PA32.{1,4} | Osteomyelitis & Paget Disease of Bone — Summary & Reflection

REFLECT

Before you proceed to the summary, take a few minutes to test your own integration of this material.

Scenario A: A 12-year-old boy presents with fever, swollen knee, and inability to walk. X-ray is normal at day 3. MRI shows T2 hyperintense signal in the distal femoral metaphysis. Blood culture grows S. aureus.
• What is your diagnosis? What morphological stage are we at?
• What will happen if IV antibiotics are started immediately vs. if treatment is delayed 2 weeks?
• At 2 weeks without treatment, what structure forms that represents dead bone? What new bone forms around it?

Scenario B: A 68-year-old man is referred to you (as the pathologist) with a biopsy from the tibia. Histology shows irregular lamellar bone fragments joined by numerous prominent basophilic cement lines. There are giant osteoclasts with >40 nuclei.
• What is your diagnosis?
• Which phase of the disease are you most likely in, given the hyperactive osteoclasts?
• What will happen to this patient's serum ALP? His 8th cranial nerve?
• What is the 1% complication that kills patients with this disease?

Write your answers in your notebook — compare with the summary below.

KEY TAKEAWAYS

Osteomyelitis — key framework:

• Classification: Route (hematogenous > contiguous > direct) × Organism (pyogenic: S. aureus 80% > TB > others) × Time (acute/subacute/chronic)
• Pathogenesis of hematogenous OM: Bacteremia → metaphyseal sinusoidal lodgment (slow flow, reduced phagocytosis) → suppuration → pressure necrosis → sequestrum (dead bone) + involucrum (reactive new bone shell) + cloaca (opening) + sinus tract
• Brodie abscess: Subacute walled-off lytic cavity with sclerotic rim; metaphysis; S. aureus; mimics tumour
• Radiology: Early = normal X-ray (bone scan + MRI positive); Late = lytic + sequestrum + involucrum + sclerosis
• Complications: Chronic OM, septic arthritis, growth disturbance, secondary AA amyloidosis (chronic sinus), Marjolin ulcer = SCC at sinus tract
• TB osteomyelitis (Pott disease): Thoracolumbar spine; caseating granulomas; cold abscess; gibbus deformity; paraplegia; no sequestrum
• Special organisms: Sickle cell → Salmonella; IV drug user → Pseudomonas

Paget Disease of Bone — key framework:

• Etiology: Paramyxovirus + genetic (SQSTM1/p62 → NF-κB → osteoclast hyperactivation)
• 3 phases: Osteolytic (osteoporosis circumscripta / blade-of-grass) → Mixed (combined lytic + sclerotic; highest ALP) → Osteosclerotic (cotton-wool skull; ivory vertebra)
• Pathognomonic micro: Mosaic/jigsaw cement-line pattern (irregular lamellar bone fragments with prominent basophilic cement lines) + giant hypernucleated osteoclasts
• Biochemistry: ALP markedly elevated (osteoblast marker); urinary hydroxyproline elevated (osteoclast/collagen breakdown marker); calcium and phosphate normal (distinguishes from hyperparathyroidism)
• Complications (5 HIGH-YIELD):
1. Chalk-stick pathological fracture (transverse)
2. Nerve compression — VIII nerve deafness most common
3. High-output cardiac failure (AV shunting through hypervascular bone)
4. Secondary osteosarcoma (~1% polyostotic — most feared)
5. Basilar invagination (brainstem compression)