This study analyzed immunohistological features of the extruded or sequestrated intervertebral disc of the lumbar spine. To clarify the pathogenesis of neovascularization, cells isolated from herniated disc were cultured and examined biologically.
The objectives of this study were to characterize the histologic features of extruded or sequestrated discs and inflammatory cells that infiltrate along the margins of the disc tissue and to clarify the pathogenesis of neovascularization observed at the edge of the disc tissue.
When some of the contents of the disc extrudes into the epidural space and is considered “foreign,” an autoimmune response develops, which can lead to a chronic inflammatory response. However, the pathogenesis of inflammatory cell infiltrations and neovascularization are not clearly defined.
The herniated discs were obtained during surgery and were stained with anti-interleukin-1, intercellular adhesion molecule-1, lymphocyte function-associated antigen, and basic fibroblast growth factor antibodies by using an indirect immunoperoxidase method. Cells isolated from herniated disc were cocultured with human endothelial cells and basic fibroblast growth factor contained by cultured disc cells were measured by radioimmunoassay.
The ingrowth of granulation tissue with vascularization, occurring at the edge of fibrocartilage fragment, was present at 11 of 16 of extruded and 3 of 5 of sequestrated discs. Anti-interleukin-1, intracellular adhesion molecule-1, lymphocyte function-associated antigen, and basic fibroblast growth factor were expressed on most of mononuclear cells infiltrating into the extruded or sequestrated disc. Cells from the extruded or sequestrated disc demonstrated significantly greater levels of basic fibroblast growth factor than those from the protruded disc, and they enhanced the proliferation of endothelial cells.
This study showed that mononuclear cells infiltrating along the margins of extruded discs expressed inflammatory mediators and might induce neovascularization and persistence of inflammation.
From the Department of Orthopedic Surgery, Kobe University School of Medicine, Kobe, Japan.
Acknowledgment date: September 16, 1994.
First revision date: February 14, 1995.
Acceptance date: March 3, 1995.
Device status category: 1.
Address reprint requests to: Minoru Doita, MD, Department of Orthopaedic Surgery; Kobe University School of Medicine; 7-5-1 Kusunoki-cho Chuo-ku; Kobe 650; Japan