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Infection of bone is called osteomyelitis and usually involves the cortex, medulla and periosteum.

The main causative organisms include Staphylococcus aureus, Escherichia coli (particularly in infants and the very elderly), Salmonella (particularly in patients with sickle-cell disease), and Mycobacterium tuberculosis.

In osteomyelitis the infective organisms gain access to the medullary cavity of the bone by two main routes:

1 Direct access through an open wound. This is an important cause after trauma, particularly when trauma has been followed by an open fracture, and can lead to failed or delayed fracture repair.

2 Blood-borne spread following bacteraemia from a focus of sepsis elsewhere, e.g. acute pyelonephritis. Tuberculous osteomyelitis is the result of blood-borne spread from a primary tuberculous infective lesion in the lung.

In all forms of osteomyelitis (except for TB) the marrow cavity becomes filled with a purulent acute inflammatory exudate, leading to necrosis of medullary bone trabeculae. Destruction of the cortical bone may lead to the discharge of pus into extraosseous connective tissue, and the infection may track through to the skin surface, producing a chronic discharging sinus. Because the infection is localized to the confined space of the marrow cavity, the pus has little chance to drain without surgical intervention; inflammation tends to become chronic, with organisms remaining viable within the marrow cavity for many years. Chronic osteomyelitis results, with extensive bone destruction, marrow fibrosis and recurrent focal suppuration. With chronicity, there is reactive new-bone formation, particularly around the inflamed periosteum, leading to a thickened and abnormally shaped bone.

In tuberculous osteomyelitis, the marrow cavity contains rapidly enlarging caseating granulomas which destroy trabecular and cortical bone.
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