Pathogenesis of Acute Osteomyelitis

This is a short powerpoint made animation video for the pathogenesis of acute osteomyelitis.

Osteomyelitis is defined as an inflammation of the bone caused by an infecting organism. The infection may be limited to a single portion of the bone or may involve numerous regions, such as the marrow, cortex, periosteum, and the surrounding soft tissue. The infection generally is due to a single organism, but polymicrobial infections can occur, especially in the diabetic foot.

Osteomyelitis presents in 3 stages with ill-defined transitions: Acute, subacute, and chronic. These transition indicates that therapeutic measures have been inadequate or inappropriate or that the organisms are especially resistant. Arbitarily, acute osteomyelitis has been defined as those with duration of less than 2 weeks, subacute as those with duration of 2-6 weeks and chronic as those with duration more than 6 weeks. A more accurate definition is that the osteomyelitis is acute as long as the predominant histological and clinical picture is that of acute infection. When chronic inflammation and the secondary changes due to dysvascularity and scarring begin, the disease is defined as chronic.1

Progression of Acute Hematogenous Osteomyelitis:

  1. Inflammation
  2. Suppuration
  3. Bone necrosis
  4. Reactive new bone formation
  5. Resolution and healing

Common causative organisms of Acute Osteomyelitis:

  • S. aureus (commonest)
  • Garm negative: increasing number of vertebral infections
  • IVDU: Pseudomonas
  • Chornically ill: Fungal
  • Sickle cell: Salmonella (diaphyseal rather than metaphyseal)
  • 2-4 weeks (neonates): GBS
  • 6 months to 4 yrs: H. influnezae
  • <4 yrs: Kingella kingae (PCR needed for diagnosis)

Transcript for the video:

The possible routes of infection can be either hematogenous from septic focus like a boil or a sore throat or it can follow direct inoculation from an open fracture or a surgery. It can also spread from the infection of the adjacent sites like odontogenic infections leading to the osteomyelitis of the jaw.

Edema and pus formation from acute inflammation leads to significant rise in the intramedullary pressure. This leads to vascular collapse resulting in ischemic necrosis of the bone.

The pressurized focus of infection can also force its way to the bone cortex and ultimately under the periosteum which can separate the it from the underlying bone leading to further compromise of the bone’s vascular supply contributing to bone ischemic necrosis. Particularly in children where bone and periosteum are loosely adhered, the infection can generate sub-periosteal abscesses or spread along sub-periosteal planes into adjacent joints. In adults, the infection can dissect through the periosteum and generate sinus tracts to the skin.

osteomyelitis pathogenesis

With progression to chronic osteomyelitis, pieces of dead necrotic bone, termed “sequestra” can be observed with shells of reactive bone forming around them, termed “involucra”, representing a healing response aimed at isolating foci of infection from surrounding healthy bone.

Common organisms causing acute osteomyelitis are Staphylococcus aureus, Escherechia coli, Streptococci, Pseudomonas and Salmonella in cases of Sickle cell disease, Hemophilus influenza, Group B Streptococci and Mixed infection in cases of inoculation.

Salmonella osteomyelitis is common in sickle cell disease due to hyposplenism, complement deficiency and bowel infarction leading to translocation of salmonella.

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