Tuberculosis of bones and joints is a granulomatous inflammation caused by Myobacterium tuberculosis. It is a localized and destructive disease that is usually blood-borne from a primary focus such as infected peribronchial or mesenteric lymph nodes.

The infection may be either of the human or the bovine type. In countries where raw milk is used extensively, bovine transmission is common, whereas in areas where milk is pasterurized and there is rigid control of dairy herds, the bovine type is extremely rare and the human type is more common.

The incidence of tuberculosis has greatly declined in the past three decades owing to the discovery of antituberculous drugs and the enforcement of strict public health measures such as pasteurization and the reporting and isolation of patients with active tuberculosis.

But in economically well-developed countries it is still prevalent.

Tuberculosis of bones and joints is more common in children, though it may occur at any age.

Pathology

The infection of a joint by the tubercle bacillus may occur by direct hematogenous infection of the synovial membrane (synovial tuberculosis) or by indirect spread from a focus in an adjacent bone, e.g., in the metaphysis or epiphysis.

Tuberculous osteomyelitis is characterized by destruction of bone with little or no tendency for new bone formation.

The tuberculous bone focus spreads with increasing centrifugal destruction of surrounding bone, finally breaking into the joint. The synovial membrane reacts first by excessive secretion of fluid and later by proliferation, thickening, studding of its inner surface with tubercles, and fibrosis of its outer surface.

The tuberculous granulation tissue soon covers the hyaline articular cartilage as a pannus 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 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. A thick fibrous wall lines the tuberculous abscess, which contains serum along with caseous necrotic tissue, tubercle bacilli, and degenerating leukocytes.

If the original focus remains active and these abscesses remain untreated, they will rupture externally through the skin to form sinuses, the results being the inevitable secondary infection by pyogenic bacteria, and complete destruction of the affected joint.

Clinical Features

Tuberculous arthritis is  monarticular in 90 percent of cases.

Typically, the child appears generally ill, is easily fatigued, and has evident weight loss. A family history of tuberculosis or a personal history of cervical adenitis or pleurisy may be obtained.

If the lesion is in the lower limb, for instance, in the hip, the initial symptom may be a slight limp due to discomfort. The affected joint will be stiff, and soon the “night-cries” develop; because irritation from the process is low-grade, muscle spasm protects the part quite satisfactorily during the day, but when the child is asleep the protective action of the muscles is lost, and on motion, pain is produced; hence, the cry.

Local physical signs vary according to the joint involved. The vertebral column is the most common site, the next in order of frequency being the hip, knee, ankle, sacroiliac, shoulder, and wrist joints.

In superficial joints, such as the knee or elbow, synovial thickening and effusion present as a fullness or bogginess. This may be difficult to detect in the deep joints such as the hip. Local heat and redness are usually absent, and tenderness is minimal. Muscle atrophy is usually marked and is often present in the early stages. Joint motion is usually limited.

Temperature elevation is ordinarily not marked.

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