Structural effects of glucosamine sulfate and risedronate on cartilage and subchondral bone in a rabbit model of osteoarthritis

Bone ◽  
2012 ◽  
Vol 50 ◽  
pp. S96
Author(s):  
D. Guede⁎ ◽  
M. López-Pena ◽  
N. Miño ◽  
M. Permuy ◽  
F. Muñoz ◽  
...  
Bone ◽  
2012 ◽  
Vol 50 ◽  
pp. S97-S98
Author(s):  
M. Permuy⁎ ◽  
M. López ◽  
N. Miño ◽  
F. Muñoz ◽  
A.G.- Cantalapiedra ◽  
...  

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Jeong-Eun Huh ◽  
Yeon-Cheol Park ◽  
Byung-Kwan Seo ◽  
Jae-Dong Lee ◽  
Yong-Hyeon Baek ◽  
...  

We sought to determine the cartilage repair capacity of WIN-34B in the collagenase-induced osteoarthritis rabbit model and in progenitor cells from subchondral bone. The cartilage protective effect of WIN-34B was measured by clinical and histological scores, cartilage area, and proteoglycan and collagen contents in the collagenase-induced osteoarthritis rabbit model. The efficacy of chondrogenic differentiation of WIN-34B was assessed by expression of CD105, CD73, type II collagen, and aggrecanin vivoand was analyzed by the surface markers of progenitor cells, the mRNA levels of chondrogenic marker genes, and the level of proteoglycan, GAG, and type II collagenin vitro. Oral administration of WIN-34B significantly increased cartilage area, and this was associated with the recovery of proteoglycan and collagen content. Moreover, WIN-34B at 200 mg/kg significantly increased the expression of CD105, CD73, type II collagen, and aggrecan compared to the vehicle group. WIN-34B markedly enhanced the chondrogenic differentiation of CD105 and type II collagen in the progenitor cells from subchondral bone. Also, we confirmed that treatment with WIN-34B strongly increased the number of SH-2(CD105) cells and expression type II collagen in subchondral progenitor cells. Moreover, WIN-34B significantly increased proteoglycan, as measured by alcian blue staining; the mRNA level of type IIα1 collagen, cartilage link protein, and aggrecan; and the inhibition of cartilage matrix molecules, such as GAG and type II collagen, in IL-1β-treated progenitor cells. These findings suggest that WIN-34B could be a potential candidate for effective anti-osteoarthritic therapy with cartilage repair as well as cartilage protection via enhancement of chondrogenic differentiation in the collagenase-induced osteoarthritis rabbit model and progenitor cells from subchondral bone.


2021 ◽  
Author(s):  
Feihua Yan ◽  
Xujun Zhao ◽  
Shisheng Duan ◽  
Aini Maimaiti ◽  
Yong Qi ◽  
...  

Abstract Purpose Knee osteoarthritis (KOA) is a common and severe disease characterized by articular cartilage degeneration, subchondral bone remodeling and inflammation. This study aimed to investigate the therapeutic effects of high fibular osteotomy (HFO) in a KOA rabbit model and to examine the molecular mechanisms involved in medial compartment KOA protective effects.Methods A rabbit model of destabilization of the medial meniscus was used to induce post-traumatic KOA. The effectiveness of HFO on protection against KOA was tested. Hematoxylin and eosin staining, Safranin O/Fast green staining and micro-CT analysis were performed to evaluate structural and morphological changes. The expression of metalloproteinase (MMP)-1, MMP-3, MMP-13, collagen type II (Col2), a disintegrin and metalloproteinase domain with thrombospondin motifs (ADAMTS)-5, aggrecan, interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α was assessed by real time PCR, western blotting and enzyme-linked immunosorbent assay. Additionally, western blotting was performed to test the expression of NFκB p65, phospho-IκBα and IκBα. Results HFO delayed the progression of articular cartilage damage and suppressed subchondral bone remodeling. HFO also decreased MMP-1, MMP-3, MMP-13 and ADAMTS-5 expression, and increased Col2 and aggrecan expression. In parallel, HFO attenuated the expression of IL-1β, IL-6 and TNF-α. Furthermore, the molecular mechanism underlying the protective effect of HFO in medial compartment KOA was related to the NFκB signaling pathway. Conclusion HFO may be a novel therapeutic approach to treating medial compartment KOA.


2017 ◽  
Vol 92 (3) ◽  
pp. 201-211 ◽  
Author(s):  
A Parrilli ◽  
G Giavaresi ◽  
A Ferrari ◽  
F Salamanna ◽  
G Desando ◽  
...  

2015 ◽  
Vol 11 (1) ◽  
Author(s):  
María Permuy ◽  
David Guede ◽  
Mónica López-Peña ◽  
Fernando Muñoz ◽  
Jose-Ramón Caeiro ◽  
...  

2009 ◽  
Vol 17 ◽  
pp. S58
Author(s):  
T. Shirai ◽  
M. Kobayashi ◽  
K. Nishitani ◽  
T. Satake ◽  
H. Kuroki ◽  
...  

2015 ◽  
Vol 67 (2) ◽  
pp. 325-333
Author(s):  
R.B. Eleotério ◽  
K.C.S. Pontes ◽  
J.P. Machado ◽  
E.C.C. Reis ◽  
P.S. Ferreira ◽  
...  

Chondroitin and glucosamine sulfate nutraceuticals are commonly used in the management of degenerative articular disease in veterinary routine. However, there are controversies on the contribution of these substances to articular cartilage. The purpose of this study was to evaluate the efficiency of a chondroitin and glucosamine sulfate-based veterinary nutraceutical on the repair of an induced osteochondral defect in a dog femoral condyle, by macroscopic, histological and histomorphometric analyses. The nutraceutical was orally administered the day following injury induction, every 24 hours (treated group, TG, n=24), compared with animals that did not receive the product (control group, CG, n=24). Six animals per group were anaesthetized for sample collection at 15, 30, 60 and 90 days after surgery. At 15 days, defects were macroscopically filled with red-pinkish tissue. After 30 days, whitish color tissue was observed, both in TG and CG animals, with firmer consistency to touch at 60 and 90 postoperative days. Histological analysis demonstrated that, in both groups, there was initial blood clot formation, which was subsequently substituted by a fibrin net, with capillary proliferation from the adjacent bone marrow and infiltration of mesenchymal cells in clot periphery. As cellular differentiation developed, repair tissue presented a fibrocartilage aspect most of the time, and new subchondral bone formation occurred in the deepest area corresponding to the defect. Histomorphometry suggested that the nutraceutical did not favor the articular cartilage repair process. It was concluded that nutraceutical did not significantly influence chondrocytes proliferation or hyaline architecture restoration.


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