Regulation of cartilage matrix synthesis by …
Cartilage synthesis | Science Buzz
Ex vivo synthesis of articular cartilage — UT San Antonio
Notice that paracetamol (acetaminophen or Tylenol) did not inhibit GAG synthesis. The researchers noted that caution must be exercised in extrapolation from in-vitro (lab) to in-vivo (person) effects of NSAIDs, but it seems possible that some highly effective anti-inflammatory agents may produce adverse effects on cartilage integrity when employed during long-term treatment.77 Other researchers have confirmed NSAIDs’ inhibitory effect on proteoglycan synthesis and have commented that “…any drug that suppresses proteoglycan synthesis and impairs the ability of the chondrocyte to repair its damaged extracellular matrix, could potentially accelerate the breakdown of the articular tissue.”78, 79
Type II collagen is a major constituent of articularcartilage, representing 90–95% of the total collagen content andforming the fibrillar structure that gives cartilage its tensilestrength (). Among severalreported biomarkers (),components of type II collagen are recognized as the most importantbiomarkers for OA (). Actually,it has been reported that CTX-II levels in patients with knee OAare significantly higher compared to levels in non-OA controls(). Moreover, correlations havebeen shown between the CTX-II levels and the stage of OA (–),the radiographic changes of OA (,),or the knee pain in symptomatic OA (). Thus, CTX-II is considered to be areliable marker of cartilage degradation. Furthermore, it has beensuggested that abnormalities in the metabolism (degradation andsynthesis) of type II collagen play a key role in the pathogenesisof OA (), and that theC-propeptide of type II procollagen (CPII), releasedextracellularly from the newly synthesized molecule, is directlyrelated to type II collagen synthesis in healthy and osteoarthriticarticular cartilages (). Thus,we utilized CPII as a type II collagen synthesis marker.
Knee cartilage replacement therapy - Wikipedia
In a follow-up study, the same research group, took femoral head articular cartilage from non-arthritic and osteoarthritic patients post-operatively after total hip replacement. The relative human cartilage metabolism was measured on 245 osteoarthritic patients and 80 normal patients’ cartilage organ cultures subjected to various NSAIDs. The commonly used NSAIDs indomethacin, ibuprofen, and naproxen were shown to significantly inhibit (from 40 to 70%) glycosaminoglycan synthesis in patients’ cartilage.76 (See Figure 12.)
At present no quantitative non-invasive method for determining the anabolic (building up) and catabolic (breaking down) activity of NSAIDs on human cartilage in vivo exists. Most information on the effects of NSAIDs on the turnover of extra-cellular matrix macromolecules comes from short-term organ culture studies. Initial evaluations into the pathophysiology of osteoarthritis concentrated on the effects of NSAIDs on glycosaminoglycan synthesis. It was established that in all but the most severe cases of osteoarthritis, the chondrocyte response to proteoglycan depletion was an increase in glycosaminoglycan synthesis.72, 73 One of the first to show that NSAIDs diminished glycosaminoglycan synthesis in aged human cartilage cells (taken during hip surgery) in vitro was a research group from the University of Sydney in 1976.74 J.T. Dingle, led several of the follow-up studies on the effects of NSAIDs on human cartilage metabolism. The initial studies revealed significant declines in glycosaminoglycan synthesis in both normal and osteoarthritic human cartilages.75 (See Figure 11.)
Cartilage supplement, vitamins, herbs, natural ways to …
From observations in animal models of OA there is substantial evidence that NSAIDs are toxic to articular cartilage. Drs. Marshall J. Palmoski and Kenneth D. Brandt from the Indiana University School of Medicine published several research papers showing that NSAIDs suppress chondrocyte proteoglycan (PRG) synthesis. Prior to these studies they had already shown that salicylate (aspirin), the drug most commonly employed in the treatment of OA at the time, reduced PRG synthesis in cultures of normal articular cartilage by about 30% and in cultures of OA cartilage by up to 99% at levels achieved in the serum of patients treated with salicylate.50 They also showed that salicylate (aspirin) accelerated the development of structure damage in the OA joint in the canine cruciate-deficient model or that caused by immobilization, and resulted in more severe pathology than that seen in the OA knees of dogs not treated with the drug.51-53 As more clinicians started using ibuprofen and other NSAIDs, instead of aspirin for OA, Drs. Palmoski and Brandt studied the effects these drugs had on canine articular cartilage. Specifically they found that fenoprofen and ibuprofen inhibited net PRG synthesis in a concentration-dependent fashion. At concentrations in the culture medium comparable to plasma concentrations seen in patients after oral administration of NSAIDs in humans, net PRG synthesis in the presence of these drugs averaged 72% and 86% of the control values, respectively (P54-56 (See Figure 10.)
Contrast agents that go beyond qualitative visualization and enable quantitative assessments of functional tissue performance represent the next generation of clinically useful imaging tools. An optimized and efficient large-scale synthesis of a cationic iodinated contrast agent (CA4+) is described for imaging articular cartilage. Contrast-enhanced CT (CECT) using CA4+ reveals significantly greater agent uptake of CA4+ in articular cartilage compared to that of similar anionic or nonionic agents, and CA4+ uptake follows Donnan equilibrium theory. The CA4+ CECT attenuation obtained from imaging ex vivo human hip cartilage correlates with the glycosaminoglycan content, equilibrium modulus, and coefficient of friction, which are key indicators of cartilage functional performance and osteoarthritis stage. Finally, preliminary toxicity studies in a rat model show no adverse events, and a pharmacokinetics study documents a peak plasma concentration 30 min after dosing, with the agent no longer present in vivo at 96 h via excretion in the urine.
Glossary | Linus Pauling Institute | Oregon State University
NuJoint DS K-9 Double Strength Hip and Joint Dog …
But I see studies online that talk about supplements that "encourage cartilage synthesis" or whatever.
Articular Cartilage - Basic Science - Orthobullets
7/30/1996 · Assays for determining cartilage synthesis associated with osteoarthritis are presented
Difference Between Bone and Cartilage | Difference …
IL-1 is a potent inducer of prostaglandin (PG) synthesis by inducing PGE2 synthesis in human chondrocytes
Disc Cartilage Regeneration | Stem Cells for Cartilage Repair, Part 2
Regulation of Chondrogenesis
In addition to general aspects of good nutrient exchange and absence of conditions like turbulent flow (43), it is possible to modulate the quantity and quality of cartilage engineered . Serum factors and various growth factors have been shown to modulate cartilage matrix synthesis in 3-D cultures, especially fibronectin (44), insulin-like growth factor-I (IGF-I; 44,45), transforming growth factor b (TGF-b; 45), and platelet-derived growth factor (PDGF; 40).
06/10/1994 · Original Article
The key requirements of bioresorbable materials are that 1) their rates of degradation must be compatible with the intended use, and 2) the products of their degradation must be nontoxic. Of the synthetic materials, polyglycolic acid (PGA), polylactic acid (PLA), and their copolymers are most widely studied. They have been used clinically since their introduction as sutures in the 1970s. Their rate of resorption is considered short in comparison to other polymers like polycaprolactone (PCL), which has a longer half-life more suited to drug delivery applications. Matrices of PGA provided a template for new cartilage formation by chondrocytes (41). With precise control of culture conditions, bioreactors may provide improved growth and matrix synthesis (42,43).
Kartogenin-Incorporated Thermogel Supports Stem …
Cartilage is well suited to adapt to the intermittent loads placed upon joints. It has been shown that mechanical compression modulates biosynthesis in cartilage slices (52,53) and in isolated chondrocytes (54). Preliminary results indicate that hydrostatic fluid pressure enhances chondrogenesis in 3-D culture (55).
What is Collagen? 7 Ways Collagen Can Boost Your …
In the normal joint, there is a balance between the continuous process of cartilage matrix degradation and repair. In OA, there is a disruption of the homeostatic state and the catabolic (breakdown) processes of chondrocytes. It is clear from the scientific literature that NSAIDs from in vitro and in vivo studies in both animals and humans have a significantly negative effect on cartilage matrix which causes an acceleration of the deterioration of articular cartilage in osteoarthritic joints. The preponderance of evidence shows that NSAIDs have no beneficial effect on articular cartilage in OA and accelerate the very disease for which they are most often used and prescribed. Some of the effects of NSAIDs on the articular cartilage in OA include inhibition of chondrocyte proliferation, synthesis of cellular matrix components, glycosaminoglycan synthesis, collagen synthesis and proteoglycan synthesis. The net effect of all or some of the above is an acceleration of articular cartilage breakdown.
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