Pathophysiology of osteomyelitis

1. Hematogenous spread from transient or sustained bacteremia, especially in children
2. Contiguous spread from adjacent soft-tissue infection, such as a diabetic foot ulcer
3. Direct inoculation after open fracture, trauma, orthopedic surgery, or an implant

Sequence of events

1. Bacterial seeding and adherence
   • Organisms lodge in bone, commonly in the metaphysis of long bones in children.
   • Metaphyseal capillary loops have slow, turbulent flow, which favors bacterial deposition.
   • S. aureus expresses adhesins that bind bone-matrix proteins such as collagen, promoting attachment.
   • In adults, direct inoculation and contiguous spread are relatively more common.
     Robbins & Kumar Basic Pathology, pp. 3787-3800.
2. Acute inflammatory response
   • Bacterial multiplication triggers influx of neutrophils, inflammatory cytokines, edema, and formation of pus within the marrow cavity.
   • The rigid bony cortex limits expansion. Therefore, rising intramedullary pressure compresses small vessels.
3. Vascular compromise and bone necrosis
   • Edema, vascular congestion, thrombosis of small vessels, and raised intramedullary pressure reduce blood supply.
   • Ischemia causes osteocyte death and necrosis of portions of bone. The resulting devitalized piece of bone is a sequestrum.
     Grainger & Allison's Diagnostic Radiology, pp. 1621-1639.
4. Cortical spread and subperiosteal abscess
   • Pus extends through Haversian and Volkmann canals to the cortex.
   • It may break through the cortex and elevate the periosteum, producing a subperiosteal abscess.
   • Periosteal elevation further impairs cortical blood supply, worsening necrosis.
5. Reactive new-bone formation
   • The lifted periosteum forms new bone around the sequestrum.
   • This shell of viable new bone is the involucrum.
   • Openings in the involucrum, called cloacae, permit pus to drain into adjacent soft tissue.
6. Chronic osteomyelitis
   • Infection may persist because the sequestrum is avascular, so host immune cells and systemic antibiotics penetrate poorly.
   • Bacteria, particularly staphylococci, can form a biofilm on necrotic bone or orthopedic implants. Biofilm reduces bacterial metabolic activity and shields organisms from immune clearance and antibiotics.
   • Persistent drainage can form a sinus tract to skin. Chronic inflammation causes marrow fibrosis, sclerosis, recurrent abscesses, and bone deformity.

Simplified flowchart

Why children often have metaphyseal disease