Treatment of spinal tuberculosis- Evolution in last 50 years

Extrapulmonary tuberculosis (EPTB), including bone and joint involvement, was historically considered an extension of pulmonary disease and managed empirically with uniform treatment protocols. Over the past five decades, this perception has undergone a major transformation with EPTB now recognized as distinct clinical entity accounting for 15-25% of all TB cases, frequently affecting children, women, and immunocompromised individuals, often without pulmonary involvement, and contributing significantly to long-term morbidity. Spinal tuberculosis (STB) represents a unique form of EPTB characterized by a complex interplay of infection, biomechanics, and functional impairment. Unlike pulmonary TB, which is a multibacillary disease occurring in oxygen-rich lung tissue, STB is a paucibacillary disease arising in relatively hypoxic cancellous bone. Its pathology is driven largely by host immune response, leading to vertebral destruction, abscess formation, spinal instability, kyphotic deformity, and neurological deficits. Healing often occurs with fibrosis and bony fusion but may leave permanent structural and functional sequelae. The diagnostic paradigm has shifted from reliance on clinical suspicion and plain radiography to advanced imaging and tissue-based confirmation. MRI has emerged as the gold standard for early detection, assessment of disease extent, neural compression, and treatment monitoring. CT provides detailed evaluation of bony destruction and facilitates image-guided biopsy. Tissue diagnosis, combining histopathology, AFB smear/culture and microbiological techniques including CBNAAT and line probe assays, is now essential to ascertain etiology and detect drug resistance. This integrated diagnostic approach has significantly improved accuracy and enabled individualized management. Therapeutically, STB management has evolved from prolonged empirical regimens and immobilization to evidence-based, multidrug chemotherapy combined with selective surgical intervention. Standard treatment for drug-sensitive STB includes an intensive phase with isoniazid, rifampicin, pyrazinamide, and ethambutol, followed by a continuation phase tailored to disease severity, typically extending to 12 months. STB to be treated till healed status is demonstrated by contrast MRI/PET scan. Molecular diagnostics have facilitated early detection of drug resistance, enabling personalized second-line therapy in drug-resistant STB. Principles of treatment emphasize daily weight-based dosing, strict adherence, and uninterrupted therapy. Surgical management has transitioned from decompression alone to comprehensive strategies integrating decompression, stabilization, and deformity correction, with instrumentation now considered safe in infected bone. A major advancement has been the shift in treatment goals from mere infection control to a composite outcome encompassing clinical recovery, normalization of inflammatory markers, radiological healing, preservation of spinal stability, prevention of deformity, and restoration of function. Early diagnosis and risk stratification are critical, particularly in children, to prevent progressive kyphosis and long-term disability. In summary, STB has evolved from a disease associated with high mortality and disability to a condition with predictable healing and improved outcomes. Advances in imaging, molecular diagnostics, chemotherapy, and surgical techniques have transformed its management into a multidisciplinary, evidence-based approach focused on early diagnosis, individualized therapy, and functional restoration.