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Pathogenesis of osteomyelitis

Authors
Jason Calhoun, MD
Madhuri M Sopirala, MD, MPH
Section Editor
Daniel J Sexton, MD
Deputy Editor
Elinor L Baron, MD, DTMH

INTRODUCTION

Osteomyelitis is a progressive infection of bone that results in inflammatory destruction followed by new bone formation. Three major categories are based upon pathogenic mechanisms of infection [1]:

Osteomyelitis secondary to a contiguous focus of infection (eg, after trauma, surgery, or insertion of a prosthetic joint)

Osteomyelitis secondary to a contiguous focus of infection associated with vascular insufficiency, primarily occurring in patients with diabetes mellitus and/or peripheral vascular disease

Osteomyelitis following hematogenous spread of infection, which is the major mechanism in vertebral osteomyelitis and in children. It was previously thought that spread of infection may occur via vertebral veins known as Batson's plexus, especially from sites of infection in bowel or urinary tract. Seeding beneath the vertebral endplate is followed by involvement of the disc and other adjoining vertebrae. Blood vessels in pediatric spine terminate within the intervertebral disc, allowing for direct extension of infection [2]. Many experts now believe that the corkscrewing of the vertebral arterial supply leads to vertebral osteomyelitis in patients with bacteremia.

Acute osteomyelitis evolves over several days to weeks and can progress to a chronic infection [1]. The hallmark of chronic osteomyelitis is the presence of dead bone (sequestrum). Other common features of chronic osteomyelitis include involucrum (reactive bony encasement of the sequestrum), local bone loss, and, if there is extension through cortical bone, sinus tracts.

        

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Literature review current through: Mar 2015. | This topic last updated: Apr 16, 2015.
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