**4. Pathogenesis**

Hematogenous infection of the long bones, which are most frequently affected, begins in the capillary loops of the metaphysic, adjacent to the cartilaginous growth plate (physis). These areas are very susceptible to hematogenous infection, because of its high vascularity and because the blood flow within the vessels is slow [22]. Bacteria can pass through gaps from the sinusoidal veins to the capillaries into the tissue, where they are provided an ideal environment to grow, resulting in abscess formation. These abscesses frequently rupture into the joint [23]. In neonates acute hematogenous osteomyelitis and septic arthritis co-exist in up to 76% of all cases as a result of this unique vascular anatomy of the epiphysis; the bone marrow compartment is seldom involved [10,24]. The epiphysis receives its blood supply directly from metaphyseal blood vessels (transphyseal vessels) and the adjacent cartilaginous growth plate is traversed by capillaries, allowing spread of the pathogenic bacteria to the physis, epiphysis and joint and resulting in slipped epiphyses, fractures, premature physeal closure and chronic infection (Figure 1) [25].

Characteristics of the neonatal bone prevent many of the features of chronic osteomyelitis: cortical sequestra are often completely absorbed due to extensive bone blood supply in the newborn and, in addition, efficient vasculature of the inner layer of the periosteum encourages early development of new bone formation [26,27]. Complete destruction of joints is rare, but serious growth disturbances may occur.
