Surface replacement arthroplasty for glenohumeral arthropathy in patients aged younger than fifty years: results after a minimum ten-year follow-up.

BACKGROUND: The role of cementless surface replacement arthroplasty (CSRA) in young individuals is currently unclear. The aim of this study was to evaluate CSRA long-term results for glenohumeral arthritis in young patients. METHODS: Between 1990 and 2003, 54 CSRAs were performed on 49 patients (25 men, 24 women) aged younger than 50 years. Mean age was 38.9 years (range, 22-50 years). Three patients (4 shoulders) died over time and 8 were lost to follow-up, leaving 38 patients (42 shoulders) with a mean follow-up of 14.5 years (range, 10-25 years). There were 17 total shoulder replacements with metal back glenoid, and 37 underwent humeral head resurfacing with microfracture of the glenoid. RESULTS: The indications were avascular necrosis, 16; rheumatoid arthritis, 20; instability arthropathy, 7; primary osteoarthritis, 5; fracture sequelae, 3; postinfection arthritis, 2; and psoriatic arthritis, 1. The mean relative Constant score increased from 11.5% to 71.8% (P < .0001), and the mean patient satisfaction at final follow-up was 8.7 of 10. The mean relative Constant score for the humeral head resurfacing with microfracture of the glenoid improved to 77.7% compared with 58.1% for total resurfacing arthroplasty. Two required early arthrodesis due to instability and deep infection. Seven were revised to stemmed prosthesis: 1 for traumatic fracture and 1 for glenoid erosion 16 years after the index procedure. Five shoulders in 4 patients (4 rheumatoid arthritis, 1 avascular necrosis) were revised at 8 to 14 years after surgery for cuff failure and loosening. Three were revised to stemless reverse total shoulder arthroplasty due to rotator cuff failure at 23, 16, and 13 years after surgery. CONCLUSIONS: CSRA provides good long-term symptomatic and functional results in the treatment of glenohumeral arthropathy in patients aged younger than 50 years in 81.6% of the patients. This improvement is maintained over more than 10 years after surgery, with high patient satisfaction (8.7 of 10). However, 10 shoulders (of 54) (18.5%) underwent revision arthroplasty. Resurfacing offers a valuable tool in treating young patients with glenohumeral arthritis, providing reasonably good long-term results in 81.6% of the patients, while allowing preservation of bone stock if the need for revision arises. All the revision arthroplasty options are preserved, including less invasive procedures.

Mechanisms underlying beta2-adrenoceptor-mediated nitric oxide generation by human umbilical vein endothelial cells.

Endothelial beta(2)-adrenoceptor (beta(2)AR) stimulation increases nitric oxide (NO) generation, but the underlying cellular mechanisms are unclear. We examined the role of l-arginine transport and of phosphorylation of NO synthase 3 (NOS-3) in beta(2)AR-mediated NO biosynthesis by human umbilical vein endothelial cells (HUVEC). To this end, we assessed l-arginine uptake, NOS activity (from l-arginine to l-citrulline conversion), membrane potential (using [(3)H]tetraphenylphosphonium), as well as serine phosphorylation of NOS-3 (by Western blotting and mass spectrometry), in HUVEC treated with betaAR agonists or cyclic AMP-elevating agents. beta(2)AR stimulation increased l-arginine transport, as did cyclic AMP elevation with either forskolin or dibutyryl cyclic AMP, and this increase was inhibitable by N-ethylmaleimide. Blockade of l-arginine uptake by l-lysine inhibited NOS activity and, conversely, blockade of NOS using N(omega)-nitro-l-arginine methyl ester (l-NAME) inhibited l-arginine transport. beta(2)AR stimulation also caused a membrane hyperpolarization inhibitable by l-NAME, suggesting that the increase in l-arginine uptake occurred in response to NO-mediated hyperpolarization. beta(2)AR activation also increased NOS activity and phosphorylation of NOS-3 on serine-1177, and these increases were attenuated by inhibition of protein kinase A (PKA), phosphatidylinositol 3-kinase (PI3K) or Akt, and abolished by coinhibition of PKA and Akt. These findings suggest that beta(2)AR-mediated NOS-3 activation in HUVEC is mediated through phosphorylation of NOS-3 on serine-1177 through both the PKA and the PI3K/Akt systems, and is sustained by an increase in l-arginine uptake resulting from NO-mediated membrane hyperpolarization.