ABSTRACT
BACKGROUND DATA: Few studies have investigated the long-term efficacy of percutaneous lumbar disc decompression (PLDD) with Dekompressor (Stryker, Kalamazoo, MI) for discogenic radicular pain that has failed conservative management. OBJECTIVE: Determine long-term outcomes of Dekompressor PLDD for discogenic radicular pain. METHODS: Prospective cohort study at a tertiary academic spine center of consecutive patients (12/2004-11/2005) with discogenic lumbosacral radicular pain who underwent PLDD with Dekompressor. Numerical Rating Scale (NRS) leg pain score and Oswestry Disability Index (ODI) score data were collected at 6 months and 1 year. These two measures, 5-point Likert scale patient satisfaction, and surgical rate data were collected at 8 years. RESULTS: Seventy patients underwent PLDD. Forty and 25 patients were successfully contacted at 1-year and 8-year follow-up, respectively. Using intention to treat analysis, at 1 year and 8 years, NRS leg pain scores were reduced >50% in 47% (95% confidence interval [CI] 35%, 59%) and 29% (95% confidence interval [CI] 18%, 40%) of patients, respectively; ODI score improved >30% in 43% (CI 32%, 55%) and 26% (CI 19%, 41%) of patients, respectively. Of the patients who followed up at 8 years, 36% (CI 17%, 55%) had undergone surgery and the median satisfaction was "4" (interquartile range 2,5). CONCLUSIONS: While limited by loss-to-follow-up, this study suggests that treatment of discogenic lumbosacral radicular pain with Dekompressor results in decreased leg pain and disability and favorable satisfaction at long-term follow-up. Further study with adequate follow-up retention is needed to confirm that Dekompressor spares open spinal surgery.
ABSTRACT
Endothelial cells are subjected to mechanical forces in the form of cyclic stretch resulting from blood pulsatility. Pulmonary artery endothelial cells (PAECs) produce factors that stimulate and inhibit pulmonary artery smooth muscle cell (PASMC) growth. We hypothesized that PAECs exposed to cyclic stretch secrete proteins that inhibit PASMC growth. Media from PAECs exposed to cyclic stretch significantly inhibited PASMC growth in a time-dependent manner. Lyophilized material isolated from stretched PAEC-conditioned media significantly inhibited PASMC growth in a dose-dependent manner. This inhibition was reversed by trypsin inactivation, which is consistent with the relevant factor being a protein(s). To identify proteins that inhibited cell growth in conditioned media from stretched PAECs, we used proteomic techniques and found that thrombospondin (TSP)-1, a natural antiangiogenic factor, was up-regulated by stretch. In vitro, exogenous TSP-1 inhibited PASMC growth. TSP-1-blocking antibodies reversed conditioned media-induced inhibition of PASMC growth. Cyclic stretched PAECs secrete protein(s) that inhibit PASMC proliferation. TSP-1 may be, at least in part, responsible for this inhibition. The complete identification and understanding of the secreted proteome of stretched PAECs may lead to new insights into the pathophysiology of pulmonary vascular remodeling.
