Osteoarthritis
Osteoarthritis is a family of degenerative joint diseases characterized by chronic pain, deformity, and progressive physical and psychological disability. Osteoarthritis without an identified cause is called primary osteoarthritis. Secondary osteoarthritis results from known precipitants such as bone ischemia, trauma, and neuropathy, among others. The common terminal state for all forms of osteoarthritis is the destruction of the joint. The diagnosis is made when a patient reports joint pain; radiographs demonstrate cartilage loss, hardening of the bone below the cartilage, and bone spur formation; and no other disease is responsible. It is essential to remember that not all patients with radiographic evidence of osteoarthritis are in pain. Some who report pain are troubled to an extent far less than suggested by the radiographs. Thus, the common dictum in musculoskeletal medicine “treat the patient, not the x-rays” is especially germane to osteoarthritis.
Primary Osteoarthritis
Primary osteoarthritis is characterized by progressive loss of articular cartilage and reactive changes in the bone, leading to the destruction and painful malfunction of the joint. It is the most common arthropathy among adults—particularly the elderly. Osteoarthritis can involve all components of the joint: synovium, articular cartilage, subchondral bone, capsule, ligaments, and periarticular muscles. The principal mechanism of the disease is the destruction of articular cartilage, but osteoarthritis is abetted by the bone’s attempt to make new bone. Specifically, it is known that bone reacts to stress concentration by remodeling. In osteoarthritis, the loss of cartilage leads to increased stress in the bone. This, in turn, promotes new bone formation, development of osteophytes, and sclerosis of the underlying bone. Because sclerotic bone is hard and less yielding, sclerosis decreases the joint’s ability to absorb and dissipate force and makes it prone to further damage.
Epidemiology and Risk Factors
Osteoarthritis is very common. More than 20 million active cases of osteoarthritis are thought to be found in the United States alone. At least 80% of individuals age65 years and older will have radiographic signs of the disease, but not all will have pain.1 Among those with symptoms, functional limitations will be reported by approximately 10% to 20%.2 Pain and difficulty with ambulation attributed to osteoarthritis may account for up to 30% of physician office visits. As the baby boomer generation ages, osteoarthritis will become an even greater public health problem.
The most important determinant of risk for osteoarthritis is age. With aging, articular cartilage loses proteoglycans and collagen. This process leads to softening of the articular cartilage, with eventual fissuring and fibrillation. Genetic transmission of osteoarthritis appears possible as well. Obesity is also considered a risk factor of osteoarthritis, but this risk is not likely the result of increased load bearing alone. The joint at the base of the thumb, which is a non–weight-bearing joint, of course, is one at highest risk for osteoarthritis in obese patients.
Ligamentous laxity and congenital bone deformity also can cause osteoarthritis, probably because of altered biomechanics and abnormal peak stress concentration. That is, joints function best when the two opposing surfaces come into near-perfect contact; however, deformity and laxity may prevent that. This is the same reason that car tires wear out prematurely if the lug nuts securing the wheel to the car are loose (laxity) or if the tire is mounted imperfectly (deformity). Repetitive normal loading of a joint may also abet the development of clinically significant osteoarthritis, but the alternative, inactivity, may have worse consequences.
Pathophysiology
In primary osteoarthritis, the homeostatic mechanisms that maintain the cartilage no longer sustain the balance between normal breakdown and synthesis (regeneration). In healthy cartilage, chondrocytes continually replace the collagen and proteoglycans that compose the matrix. Collagen provides tensile strength, and the proteoglycans—and the water bound to them—provide the cushioning. When the chondrocytes cannot synthesize enough matrix, the tissue will fail mechanically. This loss of cartilage then leads, ultimately, to exposure of the underlying bone. Weight-bearing forces on the exposed bone stimulate new bone formation. As noted, this bony sclerosis makes the bone less compliant and more apt to break than bend with load. A vicious cycle is thus established (Fig. 1
Figure 1A, Low-power magnification of a section of a glenohumeral head of osteoarthritic cartilage removed during total shoulder arthroplasty. Note the significant fibrillation and fissures. B, High-power magnification of the articular surface of a humeral head with osteoarthritis. There are clefts in the cartilage and large dead areas devoid of cells.
(Reproduced from Mankin HJ, Mow VC, Buckwalter JA: Articular cartilage repair and osteoarthritis, in Buckwalter JA, Einhorn TA, Simon SR (eds): Orthopaedic Basic Science: Biology and Biomechanics of the Musculoskeletal System, ed 2. Rosemont, IL, American Academy of Orthopaedic Surgeons, 2000, p 478.)
).
Osteoarthritis is distinct from normal aging. First, not all elderly people demonstrate the changes associated with the disease. Second, and perhaps more telling, is that in early osteoarthritis, the water content of the cartilage actually increases, whereas in aging, cartilage loses water. Water is held in the cartilage by its polar interactions with the matrix, suggesting that the primary lesion in osteoarthritis is one of matrix abnormality—either abnormal synthesis or increased production of matrix-destroying enzymes.
The pathologic findings in osteoarthritis depend on the stage. Early on, the cartilage is merely soft. As the disease progresses, there is abrasion of the cartilage, which may lead to full-thickness loss and exposure of subchondral bone. Once the protective layer of the cartilage (the lamina splendens) is lost, mechanical wear accelerates through the remaining cartilage. Also, a single small defect in the cartilage can spread geographically, as pieces of adjacent cartilage can be pulled off the bone when the edge of the defect catches on the opposing surface. This process not only enlarges the area of damage but also creates loose bodies that may inflict harm elsewhere in the joint.
Reactive changes in the bone cause it to harden, making it more likely to crack with load rather than bend (as a healthy subchondral bone would) leading to further joint destruction. Cracks in the bone create channels through which synovial fluid can enter the bone. This synovial fluid creates the subchondral cysts seen on radiographs. The bone repair process also includes new bone formation in the joint itself or at its margins in the form of bone spurs known as osteophytes.
Clinical Presentation
Physical Examination
The chief complaint of osteoarthritis is deep, aching pain, often of insidious onset. Typically, patients report pain in the interphalangeal joints and the first carpometacarpal joint of the hand, the knees and hips, the first metatarsophalangeal joint in the foot, and the spine. Patients generally report that the pain gradually becomes worse as the day goes on because mechanical load accumulates over time. Pain that is worse at the end of the day stands in contrast to the complaints of inflammatory conditions, which tend to improve as the day progresses. Other common signs and symptoms are stiffness, limited motion, and swelling. The typical patient is also at least somewhat overweight.
Obtaining a detailed medical history is important to identify the risk factors and associated problems that may affect clinical management. Most patients will have tried some form of treatment on their own, so obtaining a detailed medical history, including questions about conventional and alternative medicine therapies, is critical.
Early in the disease, there may be no objective findings. Later, the joint may be enlarged with distinct bony prominences. Joints may be slightly red, warm, and tender, reflecting the synovitis and inflammation caused by the cartilaginous debris. Osteoarthritis of the knee may produce an effusion. Range of motion should be documented. While testing range of motion, crepitus may be felt. The patient’s gait and posture should be observed for signs of muscle weakness and neurologic imbalance. Muscle testing, reflexes, and neurologic examination of the peripheral nerves should be performed, and joint stability should be assessed as well.
The key feature of the examination is to exclude other causes of pain. In the lower extremity, for example, spinal stenosis, vascular disease, or bursitis may cause pain. In the presence of osteoarthritis detected on radiographs, it may be easy to dismiss these causes and falsely attribute all of the pain to the arthritis.
Laboratory Studies
There are no specific laboratory tests for osteoarthritis, although many tests may be performed in the course of excluding other causes of the patient’s complaints. For example, a white blood cell count, erythrocyte sedimentation rate, and C-reactive protein level are obtained to exclude inflammatory arthritis.
Imaging Studies
Osteoarthritis is characterized by four cardinal features on plain radiographs: asymmetric joint space narrowing, subchondral sclerosis, osteophyte formation, and subchondral cysts (Figs. 2 and 3
Figure 2 Severe osteoarthritis of the glenohumeral joint, with large inferior osteophyte (1), loss of joint space (2), sclerotic bone formation (3), and periarticular cyst formation (4).
(Reproduced from Crosby LA (ed): Total Shoulder Arthroplasty. Rosemont, IL, American Academy of Orthopaedic Surgeons, 2000, p 18.)
Figure 3 Osteoarthritis of the hip with loss of joint space (1) and complete degeneration of the articular surfaces of the femoral head and the acetabulum. There is also marginal osteophyte formation (2) as well as a subchondral cysts in the acetabulum (3).
). Radiographs should be obtained while the patient is weight bearing to allow the opposing surfaces of the joint to come maximally close and thus outline the remaining cartilage (Fig. 4
). MRI is typically not needed, unless it is used to exclude other diagnoses, such as osteonecrosis. Any patient with osteoarthritis that is detected on radiographs will also have cartilage abnormalities; therefore, ordering MRI to identify a meniscal tear in the knee in a patient with advanced osteoarthritis is often a poor diagnostic strategy.
Differential Diagnosis
The key to diagnosis is to first establish that the patient’s complaints are caused by disease in the joint itself and not referred from other areas. Once the diagnosis of arthritis (of any sort) is made, inflammatory causes, including rheumatoid arthritis, gout, and infection, must be considered. If these causes are excluded, a diagnosis of primary or secondary osteoarthritis can be made.
Prevention and Treatment
Medical Management
There is no known cure for osteoarthritis. The mainstay of medical treatment includes pain management, maintaining mobility and function, and preventing disease progression. Nonpharmacologic options include patient education, weight reduction, physical and occupational therapy, and a general cardiovascular fitness exercise program.1 Weight reduction is beneficial in decreasing the mechanical load on painful joints. An exercise program should be followed to strengthen periarticular muscles, reduce weight, and promote general well-being. Although a strengthening regimen can be recommended on empirical grounds—fitness for its own sake—there is good reason to believe that it will mitigate the painful effects of osteoarthritis.
Normal muscle function protects the joints. Coordinated muscular contraction limits joint instability. Muscle contraction also can absorb some of the stresses in load bearing. Thus, strong and responsive muscles can replace, to some extent, dysfunctional ligaments and cartilage.
Bracing can occasionally be used to unload painful joints, especially if there is significant malalignment or associated ligamentous instability. Physical modalities such as heat or cold therapy, ultrasound treatment, and iontophoresis can be used for pain relief.
The principal pharmacologic approach to osteoarthritis has been the use of nonsteroidal anti-inflammatory drugs (NSAIDs), particularly aspirin. NSAIDs offer both pain relief and control of inflammation, but they have significant adverse effects, including impaired renal function and gastrointestinal bleeding. Therefore, long-term use demands careful monitoring. Recent guidelines have recommended the use of acetaminophen as the first-line pharmacologic treatment of pain from osteoarthritis. Published studies have demonstrated that the efficacy of acetaminophen equals that of ibuprofen for the management of mild to moderate osteoarthritis of the knee but offers a better safety profile.3 If acetaminophen alone is inadequate, an NSAID can be prescribed in combination.
Other Nonsurgical Options
Joint injection with steroids or hyaluronate may offer symptom relief. The potential adverse effects of steroid therapy, such as decreased resistance to local infection, limit the frequency with which this approach can be applied. Alternative medications (eg, nutritional supplements, such as glucosamine and chondroitin sulfate) are commonly used, but their effectiveness in treating osteoarthritis remains unproven.
Surgical Management
Many patients with osteoarthritis of the hip and knee eventually seek surgical treatment, particularly for pain relief and functional improvement. Joint replacement (arthroplasty) is highly effective in relieving pain (Fig. 5
Figure 5 The same patient as in Figure 4 after total knee arthroplasty. The articular surface and adjacent bone was removed and replaced with metal and plastic components.
). The success rate, if measured by pain-relieving effects, is greater than 90%.4 However, the success rate for functional improvement is not as high. The major limitation of joint arthroplasty is the lack of long-term durability of the prostheses. Additionally, medical complications, although rare, can be devastating. Arthroplasty is a good operation for patients with end-stage joint destruction with pain and loss of function. It is less than ideal for patients who can play 17 holes of golf but want to play 18: the biologic costs outweigh the benefits.
Osteonecrosis
Pathophysiology
Osteonecrosis is a common cause of secondary osteoarthritis. It represents the final pathologic process of a number of conditions that kill the bone from ischemia.5 Other terms used to describe this phenomenon are avascular necrosis, aseptic necrosis, and ischemic bone necrosis. Osteonecrosis results from a reduction of blood flow to bone such that its metabolic demands are not met. Once the bone dies, it cannot repair cumulative damage and is prone to collapse (Fig. 6). The collapse of bone under the cartilage produces in an irregular surface and, ultimately, destruction of the other side of the joint as well. Osteonecrosis occurs in the setting of intravascular obstruction, vascular compression, or physical disruption of vessels that supply the affected bones.6 Conditions associated with osteonecrosis include systemic lupus erythematosus, alcoholism, pancreatitis, hemoglobinopathies, Gaucher’s disease, coagulopathies, Legg-Calvé-Perthes disease, corticosteroid use, displaced fractures and joint dislocations, organ transplantation, hemophilia, obesity, and even pregnancy.6,7 Osteonecrosis can develop in some patients without a recognized cause.
Ischemia may result from processes originating within or outside of the vascular system. Intravascular obstruction by emboli or thrombosis directly leads to regions of ischemia. Infiltrative processes can indirectly compress the osseous sinusoids and lead to venous congestion and decreased blood flow.
Figure 6 A patient with osteonecrosis of the femoral head from a hemoglobinopathy. There has been significant collapse of the femoral head. In time, the irregularities of the femur will destroy the acetabulum.
Bone cannot expand under pressure. Thus, venous congestion creates a region of increased pressure analogous to a compartment syndrome of the soft tissues. Displaced fractures and dislocations may disrupt vessels near the joint. Such disruption will cause osteonecrosis when the remaining vessels cannot provide enough blood flow to meet metabolic demands.
Certain regions of the skeleton are especially prone to osteonecrosis, specifically the femoral head and condyles, the humeral head, the carpal bones (scaphoid and lunate), and the talus.6
Clinical Presentation
Physical Examination
Osteonecrosis may be painful, even before secondary osteoarthritis develops. Patients typically report that the pain develops slowly over a long period and is generally associated with load-bearing activities. With disease progression, pain may be constant. Obtaining a comprehensive medical history is essential for identifying risk factors and conditions associated with osteonecrosis. Identifying and treating these conditions may prevent osteonecrosis from occurring in other bones.
Clinical findings for osteonecrosis are similar to those for osteoarthritis. The opposite extremity should be examined carefully because the incidence of bilateral involvement of osteonecrosis can approach 50%. Care should be taken to assess for possible referred pain from adjacent joints or the spine.
Imaging Studies
Plain radiography can confirm the diagnosis when changes in the bone, such as subchondral lucency or patchy sclerosis, are present. Although bone scanning can detect changes in the affected bones before they become apparent on plain radiographs, it is not highly specific for osteonecrosis. MRI is now the modality of choice for confirming the diagnosis. It is especially useful for those patients who are at risk but remain asymptomatic. It can also estimate the size of the necrotic segment, which may help plan treatment and estimate prognosis.
Prevention and Treatment
Medical Management
The most effective treatment is prevention, which is achieved by the proper identification of risk factors and the modulation of those factors. This is done, for example, by minimizing the dose and duration of corticosteroid and cytotoxic medications. There is no specific medical treatment for osteonecrosis.
Surgical Management
Surgical treatment has been shown in retrospective reviews to be effective; however, without randomized trials, it is hard to prove that surgery alters the natural history of the disease. Surgical options include core decompression with or without bone grafting. Core decompression is a drilling procedure aimed to relieve the increased intraosseous pressure within the bone and to provide a channel for new blood vessels to develop in the necrotic segment. This approach is useful only in early osteonecrosis before significant bone collapse and joint degeneration occurs.
Posttraumatic Arthritis
Pathophysiology
Posttraumatic arthritis is a form of secondary osteoarthritis caused by a loss of joint congruence and normal joint biomechanics. The healthy joint is congruent, and its articular facets align perfectly, allowing smooth motion and even distribution of forces across these surfaces. Without such congruence and smooth flow, the joint surfaces will be abraded by constant impact—rattling like dice in a cup—and the forces of weight bearing will be concentrated on small areas.
The course of joint degeneration is much more rapid in posttraumatic arthritis than primary osteoarthritis. Causes of posttraumatic osteoarthritis include intra-articular fractures, damage to the joint surface, periarticular fractures that produce malalignment of the extremity or altered biomechanical loading of the joint, and ligament injuries that upset the normal biomechanics and motion of the joint. A special form of posttraumatic arthritis of the knee can occur after meniscal injury. The loss of the shock-absorbing effect of the normal meniscus places the joint at risk for early and progressive destruction. The findings of secondary osteoarthritis after meniscal loss are known as Fairbank’s changes (Fig. 7
Figure 7A, Clinical photograph of a 44-year-old patient 15 years after open medial menisectomy. B, Standing radiograph of the same patient demonstrates medial compartment degeneration (Fairbank’s changes).
).
Clinical Presentation
Physical Examination
Patients with posttraumatic osteoarthritis typically present with pain and limited joint mobility. Symptoms are similar in all ways to those of primary osteoarthritis, but patients with posttraumatic osteoarthritis are typically younger and have a history of trauma or injury of the affected joint. Examination should focus on identifying any deformity because the joint may yet be saved if these deformities are corrected.
Imaging Studies
Plain radiography is usually adequate for diagnostic purposes. CT and MRI can be useful adjuncts; however, once the diagnosis of posttraumatic arthritis is made, they typically provide little additional information; as such, they should be used primarily for preoperative planning or when an additional diagnosis such as a loose body is being considered.
Prevention and Treatment
The most effective measures to prevent posttraumatic arthritis are to identify the injuries, restore proper joint surface anatomy and alignment, provide soft-tissue support, and initiate rehabilitation. Treatment of intra-articular fractures focuses on reestablishing joint congruency and normal joint mechanics. For patients with established posttraumatic arthritis, treatment is similar to that for primary osteoarthritis.
Neuropathic Arthritis
Pathophysiology
A neuropathic joint is one that has been destroyed by an underlying neurologic dysfunction.8 Other terms used to describe neuropathic arthritis are Charcot arthropathy and neuropathic arthropathy.7 Some of the conditions associated with the development of neuropathic joints include the peripheral neuropathy of diabetes mellitus, syringomyelia, head or spinal trauma, meningomyelocele, multiple sclerosis, congenital insensitivity to pain, alcoholism, and familial dysautonomia.7,9 Often, the destroyed joint is not painful.
Diabetes mellitus is most commonly associated with neuropathic joints. In approximately 5% of diabetic patients with sensory neuropathy, neuropathic arthritis eventually develops.9
Two principal theories have been proposed concerning the pathophysiology of neuropathic arthritis. The first cites cumulative trauma as the initiating mechanism. Repetitive loading of a joint, left unchecked, leads to fracture of the joint surface. Ordinarily, normal sensory feedback mechanisms will signal the individual to stop the inciting activity and thus protect the joint. In neuropathy, this does not happen, and the person leaves his hand in the fire, so to speak. The second mechanism is associated with dysfunction of the sympathetic fibers innervating the smooth muscles of arterioles, which results in enhanced blood flow and hyperemia. Although patients with diabetes and peripheral vascular disease typically have decreased microcirculation, the foot itself may have increased blood flow, which can lead to increased osteoclast activity and bone resorption. This weakens the bone and predisposes it to fracture. It has yet to be explained why arthropathy develops in some patients but not in others with apparently similar patterns of neuropathy.10
The gross pathology of neuropathic arthritis is similar to that observed in severe osteoarthritis, with destruction of cartilage, sclerosis and fragmentation of bone, osteophyte formation, and loose bodies within the joint.7 The joints most commonly affected are those in the foot and ankle. In these joints, erosive synovitis develops first, possibly followed by instability and subluxation. Ultimately, the joint is completely destroyed11(Fig. 8
Figure 8 Characteristic radiographic features of the neuropathic joint demonstrating the five “Ds”: joint distention, bone debris, dislocation, disorganization, and increased bone density.
).11 In the foot, collapse of the midtarsal joints can lead to a “rocker-bottom deformity.” The shape of the foot and ankle can be dramatically altered, changing the distribution of pressure on the plantar surface. This, coupled with peripheral neuropathy, produces skin ulcerations that can progress to cellulitis, osteomyelitis, and gangrene and lead to amputation in some instances.
Clinical Presentation
Physical Examination
Patients with neuropathic joints often present with joint swelling. They also typically describe a sudden onset of symptoms, occasionally associated with an audible “pop” after a minor injury that will not resolve. Pain is often much less than that expected for the amount of swelling or deformity. Patients also often have a long-standing history diabetes with significant sensory neuropathy. Examination reveals swelling with signs of inflammation and variable degrees of bony deformity and joint laxity.
Imaging Studies
Radiographs often show findings suggestive of osteomyelitis with aggressive bony destruction. In cases of slow progression, the radiographic features may appear similar to those of osteoarthritis.
Prevention and Treatment
Medical Management
As with most forms of secondary osteoarthritis, the most effective treatment is prevention. Patient education regarding proper foot care and footwear and regular follow-up by health care providers is required. Once neuropathic arthritis has been diagnosed, treatment centers on protecting the joint to allow for healing and preventing further damage to the joint and soft tissues. Total contact casting protects the limb and allows for healing. However, casts need to be changed regularly to accommodate the reduction in swelling and to assess the potential for pressure sores. In some studies, bisphosphonates have been effective in hastening bone healing in the acute phase.8 Another important goal is to protect the unaffected extremity from overload and possible joint damage. If there is residual deformity, treatment should be focused on preventing the development of pressure ulcers. Orthotic devices can be molded to protect prominences around the foot and ankle.
Surgical Management
Surgery may be unavoidable as salvage for patients with end-stage conditions. Options include fusion (arthrodesis) of unstable joints, excision of bony prominences to reduce the risk of ulceration, correction of joint malalignment to reduce the risk of further joint destruction, and amputation.
Key Terms
Lamina splendens The protective top layer of articular cartilage
Neuropathic arthritis The chronic, progressive destruction of a joint that is caused by the loss of sensation from an underlying neurologic dysfunction; also known as Charcot arthropathy
Osteonecrosis The death of bone, often as a result of obstruction of its blood supply
Posttraumatic arthritis A form of secondary osteoarthritis caused by a loss of joint congruence and normal joint biomechanics
Primary osteoarthritis Osteoarthritis without an identified cause; characterized by progressive loss of articular cartilage and reactive changes in the bone, leading to the destruction and painful malfunction of the joint
Secondary osteoarthritis Osteoarthritis resulting from known precipitants such as bone ischemia, trauma, and neuropathy
References
1. Brandt KD: The role of analgesics in the management of osteoarthritis pain. Am J Ther 2000;7:75-90.
2. Brandt KD: (ed): Diagnosis and Nonsurgical Management of Osteoarthritis, ed 2. Caddo, OK, Professional Communications, Inc, 2000.
3. Shamoon M, Hochberg MC: The role of acetaminophen in the management of patients with osteoarthritis. Am J Med 2001;110(suppl 3A):46S-49S.
4. Katz JN: Preferences, quality, and the (under) utilization of total joint arthroplasty. Med Care 2001;39:203-205.
5. Pavelka K: Osteonecrosis. Baillieres Best Pract Res Clin Rheumatol 2000;14:399-414.
6. Mirzai R, Chang C, Greenspan A, et al: Avascular necrosis. Compr Ther 1998;24:251-255.
7. Klippel JH, Weyand CM, Wortmann RL: (eds): Primer on the Rheumatic Diseases, ed 11. Atlanta, GA, Arthritis Foundation, 1997, pp 216-221, 322-324, 378-381.
8. Klenerman L: The Charcot joint in diabetes. Diabet Med 1996;13(suppl 1):S52-S54.
9. O’Connor BL, Brandt KD: Neurogenic factors in the etiopathogenesis of osteoarthritis. Rheum Dis Clin North Am 1993;19:581-605.
10. Guyton GP, Saltzman CL: The diabetic foot: Basic mechanisms of disease. J Bone Joint Surg Am 2001;83:1084-1096.
11. Wilson M: Charcot foot osteoarthropathy in diabetes mellitus. Mil Med 1991;156:563-569.
