms at presentation must fall into this group to explain how they lived with debilitating pain obvious at initial presentation. In other words, these patients have episodes of discomfort over the years but self-treat or live with the pain until it disappears or until over several years the cycle worsens to the point that the patient presents in constant agony. The x-rays of these patients typically reveal a pattern that clearly took years to develop.
Response to previous treatment attempts can also be helpful. Most patients should have at least a temporary improvement with immobilization and NSAIDs. Previous effects of steroid injection may be a little bit harder to interpret because the most important diagnostic information is obtained immediately following the injection. Although it is relatively rare, some patients develop a flare reaction following a steroid injection. This is presumably a result of an almost goutlike reaction to the steroid crystals but negates much of the diagnostic information that could be obtained in considering the patients’ previous response to the injection. Potential “red flags” could include patients who seem to get worse with true immobilization (while immobilized) and patients who only find relief with narcotic pain medication. Workers’ compensation and ligation issues may also affect the patient’s “perception” of the effectiveness of previous treatments.
Physical Examination
Assessment of the patient’s overall persona, emotional stability, and coping skills should be included as part of the physical examination. Although this has nothing to do with the diagnosis of osteoarthritis or posttraumatic arthritis, it may offer some future insight to the patient’s response to treatment modalities. Patients with poor coping skills often do not do as well as other patients. This probably has to do with their expectation and emotional desire for complete resolution of any pain at all, whereas other patients will be satisfied with reduction of the symptoms to a tolerable and livable level. This includes surgical treatments as well. Although partial wrist fusion for radiocarpal arthritis may eliminate primary pain generators, altered wrist biomechanics and residual pathology prevent the restoration of a “normal wrist.” In comparison to preoperative discomfort, there may be marked improvement but still residual discomfort. This is similar to the problems that are seen in patients with “chronic pain”—especially when they are taking chronic narcotic pain medication. A useful analogy for this patient population is as follows: When someone not taking pain medications walks across the room and bangs their knee on the table they feel definite pain and often mutter profanities under their breath. As they rub the extremity their body releases endorphins, and after a few minutes the pain is tolerable and the person gets on with their day. In contrast, a person with chronic pain who is currently taking narcotics walks into the same table and, after the muttered profanities, rubs the extremity. However, their body does not release endorphins. This person must then take a pain pill to alleviate the same discomfort that another person’s body could easily deal with on its own. When you take this analogy and apply it to wrist pain, it is easy to see that a modality that appears to be a technical success may still be a clinical failure.
As part of this general overview, confounding factors such as lower-extremity problems requiring the use of assistive ambulation devices should also be noted. Likewise, in cases of severe arthritis other affected joints need to be addressed as well. This situation is most commonly observed and incorporated into treatment plans for inflammatory arthritis.
The bulk of the physical examination when evaluating for wrist arthritis is centered on the wrist and hand itself. Identifying swelling patterns is a good starting point. STT arthritis is usually prone to more significant swelling, and when noted on the radial aspect of the wrist, STT arthritis should be high on the differential. Midcarpal arthritis also tends to swell quite a bit, but here the swelling is located more on the dorsum of the wrist. Otherwise, swelling patterns seem to be more variable. Thumb carpometacarpal (CMC) joint arthritis and even radiocarpal arthritis may present with impressive swelling or a fairly benign initial presentation.
Finger range of motion can then be assessed. This is sometimes decreased as a result of discomfort, and a lot of encouragement is necessary to fully evaluate involvement here. Severe swelling and pain in the wrist does affect the peripheral tendons, and occasionally a patient will present with enough swelling that finger motion is compromised although there is nothing specifically wrong with the fingers. Range of motion of the wrist is considered next with attention to extension, flexion, ulnar deviation, radial deviation, supination, and pronation. There is a spectrum of what could be considered normal, and comparison to their contralateral asymptomatic side is often helpful. Motions that produce discomfort should be noted. Typically for radial carpal or midcarpal arthritis the extremes of extension and flexion seem to be problematic. With DRUJ arthritis pronation and supination are more affected. Pain from both radial styloid and STT arthritis occurs with radial deviation. Thumb motion tends to cause discomfort at primarily the thumb CMC joint but may also cause discomfort at the STT joint; however, isolated thumb motion generally does not cause discomfort at the radial styloid articulation itself.
Evaluation of digital and wrist strength is done next. Other than pain limiting effort, these should be close to normal limits. Sensation is then typically assessed by touching the fingers and asking the patient whether it feels normal or if it feels the same as the contralateral side. More definite measurements can be obtained using two-point discrimination; sharp/dull discrimination; or, when necessary, Semmes-Weinstein sensory threshold mapping. It is not uncommon to uncover a concurrent median nerve compression syndrome even if this was not part of the initial presentation.
With the general examination issues out of the way, the primary pain generators are pinpointed using digital palpation and provocative maneuvers. The point of maximum tenderness is narrowed down by carefully palpating each area of the wrist. The radial carpal joint, the scapholunate interval, the STT joint, the radial styloid articulation, the CMC joint of the thumb, the midcarpal joint, the ulnar fovea, and the DRUJ should all be separately palpated depending on where the patient’s primary complaints ( Fig. 1-5 ). Often this exercise is extremely helpful, but other times, unfortunately, the pain distributions are vague or too widespread.
