Many pathological disease processes are manifested by abnormalities in cellular signalling caused by altered protein expression. Our aims, therefore, were to determine whether ‘’degenerative disc disease’’ results in 1) altered proteome expression and 2) such changes might be used as a marker for the disease process.

Using gel electrophoresis, we analysed the proteome expression of nucleus pulposus (NP) derived from patients with scoliosis (‘normal’) compared to degenerate samples from patients with 1) back pain undergoing spinal fusion (DDD) and 2) sciatica undergoing discectomy (herniated nucleus pulposus or HNP). Normal NP tissue was also obtained from organ donor patients with no previous history of back pain. All samples were investigated in duplicate. Protein concentrations were measured qualitatively by visual analysis in a blinded manner and categorised into high, medium, low or absent. The Kruskal-Wallis analysis of variance was sued to analyse the data. Subsequent proteins of interest were determined on N-terminal protein sequencing.

15 samples each were collected each from scoliosis, DDD, and HNP, but only 4 samples from the organ donor groups. One major protein band difference was observed whose molecular weight was 15 kDa and N-terminal sequence homologous with lysozyme C (lysozyme-C-like-protein - LCLP). DDD and HNP samples exhibited significantly reduced levels of LCLP compared to scoliosis (P< 0.0001). All NP from donor patients exhibited high levels of LCLP, but numbers were too small for statistical analysis. No statistical correlation existed between age and LCLP levels.

The true physiological roles of Lysozyme C remains unclear, but it is a known ubiquitous secretory and hydrolytic protein found in saliva, milk, cerebrospinal fluid and synovial liquid, and thought to function in primary immunity. LCLP loss in degenerate disc tissue might be due to 1) lack of production, 2) increased breakdown through a specific ubiquitin-linked pathway, or 3) polymerisation with tissue-specific amyloid deposition. The inflammatory effects within the NP related to localised LCLP-amyloid deposition offers a plausible hypothesis for patho-physiology of disc degeneration and discogenic pain. Until we determine the true nature and function of LCLP, we are no further in understanding the patho-mechanisms of disc degeneration. Moreover, LCLP loss in the NP of degenerate discs may provide a potential diagnostic marker for degenerative disc disease.