scholarly journals P216 An evaluation of articular cartilage and subchondral bone architecture (Articulone) in bovine cadaver knees after high energy trauma

2007 ◽  
Vol 15 ◽  
pp. B142
Author(s):  
M.J. Langworthy
2021 ◽  
Vol 11 (15) ◽  
pp. 7118
Author(s):  
Ermina Hadzic ◽  
Garth Blackler ◽  
Holly Dupuis ◽  
Stephen James Renaud ◽  
Christopher Thomas Appleton ◽  
...  

Post-traumatic osteoarthritis (PTOA) is a degenerative joint disease, leading to articular cartilage breakdown, osteophyte formation, and synovitis, caused by an initial joint trauma. Pro-inflammatory cytokines increase catabolic activity and may perpetuate inflammation following joint trauma. Interleukin-15 (IL-15), a pro-inflammatory cytokine, is increased in OA patients, although its roles in PTOA pathophysiology are not well characterized. Here, we utilized Il15 deficient rats to examine the role of IL-15 in PTOA pathogenesis in an injury-induced model. OA was surgically induced in Il15 deficient Holtzman Sprague-Dawley rats and control wild-type rats to compare PTOA progression. Semi-quantitative scoring of the articular cartilage, subchondral bone, osteophyte size, and synovium was performed by two blinded observers. There was no significant difference between Il15 deficient rats and wild-type rats following PTOA-induction across articular cartilage damage, subchondral bone damage, and osteophyte scoring. Similarly, synovitis scoring across six parameters found no significant difference between genetic variants. Overall, IL-15 does not appear to play a key role in the development of structural changes in this surgically-induced rat model of PTOA.


2014 ◽  
Vol 32 (7) ◽  
pp. 535-538 ◽  
Author(s):  
Shahram Paydar ◽  
Armin Ahmadi ◽  
Behnam Dalfardi ◽  
Alireza Shakibafard ◽  
Hamidreza Abbasi ◽  
...  

Author(s):  
Jonathan Hammerschlag ◽  
Yehuda Hershkovitz ◽  
Itamar Ashkenazi ◽  
Zahar Shapira ◽  
Igor Jeroukhimov

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Wei Lin ◽  
Huijun Kang ◽  
Yike Dai ◽  
Yingzhen Niu ◽  
Guangmin Yang ◽  
...  

Abstract Background Patellar instability (PI) often increases the possibility of lateral patellar dislocation and early osteoarthritis. The molecular mechanism of early articular cartilage degeneration during patellofemoral osteoarthritis (PFOA) still requires further investigation. However, it is known that the NF-κB signaling pathway plays an important role in articular cartilage degeneration. The aim of this study was to investigate the relationship between the NF-κB signaling pathway and patellofemoral joint cartilage degeneration. Methods We established a rat model of PI-induced PFOA. Female 4-week-old Sprague-Dawley rats (n = 120) were randomly divided into two groups: the PI (n = 60) and control group (n = 60). The distal femurs of the PI and control group were isolated and compared 4, 8, and 12 weeks after surgery. The morphological structure of the trochlear cartilage and subchondral bone were evaluated by micro-computed tomography and histology. The expression of NF-κB, matrix metalloproteinase (MMP)-13, collagen X, and TNF-ɑ were evaluated by immunohistochemistry and quantitative polymerase chain reaction. Results In the PI group, subchondral bone loss and cartilage degeneration were found 4 weeks after surgery. Compared with the control group, the protein and mRNA expression of NF-κB and TNF-ɑ were significantly increased 4, 8, and 12 weeks after surgery in the PI group. In addition, the markers of cartilage degeneration MMP-13 and collagen X were more highly expressed in the PI group compared with the control group at different time points after surgery. Conclusions This study has demonstrated that early patellofemoral joint cartilage degeneration can be caused by PI in growing rats, accompanied by significant subchondral bone loss and cartilage degeneration. In addition, the degeneration of articular cartilage may be associated with the activation of the NF-κB signaling pathway and can deteriorate with time as a result of PI.


2013 ◽  
Vol 57 (5) ◽  
pp. 1196-1203 ◽  
Author(s):  
Andrew G. Georgiadis ◽  
Farah H. Mohammad ◽  
Kristin T. Mizerik ◽  
Timothy J. Nypaver ◽  
Alexander D. Shepard

Author(s):  
Timur B. Minasov ◽  
Ekaterina R. Yakupova ◽  
Dilmurod Ruziboev ◽  
Ruslan M. Vakhitov-Kovalevich ◽  
Ruslan F. Khairutdinov ◽  
...  

Degenerative pathology of the musculoskeletal system is one of the main reasons for decreased mobility in patients of the older age group. Increasing the life expectancy leads to predominance non-epidemic pathology in all developed countries. Therefore, degenerative diseases of musculoskeletal system have not only medical significance but also social significance. Objective is studying the morphological features of synovial environment of the decompensated osteoarthritic (OA) knee joint. Structural features of subchondral bone, hyaline cartilage of the femur and tibia, the articular capsule, menisci and ligamentous apparatus of the knee joint were studied in 64 patients who underwent total knee arthroplasty at the Department of Traumatology and Orthopedics Bashkirian State Medical University in the period from 2015 to 2020. Material selection, preparation of histological samples, staining with hematoxylin-eosin, microscopy was performed. Adaptive signs of articular cartilage of the femoral condyles manifest in the form of cartilage tissue rearrangement, which are most pronounced in the central zone of the cartilage. At the same time, the phenomena of decompensation and significant areas of destruction are noted. Also, the subchondral bone was replaced with connective tissue with subsequent sclerosis. This sclerosis subsequently led to the decompensation of structures of the hyaline cartilage in the deep and middle zones. Destructive and dystrophic processes were noted in the knee joint menisci. Articular cartilage was replaced with granulation tissue with subsequent invasion of blood vessels. Cruciate ligaments in patients with OA show signs of adaptation due to expansion of endothenonium layers between bundles of collagen fibers and an increase in the diameter of blood vessels.


2010 ◽  
Vol 18 (12) ◽  
pp. 1570-1576 ◽  
Author(s):  
A.S. Aula ◽  
J. Töyräs ◽  
V. Tiitu ◽  
J.S. Jurvelin

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