This article determines…. Assam tea is a type of black tea known for its rich, malty flavor and potential health benefits. This article tells you everything you need to know….

Antibiotics are lifesaving medications, but they may also pose problems with autoimmune conditions like rheumatoid arthritis. Infrared saunas may help people with rheumatoid arthritis heal tissue, improve mobility, and reduce pain.

There's limited evidence for cryotherapy's effectiveness for RA. However, some people report temporary pain relief and reduced joint swelling. Joints affected by rheumatoid arthritis may feel tender, painful, and stiff.

This can make it challenging to fall and stay asleep. E-stim is often used to target pain and promote muscle recovery, but its benefit to people with RA has not been proven. Learn more. A Quiz for Teens Are You a Workaholic? How Well Do You Sleep?

Health Conditions Discover Plan Connect. Rheumatoid Arthritis. Basics Pain Management Living with RA Mental Health Community Newsletter. Going Green: Green Tea for Rheumatoid Arthritis. Medically reviewed by Imashi Fernando, MS, RDN, CDCES — By Ann Pietrangelo — Updated on August 2, Green tea Research Other health benefits Preparation Supplements Interactions FAQs Bottom line Green tea contains powerful antioxidants with anti-inflammatory properties.

About green tea. What does the research say? Other health benefits of green tea. How do you take your tea? Green tea supplements. Possible interactions.

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EGCG can restore the enzymatic actions of glutathione peroxidase GPX and can regulate the levels of glutathione.

Besides that, EGCG is capable of inhibiting the production of hydrogen peroxide and nitric oxide 12 - 14 , 16 , Usually, chondrocytes keep a dynamic equilibrium between production and degradation of the extracellular matrix, such as aggrecan and type II collagen, which are the most relevant proteoglycan in the articular cartilage.

In the OA, there is a disorder of synovial joints presenting focal areas of articular cartilage damage, associated with new bone formation at the margin of the joints, modifications in the subchondral bone, synovitis, and thickening of the joint capsule.

The results for these dysfunctions depend on the severity of the damage, but the characteristic clinical symptoms are inflammation, reduced range of motion, mild-to-severe pain, and deformity. In addition to the degradation of the articular cartilage, OA also involves damages to bone and synovium in the joints and is associated with lifestyle, diet, genetics, and aging 24 , The pathophysiology of OA is not fully understood, but it is known that the pathogenesis involves inflammatory processes, oxidative stress, osteoclastogenesis, and proteolytic degradation of cartilage Figure 2.

Chondrocytes are the only cells found in the cartilage matrix and are the central regulators of matrix catabolism and anabolism in the articular cartilage.

In the presence of inductive stimuli, there is an increased activity or expression of cartilage proteinases, which are primarily synthesized by chondrocytes leading to OA Chondrocytes are also responsible for the production of pro-collagen N-proteinases, which may include disintegrin and metalloproteinase with thrombospondin motifs ADAMTS These proteinases are related to the removal of the N-terminal pro-peptide of type II pro-collagen, augmenting the cartilage matrix anabolism 26 , Increased catabolism of the cartilage matrix cartilage collagen and aggrecan results in the degeneration of articular cartilage in arthritic processes.

MMPs MMP-2 and MMP and aggrecanases ADAMTS-4 and ADAMTS-5 have been detected in OA 28 , Chondrocytes, osteoclasts, and stromal cells should also be mentioned once they produce the Receptor Activator Factor kβ Ligand RANKL.

The connection of RANK to RANKL in osteoclasts precursor cells leads to the activation of I Kappa B Kinase IKK and phosphorylation of I Kappa B alpha IkBα that are related to the activation of osteoclastogenesis. Moreover, in OA, interleukins such as IL-1β, IL-6, IL-8, IL, and TNF-α are associated with increased production of RANKL resulting in bone resorption 30 - This scenario of inflammation and increased levels of cytokines and proteases results in the death of chondrocytes and synoviocytes stimulation leading to the recruitment of mononuclear and polymorphonuclear factors collaborating to more cartilage destruction.

In addition to the increase in pro-inflammatory cytokines and TNF-α, the presence of prostaglandin-2 PGE-2 and free radicals such as reactive oxygen and nitrogen species are linked to the pathogenesis of the disease 33 , Fechtner et al.

They showed that there are different effects of the catechins on the IL-1β signal transduction pathways. The production of cytokines and MMP in human RASFs is directly associated with augmented levels of prostaglandins in response to IL-1β 35 and a study showed that EGCG inhibited the expression of TNF-α, and IL-1β-induced COX-2 in human OA chondrocytes 8 , EGCG is also related to the regulation of the expression of inducible nitric oxide synthase; it is capable of inhibiting IL-1β, induced phosphorylation, and degradation of IκBα to downregulate NFκB translocation This catechin can also inhibit the expression of MMP-1 and MMP and the catabolism of proteoglycan and type II collagen in human cartilage and can inhibit ADAMTS-1, ADAMTS-4, and ADAMTS-5 24 , 38 , Rasheed et al.

EGCG led to the inhibition of the expression of IL-1β-induced ADAMTS-5 and led to the up-regulation in the expression of hsa-miRp.

These results provided valuable insights into the molecular basis for the effects of EGCG in OA and indicated that this role in OA chondrocytes might be associated with its capacity to inhibit inflammatory pathways via modulation of miRNAs expressions.

Furthermore, EGCG can improve IL-1β-mediated suppression of the synthesis of transforming growth factor β, and can enhance the production of type II collagen and aggrecan core protein in articular chondrocytes A study performed by Comblain et al.

Their results showed that about 4, genes were differentially expressed according to inflammation, cartilage catabolism, and angiogenesis. Moreover, they observed that the mixture promoted beneficial effects on OA physiopathology due to the regulation in the release of key catabolic and inflammatory factors.

The authors postulated that these findings suggest that these natural ingredients could be used in the management of OA. Comblain et al. The inclusion criteria were the presence of clinical and radiographic signs of OA presence of subchondral bone sclerosis and osteophytes on at least one limb, and no evidence of systemic disease.

After three months of treatment, animals that received the supplemented diet presented a significant decrease in pain that was not observed in the control group. The biomarkers of OA did not present statistical differences between the treated group and placebo.

Hashempur et al. They observed that the group that received the plant presented a significant reduction in the following scores: total WOMAC, WOMAC physical function scores, and VAS pain when compared to the control group.

They did not see significant differences regarding WOMAC pain and stiffness scores between groups. No adverse effects were reported for patients included in the treated group.

These results suggest that GT could be considered as a safe adjuvant in the treatment and control of pain, and for the improvement of knee joint physical function in subjects with OA. For the reasons mentioned above, we suggest that GT and its bioactive compounds, mainly ECGC, could have a role in improving the severity of symptoms of OA Figure 2.

Due to the impressive antioxidant and anti-inflammatory effects of this plant, we were surprised by the lack of studies that had used GT in subjects with OA.