scholarly journals Effect of intraarticular injection of chondroitin sulfate into synovial joint elements in an experiment

2020 ◽  
pp. 84-89
Author(s):  
V. I. Nikolaev ◽  
D. A. Zinovkin ◽  
A. A. Tretyakov

Objective: to study morphological and morphometric changes in the epiphysis bone in a rat during the intra-articular injection of chondroitin sulfate (CS). Mаteriаl аnd methods. The object of the study was the knee joints of 36 Wistar rats. CS injections at a dose of 0.05 ml were performed once a week into one of the knee joints (experimental joint), and isotonic NaCl solution at the same volume was injected into the opposite joint (control joint). The animals in the number of 12 units were withdrawn from the experiment on the 7th, 14th, and 21st days, which corresponded to one week after one-, two-and three-fold intra-articular injections of HC and 0.9 % NaCl. The isolated knee joints were placed in a decalcifying liquid, then were fixed in 10% neutral buffered formalin. 4 micron histological sections were stained with hematoxylin and eosin. The morphometric analysis assessed the thickness of hyaline articular cartilage, the thickness of the epiphysis growth zone cartilage, and the cell content of the subchondral bone. Results. The study of the thickness of the articular cartilage, the growth zone of epiphyseal cartilage and the cellular composition of the subchondral bone has showed a statistically significant dynamic increase in these indicators after the 2nd and 3rd intra-articular injections of CS. The assessment of the thickness of the articular cartilage on the 21st day found some statistically significant differences between the experimental and control groups (p < 0.0001), the thickness of the epiphyseal cartilage had increased significantly by that time (p < 0.0001), and the cell content of bone marrow showed statistically significant differences (p = 0.002). Conclusion. The obtained data testify to a pronounced regenerative effect of CS, injected intra-articularly into articular cartilage.

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.


2021 ◽  
Author(s):  
Weiping Lin ◽  
Zhengmeng Yang ◽  
Liu Shi ◽  
Haixing Wang ◽  
Qi Pan ◽  
...  

Abstract Background: Osteoarthritis (OA) is a chronic joint disease, characterized by articular cartilage degradation, subchondral bone hardening, and inflammation of the whole synovial joint. There is no pharmacological treatment in slowing down OA progression, leading to costly surgical interventions eventually. Cell therapy using chondrocytes or progenitor cells from different sources has been reported in clinical trials for OA management with some success, but outcomes are varied. Peripheral blood derived mesenchymal stem cells (PB-MSCs) are promising cells owing to their easy collection, superior migration, and differentiation potentials. In the current study, we evaluated the effect of intra-articular administration of PB-MSCs on the progression of OA in mice.Methods: C57BL/6J mice (8-10 weeks old male) were subjected to destabilization of the medial meniscus surgeries (DMM) on their right joints following protocols as previously reported. The mice after DMM were randomly treated with saline (vehicle control), PB-MSCs, or adipose tissue derived MSCs (AD-MSCs) (n = 7 per group). The mice treated with sham surgery were regarded as sham controls (n = 7). PB-MSCs and AD-MSCs were harvested and cultured according to previous published protocols, and pre-labeled with BrdU for 48 h before use. PB-MSCs or AD-MSCs (5 × 105 cells/mouse; passage 3~5) were injected into the right knee joints thrice post-surgery (except sham surgery group). The mice were euthanized at 8 weeks post-surgery and knee joint samples were collected for micro-CT and histological examinations.Results: PB-MSCs administration significantly reduced hardening of subchondral bone comparing to vehicle controls. Safranin O staining showed that PB-MSCs treatment ameliorated degeneration of articular cartilage, which is comparable to AD-MSCs treatment. The expression of catabolic marker MMP13 was significantly reduced in articular cartilage of PB-MSCs-treated groups comparing to vehicle controls. Co-expression of BrdU and Sox9 were detected, indicating injected PB-MSCs differentiated towards chondrocytes in situ. Reduced level of IL-6 in the peripheral sera of PB-MSCs- and AD-MSCs-treated mice was also determined. Conclusions: Repetitive administration of PB-MSCs or AD-MSCs halted OA progression through inhibiting cartilage degradation and inflammation. PB-MSCs may become a promising cell source for cartilage tissue repair and alleviation of OA progression.


Bone ◽  
2003 ◽  
Vol 32 (3) ◽  
pp. 284-290 ◽  
Author(s):  
Dragica Bobinac ◽  
Josip Spanjol ◽  
Sanja Zoricic ◽  
Ivana Maric

2019 ◽  
Author(s):  
Melina Rodrigues Bellini ◽  
Michael Andrew Pest ◽  
Jae-Wook Jeong ◽  
Frank Beier

ABSTRACTBackgroundMitogen-inducible gene 6 (Mig-6) is a tumour suppressor gene that is also associated with the development of osteoarthritis (OA)-like disorder. Recent evidence from our lab and others showed that cartilage-specific Mig-6 knockout (KO) mice develop chondro-osseous nodules, along with increased articular cartilage thickness and enhanced EGFR signaling in the articular cartilage. Here, we evaluate the phenotype of mice with skeletal-specific overexpression of Mig-6.MethodsSynovial joint tissues of the knee were assessed in 12 and 36 weeks-old skeleton-specific Mig-6 overexpressing (Mig-6over/over) and control animals using histological stains, immunohistochemistry, semi-quantitative OARSI scoring, and microCT for skeletal morphometry. Measurement of articular cartilage and subchondral bone thickness were also performed using histomorphometry.ResultsOur results show only subtle developmental effects of Mig-6 overexpression. However, male Mig-6over/over mice show accelerated cartilage degeneration at 36 weeks of age, in both medial and lateral compartments of the knee. Immunohistochemistry for SOX9 and PRG4 showed decreased staining in Mig-6over/over mice relative to controls, providing potential molecular mechanisms for the observed effects.ConclusionOverexpression of Mig-6 in articular cartilage causes no major developmental phenotype but results in accelerated development of OA during aging. These data demonstrate that precise regulation of the Mig-6/EGFR pathway is critical for joint homeostasis.


2020 ◽  
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.


2020 ◽  
Author(s):  
Wei Lin ◽  
Yike Dai ◽  
Guangmin Yang ◽  
Jinghui Niu ◽  
Ming Li ◽  
...  

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.


2019 ◽  
Author(s):  
Luling Wang ◽  
Demao Zhang ◽  
Jianxun Sun ◽  
Yujia Cui ◽  
Linyi Cai ◽  
...  

Abstract Background: To clarify the expression and distribution of ADAMTS1, ADAMTS2 and ADAMTS5 in knee joints of osteoarthritis (OA) mice. Methods: OA was established via anterior cruciate ligament transection (ACLT) on the knee joints of C57BL/6J mice. The morphology change of OA was analyzed by Micro-CT. Histologic analysis was used to evaluate symptomatic change in articular cartilage and subchondral bone. Quantitative real-time PCR (qPCR) was used to analyze mRNA expressions of ADAMTS family in bone-related tissues and cells. Immunofluorescence staining was used to analyze the expressions and distributions of ADAMTS1, ADAMTS2, and ADAMTS5, as well as the condition of inflammation of OA.Results: Cartilage deterioration, significant reduction of collagen and proteoglycan components in the cartilage matrix happened in ACLT-induced OA mice, along with increased inflammatory response and osteoclast activity. Among ADAMTS, the gene expression levels of ADAMTS1, ADAMTS2 and ADAMTS5 were ranked top 5 in cartilage/chondrocytes, osteogenic tissue/osteoblasts and cortical bone/osteocytes. After ACLT surgery, the expressions of ADAMTS1, ADAMTS2 and ADAMTS5 all increased in articular cartilage, growth plate and subchondral bone of knee joints. Conclusion: The enhanced expressions of ADAMTS1, ADAMTS2 and ADAMTS5 after ACLT surgery provide a further understanding in degenerative change of OA.


2021 ◽  
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.


Sign in / Sign up

Export Citation Format

Share Document