Tuberculosis (TB) can cause joint disease primarily through the spread of Mycobacterium tuberculosis bacteria from the lungs or other primary sites of infection to the bones and joints. This process is known as extrapulmonary tuberculosis, where the bacteria disseminate via the bloodstream or lymphatic system to distant sites, including the skeletal system. Once the bacteria reach the joints, they initiate a chronic inflammatory response that leads to joint destruction and disease.
The mechanism begins when Mycobacterium tuberculosis infects the body, usually entering through the lungs. The immune system responds by forming granulomas—clusters of immune cells that wall off the bacteria to contain the infection. However, these granulomas do not eradicate the bacteria completely; instead, the bacteria can persist in a latent state. If the immune system weakens or fails to contain the infection, the bacteria can reactivate and spread. When TB bacteria enter the bloodstream, they can seed various organs, including bones and joints, causing localized infections.
In the joints, tuberculosis typically affects weight-bearing joints such as the hips, knees, and spine, but it can involve any joint. The infection usually starts in the synovium, the lining of the joint, where the bacteria multiply and provoke a chronic inflammatory reaction. This inflammation causes the synovium to thicken and produce excess fluid, leading to swelling and pain. Over time, the infection spreads to adjacent cartilage and bone, causing erosion and destruction of joint structures.
The pathological process involves the formation of tuberculous granulomas within the joint tissues. These granulomas contain infected macrophages, epithelioid cells, lymphocytes, and fibroblasts. At the center of the granuloma, caseous necrosis—a form of tissue death with a cheese-like appearance—develops due to the immune response and bacterial activity. This necrotic tissue damages the joint surfaces and underlying bone. The chronic inflammation and necrosis lead to progressive joint destruction, deformity, and loss of function if untreated.
In spinal tuberculosis, also known as Pott’s disease, the infection often affects the vertebral bodies. The bacteria spread from one vertebra to adjacent ones through the blood supply and along ligaments, causing vertebral collapse, deformity, and sometimes abscess formation. This can lead to severe complications such as spinal cord compression and neurological deficits.
The clinical manifestations of joint tuberculosis include chronic joint pain, swelling, stiffness, and reduced mobility. Because the symptoms develop slowly and mimic other joint diseases like rheumatoid arthritis or osteoarthritis, diagnosis can be delayed. The disease may also cause systemic symptoms such as fever, weight loss, and night sweats, reflecting the underlying infection.
Risk factors that increase susceptibility to joint tuberculosis include immunosuppression (due to diseases like HIV or autoimmune conditions), malnutrition, diabetes, and advanced age. Patients with rheumatic diseases who are treated with immunosuppressive drugs are particularly vulnerable to reactivation or new infection of TB in the joints.
Treatment of joint tuberculosis requires prolonged antibiotic therapy targeting Mycobacterium tuberculosis, often combined with surgical intervention to drain abscesses or stabilize damaged joints. Early diagnosis and treatment are crucial to prevent irreversible joint damage and disability.
In summary, tuberculosis causes joint disease by hematogenous or lymphatic spread of Mycobacterium tuberculosis to the joint tissues, where it induces a chronic granulomatous inflammatory response. This leads to tissue necrosis, destruction of cartilage and bone, and progressive joint dysfunction. The disease’s slow progression and nonspecific symptoms often delay diagnosis, making awareness and early intervention essential for preserving joint health.