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 re- port 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 is characterized by progressive loss of articular cartilage and re- active 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 carti- lage, 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 osteoarthri- tis, the loss of cartilage leads to increased stress in the bone. This, in turn, promotes new bone formation, development of osteo- phytes, and sclerosis of the underlying bone.
Because sclerotic bone is hard and less yield- ing, 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 age 65 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 in- creased 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.
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 cushion- ing. 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 not- ed, 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).
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—eitherabnormal synthesis or increased production of matrix-destroying enzymes.
The pathologic findings in osteoarthritis de- pend 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 car- tilage 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 de- struction. 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.
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 dis- ease, or bursitis may cause pain. In the presence of osteoarthritis detected on radiographs, it may be easy to dismiss these causes and falsely at- tribute all of the pain to the arthritis.
There are no specific laboratory tests for osteoarthritis, although many tests may be per- formed 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.
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).
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; there- fore, ordering MRI to identify a meniscal tear in the knee in a patient with advanced osteoarthritis is often a poor diagnostic strategy.
The key to diagnosis is to first establish that the patient’s complaints are caused by dis- ease 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
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 rec- ommended on empirical grounds—fitness for its own sake—there is good reason to believe that it will mitigate the painful effects of os- teoarthritis.
Normal muscle function protects the joints. Coordinated muscular contraction limits joint instability. Muscle contraction also can absorb some of the stresses in loadbearing. Thus, strong and responsive muscles can replace, to some extent, dysfunctional ligaments and cartilage.
Bracing can occasionally be used to un- load painful joints, especially if there is sig- nificant malalignment or associated ligamen- tous 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 re- lief 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 com- bination.
Other Nonsurgical Options
Joint injection with steroids or hyaluronate may offer symptom relief. The potential ad- verse 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.
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).
The success rate, if measured by pain- relieving effects, is greater than 90%.4 How- ever, 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, med- ical complications, although rare, can be de astating. 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 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 intra- vascular obstruction, vascular compression, or physical disruption of vessels that supply the affected bones.6 Conditions associated with osteonecrosis include systemic lupus erythematosus, alcoholism, pancreatitis, he- moglobinopathies, 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 orig- inating within or outside of the vascular sys- tem. Intravascular obstruction by emboli or thrombosis directly leads to regions of is- chemia. Infiltrative processes can indirectly compress the osseous sinusoids and lead to venous congestion and decreased blood flow. Bone cannot expand under pressure. Thus, venous congestion creates a region of increased pressure analogous to a compart- ment syndrome of the soft tissues. Displaced fractures and dislocations may disrupt ves- sels 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
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 os- teonecrosis can approach 50%. Care should be taken to assess for possible referred pain from adjacent joints or the spine.
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 seg- ment, which may help plan treatment and estimate prognosis.
Prevention and Treatment
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 med- ical treatment for osteonecrosis.
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 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 abrad- ed 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, peri- articular fractures that produce malalignment of the extremity or altered biomechani- cal loading of the joint, and ligament injuries that upset the normal biomechanics and mo- tion 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).
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.
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 typical- ly provide little additional information; as such, they should be used primarily for pre- operative planning or when an additional diagnosis such as a loose body is being consid- ered.
Prevention and Treatment
The most effective measures to prevent post- traumatic 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.
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 con- ditions 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 pro- posed 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 re- sorption. 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 pat- terns 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).
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.
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 re- solve. 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.
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
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 cast- ing 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 over- load 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.
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.