Skeletal tuberculosis is a form of extrapulmonary tuberculosis caused by the bacterium Mycobacterium tuberculosis. This infection specifically affects the bones, joints, and spine, and is also known as osteoarticular or bone tuberculosis. Spinal involvement is historically referred to as Pott’s disease. Although skeletal tuberculosis is a relatively rare manifestation, accounting for a small percentage of all cases, it can lead to severe destruction and deformity if not promptly diagnosed and treated.
How the Infection Reaches the Skeletal System
The journey of Mycobacterium tuberculosis from the initial site of infection, typically the lungs, to the bone occurs primarily through the bloodstream, a process known as hematogenous spread. This dissemination usually happens during a primary infection. The bacilli travel through the systemic circulation and tend to settle in areas with a rich blood supply, such as the metaphyseal regions of long bones or the vertebral bodies of the spine.
Once the bacteria reach the bone, they establish a focus of infection that can remain dormant for years before causing active disease. The highly vascularized nature of the vertebral bodies makes the spine a frequent target, accounting for approximately half of all bone and joint tuberculosis cases. The infection often manifests later as a result of the reactivation of latent bacteria, causing inflammation and tissue destruction within the bone marrow and adjacent tissues.
Recognizing the Specific Symptoms
Skeletal tuberculosis is characterized by a slow, insidious onset of symptoms, often leading to a significant delay in diagnosis. Unlike acute bacterial infections, systemic symptoms like fever or weight loss are often absent or subtle, complicating early recognition. The presentation depends heavily on the location of the infection, which most commonly involves the spine or peripheral joints like the hips and knees.
When the spine is involved (Pott’s disease), the primary symptom is progressive, chronic, non-specific back pain. As the infection destroys the vertebral bodies, their collapse can cause a characteristic forward angulation of the spine known as kyphosis or a gibbus deformity. Vertebral destruction can also result in large paraspinal abscesses, collections of pus that may track along fascial planes and present as a soft, painless swelling far from the site of infection, termed a “cold abscess.”
In advanced spinal cases, the disease can compromise the spinal cord, leading to neurological deficits such as muscle weakness, sensory changes, or paralysis (paraplegia). When the infection affects peripheral joints, it typically presents as pain, swelling, and limited range of motion, often mimicking other forms of arthritis. Tuberculous arthritis is generally “cold,” lacking the intense heat and redness seen in acute bacterial arthritis.
Confirming the Diagnosis
Confirming bone tuberculosis involves clinical suspicion, imaging studies, and definitive microbiological testing. Initial screening may use blood tests, such as a tuberculin skin test or an interferon-gamma release assay, to look for an immune response. However, these tests indicate exposure, not necessarily active skeletal disease. Imaging is performed to assess the extent of damage to the bone and surrounding soft tissues.
X-rays are often the first imaging modality used, but they may only show advanced stages of disease, such as bone destruction or joint space narrowing. Computed Tomography (CT) scans offer better detail of early bone destruction and are useful for detecting paraspinal fluid collections or abscesses. Magnetic Resonance Imaging (MRI) is considered the preferred imaging method, providing the clearest visualization of soft tissue involvement, marrow edema, and potential spinal cord compression.
Definitive diagnosis requires obtaining a tissue sample or fluid from the affected site for laboratory analysis, typically via a needle biopsy or abscess aspiration guided by CT imaging. The sample is tested using microbiological culture to grow M. tuberculosis and Nucleic Acid Amplification Tests (NAAT), such as PCR, to quickly detect the bacteria’s genetic material. Since skeletal samples are often “pauci-bacillary” (containing few bacteria), culture results may be slow or negative, making PCR and histopathological evidence of typical tuberculous granulomas important for confirmation.
Long-Term Treatment Protocols
Treatment for skeletal tuberculosis is primarily pharmaceutical, relying on a prolonged course of multi-drug anti-tuberculosis therapy. The standard regimen mirrors that used for pulmonary tuberculosis but is often extended due to slower drug penetration and reduced blood supply within the bone tissue. The initial phase typically lasts two months and involves a combination of four first-line drugs:
- Isoniazid (H)
- Rifampicin (R)
- Pyrazinamide (Z)
- Ethambutol (E)
Following the initial phase, the continuation phase involves a reduced number of drugs, usually Isoniazid and Rifampicin. The total duration of drug therapy is generally recommended to be longer than the six months used for uncomplicated pulmonary disease. Treatment often lasts between 9 to 12 months, though guidelines may suggest up to 18 months for extensive disease, drug resistance, or central nervous system involvement.
Surgery plays a supporting role and is reserved for specific complications, not as the primary treatment. Intervention may be necessary in cases of significant spinal instability, severe kyphotic deformity, or neurological deficit due to spinal cord compression. Procedures can involve debridement of infected tissue or stabilization of the spine to prevent further collapse and protect the nervous system. Monitoring the patient’s response is based on clinical improvement and follow-up imaging.