Knee Joint Tuberculosis

Knee TB, like other osteoarticular TB, is secondary, mostly from pulmonary TB. In large domestic series it ranks second after spinal TB and first among the six major joints; foreign literature places it first or second. It is most common in children under 10 with no sex predilection; long course and epiphyseal involvement often cause growth deformity. It is usually unilateral, with bilateral cases rare. Classified as simple synovial TB, simple osseous TB, and total joint TB.

Common Symptoms

Fatigue; lymphadenopathy; Yan Tie; tuberculous lymphadenitis; anorexia; night sweats; low fever; weight loss; muscle atrophy

Causes and Pathogenesis

(1) Etiology: The knee is the largest hinge joint, with mismatched hemispherical and tibial plateau articular surfaces that are unstable and easily injured. Located mid-point of the weight-bearing lower limb, it bears large lever forces and is prone to strain and sprains causing hemarthrosis and synovial injury. The knee has the richest synovium and a rich but slow terminal vascular network where bacilli lodge. Human TB is caused by human and bovine types, which do not directly invade joints but seed hematogenously after pulmonary lesions. Bacilli grow slowly and may remain latent until declining immunity allows proliferation. Thus knee TB relates to bacillary number/virulence, the joint's anatomy/mechanics, and host resistance. (2) Pathogenesis: A series of destructive processes involving synovium, bone, and cartilage, mostly secondary to pulmonary TB (often already resolved/fibrosed/calcified). Primary foci form in childhood; hematogenous emboli are mostly killed, a few walled off by fibrous tissue; later reactivation causes lesions. The knee's rich synovium means synovial TB is most common, then osseous and total. Osseous TB occurs in the distal femoral epiphysis/metaphysis and proximal tibial condyles; central type forms sequestra and cavities, marginal type (metaphyseal) has fewer sequestra. Marginal lesions near the joint easily penetrate cartilage causing total joint TB. Fibular head and tibial tubercle TB are rare; patellar TB (central or marginal) easily penetrates the articular surface. Synovial TB starts as congestion, edema, and serous effusion, later thickening. Early total joint TB has marginal cartilage/subchondral destruction with most articular cartilage intact, preserving some function if controlled. Late total joint TB destroys most articular cartilage and bone, involving menisci and cruciate ligaments; capsular/ligamentous laxity allows posterolateral tibial dislocation under hamstring/iliotibial band pull. Growth plate destruction in children causes shortening or lengthening. Untreated late disease develops cold abscesses, mixed infection, chronic sinuses, and fibrous or bony ankylosis with flexion/varus/valgus deformity, especially tibial abduction-flexion-external rotation subluxation causing lifelong disability.

Treatment

Supportive therapy, rehabilitation

Preventive Measures

This is a local manifestation of systemic TB, second among limb joint TB. Besides symptomatic treatment to improve knee function, treating the primary TB focus is key.

Department to Visit

It is recommended to visit the Orthopedic Surgery department; an appointment can be booked on this platform before the visit.

Warm reminder: The above information is for health science reference only and cannot replace professional medical diagnosis. If you have related symptoms, please seek medical attention at a regular hospital promptly.