scholarly journals Canine osteoarthritis and treatments: a review

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Stephanie D. Bland
Keyword(s):  
Synovial Membrane ◽  
Animal Species ◽  
Collagen Type ◽  
The United States ◽  
Cartilage Destruction ◽  
Degenerative Joint Disease ◽  
Joint Disease ◽  
Synovial Membrane Inflammation ◽  
Canine Osteoarthritis ◽  
Pro Inflammatory Cytokines

Arthritis is a commonly occurring chronic illness in human and animals alike. Among all domestic and pet animal species, dogs suffer from arthritis more often because of excessive running or exercise, injury, and/or genetic predisposition. Presently, one in four of 77.2 million pet dogs in the United States are diagnosed with some form of arthritis. In dogs, osteoarthritis is more common than rheumatoid arthritis and pain is the number one observation. Osteoarthritis, also known as degenerative joint disease, is a slowly progressive inflammatory disease, which is characterized by degeneration of the cartilage, hypertrophy of bone at the margins, and changes in the synovial membrane, and that eventually results in pain and stiffness of joints. Alterations in joint structures, decreased flexibility, and severe pain ensues, due to lack of hydration and inflammation. Cells within the damaged joints release pro-inflammatory cytokines, which further the inflammatory process. This causes more breakdown of the cartilage collagen type II and proteoglycans, which results in a perpetual destructive cycle. This perpetuating cycle ultimately results in cartilage destruction, subchondral bone thickening, and synovial membrane inflammation. This review focuses on osteoarthritis, the disease, causes, treatments, and presents a glimpse of some new therapies under study.

scholarly journals The pathophysiology and medical management of canine osteoarthritis : continuing education

1997 ◽  
Vol 68 (1) ◽  
Author(s):  
T. Vaughan-Scott ◽  
J.H. Taylor
Keyword(s):  
Continuing Education ◽  
Clinical Signs ◽  
Cartilage Degeneration ◽  
Degenerative Joint Disease ◽  
Joint Disease ◽  
Joint Cartilage ◽  
Pharmacological Management ◽  
Gradual Onset ◽  
Joint Surfaces ◽  
Canine Osteoarthritis

Osteoarthritis or degenerative joint disease is a condition characterised by degeneration of articular cartilage often associated with the formation of new bone at joint surfaces or margins. Commonly encountered in dogs, osteoarthritis may have a gradual onset, but may also occur acutely. Osteoarthritis can be a primary disease of joint cartilage, but is more often secondary to abnormal stresses on joints. This article describes the pathogenesis and progression of cartilage degeneration as well as the dietary, lifestyle and pharmacological management of osteoarthritis. Recent pharmacological developments allow the clinician not only to control clinical signs of the disease, but also to slow the progression of cartilage degeneration.

scholarly journals Mitochondrial Transplantation Ameliorates The Development and Progression of Osteoarthritis.

2021 ◽  
Author(s):  
A Ram Lee ◽  
Jin Seok Woo ◽  
Seon-Yeong Lee ◽  
Hyun Sik Na ◽  
Keun-Hyung Cho ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
Mitochondrial Function ◽  
Therapeutic Potential ◽  
Interleukin 1 ◽  
Cartilage Destruction ◽  
Degenerative Joint Disease ◽  
Joint Disease ◽  
Necrosis Factor Alpha ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monosodium Iodoacetate

Abstract Objective: Osteoarthritis (OA) is a common degenerative joint disease characterized by breakdown of joint cartilage. Mitochondrial dysfunction of the chondrocyte is a risk factor for OA progression. We examined the therapeutic potential of mitochondrial transplantation for OA.Methods: Mitochondria were injected into the knee joint of monosodium iodoacetate (MIA)-induced OA rats. Chondrocytes from OA rats or patients with OA were cultured to examine mitochondrial function in cellular pathophysiology.Results: Pain, cartilage destruction, and bone loss were improved in mitochondrial transplanted-OA rats. The transcript levels of interleukin 1 beta (IL-1β), tumor necrosis factor alpha (TNF-α), matrix metallopeptidase 13 (MMP13), and monocyte chemoattractant protein-1 (MCP-1) in cartilage were markedly decreased by mitochondrial transplantation. Mitochondrial function, as indicated by membrane potential and oxygen consumption rate, in chondrocytes from OA rats was improved by mitochondrial transplantation. Likewise, the mitochondrial function of chondrocytes from OA patients was improved by coculture with mitochondria. Furthermore, inflammatory cell death was significantly decreased by coculture with mitochondria.Conclusion: Mitochondrial transplantation ameliorated OA progression, which is caused by mitochondrial dysfunction. These results suggest the therapeutic potential of mitochondrial transplantation for OA.

scholarly journals MiR-24-3p Attenuates IL-1β-Induced Chondrocyte Injury Associated With Osteoarthritis by Targeting BCL2L12

2020 ◽  
Author(s):  
Jin Xu ◽  
Xiaozhong Qian ◽  
Ren Ding
Keyword(s):  
Cell Viability ◽  
Inflammatory Cytokines ◽  
Caspase 3 ◽  
Degenerative Joint Disease ◽  
Joint Disease ◽  
Luciferase Reporter ◽  
Pcr Analysis ◽  
Protective Effects ◽  
Tnf Α ◽  
Pro Inflammatory Cytokines

Abstract Background: Osteoarthritis (OA) is a chronic and degenerative joint disease prevalent in the elderly. MiR-24-3p has been reported to be involved in an OA-resembling environment. However, the functional role and underlying mechanism of miR-24-3p in chondrocyte injury associated with OA remains unknown. Methods: The expression of miR-24-3p was determined in OA cases and control patients, as well as IL-1β-stimulated chondrocyte cell line CHON-001 using reverse transcription quantitative PCR analysis. Cell viability was analyzed by CCK-8 assay. Apoptosis status was assessed by caspase-3 activity detection. The pro-inflammatory cytokines (TNF-α and IL-18) were determined using ELISA assay. The association between miR-24-3p and BCL2L12 was confirmed by luciferase reporter assay.Results: We first observed that miR-24-3p expression level was lower in the OA cases than in the control patients and IL-1β decreased the expression of miR-24-3p in the chondrocyte CHON-001. Functionally, overexpression of miR-24-3p significantly attenuated IL-1β-induced chondrocyte injury, as reflected by increased cell viability, decreased caspase-3 activity, pro-inflammatory cytokines (TNF-α and IL-18). Western blot analysis showed that overexpression of miR-24-3p weakened IL-1β-induced cartilage degradation, as reflected by reduction of MMP13 (Matrix Metalloproteinase-13) and ADAMTS5 (A Disintegrin And Metalloproteinase with Thrombospondin Motifs-5) protein expression, as well as markedly elevation of COL2A1 (collagen type II). Importantly, BCL2L12 was demonstrated to be a target of miR-24-3p. BCL2L12 knockdown imitated, while overexpression significantly abrogated the protective effects of miR-24-3p against IL-1β-induced chondrocyte injury.Conclusions: In conclusion, our work provides important insight into targeting miR-24-3p/BCL2L12 axis in OA therapy.

scholarly journals Bioregulatory drugs in osteoarthritis management

2019 ◽  
pp. 76-83
Author(s):  
O. A. Shavlovskaya
Keyword(s):  
Chronic Pain ◽  
Pain Relief ◽  
Combined Treatment ◽  
Pain Syndrome ◽  
Cartilage Destruction ◽  
Degenerative Joint Disease ◽  
Joint Disease ◽  
Functional Improvement ◽  
Chronic Pain Syndrome ◽  
Matrix Loss

Osteoarthritis (OA) is a degenerative joint disease. Modern theories consider various structural (cartilage destruction) and biophysical disorders (matrix loss of glycosaminoglycans) as the basis of acute and chronic pain syndrome. The main aim of OA therapy is pain relief and functional improvement. To manage pain syndrome in OA it is reasonable to use complex bioregulatory drugs (CBD) (Traumeel S, Zeel T, Discus compositum) both in monotherapy and in combined treatment. The effectiveness of CBD is comparable to that of NSAIDs and CS.

Upper Extremity Difficulties in the Dedicated Amateur Instrumentalisty

2001 ◽  
Vol 16 (4) ◽  
pp. 152-156 ◽  
Author(s):  
William J Dawson
Keyword(s):  
Upper Extremity ◽  
Sports Participation ◽  
The United States ◽  
Degenerative Joint Disease ◽  
Joint Disease ◽  
Patients Âgés ◽  
Thumb Carpometacarpal Joint ◽  
Inflammatory Conditions ◽  
Joint Dislocations ◽  
Thumb Carpometacarpal

There are more than 62 million amateur instrumental musicians in the United States, many of whom can be described as active, dedicated amateurs. This report details a 15-year experience with 258 such patients with upper extremity problems from the author’s hand surgical practice, and compares some epidemiological and etiological parameters of this group with a cohort of 322 professional instrumentalists. The 258 patients’ ages ranged from 10 to 87 years; 137 (53.1%) were males. More than 75% played string or keyboard instruments. Music was the cause of difficulties in only 14% overall, but this rate rose to 47.2% for overuse-related diagnoses. Inflammatory conditions and muscle–tendon strains were equally represented and constituted 85% of all overuse diagnoses. Trauma caused difficulties in 124 patients (48.1%) and resulted from sports participation in one-third of these; it was significantly more common in males under 40. Falls on the upper limb accounted for another third of the injuries. Fractures and joint dislocations were the most common traumatic diagnoses, most often affecting the digits and distal forearm/wrist. A group of 45 “other” conditions included 18 patients with various nerve compressions (13 with carpal tunnel syndrome), 12 with ganglia in the wrist or fingers, and seven with various inflammatory problems. Only 17 patients presented with arthritic conditions, all resulting from degenerative joint disease; eight had involvement of the thumb carpometacarpal joint. This dedicated amateur group was similar to the professional cohort in many epidemiologic, etiologic, and diagnostic parameters, although the professionals were more likely to present on more than one occasion with upper extremity problems, and more of their problems were related to musical practice or performance.

scholarly journals Insights into the Action Mechanisms of Traditional Chinese Medicine in Osteoarthritis

2017 ◽  
Vol 2017 ◽  
pp. 1-13 ◽  
Author(s):  
Linfu Li ◽  
Haiqing Liu ◽  
Weimei Shi ◽  
Hai Liu ◽  
Jianqiong Yang ◽  
...  
Keyword(s):  
Chinese Medicine ◽  
Traditional Chinese Medicine ◽  
Cartilage Destruction ◽  
Degenerative Joint Disease ◽  
Joint Disease ◽  
Action Mechanism ◽  
Action Mechanisms ◽  
Inflammatory Drugs ◽  
Anti Inflammation ◽  
Modern Technologies

Osteoarthritis (OA) is a chronic degenerative joint disease characterized by articular cartilage destruction, synovial inflammation, and osteophyte formation. No effective treatments are available. The current pharmacological medications such as nonsteroidal anti-inflammatory drugs (NSAIDs) and analgesics, accompanied by possible adverse effects, might ameliorate OA symptoms. But they do not arrest the progression of OA. Traditional Chinese medicine (TCM) provides medical value by modification of disease and symptoms in OA. Valuable work on exploring TCM merits for OA patients has been investigated using modern technologies, although the complicated interacting network among the numerous components indicates the uncertainty of target specification. This review will provide an overview of the action mechanism of TCM in the last 5 years, discussing the TCM activities of anti-inflammation, antiapoptosis, antioxidation, anticatabolism, and proliferation in OA. TCM is a proposed medical option for OA treatment.

scholarly journals The Role of Fibrosis in Osteoarthritis Progression

Life ◽  
2020 ◽  
Vol 11 (1) ◽  
pp. 3
Author(s):  
Yeri Alice Rim ◽  
Ji Hyeon Ju
Keyword(s):  
Knee Joint ◽  
Total Joint Replacement ◽  
Cartilage Degeneration ◽  
Critical Issue ◽  
Degenerative Joint Disease ◽  
Joint Disease ◽  
Joint Movement ◽  
Synovial Membrane Inflammation ◽  
Osteoarthritis Progression

Osteoarthritis (OA) is a chronic degenerative joint disease where the main characteristics include cartilage degeneration and synovial membrane inflammation. These changes in the knee joint eventually dampen the function of the joint and restrict joint movement, which eventually leads to a stage where total joint replacement is the only treatment option. While much is still unknown about the pathogenesis and progression mechanism of OA, joint fibrosis can be a critical issue for better understanding this disease. Synovial fibrosis and the generation of fibrocartilage are the two main fibrosis-related characteristics that can be found in OA. However, these two processes remain mostly misunderstood. In this review, we focus on the fibrosis process in OA, especially in the cartilage and the synovium tissue, which are the main tissues involved in OA.

scholarly journals 3′-Sialyllactose Protects SW1353 Chondrocytic Cells From Interleukin-1β-Induced Oxidative Stress and Inflammation

2021 ◽  
Vol 12 ◽  
Author(s):  
Ahreum Baek ◽  
So Hee Jung ◽  
Soonil Pyo ◽  
Soo Yeon Kim ◽  
Seongmoon Jo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Responses ◽  
Antioxidant Defense System ◽  
Cartilage Destruction ◽  
Degenerative Joint Disease ◽  
Interleukin 1Β ◽  
Joint Disease ◽  
Enzymatic Antioxidants ◽  
Expression Levels ◽  
Apoptotic Protein

Osteoarthritis (OA) is a major degenerative joint disease. Oxidative stress and inflammation play key roles in the pathogenesis of OA. 3′-Sialyllactose (3′-SL) is derived from human milk and is known to regulate a variety of biological functions related to immune homeostasis. This study aimed to investigate the therapeutic mechanisms of 3′-SL in interleukin-1β (IL-1β)-treated SW1353 chondrocytic cells. 3′-SL potently suppressed IL-1β-induced oxidative stress by increasing the levels of enzymatic antioxidants. 3′-SL significantly reversed the IL-1β mediated expression levels of reactive oxygen species in IL-1β-stimulated chondrocytic cells. In addition, 3′-SL could reverse the increased levels of inflammatory markers such as nitrite, prostaglandin E2, inducible nitric oxide synthase, cyclooxygenase-2, IL-1β, and IL-6 in IL-1β-stimulated chondrocytic cells. Moreover, 3′-SL significantly inhibited the apoptotic process, as indicated by the downregulation of the pro-apoptotic protein Bax, upregulation of the anti-apoptotic protein Bcl-2 expression, and significant reduction in the number of TUNEL-positive cells in the IL-1β-treated chondrocytic cells. Furthermore, 3′-SL reversed cartilage destruction by decreasing the release of matrix metalloproteinases (MMP), such as MMP1, MMP3, and MMP13. In contrast, 3′-SL significantly increased the expression levels of matrix synthesis proteins, such as collagen II and aggrecan, in IL-1β-treated chondrocytic cells. 3′-SL dramatically suppressed the activation of mitogen-activated protein kinases (MAPK) and phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT)/nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling pathways, which are related to the pathogenesis of OA. Taken together, our data suggest that 3′-SL alleviates IL-1β-induced OA pathogenesis via inhibition of activated MAPK and PI3K/AKT/NF-κB signaling cascades with the downregulation of oxidative stress and inflammation. Therefore, 3′-SL has the potential to be used as a natural compound for OA therapy owing to its ability to activate the antioxidant defense system and suppress inflammatory responses.

scholarly journals Sodium Monoiodoacetate Dose-Dependent Changes in Matrix Metalloproteinases and Inflammatory Components as Prognostic Factors for the Progression of Osteoarthritis

2021 ◽  
Vol 12 ◽  
Author(s):  
Marta Bryk ◽  
Jakub Chwastek ◽  
Jakub Mlost ◽  
Magdalena Kostrzewa ◽  
Katarzyna Starowicz
Keyword(s):  
Matrix Metalloproteinases ◽  
Synovial Membrane ◽  
Weight Bearing ◽  
Joint Inflammation ◽  
Cartilage Degeneration ◽  
Degenerative Joint Disease ◽  
Joint Disease ◽  
Inflammatory Factors ◽  
Behavioral Studies ◽  
Bone Degradation

Osteoarthritis (OA) is a degenerative joint disease that primarily affects people over 65 years old. During OA progression irreversible cartilage, synovial membrane and subchondral bone degradation is observed, which results in the development of difficult-to-treat chronic pain. One of the most important factors in OA progression is joint inflammation. Both proinflammatory and anti-inflammatory factors, as well as extracellular matrix degradation enzymes (matrix metalloproteinases (MMPs), play an important role in disease development. One of the most widely used animal OA models involves an intra-articular injection of sodium monoiodoacetate (MIA) directly into the joint capsule, which results in glycolysis inhibition in chondrocytes and cartilage degeneration. This model mimics the degenerative changes observed in OA patients. However, the dose of MIA varies in the literature, ranging from 0.5 to 4.8 mg. The aim of our study was to characterize grading changes after injection of 1, 2 or 3 mg of MIA at the behavioral and molecular levels over a 28-day period. In the behavioral studies, MIA injection at all doses resulted in a gradual increase in tactile allodynia and resulted in abnormal weight bearing during free walking sequences. At several days post-OA induction, cartilage, synovial membrane and synovial fluid samples were collected, and qPCR and Western blot analyses were performed. We observed significant dose- and time-dependent changes in both gene expression and protein secretion levels. Inflammatory factors (CCL2, CXCL1, IL-1β, COMP) increased at the beginning of the experiment, indicating a transient inflammatory state connected to the MIA injection and, in more severe OA, also in the advanced stages of the disease. Overall, the results in the 1 mg MIA group were not consistently clear, indicating that the lowest tested dose may not be sufficient to induce long-lasting OA-like changes at the molecular level. In the 2 mg MIA group, significant alterations in the measured factors were observed. In the 3 mg MIA group, MMP-2, MMP-3, MMP-9, and MMP-13 levels showed very strong upregulation, which may cause overly strong reactions in animals. Therefore, a dose of 2 mg appears optimal, as it induces significant but not excessive OA-like changes in a rat model.

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