Tuberculosis of Bone & Joint

Skeletal tuberculosis (osteoarticular TB) accounts for roughly 10–15% of all extrapulmonary TB and ~1–3% of total TB. It is almost always secondary to a primary focus (lung or lymph node), reaching bone by haematogenous spread. The spine is the most common site, and the disease is notorious for an indolent course, "cold" inflammation, and late presentation with deformity or neurological deficit. This is a perennial favourite of NEET PG examiners — both the orthopaedics and the radiology/medicine angles.

Definition & Classification

Osteoarticular TB is a chronic granulomatous infection of bone, joint, or spine caused predominantly by Mycobacterium tuberculosis (rarely M. bovis). It is paucibacillary (few organisms) but produces extensive caseation and tissue destruction.

Distribution by frequency (high-yield order):

Rank	Site	Eponym / key term
1	Spine (~50%)	Pott's disease / Pott's spine
2	Hip (~15%)	Wandering acetabulum
3	Knee (~15%)	—
4	Foot & ankle, elbow, wrist, shoulder	Caries sicca (dry caries) = shoulder

High-yield: The spine is the commonest site of skeletal TB; within the spine the lower thoracic and thoracolumbar junction (T10–L1) is most often affected. The paradiscal lesion is the commonest type.

Anatomical classification of spinal TB (Pott's):

1. Paradiscal — commonest; two adjacent vertebral end-plates + disc; arteries are end-arteries supplying metaphyseal regions.
2. Central — vertebral body collapse → may mimic tumour/vertebra plana.
3. Anterior (subligamentous) — abscess strips anterior longitudinal ligament; multiple contiguous bodies scalloped.
4. Appendiceal (posterior) — pedicle/lamina/spinous process; rare but more likely to cause cord compression early and mimic tumour.

Etiology & Pathophysiology

• Organism reaches bone via haematogenous route (Batson's venous plexus implicated in spinal spread, also arterial).
• In the spine, infection begins in the anterior part of the vertebral body near the end-plate. The disc is avascular and is destroyed secondarily by loss of nutrition from adjacent end-plates — hence disc space is relatively preserved early (a key TB-vs-pyogenic point).
• Granuloma formation → caseous necrosis → bone destruction → anterior wedging → kyphosis (gibbus).
• Pus is "cold" — lacks the heat, redness and acute features of pyogenic pus because there is little neutrophilic/acute inflammatory reaction. It tracks along fascial planes by gravity to form a cold abscess.

High-yield — cold abscess tracking:

• Cervical spine → retropharyngeal abscess (dysphagia, respiratory difficulty).
• Thoracic → paravertebral / fusiform (bird-nest) abscess.
• Lumbar → psoas abscess tracking down to Scarpa's (femoral) triangle, may point in the groin / petit triangle (lumbar triangle).

Histopathology: Epithelioid cell granulomas with Langhans giant cells and central caseous necrosis — the diagnostic triad.

Clinical Features

General: Insidious onset over weeks–months. Constitutional features — evening rise of temperature, night sweats, malaise, weight loss, loss of appetite. Pain worse at night; "night cries" in children (sudden cry due to muscle spasm relaxing during sleep, allowing inflamed surfaces to grate).

Spinal TB (Pott's disease)

• Back pain (commonest symptom), localised, with paravertebral muscle spasm and a stiff "poker" spine.
• Gibbus — sharp, angular kyphosis from anterior vertebral collapse (knuckle-like prominence).
• Cold abscess (may be the presenting feature).
• Neurological deficit — Pott's paraplegia. Test for Coin test / supporting the head: the child supports the chin/head with hands when bending (rigid spine).

High-yield — Pott's paraplegia (two timing types):

• Early-onset paraplegia (during active disease): due to pressure — abscess, granulation tissue, caseous material, sequestrum. Better prognosis, often reversible with ATT ± decompression.
• Late-onset paraplegia (years later, healed disease): due to mechanical causes — internal gibbus, fibrosis/bony ridge, or reactivation. Worse prognosis.

TB Hip

• Stages: Synovitis → early arthritis → advanced arthritis.
• Attitude evolves: initial FABER (flexion, abduction, external rotation — synovitis, joint capsule most lax) → later flexion, adduction, internal rotation (deformity stage).
• Wandering acetabulum — acetabular destruction with migration of femoral head (radiological hallmark).
• True shortening, positive Thomas test, wasting of gluteal/thigh muscles.

TB Knee

• Triple deformity: flexion, posterior subluxation of tibia, and external rotation.
• "White swelling" — pale, doughy synovial thickening without the warmth of pyogenic arthritis.
• Lobulated swelling, marked muscle (quadriceps) wasting → limb looks spindle-shaped.

Diagnosis & Investigation of Choice

Stepwise approach:

Clinical suspicion → Plain radiograph → MRI (best for spine/soft tissue & cord) → Confirmation by FNAC/biopsy with AFB stain, culture & CBNAAT/GeneXpert → Histopathology

Modality	Role / finding
Plain X-ray	First-line. Needs ≥30% bone destruction to show changes; lytic lesions, reduced disc space (late), wedging, paravertebral shadow.
MRI	Investigation of choice for spinal TB — earliest detection, marrow oedema, disc/end-plate involvement, abscess extent, cord compression, skip lesions.
CT	Best for bony detail / sequestra and image-guided biopsy.
FNAC / biopsy	Confirmatory. AFB smear (Ziehl–Neelsen), culture (gold standard for drug sensitivity), histopathology.
CBNAAT (GeneXpert MTB/RIF)	Rapid; detects MTB + rifampicin resistance in ~2 hours; now front-line in RNTCP/NTEP.
ESR / CRP	Raised, non-specific; useful to monitor response.
Mantoux / IGRA	Supportive only; positive in latent infection too.

High-yield: MRI is the investigation of choice for spinal TB (most sensitive, shows cord compression). The gold standard for confirmation is microbiological/histopathological tissue diagnosis; culture remains the reference for drug-sensitivity testing, while CBNAAT is the rapid front-line test in India.

Radiological TB-specific signs: "Aneurysmal phalangis / spina ventosa" (TB dactylitis — fusiform expansion of a short tubular bone in children). In spine — vertebra plana in central type, anterior scalloping in subligamentous type.

TB vs Pyogenic Spondylodiscitis (must-know comparison)

Feature	Tuberculous spine	Pyogenic spondylodiscitis
Onset	Insidious (weeks–months)	Acute (days)
Systemic toxicity	Low-grade, chronic	High fever, septic
Disc space	Preserved early (destroyed late)	Early destruction of disc
Vertebrae involved	Multiple, contiguous; skip lesions possible	Usually two adjacent
Abscess	Large, cold, well-defined thin smooth wall, calcification	Smaller, thick irregular enhancing wall, no calcification
Site	Anterior body, paradiscal	Disc-centred
Bone sclerosis/new bone	Minimal	Prominent reactive sclerosis
Common organism	M. tuberculosis	Staph. aureus

High-yield: Relative disc preservation with anterior body destruction, large calcified cold abscess, and a smooth thin abscess wall point to TB; early disc destruction with reactive sclerosis points to pyogenic infection.

Management & Drug of Choice

Cornerstone = Anti-tubercular therapy (ATT). Most osteoarticular TB heals with chemotherapy alone; surgery is selective.

ATT regimen (DOTS / NTEP — weight-band, daily fixed-dose combination):

• Intensive phase (2 months): HRZE — Isoniazid (H) + Rifampicin (R) + Pyrazinamide (Z) + Ethambutol (E).
• Continuation phase: HRE (or HR) — for bone & joint TB extended duration.

High-yield — duration: Skeletal/spinal TB is treated for a prolonged course, generally 9–12 months (extended from the standard 6 months). The intensive phase is 2 months HRZE, continuation 7–10 months. Spinal TB in particular often gets 12 months.

First-line drug toxicities (frequently asked):

Drug	Key adverse effect	Note
Isoniazid (H)	Peripheral neuropathy, hepatitis	Give pyridoxine (B6) prophylaxis
Rifampicin (R)	Hepatotoxicity, orange-red secretions, drug interactions (CYP inducer)	Most potent sterilising drug
Pyrazinamide (Z)	Hepatotoxicity, hyperuricaemia/arthralgia	Best in acidic/intracellular environment
Ethambutol (E)	Retrobulbar (optic) neuritis — colour vision loss	Dose-related; check vision
Streptomycin	Ototoxicity (CN VIII), nephrotoxicity	Second-line injectable

Adjuncts: Rest/immobilisation (brace, traction), nutritional support, analgesia, graded mobilisation.

Surgical indications

Mnemonic for spinal surgery indications:

1. Neurological deficit not improving (or worsening) after a trial of ATT — or progressive deficit.
2. Drainage of a large/compressive cold abscess.
3. Instability / progressive deformity (severe kyphosis, panvertebral disease).
4. Doubtful diagnosis — need for tissue (biopsy).
5. Failure of conservative treatment / non-response.

High-yield: Anterior debridement + decompression with strut bone grafting is the classic Hong Kong operation for spinal TB with cord compression. The "middle-path regimen" of Tuli: ATT for all, with surgery reserved for specific indications — a favourite exam concept.

Joint TB (hip/knee): ATT + rest; arthrodesis for a painful destroyed joint in young adults; total joint arthroplasty can be considered in quiescent/healed disease (some advocate after disease control with ATT cover).

Paradoxical Reaction

A transient clinical/radiological worsening (enlarging abscess, new lesions, increasing oedema on MRI) despite appropriate ATT, occurring weeks–months into treatment — due to an enhanced immune response to mycobacterial antigens (an IRIS-like phenomenon, especially in HIV co-infection after starting ART).

High-yield — Paradoxical reaction: It is NOT treatment failure or drug resistance. Confirm adherence, rule out resistance/secondary infection, continue the same ATT; consider a short course of corticosteroids and aspiration if symptomatic. Do not abandon the regimen.

Complications

• Neurological: Pott's paraplegia (early/late), bladder–bowel involvement, quadriplegia (cervical).
• Deformity: Gibbus, severe kyphosis, scoliosis; cosmetic and cardiopulmonary effects in children (kyphos > growth-related deterioration).
• Cold abscess → may burst → sinus formation → secondary pyogenic infection.
• Joint destruction → ankylosis, limb-length discrepancy, fixed deformities.
• Amyloidosis in long-standing chronic suppuration.
• Drug resistance (MDR/XDR-TB) with non-adherence.

Key Differentials

• Pyogenic spondylodiscitis / osteomyelitis (see table above) — early disc loss, acute, sclerosis.
• Brucellar spondylitis — endemic areas, lower lumbar, less deformity, "parrot's beak" osteophyte; minimal kyphosis.
• Metastasis / multiple myeloma — pedicle destruction with disc preservation, no paravertebral cold abscess (but central TB can mimic).
• Fungal spondylitis, typhoid spine.
• Hip: Perthes disease, transient synovitis, juvenile idiopathic arthritis, pyogenic arthritis.
• Knee: Monoarticular JIA, pigmented villonodular synovitis, haemophilic arthropathy.

High-yield: Pedicle (posterior element) destruction with a preserved disc → think metastasis/myeloma, whereas anterior body + disc with a paravertebral/psoas cold abscess → think TB.

Recently asked / exam angle

• Investigation of choice for spinal TB → MRI. Earliest, shows cord compression and abscess extent.
• Commonest site of skeletal TB → spine; commonest spinal type → paradiscal; commonest region → thoracolumbar (D10–L1).
• Disc space preserved early in TB; destroyed early in pyogenic — classic single-best-answer discriminator.
• Early vs late Pott's paraplegia — early due to pressure (good prognosis), late due to mechanical/healed disease (poor prognosis).
• Cold abscess from lumbar spine → psoas abscess → femoral triangle.
• Ethambutol → optic neuritis; Isoniazid → peripheral neuropathy (give pyridoxine).
• Paradoxical reaction = continue ATT, not failure — increasingly tested with HIV/IRIS.
• Tuli's middle-path regimen / Hong Kong (anterior) procedure — surgery concept.
• Spina ventosa = TB dactylitis (short tubular bones in children).
• Caries sicca = TB of the shoulder (dry, little abscess/destruction).
• Wandering acetabulum = TB hip radiological sign.
• CBNAAT/GeneXpert rapidly detects MTB + rifampicin resistance — front-line in India's NTEP.

Rapid revision

1. Skeletal TB is secondary & haematogenous; spine > hip > knee.
2. Commonest spinal lesion is paradiscal at the thoracolumbar junction; central type → vertebra plana.
3. Disc preserved early in TB, destroyed late — opposite of pyogenic.
4. MRI = investigation of choice; FNAC/biopsy + culture/CBNAAT = confirmation; culture = gold standard for sensitivity.
5. Histology = caseating granuloma with Langhans giant cells.
6. Gibbus = angular kyphosis from anterior collapse; cold abscess tracks along fascia (lumbar → psoas → groin).
7. Early Pott's paraplegia (pressure, good prognosis) vs late (mechanical/healed, poor prognosis).
8. ATT = 2 HRZE + continuation, total 9–12 months for bone/spine.
9. Ethambutol → optic neuritis; INH → neuropathy (give B6); pyrazinamide → hyperuricaemia; rifampicin → orange urine + hepatitis.
10. Surgery indications: progressive/non-responding deficit, abscess drainage, instability/deformity, diagnostic doubt, conservative failure — Tuli's middle-path regimen; anterior decompression + strut graft = Hong Kong operation.
11. Paradoxical reaction = worsening on correct ATT → continue therapy, add steroids if needed; NOT failure.
12. Mimics: metastasis/myeloma destroy pedicles with disc sparing; brucella causes minimal deformity; caries sicca = shoulder, spina ventosa = dactylitis, wandering acetabulum = hip.