Quantitative investigations of regeneration patterns in lumbar human discs; correlation of regeneration and occupational load

Status:

completed 12/2009

Aims:

The first study on disc regeneration revealed fibroblast mediated intradiscal scar formation in about 50% of the discs and about 30% of relevant amounts of chondrocyte proliferation clusters. The present study quantified growth factor expression, surface markers and inflammation indicators of cluster of different age. Study material was collected from patients who underwent open disc surgery. All results were correlated with patient data on occupational load from this patients.

Activities/Methods:

We report on the relationship of workload and histological features like chondrocyte regeneration, intra-discal scar formation and tissue degeneration. Study Design: prospective Patient Sample: Specimen were collected from patients suffering from lumbar disc prolapse (n = 90) or spinal osteochondrosis (n = 19). Methods: Histomorphologic features were graded using semi-quantitative scoring. Occupational data were collected in a structured standardized patient interview assessing lifting and carrying loads. In this way, the exposure was assessed for each test subject's entire working life until surgery.

Results:

There was no association between cumulative workload and the histological patterns matrix degeneration, chondrocyte proliferation and scar formation. In a subgroup of patients with a heavy workload period of twelve months prior to surgery a relevant growth of chondrocyte clusters (p = 0.055) was apparent. Chondrocyte cluster formation was found in 83% (n = 74) of the prolapse patients and in 58% (n = 11) of the osteochondrosis patients (p = 0.02). Fibrocyte mediated scar formation was found in 55% of the prolapse patients and in 45% of the spinal stenosis patients. Chondrocyte cluster and its de novo collagen matrix surrounding did not integrate biomechanically sufficient with collagen fibers of the disc. Disintegration of cluster from disc matrix and formation of intra-discal sequesters were observed. Discussion and conclusions: Matrix degeneration was a common finding but displayed no relationship to occupational workload or other histological features. Scar formation was observed in every second specimen as a likely consequence of an endplate trauma but did also not correlate positively with work load. Regenerative chondrocyte cluster proliferation was identified as a common feature in disc specimen even in patients beyond 80 years. It was the only parameter positively and nearly significantly correlated with workload. This supports the hypothesis that the disc reacts on supra marginal workload with cell and matrix production. A workload threshold that indicates critical work load may exist for individuals but could not be identified in our data set. The neo matrix did not connect sufficiently to the existing matrix. Fissures between old and new matrix appeared and even the complete dissociation of the new chondrocyte cluster form the preformed matrix was frequently observed. Thus chondrocyte proliferation may not be a sufficient repair mechanism in degenerative disc disease but even the starter of disc prolapse.

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