IntroductionActivated fibroblast-like synoviocytes (FLSs) in rheumatoid arthritis (RA) share many characteristics with tumour cells and are key mediators of synovial tissue transformation and joint destruction. The glycoprotein podoplanin is upregulated in the invasive front of several human cancers and has been associated with epithelial-mesenchymal transition, increased cell migration and tissue invasion. The aim of this study was to investigate whether podoplanin is expressed in areas of synovial transformation in RA and especially in promigratory RA-FLS.MethodsPodoplanin expression in human synovial tissue from 18 RA patients and nine osteoarthritis (OA) patients was assessed by immunohistochemistry and confirmed by Western blot analysis. The expression was related to markers of synoviocytes and myofibroblasts detected by using confocal immunofluoresence microscopy. Expression of podoplanin, with or without the addition of proinflammatory cytokines and growth factors, in primary human FLS was evaluated by using flow cytometry.ResultsPodoplanin was highly expressed in cadherin-11-positive cells throughout the synovial lining layer in RA. The expression was most pronounced in areas with lining layer hyperplasia and high matrix metalloproteinase 9 expression, where it coincided with upregulation of α-smooth muscle actin (α-sma). The synovium in OA was predominantly podoplanin-negative. Podoplanin was expressed in 50% of cultured primary FLSs, and the expression was increased by interleukin 1β, tumour necrosis factor α and transforming growth factor β receptor 1.ConclusionsHere we show that podoplanin is highly expressed in FLSs of the invading synovial tissue in RA. The concomitant upregulation of α-sma and podoplanin in a subpopulation of FLSs indicates a myofibroblast phenotype. Proinflammatory mediators increased the podoplanin expression in cultured RA-FLS. We conclude that podoplanin might be involved in the synovial tissue transformation and increased migratory potential of activated FLSs in RA.
Background and purpose — We hypothesized that an ultra-short stem would load the proximal femur in a more physiological way and could therefore reduce the adaptive periprosthetic bone loss known as stress shielding.Patients and methods — 51 patients with primary hip osteoarthritis were randomized to total hip arthroplasty (THA) with either an ultra-short stem or a conventional tapered stem. The primary endpoint was change in periprosthetic bone mineral density (BMD), measured with dual-energy x-ray absorptiometry (DXA), in Gruen zones 1 and 7, two years after surgery. Secondary endpoints were change in periprosthetic BMD in the entire periprosthetic region, i.e. Gruen zones 1 through 7, stem migration measured with radiostereometric analysis (RSA), and function measured with self-administered functional scores.Results — The periprosthetic decrease in BMD was statistically significantly lower with the ultra-short stem. In Gruen zone 1, the mean difference was 18% (95% CI: −27% to −10%). In zone 7, the difference was 5% (CI: −12% to −3%) and for Gruen zones 1–7 the difference was also 5% (CI: −9% to −2%). During the first 6 weeks postoperatively, the ultra-short stems migrated 0.77 mm more on average than the conventional stems. 3 months after surgery, no further migration was seen. The functional scores improved during the study and were similar in the 2 groups.Interpretation — Up to 2 years after total hip arthroplasty, compared to the conventional tapered stem the ultra-short uncemented anatomical stem induced lower periprosthetic bone loss and had equally excellent stem fixation and clinical outcome.
Perioperative problems can be overcome with patience, empathy and profound knowledge of how patients with dementia respond prior to surgery. Our results may serve as a source for future care and provide information about hospital settings for better perioperative care in patients with dementia.
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