Implantation of amniotic membrane to reduce postlaminectomy epidural adhesions.
Eur Spine J. 2009 Apr 30; Tao H, Fan HPostlaminectomy epidural adhesion is implicated as a main cause of "failed back surgery syndrome" and associated with increased risk of complications during revision surgery. Various materials acting as mechanical barriers to reduce fibroblasts infiltration into epidural space have met with limited success. In present research, amniotic membrane (AM) was studied to investigate its effects on reducing epidural scar adhesion after laminectomy in a canine model. Laminectomy sites were created at L-1, L-3, L-5, and L-7 levels in 24 adult mongrel dogs. Freeze dried AM (FAM), cross-linked AM (CAM), and autologous free fat (AFF) were implanted, respectively, at a randomly assigned site in each dog with the remaining untreated site serving as internal control. The animals were sacrificed at 1, 6, and 12 weeks postoperatively. Then, gross pathologic observation including scar amount and adhesion tenacity, qualitative histology evaluation, and quantitative histology analysis were compared. Gross observation demonstrated that scar amount and adhesion tenacity of CAM group were significantly lower in comparison with those of FAM and non-treatment groups. A white, slightly vascularized CAM layer covered the dura mater without tenacious scar adhesion. The histology analysis also indicated reduced fibroblasts infiltration and consequent epidural fibrosis, which were similar to the results of AFF group. In conclusion, the CAM is effective in reducing epidural fibrosis and scar adhesion after laminectomy in canine model. It is a promising biomaterial for future clinical applications.
The connexin43 carboxyl-terminal peptide ACT1 modulates the biological response to silicone implants.
Plast Reconstr Surg. 2009 May; 123(5): 1440-51Soder BL, Propst JT, Brooks TM, Goodwin RL, Friedman HI, Yost MJ, Gourdie RGBACKGROUND: The implantation of a biomedical device elicits a wound-healing response that progresses through the three phases of wound healing: inflammation, cellular proliferation, and matrix remodeling. This response culminates in a fibrous collagen encapsulation of the implant. Subsequent contraction of this "scar-like" tissue can lead to physical disfigurement, implant extrusion, or impairment of implant function, necessitating surgical revision or removal. ACT1 is a synthetic peptide derived from the carboxyl-terminal sequence of the cellular gap junction protein connexin43. This novel peptide has recently been shown to modulate cutaneous wound healing, reduce scarring, and promote regenerative repair of the skin following injury. In this study, the authors investigated the ability of the ACT1 peptide to modulate the wound-healing response to biomedical device implantation. METHODS: Silicone disks coated with either vehicle control or ACT1 peptide were implanted submuscularly into male Sprague-Dawley rats. Capsulectomies were performed on days 1, 2, 3, 14, and 28. The implant capsules and surrounding tissue were analyzed histologically and biochemically. RESULTS: ACT1 modulated the wound-healing response to silicone implants by attenuating neutrophil infiltration, increasing vascularity of the capsule tissue, reducing type I collagen deposition around the implant, and reducing the continued presence of contractile myofibroblasts. CONCLUSION: ACT1 may provide an enabling technology for modulating the wound-healing response to implants, promoting integration of implanted materials and tissue-engineered devices in the human body.
