scholarly journals Intra-Articular Injections of Curcumin Monoglucuronide TBP1901 Suppresses Articular Cartilage Damage and Regulates Subchondral Bone Alteration in an Osteoarthritis Rat Model

Cartilage ◽  
2021 ◽  
pp. 194760352110432
Author(s):  
Akihiro Nakahata ◽  
Akira Ito ◽  
Ryo Nakahara ◽  
Atsuhiro Kishimoto ◽  
Atsushi Imaizumi ◽  
...  
Keyword(s):  
Articular Cartilage ◽  
Acute Phase ◽  
Subchondral Bone ◽  
Rat Model ◽  
Saline Solution ◽  
Cartilage Damage ◽  
Chronic Phase ◽  
Synovial Inflammation ◽  
Free Form ◽  
Articular Cartilage Damage

Objective Curcumin monoglucuronide (TBP1901) is highly water soluble and can convert to free form curcumin, which has pharmacological effects, on intravenous administration. This study aimed to investigate the effectiveness of TBP1901 intra-articular injections in an osteoarthritis (OA) rat model. Methods Sixty-four male Wistar rats (12 weeks old) who underwent destabilized medial meniscus (DMM) surgery were randomly separated into the TBP1901 injection or saline solution (control) injection group. They were sacrificed at 1, 2, 6, or 10 weeks postoperatively (weeks 1, 2, 6, and 10; n = 8 for each group). TBP1901 (30 mg/mL) or saline solution of 50 μL was injected into the knee joints twice a week during weeks 1 and 2 to investigate the effects in the acute phase of posttraumatic (PT) OA or once a week during weeks 6 and 10 to investigate it in the chronic phase of PTOA. Histology, immunohistochemistry, and micro-computed tomography were performed to evaluate the changes in OA. Results TBP1901 injections significantly reduced synovial inflammation at weeks 1 and 2, and tumor necrosis factor-α expression in the articular cartilage at week 6. The TBP1901 injections also significantly suppressed articular cartilage damage, subchondral bone (SB) plate thickening, SB plate perforation, and osteophyte formation at week 10. Conclusions TBP1901 intra-articular injections suppressed synovial inflammation in the acute phase of PTOA in DMM rats. In the chronic phase, TBP1901 suppresses articular cartilage damage and regulates SB plate changes.

scholarly journals Blockade of TRPM7 Alleviates Chondrocyte Apoptosis and Articular Cartilage Damage in the Adjuvant Arthritis Rat Model Through Regulation of the Indian Hedgehog Signaling Pathway

2021 ◽  
Vol 12 ◽  
Author(s):  
Ganggang Ma ◽  
Yang Yang ◽  
Yong Chen ◽  
Xin Wei ◽  
Jie Ding ◽  
...  
Keyword(s):  
Articular Cartilage ◽  
Signaling Pathway ◽  
Rat Model ◽  
Adjuvant Arthritis ◽  
Hedgehog Signaling ◽  
Cartilage Damage ◽  
Chondrocyte Apoptosis ◽  
Indian Hedgehog ◽  
Hedgehog Signaling Pathway ◽  
Articular Cartilage Damage

Articular cartilage damage with subsequent impairment of joint function is a common feature of articular diseases, in particular, rheumatoid arthritis and osteoarthritis. While articular cartilage injury mediated by chondrocyte apoptosis is a known major pathological feature of arthritis, the specific mechanisms remain unclear at present. Transient receptor potential melastatin-like seven channel (TRPM7) is reported to play an important regulatory role in apoptosis. This study focused on the effects of TRPM7 on arthritic chondrocyte injury and its underlying mechanisms of action. Sodium nitroprusside (SNP)-induced rat primary chondrocyte apoptosis and rat adjuvant arthritis (AA) were used as in vitro and in vivo models, respectively. Blockage of TRPM7 with 2-APB or specific siRNA resulted in increased chondrocyte viability and reduced toxicity of SNP. Moreover, treatment with 2-APB enhanced the Bcl-2/Bax ratio and reduced cleaved PARP and IL-6, MMP-13 and ADAMTS-5 expression in SNP-treated chondrocytes. Activation of Indian Hedgehog with purmorphamine reversed the protective effects of 2-APB on SNP-induced chondrocyte apoptosis. Blockage of TRPM7 with 2-APB relieved the clinical signs of AA in the rat model and reduced the arthritis score and paw swelling. Similar to findings in SNP-treated chondrocytes, 2-APB treatment increased the Bcl-2/Bax ratio and suppressed cleaved PARP, IL-6, MMP-13, ADAMTS-5, TRPM7, and Indian hedgehog expression in articular cartilage of AA rats. Our collective findings suggest that blockade of TRPM7 could effectively reduce chondrocyte apoptosis and articular cartilage damage in rats with adjuvant arthritis through regulation of the Indian Hedgehog signaling pathway.

scholarly journals Genetic Deletion of Interleukin-15 Is Not Associated with Major Structural Changes Following Experimental Post-Traumatic Knee Osteoarthritis in Rats

2021 ◽  
Vol 11 (15) ◽  
pp. 7118
Author(s):  
Ermina Hadzic ◽  
Garth Blackler ◽  
Holly Dupuis ◽  
Stephen James Renaud ◽  
Christopher Thomas Appleton ◽  
...  
Keyword(s):  
Articular Cartilage ◽  
Subchondral Bone ◽  
Structural Changes ◽  
Cartilage Damage ◽  
Wild Type ◽  
Significant Difference ◽  
Post Traumatic ◽  
Interleukin 15 ◽  
Joint Trauma ◽  
Surgically Induced

Post-traumatic osteoarthritis (PTOA) is a degenerative joint disease, leading to articular cartilage breakdown, osteophyte formation, and synovitis, caused by an initial joint trauma. Pro-inflammatory cytokines increase catabolic activity and may perpetuate inflammation following joint trauma. Interleukin-15 (IL-15), a pro-inflammatory cytokine, is increased in OA patients, although its roles in PTOA pathophysiology are not well characterized. Here, we utilized Il15 deficient rats to examine the role of IL-15 in PTOA pathogenesis in an injury-induced model. OA was surgically induced in Il15 deficient Holtzman Sprague-Dawley rats and control wild-type rats to compare PTOA progression. Semi-quantitative scoring of the articular cartilage, subchondral bone, osteophyte size, and synovium was performed by two blinded observers. There was no significant difference between Il15 deficient rats and wild-type rats following PTOA-induction across articular cartilage damage, subchondral bone damage, and osteophyte scoring. Similarly, synovitis scoring across six parameters found no significant difference between genetic variants. Overall, IL-15 does not appear to play a key role in the development of structural changes in this surgically-induced rat model of PTOA.

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.

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