Arthritis Associated with Systemic Disease and Other Arthritides (Disorders of the Joints and Adjacent Tissues) (Rheumatology) Part 1

Arthritis Associated With Systemic Disease

Arthropathy of Acromegaly

Acromegaly is the result of excessive production of growth hormone by an adenoma in the anterior pituitary gland. Middle-aged persons are most often affected. The excessive secretion of growth hormone along with insulin-like growth factor I stimulates proliferation of cartilage, periarticular connective tissue, and bone, resulting in several musculoskeletal abnormalities, including osteoarthritis, back pain, muscle weakness, and carpal tunnel syndrome.

An arthropathy resembling osteoarthritis is a common feature, affecting most often the knees, shoulders, hips, and hands. Single or multiple joints may be affected. The overgrowth of cartilage initially produces widening of the joint space. The newly synthesized cartilage is not developed in an organized manner, making it susceptible to fissuring, ulceration, and destruction. Ligamental laxity of the joint resulting from the growth of connective tissue also contributes to the development of osteoarthritis. With breakdown and loss of cartilage,the joint space narrows, and subchondral sclerosis and osteophytes appear on radiographs. Joint examination reveals marked crepitus and hypermobility.Joint fluid is noninflammatory. Calcium pyrophosphate dihydrate crystals are found in the cartilage in some cases of acromegaly arthropathy and, when shed into the joint, can produce attacks of pseudogout. Chondrocalcinosis may also be observed radiographically. Approximately half of the patients with acromegaly experience back pain, which is predominantly lumbosacral. Hypermobility of the spine may be a contributing factor in back pain. Radiograph of the spine shows normal or increased intervertebral disk spaces, hypertrophic anterior osteophytes, and ligamental calcification. These changes are similar to those observed in patients with diffuse idiopathic skeletal hyperostosis. Dorsal kyphosis in conjunction with elongation of the ribs contributes to the development of the barrel chest seen in acromegalic patients. The hands and feet become enlarged owing to soft-tissue proliferation. The fingers are thickened and have spade-like distal tufts. One-third of patients have a thickened heel pad. Approximately 25% of patients have Raynaud’s phenomenon.

Carpal tunnel syndrome occurs in about half of patients. The median nerve is compressed by the excessive growth of connective tissue in the carpal tunnel. The median nerve also becomes enlarged. Patients with acromegaly also develop proximal muscle weakness, which is thought to be caused by the effect of growth hormone on muscle. Results of muscle enzyme assays and electromyography are normal. Muscle biopsy specimens show muscle fibers of varying size and no inflammatory changes.

Arthropathy of Hemochromatosis

Hemochromatosis is a disorder of iron storage. Excessive amounts of iron are absorbed from the intestine, leading to iron deposition in parenchymal cells, which results in tissue damage and impairment of organ function. Symptoms of hemochromatosis usually begin between the ages of 40 and 60 but can occur earlier. Arthritis, which occurs in 20-40% of patients, usually begins after the age of 50 and may be the first clinical feature of hemochromatosis. The arthropathy is an osteoarthritis-like disorder affecting the small joints of the hands, followed later by larger joints such as knees, ankles, shoulders, and hips. The second and third metacarpophalangeal joints of both hands are often the first joints affected; they can provide an important clue to the possibility of hemochromatosis. Patients experience stiffness and pain. Morning stiffness usually lasts less than half an hour. The affected joints are enlarged and mildly tender. Synovial tissue is not appreciably increased. Radiographs show irregular narrowing of the joint space, subchondral sclerosis, and subchondral cysts. There is jux-taarticular proliferation of bone, with frequent hook-like osteophytes. The synovial fluid is noninflammatory. The synovium shows mild to moderate proliferation of lining cells, fibrosis, and a low number of inflammatory cells, which are mononuclear. In approximately half of patients, there is evidence of calcium pyrophosphate deposition disease (CPPD), and patients may experience episodes of pseudogout. Iron can be demonstrated in the lining cells of the synovium and also in chondrocytes.

Iron may damage the articular cartilage in several ways. Iron catalyzes superoxide-dependent lipid peroxidation, which may play a role in joint damage. In animal models, ferric iron has been shown to interfere with collagen formation. Iron has also been shown to increase the release of lysosomal enzymes from cells in the synovial membrane. Iron may also play a role in the development of chondrocalcinosis. Iron inhibits synovial tissue pyrophosphatase in vitro and, therefore, may inhibit pyrophosphatase in vivo, resulting in chondrocalcinosis. Iron in synovial cells may also inhibit the clearance of calcium pyrophosphate from the joint.


Arthropathy of Hemochromatosis

The treatment of hemochromatosis is repeated phlebotomy. Unfortunately,this treatment has little effect on the arthritis, which, along with chondrocalcinosis, usually continues to progress. Treatment of the arthritis consists of administration of acetaminophen and nonsteroidal anti-inflammatory drugs (NSAIDs). Acute pseudogout attacks are treated with higher doses of an NSAID or a short course of glucocorticoids. Placement of a hip or knee prosthesis has been successful in advanced disease.

Hemophilic Arthropathy

Hemophilia is a sex-linked recessive genetic disorder characterized by the absence or deficiency of factor VIII (hemophilia A, or classic hemophilia) or factor IX (hemophilia B, or Christmas disease). Hemophilia A is by far the more common type, constituting 85% of cases. Spontaneous hemarthrosis is a common problem with both types of hemophilia and can lead to a chronic deforming arthritis. The frequency and severity of hemarthrosis are related to the degree of clotting factor deficiency. Hemarthrosis is not common in other inherited disorders of coagulation, such as von Willebrand disease or factor V deficiency.

Hemarthrosis becomes evident after 1 year of age, when the child begins to walk and run. In order of frequency, the joints most commonly affected are the knees, ankles, elbows, shoulders, and hips. Small joints of the hands and feet are occasionally involved.

In the initial stage of arthropathy, hemarthrosis produces a warm, tensely swollen, and painful joint. The patient holds the affected joint in flexion and guards against any movement. Blood in the joint remains liquid because of the absence of intrinsic clotting factors and the absence of tissue thromboplastin in the synovium. The blood in the joint space is resorbed over a period of a week or longer, depending on the size of the hemarthrosis.Joint function usually returns to normal or baseline in about 2 weeks.

Recurrent hemarthrosis leads to the development of a chronic arthritis. The involved joints remain swollen, and flexion deformities develop. In the later stages of arthropathy, joint motion is restricted and function is severely limited. Joint ankylosis, subluxation, and laxity are features of end-stage disease.

Bleeding into muscle and soft tissue also causes musculoskeletal disorders. When bleeding into the iliopsoas muscle occurs, the hip is held in flexion because of the pain, resulting in a hip flexion contracture. Rotation of the hip is preserved, which distinguishes this problem from intraarticular hemorrhage. Expansion of the hematoma may place pressure on the femoral nerve, resulting in a femoral neuropathy. Another problem is shortening of the heel cord secondary to bleeding into the gastrocnemius. Hemorrhage into a closed compartment space, such as the volar compartment in the forearm,can result in muscle necrosis, neuropathy, and flexion deformities of the wrist and fingers. When bleeding involves periosteum or bone, a pseudotumor forms. These occur distal to the elbows or knees in children and improve with treatment of the hemophilia. Surgical removal is indicated if the pseudotumor continues to enlarge. In adults, they occur in the femur and pelvis and are usually refractory to treatment. When bleeding occurs in muscle, cysts may develop within the muscle. Needle aspiration of a cyst is contraindicated because it can induce bleeding.

Septic arthritis can occur in hemophilia and is difficult at times to distinguish from acute hemarthrosis on physical examination. Whenever there is suspicion of an infected joint, the joint should be aspirated immediately, the fluid cultured, and the patient started on antibiotics that provide broad coverage until the results of the culture are known. The patient should be infused with the deficient clotting factor before the joint is tapped to decrease the risk of further bleeding.

Radiographs of joints reflect the stage of disease. In early stages there is only capsule distention; later, juxtaar-ticular osteopenia, marginal erosions, and subchondral cysts develop. In late disease, the joint space is narrowed and there is bony overgrowth. The changes are similar to those observed in osteoarthritis. Unique features of hemophilic arthropathy are widening of the femoral intercondylar notch, enlargement of the proximal radius, and squaring of the distal end of the patella.

Recurrent hemarthrosis produces synovial hyperplasia and hypertrophy. A pannus covers the cartilage. Cartilage is damaged by collagenase and other degradative enzymes released by mononuclear cells in the overlying synovium. Hemosiderin is found in synovial lining cells, the subsynovium, and chondrocytes and may also play a role in cartilage destruction.



The treatment of hemarthrosis is initiated with the immediate infusion of factor VIII or IX at the first sign of joint or muscle hemorrhage.The patient is placed at bed rest, with the involved joint in as much extension as the patient can tolerate. Analgesic doses of an NSAID and local icing may help with the pain. NSAIDs can be given safely for short periods even though they have a stabilizing effect on platelets. Studies have shown no significant abnormalities in platelet function or bleeding time in hemophiliacs receiving ibuprofen.The cyclooxygenase-2 inhibitors do not interfere with platelet function and can be safely given for pain where their use is felt to be safe and indicated based upon the risks versus benefits. Synovectomy, open or arthroscopic, may be indicated in patients with chronic synovial proliferation and recurrent hemarthrosis. Hypertrophied synovium is very vascular and subject to bleeding. Both types of synovectomy reduce the number of hemarthroses and slow the roentgenographic progression of hemophilic arthropathy. Open surgical synovectomy, however, is associated with some loss of range of motion. Radiosynovectomy with either yttrium 90 silicate or phosphorus 31 colloid also has been effective and may be a useful alternative when surgical synovectomy is not practical. Total joint replacement is indicated for severe joint destruction and incapacitating pain. Because of the young age of hemophilic patients,total-joint prostheses may need to be replaced more than once during their lives.

Arthropathies Associated With Hemoglobinopathies

Sickle Cell Disease

Sickle cell disease is associated with several musculoskeletal abnormalities (Table 22-1). Children under the age of 5 may develop diffuse swelling, tenderness, and warmth of the hands and feet lasting from 1 to 3 weeks. The condition, referred to as sickle cell dactylitis or handfoot syndrome, has also been observed in sickle cell disease and sickle cell thalassemia. Dactylitis is believed to result from infarction of the bone marrow and cortical bone leading to periostitis and soft-tissue swelling. Radiographs show periosteal elevation, subperiosteal new bone formation, and areas of radiolucency and increased density involving the metacarpals, metatarsals, and proximal phalanges. These bone changes disappear after several months. The syndrome leaves little or no residual damage. Because hematopoiesis ceases in the small bones of hands and feet with age, the syndrome is rarely seen after age 4 or 5 and does not occur in adults.

Sickle cell crisis is often associated with periarticular pain and joint effusions.The joint and periarticular area are warm and tender. Knees and elbows are most often affected, but other joints can be involved.Joint effusions are noninflammatory, with white cell counts <1000^L; mononuclear cells predominate. There have been a few reports of sterile inflammatory effusion with high cell counts consisting of mostly polymorphonuclear white cells. Synovial biopsies have shown mild lining cell proliferation and microvascular thrombosis. Scintigraphic studies have shown decreased marrow uptake adjacent to the involved joint.The joint effusion and periarticular pain are considered to be the result of ischemia and infarction of the synovium and adjacent bone and bone marrow.The treatment is that for sickle cell crisis.

TABLE 22-1


Sickle cell dactylitis

Avascular necrosis

Joint effusions in sickle cell crises

Bone changes secondary to marrow hyperplasia


Infarction of bone

Septic arthritis

Infarction of bone marrow

Gouty arthritis

Patients with sickle cell disease may also develop osteomyelitis, which commonly involves the long tubular bones. These patients are particularly susceptible to bacterial infections, especially Salmonella infections, which are found in more than half of cases. The most common isolate is S. typhimurium. Radiographs of the involved site show periosteal elevation initially, followed by disruption of the cortex. Treatment of the infection results in healing of the bone lesion. Sickle cell disease is also associated with bone infarction resulting from thrombosis secondary to the sickling of red cells. Bone infarction also occurs in hemoglobin sickle cell disease and sickle cell thalassemia. The bone pain in sickle cell crisis is due to bone and bone marrow infarction. In children, infarction of the epiphyseal growth plate interferes with normal growth of the affected extremity. Radiographically, infarction of the bone cortex results in periosteal elevation and irregular thickening of the bone cortex. Infarction in the bone marrow leads to lysis, fibrosis, and new bone formation.

Avascular necrosis of the head of the femur is seen in ~5% of patients. It also occurs in the humeral head and less commonly in the distal femur, tibial condyles, distal radius, vertebral bodies, and other juxtaarticular sites. The mechanism for avascular necrosis is most likely the same as for bone infarction. Subchondral hemorrhage may play a role in the deterioration of articular cartilage. Irregularity of the femoral head or of other bone surfaces affected by avascular necrosis eventually results in degenerative joint disease. Radiograph of the affected joint may show patchy radiolucency and density followed by flattening of the bone. MRI is a sensitive technique for detecting early avascular necrosis as well as bone infarction elsewhere. Total hip replacement and placement of prostheses in other joints may improve function and relieve pain in those patients with severe joint destruction.

Septic arthritis is occasionally encountered in sickle cell disease (Chap. 20). Multiple joints may be infected. Joint infection may result from hematogenous spread or from spread of contiguous osteomyelitis. Microorganisms identified include Staphylococcus aureus, Streptococcus, Escherichia coli, and Salmonella. The latter is not seen as frequently in septic arthritis as it is in osteomyelitis. Acute gouty arthritis is uncommon in sickle cell disease, even though 40% of patients are hyperuremic. Hyperuricemia is due to overproduction of uric acid secondary to increased red cell turnover. Attacks may be polyarticular.

The bone marrow hyperplasia in sickle cell disease results in widening of the medullary cavities, thinning of the cortices, and coarse trabeculations and central cupping of the vertebral bodies. These changes are also seen to a lesser degree in hemoglobin sickle cell disease and sickle cell thalassemia. In normal individuals, red marrow is located mostly in the axial skeleton, but in sickle cell disease, red marrow is found in the bones of the extremities and even in the tarsal and carpal bones. Vertebral compression may lead to dorsal kyphosis, and softening of the bone in the acetabulum may result in protrusio acetabuli.


β-Thalassemia is a congenital disorder of hemoglobin synthesis characterized by impaired production of β chains. Bone and joint abnormalities occur in ß-thalassemia, being most common in the major and intermedia groups. In one study, ~50% of patients with ß-thalassemia had evidence of symmetric ankle arthropathy, characterized by a dull aching pain aggravated by weight bearing. The onset was most often in the second or third decade of life. The degree of ankle pain in these patients varied. Some patients experienced self-limited ankle pain, which occurred only after strenuous physical activity and lasted several days to weeks. Other patients had chronic ankle pain, which became worse with walking. Symptoms eventually abated in a few patients. Compression of the ankle, calcaneus, or forefoot was painful in some patients. Synovial fluid from two patients was noninflammatory. Radiographs of ankle showed osteopenia, widened medullary spaces, thin cortices, and coarse trabeculations. These findings were largely the result of bone marrow expansion. The joint space was preserved. Specimens of bone from three patients revealed osteomalacia, osteopenia, and microfractures. Increased osteoblasts as well as increased foci of bone resorption were present on the bone surface. Iron staining was found in the bone trabeculae, in osteoid, and in the cement line. Synovium showed hyperplasia of lining cells, which contained deposits of hemosiderin. This arthropathy was considered to be related to the underlying bone pathology. The role of iron overload or abnormal bone metabolism in the pathogenesis of this arthropathy is not known. The arthropathy was treated with analgesics and splints. Patients were also transfused to decrease hematopoiesis and bone marrow expansion.

Patients with ß-thalassemia major and intermedia also have involvement of other joints, including the knees, hips, and shoulders. Acquired hemochromatosis with arthropathy has been described in a patient with thalassemia. Gouty arthritis and septic arthritis can occur. Avascular necrosis is not a feature of thalassemia because there is no sickling of red cells leading to thrombosis and infarction.

ß-Thalassemia minor (trait) is also associated with joint manifestations. Chronic seronegative oligoarthritis affecting predominantly ankles, wrists, and elbows has been described. These patients had mild persistent synovitis without large effusions. Joint erosions were not seen. Recurrent episodes of an acute asymmetric arthritis have also been reported; episodes last less than a week and may affect knees, ankles, shoulders, elbows, wrists, and metacarpal phalangeal joints. The mechanism for this arthropathy is unknown. Treatment with nonsteroidal drugs was not particularly effective.

Musculoskeletal Disorders Associated With Hyperrlipidemia

Musculoskeletal manifestations may be the first indication of a hereditary disorder of lipoprotein metabolism. Patients with familial hypercholesterolemia (previously referred to as type II hyperlipoproteinemia) may have recurrent migratory polyarthritis involving knees and other large peripheral joints and, to a lesser degree, peripheral small joints. In a few patients, the arthritis is monarticular. Fever may accompany the arthritis. Pain ranges from moderate to very severe to incapacitating. The involved joints can be warm, erythematous, swollen, and tender. Arthritis usually has a sudden onset, lasts from a few days to 2 weeks, and does not cause joint damage. Episodes may suggest acute gout attacks. Several attacks occur per year. Synovial fluid from involved joints is not inflammatory and contains few white cells and no crystals. Joint involvement may actually represent inflammatory periarthritis or peritendinitis and not intraarticular disease. The recurrent, transient nature of the arthritis may suggest rheumatic fever, especially since patients with hyperlipoproteinemia have an elevated erythrocyte sedimentation rate and a falsely elevated antistreptolysin O titer. Patients may also experience Achilles tendinitis, which can be very painful. Attacks of tendinitis come on gradually and last only a few days. Fever is not present. Patients may be asymptomatic between attacks. During an attack the Achilles tendon is warm, erythematous, swollen, and tender to palpation. Achilles tendinitis and other joint manifestations often precede the appearance of xanthomas and may be the first clinical indication of hyperlipoproteinemia. Attacks of tendinitis may occur following treatment with a lipid-lowering drug. Patients can also have tendinous xanthomas in the Achilles, patellar, and extensor tendons of the hands and feet. Xanthomas have also been reported in the peroneal tendon, the plantar aponeurosis, and the periosteum overlying the distal tibia. These xanthomas are located within tendon fibers. Tuberous xanthomas are soft subcutaneous masses located over the extensor surfaces of the elbows, knees, and hands, as well as on the buttocks. They appear in childhood in homozygous patients and after the age of 30 in heterozygous patients. Patients with elevated plasma levels of very low-density lipoprotein (VLDL) and triglyceride (previously referred to as type IV hyperlipoproteinemia) may also have a mild inflammatory arthritis affecting large and small peripheral joints, usually in an asymmetric pattern with only a few joints involved at a time. The onset of arthritis is usually in middle age. Arthritis may be persistent or recurrent, with episodes lasting a few days to weeks. Joint pain is severe in some patients. Patients may experience morning stiffness. Joint tenderness and periarticular hyperesthesia may also be present, as may synovial thickening. Joint fluid is usually noninflammatory and without crystals but may have increased white blood cell counts with predominantly mononuclear cells. The fluid is occasionally lactescent. Radiographs may show juxtaarticular osteopenia and cystic lesions. Large bone cysts have been noted in a few patients. Xanthoma and bone cysts are also observed in other lipoprotein disorders. The pathogenesis of arthritis in patients with familial hypercholesterolemia or with elevated levels of VLDL and triglyceride is not well understood. Salicylates, other NSAIDs, or analgesics usually provide relief of symptoms. Clinical improvement may also occur in patients treated with lipid-lowering agents; however, patients treated with an HMG-CoA reductase inhibitor may experience myalgias, and a few patients may develop polymyositis or even rhabdomyolysis. Myositis has also been reported with the use of niacin.

Other Arthritides

Neuropathic Joint Disease

Neuropathic joint disease (Charcot’s joint) is a progressive destructive arthritis associated with loss of pain sensation, proprioception, or both. In addition, normal muscular reflexes that modulate joint movement are decreased. Without these protective mechanisms, joints are subjected to repeated trauma, resulting in progressive cartilage and bone damage. Neuropathic arthropathy was first described by Jean-Martin Charcot in 1868 in patients with tabes dorsalis. The term Charcot’s joint is commonly used interchangeably with neuropathic joint. Today, diabetes mellitus is the most frequent cause of neuropathic joint disease (Fig. 22-1).A variety of other disorders are associated with neuropathic arthritis including leprosy, yaws, syringomyelia, meningomyelocele, congenital indifference to pain, peroneal muscular atrophy (Charcot-Marie-Tooth disease), and amyloidosis. An arthritis resembling neuropathic joint disease is seen in patients who have received frequent intraarticular glucocorticoid injections into a weight-bearing joint and in patients with CPPD. The distribution of joint involvement depends on the underlying neurologic disorder (Table 22-2). In tabes dorsalis, knees, hips, and ankles are most commonly affected; in syringomyelia, the glenohumeral joint, elbow, and wrist; and in diabetes mellitus, the tarsal and tarsometatarsal joints.

Charcot arthropathy associated with diabetes mellitus.Lateral foot radiograph demonstrating complete loss of the arch due to bony fragmentation and dislocation in the midfoot.


Charcot arthropathy associated with diabetes mellitus.Lateral foot radiograph demonstrating complete loss of the arch due to bony fragmentation and dislocation in the midfoot.

Pathology and Pathophysiology

The pathologic changes in the neuropathic joint are similar to those found in the severe osteoarthritic joint. There is fragmentation and eventual loss of articular cartilage with eburnation of the underlying bone. Osteophytes are found at the joint margins. With more advanced disease, erosions are present on the joint surface. Fractures, devitalized bone, and intraarticular loose bodies may be present. Microscopic fragments of cartilage and bone are seen in the synovial tissue.

At least two underlying mechanisms are believed to be involved in the pathogenesis of neuropathic arthritis. An abnormal autonomic nervous system is thought to be responsible for the increased blood flow to the joint and subsequent resorption of bone. Loss of bone, particularly in the diabetic foot, may be the initial manifestation. With the loss of deep pain, proprioception, and protective neuromuscular reflexes, the joint is subjected to repeated injuries including ligamental tears and bone fractures. The mechanism of injury that occurs following frequent intraarticular glucocorticoid injections is thought to be due to the analgesic effect of glucocorticoids leading to overuse of an already damaged joint, which results in accelerated cartilage damage. It is not understood why only a few patients with neuropathies develop neuropathic arthritis.

TABLE 22-2


Diabetes mellitus


Tabes dorsalis



Congenital indifference to pain


Peroneal muscular atrophy

Clinical Manifestations

Neuropathic joint disease usually begins in a single joint and then progresses to involve other joints, depending on the underlying neurologic disorder. The involved joint progressively becomes enlarged from bony overgrowth and synovial effusion. Loose bodies may be palpated in the joint cavity. Joint instability, subluxation, and crepitus occur as the disease progresses. Neuropathic joints may develop rapidly, and a totally disorganized joint with multiple bony fragments may evolve in a patient within weeks or months. The amount of pain experienced by the patient is less than would be anticipated based on the degree of joint involvement. Patients may experience sudden joint pain from intraarticular fractures of osteophytes or condyles.

Neuropathic arthritis is encountered most often in patients with diabetes mellitus, with the incidence estimated in the range of 0.5%. The usual age of onset is >50 years following several years of diabetes, but exceptions occur. The tarsal and tarsometatarsal joints are most often affected, followed by the metatarsophalangeal and talotibial joints. The knees and spine are occasionally involved. In about 20%, neuropathic arthritis may be present in both feet. Patients often attribute the onset of foot pain to antecedent trauma such as twisting their foot. Neuropathic changes may develop rapidly following a foot fracture or dislocation. Swelling of the foot and ankle are often present. Downward collapse of the tarsal bones leads to convexity of the sole, referred to as a “rocker foot.” Large osteophytes may protrude from the top of the foot. Calluses frequently form over the metatarsal heads and may lead to infected ulcers and osteomyelitis. Radiographs may show resorption and tapering of the distal metatarsal bones. The term Lisfranc fracture-dislocation is sometimes used to describe the destructive changes at the tarsometatarsal joints.


The diagnosis of neuropathic arthritis is based on the clinical features and characteristic radiographic findings in a patient with an underlying sensory neuropathy. The differential diagnosis of neuropathic arthritis includes osteomyelitis, osteonecrosis, advanced osteoarthritis, stress fractures, and CPPD. Radiographs in neuropathic arthritis initially show changes of osteoarthritis with joint space narrowing, subchondral bone sclerosis, osteophytes, and joint effusions followed later by marked destructive and hypertrophic changes. Soft-tissue swelling, bone resorption, fractures, large osteophytes, extraarticular bone fragments, and subluxation are present with advanced arthropathy. The radiographic findings of neuropathic arthritis may be difficult to differentiate from those of osteomyelitis, especially in the diabetic foot. The joint margins in a neuropathic joint tend to be distinct, while in osteomyelitis, they are blurred. Imaging studies and cultures of fluid and tissue from the joint are often required to exclude osteomyelitis. MRI is helpful in differentiating these disorders. Another useful study is a bone scan using indium 111-labeled white blood cells or indium 111-labeled immunoglobulin G, which will show an increased uptake in osteomyelitis but not in a neuropathic joint. A technetium bone scan will not distinguish osteomyelitis from neuropathic arthritis, as increased uptake is observed in both. The joint fluid in neuropathic arthritis is noninflammatory; may be xanthochromic or even bloody; and may contain fragments of synovium, cartilage, and bone. The finding of calcium pyrophosphate dihydrate crystals suggests the diagnosis of a crystal-associated neuropathic-like arthropathy. In the absence of such crystals, the presence of an increased number of leukocytes may indicate osteomyelitis.

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