• Takashi Furukawa, Kazuo Ito, Satoshi Nuka, Junichi Hashimoto, Hiroshi Takei, Masatoshi Takahara, Toshihiko Ogino, Marian F Young, and Tamayuki Shinomura.
• Department of Orthopaedic Surgery, Yamagata University School of Medicine, Yamagata, Japan.
• Spine. 2009 Dec 1; 34 (25): E911-7.

Study DesignA study of the histologic changes of the intervertebral discs (IVDs) in biglycan (Bgn)-deficient mice.ObjectiveIn this study, we investigate whether the absence of Bgn accelerates the degenerative process in mouse intervertebral disc (IVD).Summary Of Background DataProteoglycans and collagen fibrils are major components in the extracellular matrix (ECM) composition of IVD. The ECM of IVD contains several members of the small leucine repeat proteoglycans (SLRPs) family. Bgn is one member of SLRPs family, and showed a unique expression with age and degeneration in the human IVD. To date, there have been no in vivo studies to see whether SLRPs have a role in maintaining the structural integrity of IVD. To explore the functions of Bgn in the IVD, we examined discs in Bgn-deficient mice.MethodsA total of 30 spine specimens were harvested from wild-type (WT) and Bgn-deficient mice. Five specimens for each genotype at 4-, 6-, and 9-month old were examined in the experiments. Histologic analysis of the IVD was performed. Histologic gradings were performed separately on nucleus pulposus, anulus fibrosus, and endplate according to the classification system proposed by Boos et al.ResultsWe found that Bgn-deficient mice developed an early onset of disc degeneration compared with WT mice. The degenerative scores of Bgn-deficient mice were significantly higher than those of WT mice at 4- and 9-month-old. High scores for nucleus pulposus and anulus fibrosus in Bgn-deficient mice significantly affected the difference in total degenerative scores at 9 months of age.ConclusionBgn deficiency significantly accelerated disc degeneration.

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