Abstract
Data from studies in other diseases state implicate cellular adhesion molecules as mediators of fibrosis and scarring. We sought to explore and assess the effect of using monoclonal antibodies against intercellular adhesion molecule-1 (ICAM-1) and its ligand CD-18 to decrease epidural fibrosis in an animal spinal surgery model.
We hypothesize that use of antiadhesion molecules (anti–ICAM-1 and anti–CD-18) decreases epidural fibrosis in rats after spinal surgery compared with nontreated group and monoclonal anti human immunoglobulin (Ig)G group.
Experimental animal spine surgery (laminectomy) protocol with application of antiadhesion molecules (anti–ICAM-1 and anti–CD-18 group as a specific monoclonal antibody) to surgical site in test group compared with monoclonal antihuman IgG group (as a nonspecific monoclonal antibody) and nontreated group.
Thirty Sprague Dawley male or female rats weighing 175 to 250 g were used randomly for three groups (nontreated, anti–ICAM-1 and anti–CD-18, monoclonal antihuman IgG). Laminectomy was performed at level L4 in all animal groups. After injection of materials (except nontreated group), the surgical sites were closed in layers. Three weeks later, all rats were killed. Twenty-seven rats were available for histological analysis. The histological sections were evaluated for fibroblast numbers of fibrous tissue within the laminectomy side, adhesion degree between dura mater and fibrous tissue, and new bone formation in the laminectomy region.
Comparing the fibroblast numbers in fibrous tissue within groups, the number of fibroblasts were significantly less in anti–ICAM-1 and anti–CD-18 group than nontreated group (p=.037). The number of fibroblasts of monoclonal anti human IgG group was not significantly different from anti–ICAM-1 and anti–CD-18 (p=.608) and the nontreated group (p=.508). In the anti–ICAM-1 and anti–CD-18 applied group, adhesion degree was found significantly less than monoclonal antihuman IgG (p=.036) and nontreated group (p=.036) statistically. There were no significant difference between the monoclonal antihuman IgG group and the nontreated group about adhesion degree (p=.645).
Therapy that targets ICAM-1 could be valuable in the management of epidural fibrosis. Blocking the function of ICAM-1 may provide cellular protection against epidural fibrosis and also it may serve as an important component in this period, acting to promote leukocyte migration across epidural area after laminectomy.