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10.1136/annrheumdis-2015-208268 http://scihub22266oqcxt.onion/10.1136/annrheumdis-2015-208268 C5099200!5099200!26698846     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Ann+Rheum+Dis 2016 ; 75 (11): 1989-97 Nephropedia Template TP {{tp|p=26698846|t=2016. Proteinase-activated receptor 2 modulates OA-related pain, cartilage and bone pathology |pdf=|usr=}}{{26698846}} gab.com Text Proteinase-activated receptor 2 modulates OA-related pain, cartilage and bone pathology JO: Ann Rheum Dis http://www.kidney.de/pget.php?&tw=1&pmid=26698846 #FOAvip Objective: Proteinase-activated receptor 2 (PAR2) deficiency protects against cartilage degradation in experimental osteoarthritis (OA). The wider impact of this pathway upon OA-associated pathologies such as osteophyte formation and pain is unknown. Herein, we investigated early temporal bone and cartilage changes in experimental OA in order to further elucidate the role of PAR2 in OA pathogenesis. Methods: OA was induced in wild-type (WT) and PAR2-deficient (PAR2?/?) mice by destabilisation of the medial meniscus (DMM). Inflammation, cartilage degradation and bone changes were monitored using histology and microCT. In gene rescue experiments, PAR2?/? mice were intra-articularly injected with human PAR2 (hPAR2)-expressing adenovirus. Dynamic weight bearing was used as a surrogate of OA-related pain. Results: Osteophytes formed within 7?days post-DMM in WT mice but osteosclerosis was only evident from 14?days post induction. Importantly, PAR2 was expressed in the proliferative/hypertrophic chondrocytes present within osteophytes. In PAR2?/? mice, osteophytes developed significantly less frequently but, when present, were smaller and of greater density; no osteosclerosis was observed in these mice up to day 28. The pattern of weight bearing was altered in PAR2?/? mice, suggesting reduced pain perception. The expression of hPAR2 in PAR2?/? mice recapitulated osteophyte formation and cartilage damage similar to that observed in WT mice. However, osteosclerosis was absent, consistent with lack of hPAR2 expression in subchondral bone. Conclusions: This study clearly demonstrates PAR2 plays a critical role, via chondrocytes, in osteophyte development and subchondral bone changes, which occur prior to PAR2-mediated cartilage damage. The latter likely occurs independently of OA-related bone changes. Twit Text FOAVip Proteinase-activated receptor 2 modulates OA-related pain, cartilage and bone pathology ????Ann Rheum Dis http://www.kidney.de/pget.php?&tw=1&pmid=26698846 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26698846 #FOAvip English Wikipedia <ref>{{Cite pmid|26698846}}</ref> Proteinase-activated receptor 2 modulates OA-related pain, cartilage and bone pathology #MMPMID26698846 Huesa C; Ortiz AC; Dunning L; McGavin L; Bennett L; McIntosh K; Crilly A; Kurowska-Stolarska M; Plevin R; van ?t Hof RJ; Rowan AD; McInnes IB; Goodyear CS; Lockhart JC; Ferrell WR Ann Rheum Dis 2016[Nov]; 75 (11): 1989-97 PMID26698846show ga Objective: Proteinase-activated receptor 2 (PAR2) deficiency protects against cartilage degradation in experimental osteoarthritis (OA). The wider impact of this pathway upon OA-associated pathologies such as osteophyte formation and pain is unknown. Herein, we investigated early temporal bone and cartilage changes in experimental OA in order to further elucidate the role of PAR2 in OA pathogenesis. Methods: OA was induced in wild-type (WT) and PAR2-deficient (PAR2?/?) mice by destabilisation of the medial meniscus (DMM). Inflammation, cartilage degradation and bone changes were monitored using histology and microCT. In gene rescue experiments, PAR2?/? mice were intra-articularly injected with human PAR2 (hPAR2)-expressing adenovirus. Dynamic weight bearing was used as a surrogate of OA-related pain. Results: Osteophytes formed within 7?days post-DMM in WT mice but osteosclerosis was only evident from 14?days post induction. Importantly, PAR2 was expressed in the proliferative/hypertrophic chondrocytes present within osteophytes. In PAR2?/? mice, osteophytes developed significantly less frequently but, when present, were smaller and of greater density; no osteosclerosis was observed in these mice up to day 28. The pattern of weight bearing was altered in PAR2?/? mice, suggesting reduced pain perception. The expression of hPAR2 in PAR2?/? mice recapitulated osteophyte formation and cartilage damage similar to that observed in WT mice. However, osteosclerosis was absent, consistent with lack of hPAR2 expression in subchondral bone. Conclusions: This study clearly demonstrates PAR2 plays a critical role, via chondrocytes, in osteophyte development and subchondral bone changes, which occur prior to PAR2-mediated cartilage damage. The latter likely occurs independently of OA-related bone changes. äProteinase-activated receptor 2 modulates OA-related pain, cartilage a(epmc).pdf DeepDyve Pubget Overpricing