Page 2 of 20

PA32.{1,4} | Osteomyelitis & Paget Disease of Bone — SDL Guide (Part 2)

Radiological Features of Osteomyelitis

Radiology follows a temporal sequence that directly mirrors the pathology:

Acute phase (days 1–10 — X-ray may be NORMAL)
• X-rays: soft tissue swelling only; bone changes appear only after 30–50% of bone is destroyed — this is the clinical trap from the opening story
• Bone scan (Tc-99m) is positive within 24–48 hours — the gold standard for early detection
• MRI is the most sensitive early imaging: marrow edema (T2 hyperintense signal) before X-ray changes

Subacute to chronic phase
• Periosteal reaction — new bone laid down by the periosteum (involucrum) appears as a thin or thick line parallel to the cortex
• Lytic lesion — focal area of bone destruction within the metaphysis
• Dense sequestrum — high-density dead bone fragment within the lytic cavity (pathognomonic when present)
• Cortical thickening and sclerosis — in chronic disease, reactive bone formation predominates

CT scan is excellent for detailing sequestrum morphology and planning surgery (debridement, sequestrectomy).

Feature	Acute OM	Chronic OM
X-ray	Normal or soft tissue swelling	Lytic cavity + dense sequestrum + sclerosis
Periosteum	Early elevation	Thick involucrum
Bone scan	Positive early	Positive (less specific)
MRI	Marrow edema (T2↑)	Complex mixed signal, sinus tracts

Radiological Features of Acute vs Chronic Osteomyelitis

Complications of Osteomyelitis

Missed or inadequately treated osteomyelitis carries serious long-term consequences:

Local complications:
• Chronic osteomyelitis — the most common complication; persistent infection with intermittent flares; difficult to eradicate without surgical removal of the sequestrum
• Septic arthritis — pus breaches the joint; common in infants where metaphyseal vessels cross the epiphyseal plate; also at hip (where metaphysis is intracapsular)
• Pathological fracture — weakened bone fractures through the infected zone
• Growth disturbance — infection at or near the growth plate → premature fusion → limb length discrepancy in children

Sinus tract complications:
• Secondary (AA) amyloidosis — chronic suppuration drives sustained acute-phase response → overproduction of serum amyloid A (SAA) → SAA deposits as amyloid fibrils in kidney, liver, spleen → proteinuria, nephrotic syndrome, renal failure
• Marjolin ulcer — squamous cell carcinoma (SCC) arising in the chronically inflamed, epithelialised sinus tract; latency period 20–40 years; highly aggressive, metastasises early. This is a classic "chronic wound → malignancy" transformation and a high-yield exam question.

Systemic:
• Septicaemia and septic shock — in acute, inadequately treated cases
• Endocarditis, meningitis, pneumonia — via hematogenous seeding from the infected focus

Renal AA Amyloidosis — Congo Red Stain (Bright Field and Polarised Light)

Tuberculous Osteomyelitis: Pott Disease of the Spine

Tuberculous osteomyelitis is caused by Mycobacterium tuberculosis reaching bone via hematogenous spread from a primary (usually pulmonary) focus. In India, it is the most important form of bone TB and a major cause of preventable paraplegia.

Site predilection: Vertebral column — thoracolumbar junction (T10–L2) is most commonly affected, though any vertebra can be involved. This is "Pott disease" (named after Percivall Pott, 1779).

Pathogenesis:
1. Bacteria seed the anterior subchondral bone of a vertebral body via arterial supply
2. Caseating granulomatous inflammation destroys vertebral bone — note: no sequestrum (TB causes caseation, not pus; organisms survive in caseous material)
3. Infection spreads under the anterior longitudinal ligament to adjacent vertebrae → characteristic involvement of two or more adjacent vertebral bodies ("skip lesions" are unusual in TB, unlike pyogenic OM)
4. Infected caseous material tracks along fascial planes → cold (paraspinal) abscess — "cold" because there is no heat, redness, or tenderness (granulomatous inflammation, not acute suppuration)

Morphology:
• Caseating granulomas — central caseous necrosis surrounded by epithelioid macrophages, Langhans giant cells, lymphocytes
• No sequestrum; the destroyed bone is replaced by caseous material
• Intervertebral disc destruction — unlike pyogenic vertebral OM, which often spares the disc early; TB destroys the disc along with bone

Radiological features:
• Anterior vertebral body erosion → vertebral collapse → wedge deformity
• "Gibbus" deformity — sharp angular kyphosis at the site of collapse ("hunchback" — historic term)
• Paraspinal cold abscess — fusiform soft-tissue shadow beside the spine on AP chest X-ray ("psoas abscess" at lumbar levels)
• Disc space loss (early, distinguishes from metastasis)

Complications: Paraplegia ("Pott paraplegia") from cord compression by abscess or bone collapse; sinus tract; secondary amyloidosis in prolonged cases.

Pott Disease — Lateral Spinal X-ray Features & Wedge Collapse Mechanism