RESUMEN
BACKGROUND: Scapular notching is a radiographic finding of unknown clinical significance following reverse total shoulder arthroplasty (RTSA). The purpose of this study was to determine how baseplate position affects the incidence of scapular notching and measure the clinical outcomes. HYPOTHESIS: We hypothesized that low base plate position on the glenoid and new prosthesis design with a higher humeral inclination angle would decrease the incidence of notching at 2 years follow-up. MATERIALS AND METHODS: A total of 54 patients with an average follow-up of 30 months met inclusion criteria and underwent radiographic analysis of scapular notching and radiographic measures to determine glenoid component placement. Clinical measures including visual analog score, American Shoulder and Elbow Surgeons (ASES) scores, and range of motion (ROM) were prospectively collected. RESULTS: Thirty-nine of the 54 patients had no notching. 7 had Grade 1 notching, 7 had Grade 2 notching, one had Grade 3, and one had Grade 4 notching. Notching was associated with higher placement of the glenoid component as measured by peg-glenoid rim distance and base plate distance. All patients with no evidence of notching at 1-year, continued to have no notching after multi-year follow-up. Clinical outcome measures including ASES scores, ROM, and visual analog pain scores were improved at follow-up. CONCLUSION: We concluded that lower neck-shaft angle and low baseplate positioning led to a low incidence of significant scapular notching as only 6 out of 57 (16%) patients had notching Grade 2 and above. At short-term follow-up, this RTSA results in excellent clinical outcomes and a significantly lower scapular notching rate than traditional techniques.
RESUMEN
The activating receptor NKG2D, expressed by natural killer (NK) cells and CD8(+) T cells, has a role in the specific killing of transformed cells. We examined NKG2D expression in patients with glioblastoma multiforme and found that NKG2D was downregulated on NK cells and CD8(+) T cells. Expression of NKG2D on lymphocytes significantly increased following tumor resection and correlated with an increased ability to kill NKG2D ligand-positive tumor targets. Despite the presence of soluble NKG2D ligands in the sera of glioblastoma patients, NKG2D downregulation was primarily caused by tumor-derived tumor growth factor-beta, suggesting that blocking of this cytokine may have therapeutic benefit.