Tuberculous arthritis is granulomatous inflammation of the joint caused by the tuberculosis bacteriae. Mycobacterium tuberculosis os the most common pathogen. Tubercular arthritis is more common in children, though it may occur at any age.
It can also be called as tubercular arthropathy.
Tuberculosis of joints is a localized and destructive disease. It is generally spread through the bloodstream from a primary focus. It is never a primary lesion in a previously healthy joint
Unlike septic or bacterial arthritis that presents often with severe joint pain and fever, the symptoms of tuberculous arthritis are quite indolent. This may lead to a delay in diagnosis making.
Therefore, tuberculosis as diagnosis should be considered in any joint lesion where the diagnosis is not certain.
Tuberculous arthritis is more common in developing countries than developed ones.
There is no sex predilection for the disease.
Skeletal involvement is seen in 1% to 3% of patients with tuberculosis. About half the cases of musculoskeletal tuberculosis are involved the spine. The joints account for less than half of these musculoskeletal cases.
Hip is the most common joint involved in tubercular arthritis and is followed by the knee, ankle, elbow, and shoulder.
Xray of Tuberculous Arthritis Hip
Pathology of Tubercular Arthritis
The primary causative organism is mycobacterium tuberculosis. Atypical mycobacterie are also known to cause tuberculous arthritis especially in persons with compromised immunity. These are namely
Mycobacterium kansasii
M. xenopi
M. avium intracellulare
The infection in the joint can either be through blood or spread from the adjacent bone.
From the bone, tuberculosis spreads with increasing destruction of the surrounding bone and finally breaking into the joint. The synovial membrane reacts first by excessive secretion of fluid and later by proliferation.
With time synovial membrane gets thickened, its inner surface gets studded with tubercles, and fibrosis of its outer surface.
A pannus [granulation tissue layer] forms over the articular cartilage that eventually destroys the underlying articular cartilage and subchondral bone. The destruction of articular surfaces is most extensive around the periphery in areas where tuberculous granulations involve the synovial membrane.
With the progression of the disease, increasing amounts of caseous necrotic material and tuberculous exudates are produced.
The pus spreads by dissecting along tissue planes between muscles or between muscle sheaths, being limited by the deep fascia. With increasing tension, the deep fascia perforates and the abscess becomes subcutaneous.
If the original focus remains active and these abscesses remain untreated, they will rupture externally through the skin to form sinuses.
The spine is the most common site of affection.
Other joints which are commonly involved are
Hip
Knee
Ankle
Sacroiliac joints
Sternoclavicular joint
Elbow joint
Wrist joint
Clinical Features of Tuberculous Arthritis
Tubercular arthritis is monoarticular [involves single joint] in 90 percent of cases.
The disease is of insidious onset. Joint pain is the main complaint. In weight bearing joints, the pain increasses on weight-bearing.
The pain may be accompanied by stiffness that increases with time.
Some patients may complain of fatigue and weight loss. A family history of tuberculosis may be obtained.
[It is also important to know about the place of residence as tuberculosis is endemic in some regions.
Joint swelling may occur in later times. Limp may occur in case the joint of the lower limb is involved.
The involved limb may get wasted as compared to the opposite limb.
Though less common the presentation may just consist of swelling [cold abscess].
In superficial joints, such as the knee or elbow, synovial thickening, and effusion present as a fullness or bogginess.
The joint deformity may occur. The deformities are typical to the joint and are noted late stages [see below].
Systemic symptoms of fever, weight loss, and night sweat may or may not be present
Tuberculous arthritis has been classified into 5 stages based on x-ray findings are discussed there.
Lab Studies
Blood investigations may be normal or may chow chronic inflammatory changes
Following findings are nonspecific and may also be neoted in tuberculous arthritis
Hypochromic anemia is common.
Leukocytosis
Elevated erythrocyte sedimentation rate
The synovial fluid shows an elevated leukocyte count, a lowered sugar level, and poor mucin.
Microscopic examination may reveal tubercle bacilli but is not a constant finding. Cultural studies and guinea pig inoculations [not done for diagnostic purposes now commonly] will be positive for tuberculosis.
Relevant investigations are discussed below
Bacteriological Confirmation
A confirmation of acid-fast bacillus [Mycobacteria are called acid-fast because they resist decolorization with acid alcohol] from any body fluid or tissue is the gold standard for the diagnosis of tuberculosis.
However, the positivity rate is not very high and multiple samples may be required. Despite that, a negative test does not confirm the absence of tuberculosis.
The routinely used method is Ziehl-Neelsen stain and it can reveal acid-fast bacteriae only if the sample contains greater than 10,000 bacilli per mL. Because musculoskeletal tuberculosis is oligobacillar [contains less number of bacteriae.]
Tuberculin Skin Test or Montoux Test
Tuberculin skin test consists of intradermal installation of purified protein derivative of mycobacteriae and tests for the body’s sensitivity to past present disease. It is prone to subjective interpretation and lacks both sensitivity and specificity.
Interferon Gamma Release Assays
These are T-cell assays that rely on the stimulation of host blood cells with M. tuberculosis-specific antigens and measure the production of interferon ?.
However, the tests are quite expensive. Their interpretation also requires clinical context.
Polymerase Chain Reaction
Polymerase chain reaction uses nucleic acid amplification to detect the bacilli but cannot differentiate living bacilli from dead bacilli. Therefore, the test could be positive in the past cured infections as well.
Synovial Fluid Examination
Synovial fluid in tuberculous arthritis has the following features
Usually nonhemorrhagic and turbid
Moderate Leukocytosis
10,000-20,000 cells/mL
Mainly polymorphonuclear leukocyte.
Other tests on synovial fluid aspirations
Culture for mycobacteria – Positive in 20-40%
PCR analysis
Synovial Biopsy
Gold standard
Positive in 80% of cases
Findings
Caseating granulomas
Lymphocytes,
Giants cells
Imaging
X-rays
X-ray changes are generally noted 2 to 5 months after disease onset. Therefore, an x-ray is not a good modality for early diagnosis. In case of high suspicion, MRI is the best imaging to find out joint changes early.
The earliest findings in the radiograms are regional bone atrophy, soft-tissue swelling, and capsular distention. These changes are due to synovitis and are nonspecific. As a rule, the bone decalcification in tuberculous arthritis is widespread, extending 3 to 5 cm from the joint.
The joint space is widened and is preserved until late in the course of the disease.
Classical findings in tuberculous arthritis are known as Phemister’s triad and include
Peri-articular osteoporosis
Peripherally located osseous erosion
Gradual decrease in the joint space
Destruction of the hyaline cartilage by the tuberculous granulation tissue is a slow process in contrast to pyogenic arthritis, in which the destruction of articular cartilage and narrowing of the joint space take place early in the course of the disease.
Bone destruction can be seen in the epiphysis or metaphysis as areas of radiolucency in which the normal trabecular structure of bone has disappeared
The reactive new bone formation is characteristically absent in the early stages of tuberculous arthritis. It is only in the late healing stages that it develops.
Sequestra may occasionally be present.
Eventually, in an untreated case, the entire articular cartilage will eventually be eroded and extensive destruction of subjacent bone will take place, resulting in the gross deformity of the joint.
Stages of Tuberculous Arthritis
Stage I [Synovitis]
Soft tissue swelling, no bony lesion, localized osteoporosis
joint space widening (due to joint effusion)
Excellent outcome
Stage II [Early arthritis]
Marginal erosions
Decrease of joints space
Good outcome with only residual mild stiffness.
Stage III [Advanced arthritis]
Subperichondral cyst
Loss of joint space
Fair outcome with a notable loss of motion.
Stage IV – [Advanced arthritis with joint destruction]
No motion at the joint after treatment.
Stage V [anlylosis]
Fibrous or bony ankylosis of joint.
CT
CT shows the extent of bony destruction better than x-rays. It even catches the presence of sequestrum earlier than x-rays.
MRI
In MRI T1 sequence the lesions are typically hyperintense whereas in T2 sequence are hypointense.
Gadolinium-enhanced MRI shows a brilliant enhancement due to presence of blood degradation products, inflammation, necrosis and fibrosis. [Differentiates tuberculous arthritis from other arthropathies where these findings are less common.
MRI also can assess other pathologies like
Osteomyelitis
Myositis
Cellulitis
Para-articular abscess
Tenosynovitis
Bursitis
Skin ulceration
Sinus tract
Differential Diagnosis
Erosive arthritis
Rheumatoid arthritis
Septic arthritis
Ankylosing spondylitis
Osteoarthritis
Synovial osteochondromatosis
Pigmented villonodular synovitis
Hemophilic arthropathy
Treatment of Tuberculous Arthritis
The mainstay of treatment of tubercular infection is antitubercular chemotherapy. This holds true for joint tuberculosis too.
Treatment consists of general medical measures, chemotherapy, local conservative orthopedic care, and surgery. Rest, splintage, and surgery are additional options and used as needed.
Antitubercular Drugs
Antitubercular drugs have radically improved the prognosis of tubercular arthritis and the mainstay treatment of tuberculous arthritis is appropriate antitubercular drug therapy.
Early institution of therapy can result in near-complete resolution and preservation of function. I
The drug treatment n general should be of at least 12-18 months though shorter regimens of 9 months to years are also being given.
Splints are used to provide the rest to the involved joint. For example, in tuberculous arthritis of the ankle, a below-knee splint helps to immobilize ankle and thus provide rest.
The duration of splint depends on severity and resolution of the disease.
Surgery
It is less commonly required and is indicated in cases not responding to antitubercular chemotherapy. The therapeutic surgeries can consist of
Open or arthroscopic debridement
Incision and drainage of abscess
Synovectomy
Decompression of spinal structures
References
Jain AK. Tuberculosis of the skeletal system (bones, joints, spine and bursal sheaths). Indian J Orthop. 2010;44(3):356.
Rajasekaran S. Tuberculosis of Bones, Joints, and Spine: Evidence-based Management Guide. Indian J Orthop. 2017;51(6):721. doi:10.4103/ortho.IJOrtho_502_17
Sequeira W, Co H, Block JA. Osteoarticular tuberculosis: current diagnosis and treatment. Am J Ther. 2000 Nov;7(6):393-8.
API Consensus Expert Committee API TB Consensus Guidelines 2006: Management of pulmonary tuberculosis, extra-pulmonary tuberculosis and tuberculosis in special situations. .J Assoc Physicians India. 2006 Mar; 54:219-34.
Arun Pal Singh is an orthopedic and trauma surgeon, founder and chief editor of this website. He works in Kanwar Bone and Spine Clinic, Dasuya, Hoshiarpur, Punjab.
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