Some years ago, childhood spondylodiscitis was used to describe a continuum of primary pyogenic spinal infections (PPSIs), from discitis to vertebral osteomyelitis, including spondylodiscitis with its occasional associated soft-tissue abscesses. The pathophysiology of PPSIs has, nevertheless, become clearer and less controversial. The theory suggesting that spondylodiscitis was a self-limiting inflammatory condition is now considered completely obsolete. A better understanding of pathophysiological processes has made it possible to differentiate forms of childhood PPSI according to patients’ ages, their immune system development, better knowledge of their bacterial etiology, and the vascularization of their vertebrae and disks. The different clinical forms of PPSI have now been categorized in various ways that physicians and pediatricians should know.

The first classification is based on the child’s age and the development of their immune system, and it distinguishes three main clinical forms of childhood PPSI. The neonate form of spondylodiscitis generally affects infants under 6 months old and is recognized as the most severe manifestation of the disease: patients often present with septicemia and multiple infectious foci. Fortunately, this is the rarest form of the disease. The infantile form concerns children from 6 to 48 months old (a period during which maternally derived immunity decreases and stops), the age group representing 60%–80% of cases of childhood spondylodiscitis. Finally, in the third form, affecting children above 4 years old, patients are more prone to being febrile and appearing very ill.

The second classification can be superimposed on the first and assigns each age group a bacterial probability of spondylodiscitis. Approximately 80% of spondylodiscitis cases in children younger than 6 months are due to S. aureus. For children from 6 to 48 months old, there are now robust arguments supporting the hypothesis that K. kingae should be considered the primary etiological pathogen for spondylodiscitis. The third form affects children older than 4 years of age, and S. aureus is the predominant pathogen.

Finally, a third classification is based on the anatomical characteristics of the patient’s vertebral endplate and disk vascularization. Many studies have demonstrated that the vertebral endplates and the superficial portion of the disks share a common blood supply at birth that gradually regresses during infancy. In children, the metaphysis of the vertebral body has a rich blood flow, with an incomplete vascular ring ending at the pedicle’s base. Otherwise, it has been shown that several fine anastomotic branches exist between the upper and lower metaphyseal rings of two adjacent vertebrae, mostly present around the disk’s posterolateral region, providing its blood flow. It is also commonly accepted that infection starts under the vertebral endplates, that it subsequently and successively crosses both the vertebral endplate and the disk’s surface via those fine anastomotic branches, reaching the adjacent vertebral body and, lastly, the disk space between the two affected vertebral bodies. Interestingly, the blood vessels which cross the vertebral endplates evolve at around 7 or 8 years old.

These anatomical observations lead to two conclusions. First, it becomes reasonable to think that pure discitis, as some authors have suggested, cannot occur. Secondly, it seems highly likely that children will tend to have spondylodiscitis before the age of 7 to 8 years old and, afterwards, that older children and adolescents are more likely to develop vertebral osteomyelitis, providing that the infection is not neglected.

Unfortunately, these concepts do not yet appear in textbooks or university curricula, thus perpetuating enormous confusion about these infections.