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Possible Pathogenesis of Painful Intervertebral Disc Degeneration

Peng, Baogan, MD, PhD*; Hao, Jianhua, MD; Hou, Shuxun, MD*; Wu, Wenwen, MD*; Jiang, Duyin, MD, PhD; Fu, Xiaobing, PhD; Yang, Yi, MD§

doi: 10.1097/01.brs.0000201324.45537.46
Epidemiology
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Study Design. We collected the specimens of lumbar intervertebral disc (i.e., the symptomatic degenerative disc) from patients with discogenic low back pain to study the histopathologic features and growth factor expressions.

Objectives. To study the pathogenesis of disc degeneration, meanwhile discriminating between common disc degeneration (aging disc) (i.e., black asymptomatic disc, not clinically relevant) and painful disc degeneration (i.e., symptomatic disc, clinically relevant).

Summary of Background Data. The pathogenesis of intervertebral disc degeneration is poorly understood, mainly because of the difficulty to establish the experimental model with good reproducibility. Recently, the popularity of spinal fusion leads to more opportunities to obtain disc specimens, which could be applied to explore the pathogenesis of disc degeneration with modern biologic techniques.

Methods. There were 21 specimens of lumbar intervertebral discs from 15 patients with discogenic low back pain during posterior lumbar interbody fusion, 16 aging discs from patients without low back pain, and 10 normal discs as control collected for the study of their histopathologic features, as well as the expressions of basic fibroblast growth factor (bFGF) and its receptor (Flg), transforming growth factor-β1 (TGF-β1) and its receptor (TGF-βRI) by immunohistochemistry. The distribution of macrophages and mast cells was also noted. Proliferating cell nuclear antigen was assessed to evaluate proliferating activities of disc cells.

Results. The distinct histologic characteristic of the disc from the patient with discogenic low back pain was the ingrowth of vascularized granulation tissue along torn fissures, extending from the external layer of the anulus fibrosus into the nucleus pulposus. The immunohistochemical staining showed that there were strong expressions of bFGF and TGF-β1 and their receptors, as well as a strong expression of proliferating cell nuclear antigen in the zones of granulation tissue in the painful discs. However, there were only weak expressions in the nongranulation tissue zones in the painful discs and aging discs, and no expression in the control discs. In addition, abundant macrophages and mast cells were found in the granulation tissue zones of painful discs but absent in the nongranulation tissue zones of painful discs or aging discs and the normal control discs.

Conclusions. The findings indicated that degeneration of the painful disc might originate from the injury and subsequent repair of anulus fibrosus. Growth factors, such as bFGF and TGF-β1, macrophages and mast cells might play a key role in the repair of the injured anulus fibrosus and subsequent disc degeneration.

There were 21 specimens of painful lumbar intervertebral discs collected for the study of the pathogenesis of disc degeneration. The studies found that the distinct histologic characteristic of the painful disc was the ingrowth of vascularized granulation tissue along torn fissures, extending from the external layer of the anulus fibrosus into the nucleus pulposus. There were strong expressions of basic fibroblast growth factor and transforming growth factor-β1 and their receptors, as well as a strong expression of proliferating cell nuclear antigen in the zones of granulation tissue in the painful discs. In addition, abundant macrophages and mast cells were found in the same area. The findings indicated that the degeneration of painful disc might originate from the injury and subsequent repair of anulus fibrosus.

From the *Department of Orthopaedics, †Department of Anesthesiology, ‡Institute of Wound and Repair, and §Department of Pathology, 304th hospital, Beijing, China.

Acknowledgment date: January 5, 2005. First revision date: February 12, 2005. Second revision date: February 25, 2005. Third revision date: March 3, 2005. Acceptance date: March 7, 2005.

The manuscript submitted does not contain information about medical device(s)/drug(s).

Foundation funds were received in support of this work. No benefits in any form have been or will be received from a commercial party related directly or indirectly to the subject of this manuscript.

Address correspondence and reprint requests to Baogan Peng, MD, PhD, Department of Orthopaedics, 304th Hospital, 51 Fucheng Road, Beijing, 100037, P.R. China; E-mail: pengbaogan@163.com

© 2006 Lippincott Williams & Wilkins, Inc.