In addition to causing significant pulmonary disease, Mycobacterium tuberculosis can cause a variety of extrapulmonary manifestations. In a series of articles, we have reviewed pleural, lymph node, neurologic, and abdominal tuberculosis. In this article, we will discuss tuberculosis that affects the spine and peripheral joints. OVERVIEW Skeletal tuberculosis is a hematogenous infection that can affect almost any bone. The infection can begin in either bone or synovium. Usually, an active focus forms in the metaphysis in children and in the epiphysis in adults. The most common form of osteoarticular involvement is spinal tuberculosis. Lower thoracic and lumbar vertebrae are the most common sites, followed by middle thoracic and cervical vertebrae. Usually, 2 contiguous vertebrae are involved, but several vertebrae may be affected. Infrequently, skip lesions may occur. After spinal tuberculosis, infection of the hip joint is the next most common form of osteoarticular tuberculosis. The knee joint is the third most common site of osteoarticular tuberculosis. The other peripheral joints are rarely involved. Most patients with skeletal tuberculosis have pain at the joint of involvement, particularly on weight bearing. Most patients have constitutional symptoms, such as fever, for weeks before the development of joint pain. In addition to the clinical presentation and findings on plain radiographs, CT or MRI can be helpful in making the diagnosis, especially in patients who have spinal tuberculosis and paraspinal abscess. When the diagnosis is in doubt, biopsy of the involved vertebrae or bone, for histopathologic and microbiologic examination, may be required. Concomitant pulmonary involvement can help establish the diagnosis, but it is not essential. SPINAL TUBERCULOSIS In spinal tuberculosis, the infection begins in the cancellous area of the vertebral body, commonly in the epiphysis. The vertebral body becomes soft and is easily compressed, producing wedging or total collapse. Anterior wedging is commonly seen in the thoracic spine, where the normal kyphotic curve accentuates the pressure on the anterior part of vertebrae. Wedging is minimal in the cervical and lumbar spine, where the center of gravity is posteriorly located because of lordotic curve. Vertebral tuberculosis develops as an exudative lesion, which can penetrate the ligaments and follow the path of least resistance along fascial planes, blood vessels, and nerves from the original bony lesion to distant sites. In the cervical region, the exudate collects behind prevertebral fascia and may protrude as a retropharyngeal abscess. The exudative lesionmay spread down the mediastinum or spread laterally into the sternomastoid muscle and form an abscess in the neck. In the thoracic spine, the exudate may remain confined locally for several months and may appear radiographically as a fusiform or bulbous paravertebral abscess. The pressure may force the exudate to enter the spinal canal and compress the spinal cord. The exudate formed at lumbar vertebrae most commonly enters the psoas sheath. This manifests radiologically as a psoas abscess or clinically as a palpable abscess in the iliac fossa. Pott's paraplegia is the most serious complication of spinal tuberculosis, occurring in almost 30% of patients. The dorsal spine is most commonly involved, since the spinal canal is narrowest in the dorsal region. Early-onset paraplegia develops during the active phase of infection. Paraplegia of late onset appears many years after the disease has become quiescent. In most cases, early-onset paraplegia is caused by cord compression resulting from inflammatory edema, caseous material, tuberculous pus, and granulation tissue. The recovery is usually favorable. Late-onset paraplegia occurs as a result of long-standing persistent mechanical pressure. It includes internal gibbus, severe kyphotic deformity, dural fibrosis, and steno-sis of the spinal canal. The prognosis in these cases is much less favorable.1,2 Clinical presentation Spinal tuberculosis typically occurs in the first 3 decades of life. It is also being reported in middle-aged patients. The protean constitutional symptoms precede the symptoms related to the spine. Localized pain over the site of involvement is the most common early symptom. This pain may worsen on movement. Careful palpation will reveal tenderness over the affected vertebrae. In patients who do not present until vertebral wedging and collapse have occurred, a localized knuckle kyphosis is obvious, especially in the dorsal spine. Occasionally, patients with dorsal spine disease present very late with extensive vertebral destruction. These patients have deformity of the thoracic cage with a large gibbus. Retropharyngeal abscess may cause local pressure effects, such as dysphagia, dyspnea, and hoarseness. A flexion deformity of the hip may result from psoas abscess. The abscesses may be visible and palpable if they are superficially located. Rarely, paraplegia may be the presenting symptom. In most cases, however, the diagnosis of tuberculosis of the spine is already established when paraplegia develops. The earliest signs of neurologic involvement are spontaneous twitching of muscles in lower limbs, clumsiness in walking because of muscle weakness, and spasticity. Paraplegia in extension, paraplegia in flexion, sensory loss, and loss of sphincteric control may subsequently occur.1,2 Radiologic features The main sites of infection are the paradiskal, central, anterior, and appendicial vertebrae (Figures 1 and 2). Vertebral involvement is most commonly paradiskal. The appendicial type includes involvement of the pedicle, lamina, spinous process, and transverse process. There may be erosion of some vertebral bodies as a result of the pressure effect of the paravertebral abscess. It takes about 3 to 5 months for bony destruction to become visible on plain radiographs. More than 30% of mineral contentmust be removed from bone for a radiolucent lesion to be discernible on the plain radiograph. CT and MRI allow identification of bony lesions at an early stage. Prevertebral and paravertebral abscess shadows may be seen.3 Management Antituberculosis drug treatment for spinal tuberculosis is essentially the same as it is for tuberculous infection elsewhere in the body. However, there is disagreement about the duration of therapy. The consensus recommendation is for 18 to 24 months of therapy, depending on the patient's response.Short-course chemotherapy for 9 months has been shown to be equally effective in patients who receive a relatively early diagnosis.1,2,4 The indications for surgery are limited because antituberculosis therapy is usually effective. Potential indications for surgery include radiologic evidence of progression of the bony lesion and/or paraspinal abscess shadow, imminent vertebral collapse, instability of the spine, and subluxation or dislocation of the vertebral body. Surgery may also be indicated for the prevention of severe kyphosis. The common procedures consist of anterolateral decompression with interbody bone grafting, costotransversectomy with decompression, anterior debridement, anterior interbody fusion, and posterior fusion of affected vertebrae. The additional use of metallic implants and titanium cage filled with cancellous bone grafts may be required in some patients.1,2 TUBERCULOSIS OF PERIPHERAL JOINTS In this form of tuberculosis, an inflammatory reaction initially develops in the synovium, followed by formation of granulation tissue. The cartilage becomes eroded, and granulation tissue separates the cartilage and the subchondral bone. The osseous surface becomes exposed as a result of destruction of subchondral bone and trabeculae, leading to demineralization and necrosis of the bone. In tuberculous arthritis, the joint space is characteristically preserved. In advanced and late disease, paraosseous cold abscesses develop, surrounding the joints. Clinical presentation An insidious onset of slowly progressive, painful, and swollen monoarthropathy is characteristic of peripheral joint tuberculosis. Limitation of motion may cause a flexion abnormality of the knee, and the hip may display a flexion-adduction deformity. The involvement of multiple joints has been reported.3 Diagnosis The radiologic characteristics include the classic triad of juxta- articular osteoporosis, peripheral osseous erosion, and gradual narrowing of the interosseous space. The joint space is relatively preserved in early arthritis, in contrast to rheumatoid arthritis, in which the articular space is lost early. CT scanning gives a precise picture of bony destruction or soft tissue involvement. MRI is the best study for demonstrating early inflammation and abnormalities in the periarticular soft tissue. Synovial fluid analysis is a valuable tool for the evaluation of arthritis. In synovitis (without bone or cartilage involvement), the synovial fluid has the general appearance of any chronic effusion. It is xanthochromic and typically not hemorrhagic. As the disease progresses and bone and joint destruction occurs, the synovial fluid may have a yellowish white, almost gelatinous appearance that does not settle out into layers, even with centrifugation.The synovial fluid protein level is elevated, and the sugar level is low. The white blood cell count and differential are not helpful in making a specific diagnosis of tuberculosis. Acid-fast bacilli staining of synovial fluid is positive in 20% of cases; culture for M tuberculosis is positive in 80% of patients with tuberculous arthritis.5 Management The combination of isoniazid, rifampin, and pyrazinamide is the basis of treatment for tuberculous arthritis (Table). The duration of therapy is similar to that for spinal tuberculosis. Immobilization and rest are used to relieve pain during the acute phase and should be followed by early and active mobilization. Surgery is indicated only when it is necessary to drain a large abscess to relieve pressure. Recent technical developments and new materials have stimulated interest in arthroplasty for ankylosis caused by old tuberculous arthritis of the knee and hip.4,5 References: REFERENCES 1. Berger JR, Sabet A. Infectious myelopathies. Semin Neurol . 2002;22:133-142. 2. Carrol ED, Clark JE, Cant AJ. Non-pulmonary tuberculosis. Paediatr Respir Rev. 2002;2:113-119. 3. Buxi TB, Sud S, Vohra R. CT and MRI in the diagnosis of tuberculosis. Indian J Paediatr. 2002;69:965-972. 4. Maher D, Chaulet P, Spinacci S, Harries A. Global Tuberculosis Program. 2nd ed. Geneva: World Health Organization; 1997. 5. Ellis ME, el-Ramahi KM, al-Dalaan AN. Tuberculosis in peripheral joints: a dilemma in diagnosis. Tuber Lung Dis. 1993;74:399-404.
