Benzo(a)pyrene induce the inflammation, nitrosative stress and matrix degradation in articular cartilage

2016 ◽  
Author(s):  
Tsung-Hsun Hsieh
Author(s):  
Peter M. van der Kraan ◽  
Esmeralda N. Blaney Davidson

This chapter provides an overview of tissues unique to synovial joints, articular cartilage, and meniscus. The development and cellular and (bio)chemical composition are described, as well as the role of mechanical stimuli. In addition, the role of growth factors in cartilage and meniscus homeostasis, cellular differentiation, and chondrocyte hypertrophy are discussed. Furthermore, the involvement of aggrecanases and matrix metalloproteinases in cartilage and meniscus matrix degradation and osteoarthritis are described. Finally, the current status of repair of articular cartilage and meniscus is provided. This chapter reflects the changes in cellular differentiation, growth factor signalling, and altered matrix composition that contribute to osteoarthritis.


2016 ◽  
Vol 24 (11) ◽  
pp. 1981-1988 ◽  
Author(s):  
P. Behrendt ◽  
A. Preusse-Prange ◽  
T. Klüter ◽  
M. Haake ◽  
B. Rolauffs ◽  
...  

Author(s):  
Chih-Tung Chen ◽  
Peter A. Torzilli

Chondrocyte injury and death in articular cartilage can cause matrix degradation and is a risk factor for secondary osteoarthritis [1,3–5]. Chondrocyte death can occur due to excessive mechanical loading, such as with a single high traumatic impact load (≥20 MPa), repeated sub-impact loads (≥5 MPa), or extensive cyclic loads (≥1 MPa) [1–5]. Several recent studies have shown that chondrocyte death depends not only on the stress magnitude [2] but also on the stress rate [3], strain rate [5] and load duration [1–2].


2010 ◽  
Vol 18 ◽  
pp. S35
Author(s):  
L. Patel ◽  
W. Sun ◽  
K.E. Georgiadis ◽  
E.A. Morris ◽  
C.R. Flannery ◽  
...  

1995 ◽  
Vol 96 (5) ◽  
pp. 2454-2460 ◽  
Author(s):  
V M Baragi ◽  
R R Renkiewicz ◽  
H Jordan ◽  
J Bonadio ◽  
J W Hartman ◽  
...  

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Rui Dong ◽  
Jun Ying ◽  
Taotao Xu ◽  
Songfeng Hu ◽  
Peng Zhang ◽  
...  

Objective. To investigate the effect and underlying mechanism of Bushenhuoxue (BSHX) formula on articular cartilage repair. Methods. Twenty-four full-thickness cartilage defect rats were divided into two groups: model group and BSHX group (treated with BSHX formula). Macroscopic observation and histopathological study were conducted after 4- and 8-week treatment. Additionally, we also evaluated chondrocyte proliferation, extracellular matrix (ECM) deposition, cartilage degradation, and chondrocyte hypertrophy-related genes expression in chondrogenic ATDC5 cells cultured in BSHX formula-mediated serum. Moreover, we assessed aforementioned genes expression and pSMAD2/3 protein level in Tgfβr2 siRNA transfected chondrogenic ATDC5 cells in order to address whether BSHX formula exerts cartilage repairing effect through TGF-β signaling. Results. Neocartilage regeneration promotion effect was observed in cartilage defect rats after BSHX formula treatment, with increases in Col2 and pSMAD2 and decreases in Mmp13 and Runx2. Moreover, cell proliferation, the elevated Col2a1, Aggrecan and pSMAD2/3, reduced Mmp13, Adamts5, Col10a1, and Runx2 expression were also observed in chondrogenic ATDC5 cells cultured in BSHX formula-mediated serum. Besides, the expression alteration of ECM deposition, cartilage degradation, chondrocyte hypertrophy-related genes, and pSMAD2/3 protein levels presented in Tgfβr2 downregulated chondrogenic ATDC5 cells couldn’t be adjusted by BSHX formula treatment. Conclusion. By activation of TGF-β signaling, BSHX formula can promote articular cartilage repair by accelerating chondrocyte proliferation and maintaining chondrocyte phenotype, upregulate ECM accumulation, and inhibit matrix degradation.


2010 ◽  
Vol 18 (1) ◽  
pp. 97-105 ◽  
Author(s):  
P.A. Torzilli ◽  
M. Bhargava ◽  
S. Park ◽  
C.T.C. Chen

Arthritis ◽  
2011 ◽  
Vol 2011 ◽  
pp. 1-16 ◽  
Author(s):  
Elena V. Tchetina

Osteoarthritis is the most common arthritic condition, which involves progressive degeneration of articular cartilage. The most recent accomplishments have significantly advanced our understanding on the mechanisms of the disease development and progression. The most intriguing is the growing evidence indicating that extracellular matrix destruction in osteoarthritic articular cartilage resembles that in the hypertrophic zone of fetal growth plate during endochondral ossification. This suggests common regulatory mechanisms of matrix degradation in OA and in the development and can provide new approaches for the treatment of the disease by targeting reparation of chondrocyte phenotype.


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