Hematogenous osteomyelitis

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Despite the availability of potent antimicrobial drugs, improved diagnostic techniques, and effective surgical procedures, hematogenous osteomyelitis continues to provide difficulties in diagnosis, complex problems in management, serious morbidity and even mortality. In recent years, changes have occurred in the clinical setting, presenting manifestations and the types of causative microorganisms.1, 2 Microorganisms that rarely caused infection in the past have emerged as significant bone pathogens. New clinical syndromes, unusual locations of bone infection, and additional pathogenetic mechanisms have been documented. Although chronic osteomyelitis has long been known to be a difficult lesion to produce in laboratory animals, recent experimental models of chronic osteomyelitis that mimic human disease have been devised.3–7 New information is available concerning defects in host resistance which may predispose to some forms of osteomyelitis. Furthermore, knowledge of some of the microbial factors related to virulence of certain bone pathogens is increasing. The purpose of this report is to review briefly, in view of current developments, selected aspects of the problem of hematogenous osteomyelitis.

General considerations

Given the appropriate predisposing factors, osteomyelitis may develop in any bone of the body. In the human skeleton, at least 206 bones develop which vary in location, size, shape, structure, and function. In general, bones are composed of a cortex of compact (lamellar) bone and a medulla of spongy or cancellous bone. With respect to general architecture, Jaffe8 has grouped bones into four categories: (1) tubular (long and short), (2) short (cuboidal), (3) flat, and (4) irregular. The tubular bones include the. . .



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