Introduction: Ponseti and Friedman suggest that curve type is genetically determined and that curve types do not change throughout its course. In current clinical practice scoliosis is seen as a more dynamic process. Therefore we like to postulate that the natural history of idiopathic scoliosis can change during growth when left untreated.

Aim of the Study: This study focused on the shift of curve patterns as result of age, especially in patients younger than ten years. It was assessed whether age is a factor in the dynamic progression of idiopathic scoliosis. We evaluated patients records as well as radiographic images and clinical measures.

Materials and Methods: 48 Patients with idiopathic scoliosis who visited the scoliosis team between 1990 and 2007 were included. The criteria for inclusion were a curve less than 30° and not treated with brace or operative procedures. Curve pattern changes were classified according to the Scoliosis Research Society classification and the Lenke classification.

Results: The forty-eight patient records demographics consisted of eleven males and thirty-seven females. Their mean age at the start of follow-up was 11,2 years (range 4–17). Mean follow-up lasted 3,4 years (range 1–11,2). Thirteen patients were diagnosed with juvenile idiopathic scoliosis and thirty-five patients were diagnosed with an adolescent idiopathic scoliosis. Eight from the forty-eight patients, showed curve pattern changes according the SRS classification: six females and two males. Six of the thirtteen patients with juvenile scoliosis showed a shift of the scoliosis curves (46%). Two of the thirty-five patients with the adolescent scoliosis showed a shift of the scoliosis curves (6%; p< 0,05).

In eleven patients with juvenile scoliosis(84,6%) there was a shift in the Lenke classification, while this only occurred in eighttteen patients with adolescent scoliosis(51,4%) (p< 0,05). No curve pattern changes occurred in two patients with juvenile idiopathic scoliosis(15,4%) and in twelve patients of the adolescent idiopathic scoliosis(34,3%) (p< 0,05).

Conclusion: There is evidence that idiopathic scoliosis has an genetic origin, but not all elements of the scoliosis formation can be explained. We found changes in curve patterns which suggest that idiopathic scoliosis is not a fixed deformity, but a dynamic process especially in patients younger than 10 years.

We removed 23 Charité artificial discs in 19 patients due to severe back-and legpain and performed an anterior as well posterior fusion. Mean interval between insertion and retrieval is 8,4 years (3,0–16,0 years). The mean age at retrieval is 49,4 years (40–72 years). The cause of persistent or recurrent pain was one or more of several problems thought to be related to the pain: subsidence, migration, wear with or without breakage of the metal marker ring, facetjoint or adjacent degeneration. In all cases wear of the polyethylene core was seen in major or minor degree. The wear was related to posterior impingement possibly due to hyperlordosis and extension instability and was subsequently more pronounced in the peripheral rim than in the central dome. Also a relationship was noted to in vivo oxidation of the polyethylene, especially in the rim. In the periprosthetic tissue an inflammatory reaction was found, more in the severe wear cases. Polyethylene loaded macrophages were seen, also polyethylene particles lying freely in the tissue. The macrophages proved positive for Interleukin 6. The wear pattern and the inflammatory reaction resembles the pattern seen in total hips and knees. Probably a substantial number of patients will exhibit these wear changes some years after insertion. It is questionable whether changes in sterilization and packaging and better insertion and sizing techniques will prevent wear development in the future.