Pathogenesis

In the hematogenous form, the infective process classically starts in the metaphysis of long bone by the lodgment of organisms in endarteries, in which a slow blood flow facilitates their entrapment. As bone and bone marrow become the loci of bacterial proliferation, tissues

Blood Supply Long Bones

Fig. 6.1A-C Schematic presentation of changing vascular supplies in long bone according to the three different age groups. Basically, the main blood supply to long bone ends derives from the nutrient artery. A In an infant under the age of 18 months small arteries penetrate the growth cartilage to reach the epiphysis. B After 18 months, with the involution of the physeal vessels, the vascular supply in the epiphysis derives from the epiphyseal arteries and becomes separated from that in the metaphysis by the cartilaginous barrier. C Following physeal fusion the nutrient arterial branches joined by the epiphyseal branches distribute throughout the whole bone end. The blood supply in the cortex derives from the periosteal artery in the outer zone and from the nutrient artery in the inner zone (adapted from Rogers 1987)

Fig. 6.1A-C Schematic presentation of changing vascular supplies in long bone according to the three different age groups. Basically, the main blood supply to long bone ends derives from the nutrient artery. A In an infant under the age of 18 months small arteries penetrate the growth cartilage to reach the epiphysis. B After 18 months, with the involution of the physeal vessels, the vascular supply in the epiphysis derives from the epiphyseal arteries and becomes separated from that in the metaphysis by the cartilaginous barrier. C Following physeal fusion the nutrient arterial branches joined by the epiphyseal branches distribute throughout the whole bone end. The blood supply in the cortex derives from the periosteal artery in the outer zone and from the nutrient artery in the inner zone (adapted from Rogers 1987)

react intensely with hyperemia, edema, cell infiltration, and suppuration, creating a milieu under pressure within the closed space of the bone marrow. Both the elevated intramedul-lary pressure and the proteolytic action of the offenders cause infective material to leak through the haversian and Volkmann's canals of the cortex out to the subperiosteal layer, to produce an abscess. As a result, the affected bone becomes necrotized and the periosteum reacts with brisk new bone formation. The former is known as sequestrum and the latter in-

volucrum. As shown in Fig. 6.1, the metaphyseal vascular supply, periosteal attachment, and histological characteristics of the physis in the long bone differ among infants under 1 year of age, children aged up to 16 years, and adults after bone fusion. During infancy, some of the metaphyseal arteries penetrate the growth cartilage to enter the epiphysis, carrying bacteria to that part. In children, however, such a tran-schondral vasculature ceases to exist and, instead, more mature growth cartilage resists the bacterial spread from the metaphysis. This barrier delimits the infection to the metaphysis in the initial stage of an acute osteomyelitis (Fig. 6.2).

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