scholarly journals Miniaturized Water-Jet Ultrasound Indentation System for Quantitative Assessment of Articular Cartilage Degeneration: A Validation Study

2020 ◽  
Vol 2020 ◽  
pp. 1-13
Author(s):  
Yan-Ping Huang ◽  
Yong-Ping Zheng

Osteoarthritis is a common joint disease affecting a large population especially the elderly where cartilage degeneration is one of its hallmark symptoms. There is a need to develop new devices and instruments for the early detection and treatment of cartilage degeneration. In this study, we describe the development of a miniaturized water-jet ultrasound indentation probe for this purpose. To evaluate the system, we applied it to characterize the degeneration of articular cartilage with the measurement of its morphologic, acoustic, and mechanical properties, using the enzymatic digestions of cartilage as a model of OA. Fifty cartilage samples were tested with 10 of them used for the reproducibility study and the other 40 for collagenase and trypsin digestions. Thickness, integrated reflection coefficient (IRC), effective stiffness, and energy dissipation ratio (EDR) were used to quantify the change of articular cartilage before and after degeneration. The measurement reproducibility as represented by the standardized coefficient of variation (SCV) was 2.6%, 10.2%, 11.5%, and 12.8% for thickness, IRC, stiffness, and EDR, respectively. A significant change of IRC, stiffness, and EDR was detected after degeneration by the designed probe (p<0.05). There was also a significant difference of IRC, stiffness, and EDR between trypsin and collagenase digestions (p<0.001). In conclusion, a miniaturized water-jet ultrasound indentation probe has been designed, which has been successfully used to detect and differentiate cartilage degeneration simulated by enzymatic digestions. This probe, with future development, can be potentially suitable for quantitative assessment of cartilage degeneration with an arthroscopic operation.

Author(s):  
Patchava Apparao ◽  
Sudhakar S ◽  
Ganapathi Swamy Ch ◽  
Ravi Shankar Reddy

Objectives: To determine the effectiveness of knee joint stabilization exercises in minimizing articular cartilage degeneration and to examine theeffectiveness of knee joint stabilization exercises on decreasing pain, improving range of motion (ROM) and muscle strength.Methods: About 20 volunteer subjects (age 35-65 years) with primary osteoarthritis fulfilled the inclusion criteria given the knee stabilizationexercises for 8 weeks. Pain, muscle strength, functional outcome score, and serum cartilage oligomeric matrix protein (COMP) values were measuredpre- and post-intervention using visual analog scale, dynamometer, and ELISA test. Data were analyzed using a paired t-test with Statistical Packagefor the Social Sciences version 20 to find out the difference between the pre- and post-test.Results: The results of the study have shown that significant difference between pre- and post-test values of pain, ROM, muscle strength and functionaloutcome score with p<0.05, and there is statistical in significance in serum COMP value (p<0.05).Conclusion: Stabilization exercises of knee joint were shown to be beneficial for decreasing pain, improving ROM and muscle strength, and there wasno effect on articular cartilage changes in degenerative tibiofemoral joint disease.Keywords: Serum cartilage oligomeric matrix protein, Knee stabilization exercises, Proprioception exercises, Muscle strength.  


2008 ◽  
Vol 37 (1) ◽  
pp. 164-175 ◽  
Author(s):  
M.-H. Lu ◽  
Y. P. Zheng ◽  
Q.-H. Huang ◽  
C. Ling ◽  
Q. Wang ◽  
...  

2020 ◽  
Author(s):  
Melina Bellini ◽  
Michael Andrew Pest ◽  
Manuela Miranda Rodrigues ◽  
Ling Qin ◽  
Jae-Wook Jeong ◽  
...  

Abstract Background: Osteoarthritis (OA) is the most common form of arthritis and characterized by degeneration of articular cartilage. Mitogen-inducible gene 6 (Mig-6) has been identified as a negative regulator of the Epidermal Growth Factor Receptor (EGFR). Cartilage-specific Mig-6 knockout (KO) mice display increased EGFR signaling, an anabolic buildup of articular cartilage and formation of chondro-osseous nodules. Since our understanding of the EGFR/Mig-6 network in cartilage remains incomplete, we characterized mice with cartilage-specific overexpression of Mig-6 in this study. Methods: Utilizing knee joints from cartilage-specific Mig-6 overexpressing (Mig-6over/over) mice (at multiple time points), we evaluated the articular cartilage using histology, immunohistochemical staining and semi-quantitative histopathological scoring (OARSI) at multiple ages. MicroCT analysis was employed to examine skeletal morphometry, body composition, and bone mineral density.Results: Our data show that cartilage-specific Mig-6 overexpression did not cause any major developmental abnormalities in articular cartilage, although Mig-6over/over mice have slightly shorter long bones compared to the control group. Moreover, there was no significant difference in bone mineral density and body composition in any of the groups. However, our results indicate that Mig-6over/over male mice show accelerated cartilage degeneration at 12 and 18 months of age. Immunohistochemistry for SOX9 demonstrated that the number of positively stained cells in Mig-6over/over mice was decreased relative to controls. Immunostaining for MMP13 appeared increased in areas of cartilage degeneration in Mig-6over/over mice. Moreover, staining for phospho-EGFR (Tyr-1173) and lubricin (PRG4) was decreased in the articular cartilage of Mig-6over/over mice. Conclusion: Overexpression of Mig-6 in articular cartilage causes no major developmental phenotype; however, these mice develop earlier OA during aging. These data demonstrate that Mig-6/EGFR pathways is critical for joint homeostasis and might present a promising therapeutic target for OA.


Cells ◽  
2020 ◽  
Vol 9 (4) ◽  
pp. 927 ◽  
Author(s):  
Szu-Yu Chien ◽  
Chun-Hao Tsai ◽  
Shan-Chi Liu ◽  
Chien-Chung Huang ◽  
Tzu-Hung Lin ◽  
...  

Osteoarthritis (OA) is a chronic inflammatory and progressive joint disease that results in cartilage degradation and subchondral bone remodeling. The proinflammatory cytokine interleukin 1 beta (IL-1β) is abundantly expressed in OA and plays a crucial role in cartilage remodeling, although its role in the activity of chondrocytes in cartilage and subchondral remodeling remains unclear. In this study, stimulating chondrogenic ATDC5 cells with IL-1β increased the levels of bone morphogenetic protein 2 (BMP-2), promoted articular cartilage degradation, and enhanced structural remodeling. Immunohistochemistry staining and microcomputed tomography imaging of the subchondral trabecular bone region in the experimental OA rat model revealed that the OA disease promotes levels of IL-1β, BMP-2, and matrix metalloproteinase 13 (MMP-13) expression in the articular cartilage and enhances subchondral bone remodeling. The intra-articular injection of Noggin protein (a BMP-2 inhibitor) attenuated subchondral bone remodeling and disease progression in OA rats. We also found that IL-1β increased BMP-2 expression by activating the mitogen-activated protein kinase (MEK), extracellular signal-regulated kinase (ERK), and specificity protein 1 (Sp1) signaling pathways. We conclude that IL-1β promotes BMP-2 expression in chondrocytes via the MEK/ERK/Sp1 signaling pathways. The administration of Noggin protein reduces the expression of IL-1β and BMP-2, which prevents cartilage degeneration and OA development.


2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Yasuhito Sogi ◽  
Yutaka Yabe ◽  
Yoshihiro Hagiwara ◽  
Masahiro Tsuchiya ◽  
Yoshito Onoda ◽  
...  

Abstract Background Joint hemorrhage is caused by trauma, ligament reconstruction surgery, and bleeding disorders such as hemophilia. Recurrence of hemorrhage in the joint space induces hemosiderotic synovitis and oxidative stress, resulting in both articular cartilage degeneration and arthropathy. Joint immobilization is a common treatment option for articular fractures accompanied by joint hemorrhage. Although joint hemorrhage has negative effects on the articular cartilage, there is no consensus on whether a reduction in joint hemorrhage would effectively prevent articular cartilage degeneration. The purpose of this study was to investigate the effect of joint hemorrhage combined with joint immobilization on articular cartilage degeneration in a rat immobilized knee model. Methods The knee joints of adult male rats were immobilized at the flexion using an internal fixator from 3 days to 8 weeks. The rats were randomly divided into the following groups: immobilized blood injection (Im-B) and immobilized-normal saline injection (Im-NS) groups. The cartilage was evaluated in two areas (contact and non-contact areas). The cartilage was used to assess chondrocyte count, Modified Mankin score, and cartilage thickness. The total RNA was extracted from the cartilage in both areas, and the expression of metalloproteinase (MMP)-8, MMP-13, interleukin (IL)-1β, and tumor necrosis factor (TNF)-α was measured by quantitative real-time polymerase chain reaction. Results The number of chondrocytes in the Im-B group significantly decreased in both areas, compared with that in the Im-NS group. Modified Mankin score from 4 to 8 weeks of the Im-B group was significantly higher than that of the Im-NS group only in the contact area. The expression of MMP-8 and MMP-13 from 2 to 4 weeks and TNF-α from 2 to 8 weeks significantly increased in the Im-B group compared with those in the Im-NS group, but there was no significant difference in IL-1β expression. Conclusions The results showed that joint hemorrhage exacerbated immobilization-induced articular cartilage degeneration. Drainage of a joint hemorrhage or avoidance of loading may help prevent cartilage degeneration during joint immobilization with a hemorrhage.


2020 ◽  
Author(s):  
Melina Bellini ◽  
Michael Andrew Pest ◽  
Manuela Miranda Rodrigues ◽  
Ling Qin ◽  
Jae-Wook Jeong ◽  
...  

Abstract Background: Osteoarthritis (OA) is the most common form of arthritis and characterized by degeneration of articular cartilage. Mitogen-inducible gene 6 (Mig-6) has been identified as a negative regulator of the Epidermal Growth Factor Receptor (EGFR). Cartilage-specific Mig-6 knockout (KO) mice display increased EGFR signaling, an anabolic buildup of articular cartilage and formation of chondro-osseous nodules. Since our understanding of the EGFR/Mig-6 network in cartilage remains incomplete, we characterized mice with cartilage-specific overexpression of Mig-6 in this study. Methods : Utilizing knee joints from cartilage-specific Mig-6 overexpressing ( Mig- 6over/over ) mice (at multiple time points), we evaluated the articular cartilage using histology, immunohistochemical staining and semi-quantitative OARSI scoring at multiple ages. MicroCT analysis was employed to examine skeletal morphometry, body composition, and bone mineral density. Results: Our data show that cartilage-specific Mig-6 overexpression did not cause any major developmental abnormalities in articular cartilage, although Mig-6 over/over mice have slightly shorter long bones compared to the control group. Moreover, there was no significant difference in bone mineral density and body composition in any of the groups. However, our results indicate that Mig-6 over/over male mice show accelerated cartilage degeneration at 12 and 18 months of age. Immunohistochemistry for SOX9 demonstrated that the number of positively stained cells in Mig-6 over/over mice decreased relative to controls. Immunostaining for MMP13 staining is increased in areas of cartilage degeneration in Mig-6 over/over mice. Moreover, staining for phospho-EGFR (Tyr-1173) and lubricin (PRG4) was decreased in the articular cartilage of Mig-6 over/over mice. Conclusion: Overexpression of Mig-6 in articular cartilage causes no major developmental phenotype; however these mice develop earlier OA during aging. These data demonstrate that Mig-6/EGFR pathways is critical for joint homeostasis and might present a promising therapeutic target for OA.


2017 ◽  
Vol 4 (2) ◽  
pp. 450
Author(s):  
Hakan Cift ◽  
Ali Seker ◽  
Bulent Kilic ◽  
Murat Demiroglu ◽  
Asli Erdogan Cakir ◽  
...  

Background: Osteoarthritis (OA) of the knee is among the most common disabling diseases which may cause pain and decrease in functional status. It is the commonest form of arthritis and is most prevalent in the elderly, with 50% of adults aged 65-75 years and almost 70% of those 75+ years suffer from this disease. The aim of this study was to investigate consistency of radiologic findings with histomorphologic structure of bone in patients with severe gonarthrosis.Methods: 62 knees of 57 patients over 60 years old who had stage 3-4 gonarthrosis according to Kellgren-Lawrence classification were included in the study. Patients were separated into two groups as having stage 3 or stage 4 gonarthrosis. All the patients underwent total knee replacement procedure. During the operation distal femoral medial/lateral condyle and proximal tibial medial/lateral plateau were removed and sent to histologic examination for the measurement of thickness of cartilage layer and subchondral bone, number and thickness of trabeculae, space between two trabeculae.Results: Average thickness of subchondral bone was measured at stage 3 gonarthrosis and at stage 4 gonarthrosis. Only the difference between medial tibial condyle values of two groups was statistically significant. Average trabecula thickness was measured both at stage 3 and at stage 4 gonarthrosis. Only the difference between lateral tibial condyle values of two groups was statistically significant. Furthermore, as for the number of trabeculas and cavity between trabeculae, a significant difference couldn’t be found.Conclusions: Despite having radiological differences two groups can be said to show similar histopathological characteristics.


2017 ◽  
Vol 8 (10) ◽  
pp. 3737-3744 ◽  
Author(s):  
Zhenhua Feng ◽  
Xiaobin Li ◽  
Jian Lin ◽  
Wenhao Zheng ◽  
Zhichao Hu ◽  
...  

Osteoarthritis (OA) is the most common form of joint disease and is widespread in the elderly population and is characterized by erosion of articular cartilage, subchondral bone sclerosis and synovitis.


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