Introduction: With the advent of thoracoscopy, anterior release procedures in adolescent idiopathic scoliosis (AIS) have come into more frequent use, however, the indication criteria for an anterior release in thoracic AIS are still controversial in the literature. The aim is to achieve a better coronal correction but the benefit as compared to a single posterior approach is not yet clarified.

Material and Methods: Two groups of 15 patients each were matched for sex, age and cobb angle. Patients of group 1 were operated with a staged procedure of an anterior release followed by posterior instrumentation (anterior-posterior spinal fusion, APSF) and patients of group 2 were operated by a single posterior spinal fusion (PSF) with performance of concave sided rib osteotomies (concave thoracoplasty, CTP).

Results: Mean age: 16.2 y (APSF), 17.6 y (PSF). Mean preop curve: 81.7° ± 10.1° (APSF), 84.2° ± 14.1° (PSF). Mean postop curve: 34.9° ± 15.5° (APSF), 34.3° ± 12.2° (PSF) (p=0,49).

Conclusion: The single posterior approach gave the same coronal correction rate as compared to patients operated with a two stage procedure with preceding anterior release. A posterior release with CTP is more effective in increasing spinal flexibility than disc excision. According to our clinical experience, an anterior release prior to posterior instrumentation in AIS should only be considered in hyperkyphosis, coronal imbalance or massive curves.

Study Design: Experimental in vivo study on New Zealand white rabbits.

Summary of Background Data: Bone Morphogenetic Protein 2 (BMP-2) is of increasing orthopaedic interest due to its osteo-inductive potency. Currently it is used in human and animal studies for posterolateral spinal fusions. However, little data is available concerning the pathophysiologic role of BMP-2 in normal and degenerated discs.

Methods: A recently established animal model was used to create mechanically induced disc degeneration of one single segment. In 6 animals, an external disc compression device was attached for 28 days. For comparison 8 animals underwent a sham operation.

Outcome Measures: The discs were analysed by a) immunohistology to determine protein content of BMP-2 and b) real time RT-PCR to quantify RNA content of BMP-2.

Results: Sham controls showed a homogeneous distribution of BMP-2 throughout the annulus fibrosus and cluster-like accumulation within the nucleus pulposus. Mechanically degenerated discs determined a reduction of positive cells with areas lacking BMP-2. Real time RT-PCR results demonstrated a statistically significant (7.92 times) upregulation of BMP-2 as compared with shams (p=0.033).

Conclusions: Mechanically induced disc degeneration is associated with a loss of BMP-2 protein. Disc cells respond with a stimulation of BMP-2 gene expression. This data confirms the role of BMP-2 in the pathophysiology of disc remodeling. It remains unclear if this mechanism of BMP-2 stimulation contributes to the disc reorganization alone or if it may also play a role in osteo-inductive processes like osteophyte formation or endplate sclerosis.

Study Design: Experimental in vivo study on New Zealand White Rabbits.

Summary of Background Data: We have developed an in-vivo rabbit model of lumbar disc degeneration. This model provides a defined loading of one single disc. However, the molecular mechanism that leads to mechanically-induced disc degeneration remains unclear.

Objective: To investigate the process of mechanically induced disc degeneration in New Zealand White Rabbits with respect to remodeling on the gene and the level of protein expression.

Subjects: Seven animals were treated with an external compression-device applying 200N on segment L3/4. Eight animals underwent sham surgery.

Outcome Measures: After 28 days discs were harvested and cut into two pieces in a sagittal plain. One piece was used for protein analysis utilizing immunohistochemical protocols for collagen I, II and aggrecan. The other half of the disc was used for quantitative real-time RT-PCR to determine gene expression of selected matrix genes.

Results: In the compression group matrix genes were upregulated: collagen I (6.46x; p=0,018), collagen II (2.14x), biglycan (2.97x; p=0,049), decorin (4.64x; p=0,043), aggrecan (1.2x), osteonectin (2.03x), fibronectin (3.48x), fibromodulin (2.6x; p=0,037). The MMP-13 gene could only be detected in compressed discs. Gene transcripts of the metalloproteinase-inhibitor TIMP-1 were 4.5 times upregulated (p=0,007). Immunohistochemical analysis revealed a decrease of aggrecan and collagen I.

Conclusions: In our animal model mechanical loading caused degradation of the matrix proteins collagen I and aggrecan. Metalloproteinases like MMP-13 trigger this degenerative process. The elevated expression of matrix genes and TIMP-1 transcripts may characterize a mechanism of compensation.