scholarly journals Synovial fluid biomarker levels predict articular cartilage damage following complete medial meniscectomy in the canine knee

2002 ◽  
Vol 20 (1) ◽  
pp. 92-100 ◽  
Author(s):  
Cathy S. Carlson ◽  
Farshid Guilak ◽  
Thomas P. Vail ◽  
Jean F. Gardin ◽  
Virginia B. Kraus
Keyword(s):  
Articular Cartilage ◽  
Synovial Fluid ◽  
Cartilage Damage ◽  
Articular Cartilage Damage ◽  
Medial Meniscectomy ◽  
Fluid Biomarker

scholarly journals Changes in Hematobiochemical, Radiological, and Synovial Fluid Parameter in Patients of Osteoarthritis Knee with Effusion: A Prospective Observational Study

2021 ◽  
Vol 11 (8) ◽  
Author(s):  
Sachin Jain ◽  
Sameer Gupta ◽  
Tarun Naugraiya
Keyword(s):  
Articular Cartilage ◽  
Tumor Necrosis Factor ◽  
Synovial Fluid ◽  
Tumor Necrosis ◽  
Cartilage Damage ◽  
Definitive Treatment ◽  
Articular Cartilage Damage ◽  
Synovial Effusion ◽  
Early Oa ◽  
Necrosis Factor

Introduction: A joint is the point of connection between two bones in our body. Inflammation of joint leads to several diseases, including osteoarthritis (OA). OA is a common condition of debilitating joint disease mainly affecting the elderly. Case Report:e In this study, we had studied correlation the cases (OA with synovial effusion) and control (OA without synovial effusion) with blood parameters, radiological and synovial fluid parameters (tumor necrosis factor-? [TNF]-? levels), and the incidence of synovial effusion in radiological staging of disease. Out of 100 patients, 50 patients with OA knee with effusion and 50 patients OA knee without effusion. We concluded that incidence of synovitis knee along with raised markers of inflammation, that is, C-reactive protein, erythrocyte sedimentation rate, and synovial fluid TNF-? levels was significantly higher in Stage II of OA knee, indicating that inflammation is significant part of early OA knee. Inflammation in early part of disease can lead to articular cartilage damage and rapid progression of osteoarthritic changes. Conclusion:Our study concluded that OA is not only a degenerative disease but also there is significant contribution of inflammation in disease process. Targeting inflammation in synovium may delay/prevent articular cartilage damage and osteophytes formation, especially in early OA. Anti-TNF-? agents and anti-inflammatory drugs may be considered for definitive treatment of OA. Keywords: Tumor necrosis factor-alpha, osteoarthritis, Kellgren Lawrence.

Efficacy Treatment of Osteoarthritis with Combine Chondroitin and Glucosamine

2021 ◽  
Vol 23 (3) ◽  
pp. 239-244
Author(s):  
Maciej Materkowski
Keyword(s):  
Articular Cartilage ◽  
Cartilage Damage ◽  
Main Principle ◽  
Articular Cartilage Damage ◽  
Spontaneous Regeneration

Osteoarthritis led to the articular cartilage damage and cause different kind of problems – from social to biological. The analysis of existing research unfortunately subjected questioned the reliability of spontaneous regeneration of damaged cartilage, which makes it necessary to focus on the possibilities of protection of the tissue from further its degradation. Treatment of osteoarthritis require to use many drugs, which would lead to slowdown the this process. The aim of below publication is to analyse the practical, clinical biological possibilities of articular cartilage protection with a usage of SYSADOA – (symptomatic slow acting drugs of OA). Osteoarthritis is most frequent disease of the joints and prescription of the SYSADOA should be main principle of that treatment.

Biologic injections for osteoarthritis and articular cartilage damage: can we modify disease?

2017 ◽  
Vol 45 (3) ◽  
pp. 203-223 ◽  
Author(s):  
Weilong J. Shi ◽  
Fotios P. Tjoumakaris ◽  
Mayan Lendner ◽  
Kevin B. Freedman
Keyword(s):  
Articular Cartilage ◽  
Cartilage Damage ◽  
Articular Cartilage Damage

scholarly journals Traumatic Joint Injury Induces Acute Catabolic Bone Turnover Concurrent with Articular Cartilage Damage in a Rat Model of Post-Traumatic Osteoarthritis

2020 ◽  
Author(s):  
Tristan Maerz ◽  
Michael D. Newton ◽  
Mackenzie Fleischer ◽  
Samantha E. Hartner ◽  
Karissa Gawronski ◽  
...  
Keyword(s):  
Articular Cartilage ◽  
Bone Formation ◽  
Bone Turnover ◽  
Bone Remodeling ◽  
Cartilage Damage ◽  
Post Injury ◽  
Bone Formation Rate ◽  
Articular Cartilage Damage ◽  
Group I ◽  
Sustained Reduction

ABSTRACTObjectiveAssess acute alterations in bone turnover, microstructure, and histomorphometry following noninvasive anterior cruciate ligament rupture (ACLR).MethodsTwelve female Lewis rats were randomized to receive noninvasive ACLR or Sham loading (n=6/group). In vivo μCT was performed at 3, 7, 10, and 14 days post-injury to quantify compartment-dependent subchondral (SCB) and epiphyseal trabecular bone remodeling. Near-infrared (NIR) molecular imaging was used to measure in vivo bone anabolism (800 CW BoneTag) and catabolism (Cat K 680 FAST). Metaphyseal bone remodeling and articular cartilage morphology was quantified using ex vivo μCT and contrast-enhanced µCT, respectively. Calcein-based dynamic histomorphometry was used to quantify bone formation. OARSI scoring was used to assess joint degeneration, and osteoclast number was quantified on TRAP stained-sections.ResultsACLR induced acute catabolic bone remodeling in subchondral, epiphyseal, and metaphyseal compartments. Thinning of medial femoral condyle (MFC) SCB was observed as early as 7 days post-injury, while lateral femoral condyles (LFC) exhibited SCB gains. Trabecular thinning was observed in MFC epiphyseal bone, with minimal changes to LFC. NIR imaging demonstrated immediate and sustained reduction of bone anabolism (∼15-20%), and a ∼32% increase in bone catabolism at 14 days, compared to contralateral limbs. These findings were corroborated by reduced bone formation rate and increased osteoclast numbers, observed histologically. ACLR-injured femora had significantly elevated OARSI score, cartilage thickness, and cartilage surface deviation.ConclusionACL rupture induces immediate and sustained reduction of bone anabolism and overactivation of bone catabolism, with mild-to-moderate articular cartilage damage at 14 days post-injury.

Risk factors for progression of articular cartilage damage after anatomical anterior cruciate ligament reconstruction

2018 ◽  
Vol 100-B (3) ◽  
pp. 285-293 ◽  
Author(s):  
A. Nakamae ◽  
N. Adachi ◽  
M. Deie ◽  
M. Ishikawa ◽  
T. Nakasa ◽  
...  
Keyword(s):  
Risk Factors ◽  
Anterior Cruciate Ligament ◽  
Articular Cartilage ◽  
Acl Reconstruction ◽  
Cruciate Ligament ◽  
Cartilage Damage ◽  
Significant Risk ◽  
Articular Cartilage Damage ◽  
Anterior Cruciate

Aims To investigate the risk factors for progression of articular cartilage damage after anatomical anterior cruciate ligament (ACL) reconstruction. Patients and Methods A total of 174 patients who underwent second-look arthroscopic evaluation after anatomical ACL reconstruction were enrolled in this study. The graded condition of the articular cartilage at the time of ACL reconstruction was compared with that at second-look arthroscopy. Age, gender, body mass index (BMI), ACL reconstruction technique, meniscal conditions, and other variables were assessed by regression analysis as risk factors for progression of damage to the articular cartilage. Results In the medial compartment, multivariable logistic regression analysis indicated that partial medial meniscectomy (odds ratio (OR) 6.82, 95% confidence interval (CI) 2.11 to 22.04, p = 0.001), pivot-shift test grade at the final follow-up (OR 3.53, CI 1.39 to 8.96, p = 0.008), BMI (OR 1.15, CI 1.03 to 1.28, p = 0.015) and medial meniscal repair (OR 3.19, CI 1.24 to 8.21, p = 0.016) were significant risk factors for progression of cartilage damage. In the lateral compartment, partial lateral meniscectomy (OR 10.94, CI 4.14 to 28.92, p < 0.001) and side-to-side differences in anterior knee laxity at follow-up (OR 0.63, p = 0.001) were significant risk factors. Conclusion Partial meniscectomy was found to be strongly associated with the progression of articular cartilage damage despite r anatomical ACL reconstruction. Cite this article: Bone Joint J 2018;100-B:285–93.

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