Osteoarthritis occurs when your joint cartilage wears down due to repetitive use and load over time. Follow my tips here to lower your risk of this condition.
As Dr. Mercola reports, metabolic syndrome is connected to many diseases, including osteoarthritis. In a review, MRI studies supported causal associations of osteoarthritis (OA) with higher levels of adiposity, bone mineral density, and sleep disturbances, and lower levels of serum calcium and low-density lipoprotein cholesterol. One study observed symptomatic knee OA in approximately 4.9% and 16.7% of participants older than 26 and 45 years, respectively. Another study showed that the lifetime risk of developing symptomatic knee OA is 44.7%, and obesity increases this risk to approximately 60% in the case of a body mass index greater than 30.
Chronic low-grade inflammation plays an important and vital role in the pathogenesis of OA. But chronic inflammation is not exclusive to OA. It is also a distinctive characteristic of other diseases such as Alzheimer's disease (AD) and contributes to neurodegenerative processes. In Fig 1., the second link molecular mechanisms that link OA with AD.
Proteolytic enzymes have anti-inflammatory effects because they help improve intestinal health and overall immunity. These enzymes can decrease pain and swelling associated with rheumatoid arthritis, increase mobility in people with osteoarthritis, and fight infections. Trypsin and chymotrypsin (both produced by the pancreas), papain, bromelain and serratiopeptidase. The results of one study suggest that this combination is as effective as NSAIDs in the treatment of osteoarthritis, without the associated adverse events.
Study highlights that physical activity is associated with less severity of knee osteoarthritis symptoms and suggests that physical activity may be beneficial in controlling OA symptoms and improving quality of life among people with knee OA . Another study highlights that strength training is associated with less knee osteoarthritis.
Determine the effect of supplementation with turmeric, black pepper and ginger extract on prostaglandin E 2 (PGE 2), which plays an important role in modulating the immune response and the inflammatory process. in patients with chronic knee osteoarthritis, compared with naproxen. The results of this study indicated that taking the selected herbs twice a day for 4 weeks can improve PGE 2 levels in patients with chronic knee osteoarthritis similar to the drug naproxen without the side effects.
Studies have shown that commonly used ginger and its phytochemicals, including 6-shogaol, zingerone, and cedrol, are effective antirheumatic agents. They alter signaling pathways that are important in the pathophysiology of osteoarthritis and rheumatoid arthritis and result in the suppression of proinflammatory cytokines.
Natural plant extracts and nutraceuticals have been hailed as potent alternative therapies for OA due to their intrinsic anti-inflammatory and antioxidant properties. Recent evidence has shown that they are effective in relieving pain by inhibiting pro-inflammatory pathways such as NF-κB, protecting cartilage and activating autophagy. In Table 2 nutraceuticals to improve pain scores and lead to better physical function in patients with OA.
In this study, we aimed to investigate whether there is a change in the levels of vitamin D, vitamin B12, folic acid, which are important for metabolism, and homocysteine levels. In homocysteine levels; A statistically significant increase was found in the osteoarthritis group. In folic acid, vitamin B12, vitamin D levels; A statistically significant decrease was detected in the osteoarthritis group. Another study also concluded that genetically predicted homocysteine was causally associated with an increased risk of OA, especially in weight-bearing joints and in women.
In this study, we demonstrated that downregulation of SIRT1/AMPK/PGC-1α as a result of elevated homocysteine (Hcy) in chondrocytes resulted in mitochondrial dysfunction with increased proapoptotic response and oxidative stress. Furthermore, aberrant SIRT1/AMPK/PGC-1α signaling caused an increase in NF-κB expression, thereby increasing pro-inflammatory conditions in Hcy-treated chondrocytes. Overall, we demonstrated that Hcy was another factor that induced an impairment of mitochondrial function and caused an increase in ROS production and apoptosis in chondrocytes. Our findings also revealed that Hcy-reduced SIRT1 could possibly contribute to the cartilage degradation process and provide insights into the etiology of OA.
This research has summarized the global state of research on mitochondria and osteoarthritis in the last two decades, which will contribute to the field of research and the development of new treatment strategies for OA.
Chondrocytes are the only cell type present in mature cartilage and change pathologically when OA occurs. Multiple factors can cause OA, including inflammatory cytokines, mechanical stress, aging, metabolic factors, and other pathological changes, which could increase reactive oxygen species (ROS), induce oxidative stress in mitochondria, and cause damage to mitochondrial DNA. (mtDNA). , cause mitochondrial damage and shorten the lifespan of chondrocytes. Obvious changes in the morphology and function of mitochondria have been demonstrated in aging cells, and mitochondrial dysfunction is a key factor in cellular senescence, demonstrating that mitochondria can be a therapeutic target for anti-aging treatment and reduce OA morbidity in the elderly population
Mitochondria are not only the organelle for ATP production and signal transduction, but they can also maintain redox status and calcium homeostasis, regulate programmed cell death, and perform bioenergetic metabolism, stem cell reprogramming, responses related to aging, innate immunity and biosynthesis.
The report describes the benefits of some effective antioxidants on mitochondrial function in OA. Taurine can ameliorate ROS-induced chondrocyte damage and exert chondroprotective properties, including the deposition of extracellular matrix components and chondrocyte proliferation. Taurine could reduce mitochondrial superoxide anion production by activating Nrf2 and inhibit chondrocyte apoptosis and reduce OA.
Resveratrol alleviated chondrocyte damage through the NF-κB signaling pathway. Furthermore, resveratrol has been considered as a potent activator of SIRT1, which can prevent apoptosis of human chondrocytes under cellular stress, including nutritional stress, catabolic stress, and mechanical stress, and inhibit damage to mitochondria.
Chondroitin sulfate inhibited caspase-3 and caspase-9 levels by reducing mitochondrial fission, which decreased chondrocyte apoptosis. It appears that chondroitin sulfate also has the potential to treat OA through the mitochondrial pathway.
Quercetin inhibited the accumulation of nitric oxide (NO), matrix metalloproteinase 3 (MMP-3) produced by inflammation through AMPK/SIRT1 signaling, playing a key role in inhibiting extracellular matrix degeneration. Quercetin also decreased chondrocyte apoptosis by inhibiting the caspase signaling pathway. Therefore, quercetin is a potential therapeutic drug for OA that acts through the mitochondrial pathway. More phytochemicals in the link
As Dr. Mercola reports, metabolic syndrome is connected to many diseases, including osteoarthritis. In a review, MRI studies supported causal associations of osteoarthritis (OA) with higher levels of adiposity, bone mineral density, and sleep disturbances, and lower levels of serum calcium and low-density lipoprotein cholesterol. One study observed symptomatic knee OA in approximately 4.9% and 16.7% of participants older than 26 and 45 years, respectively. Another study showed that the lifetime risk of developing symptomatic knee OA is 44.7%, and obesity increases this risk to approximately 60% in the case of a body mass index greater than 30.
Chronic low-grade inflammation plays an important and vital role in the pathogenesis of OA. But chronic inflammation is not exclusive to OA. It is also a distinctive characteristic of other diseases such as Alzheimer's disease (AD) and contributes to neurodegenerative processes. In Fig 1., the second link molecular mechanisms that link OA with AD.
https://acrjournals.onlinelibrary.wiley.com/doi/abs/10.1002/acr.25252 (2024).--
https://www.mdpi.com/1422-0067/25/5/3044 (2024).--
Proteolytic enzymes have anti-inflammatory effects because they help improve intestinal health and overall immunity. These enzymes can decrease pain and swelling associated with rheumatoid arthritis, increase mobility in people with osteoarthritis, and fight infections. Trypsin and chymotrypsin (both produced by the pancreas), papain, bromelain and serratiopeptidase. The results of one study suggest that this combination is as effective as NSAIDs in the treatment of osteoarthritis, without the associated adverse events.
https://scindeks.ceon.rs/article.aspx?artid=2490-33292401079A (2024).—
https://www.researchgate.net/publication/373289830_The_effects_of_bromelain_on_osteoarthritis_symptoms_A_systematic_review (2024).--
https://link.springer.com/article/10.1007/s40744-022-00472-7 (2022).-
Study highlights that physical activity is associated with less severity of knee osteoarthritis symptoms and suggests that physical activity may be beneficial in controlling OA symptoms and improving quality of life among people with knee OA . Another study highlights that strength training is associated with less knee osteoarthritis.
https://jhrlmc.com/index.php/home/article/view/408 (2024).--
https://acrjournals.onlinelibrary.wiley.com/doi/abs/10.1002/art.42732 (2024).--
Determine the effect of supplementation with turmeric, black pepper and ginger extract on prostaglandin E 2 (PGE 2), which plays an important role in modulating the immune response and the inflammatory process. in patients with chronic knee osteoarthritis, compared with naproxen. The results of this study indicated that taking the selected herbs twice a day for 4 weeks can improve PGE 2 levels in patients with chronic knee osteoarthritis similar to the drug naproxen without the side effects.
https://onlinelibrary.wiley.com/doi/abs/10.1002/ptr.6671 (2020).--
Studies have shown that commonly used ginger and its phytochemicals, including 6-shogaol, zingerone, and cedrol, are effective antirheumatic agents. They alter signaling pathways that are important in the pathophysiology of osteoarthritis and rheumatoid arthritis and result in the suppression of proinflammatory cytokines.
https://www.mdpi.com/2072-6643/16/5/741 (2024).--
Natural plant extracts and nutraceuticals have been hailed as potent alternative therapies for OA due to their intrinsic anti-inflammatory and antioxidant properties. Recent evidence has shown that they are effective in relieving pain by inhibiting pro-inflammatory pathways such as NF-κB, protecting cartilage and activating autophagy. In Table 2 nutraceuticals to improve pain scores and lead to better physical function in patients with OA.
https://www.mdpi.com/1467-3045/46/5/251 (2024).--
In this study, we aimed to investigate whether there is a change in the levels of vitamin D, vitamin B12, folic acid, which are important for metabolism, and homocysteine levels. In homocysteine levels; A statistically significant increase was found in the osteoarthritis group. In folic acid, vitamin B12, vitamin D levels; A statistically significant decrease was detected in the osteoarthritis group. Another study also concluded that genetically predicted homocysteine was causally associated with an increased risk of OA, especially in weight-bearing joints and in women.
https://dergipark.org.tr/en/pub/nwsamed/issue/62054/874929 (2021).--
https://www.mdpi.com/2072-6643/15/7/1636 (2023).-
In this study, we demonstrated that downregulation of SIRT1/AMPK/PGC-1α as a result of elevated homocysteine (Hcy) in chondrocytes resulted in mitochondrial dysfunction with increased proapoptotic response and oxidative stress. Furthermore, aberrant SIRT1/AMPK/PGC-1α signaling caused an increase in NF-κB expression, thereby increasing pro-inflammatory conditions in Hcy-treated chondrocytes. Overall, we demonstrated that Hcy was another factor that induced an impairment of mitochondrial function and caused an increase in ROS production and apoptosis in chondrocytes. Our findings also revealed that Hcy-reduced SIRT1 could possibly contribute to the cartilage degradation process and provide insights into the etiology of OA.
https://www.sciencedirect.com/science/article/pii/S2213231718300375 (2018).--
This research has summarized the global state of research on mitochondria and osteoarthritis in the last two decades, which will contribute to the field of research and the development of new treatment strategies for OA.
Chondrocytes are the only cell type present in mature cartilage and change pathologically when OA occurs. Multiple factors can cause OA, including inflammatory cytokines, mechanical stress, aging, metabolic factors, and other pathological changes, which could increase reactive oxygen species (ROS), induce oxidative stress in mitochondria, and cause damage to mitochondrial DNA. (mtDNA). , cause mitochondrial damage and shorten the lifespan of chondrocytes. Obvious changes in the morphology and function of mitochondria have been demonstrated in aging cells, and mitochondrial dysfunction is a key factor in cellular senescence, demonstrating that mitochondria can be a therapeutic target for anti-aging treatment and reduce OA morbidity in the elderly population
Mitochondria are not only the organelle for ATP production and signal transduction, but they can also maintain redox status and calcium homeostasis, regulate programmed cell death, and perform bioenergetic metabolism, stem cell reprogramming, responses related to aging, innate immunity and biosynthesis.
The report describes the benefits of some effective antioxidants on mitochondrial function in OA. Taurine can ameliorate ROS-induced chondrocyte damage and exert chondroprotective properties, including the deposition of extracellular matrix components and chondrocyte proliferation. Taurine could reduce mitochondrial superoxide anion production by activating Nrf2 and inhibit chondrocyte apoptosis and reduce OA.
Resveratrol alleviated chondrocyte damage through the NF-κB signaling pathway. Furthermore, resveratrol has been considered as a potent activator of SIRT1, which can prevent apoptosis of human chondrocytes under cellular stress, including nutritional stress, catabolic stress, and mechanical stress, and inhibit damage to mitochondria.
Chondroitin sulfate inhibited caspase-3 and caspase-9 levels by reducing mitochondrial fission, which decreased chondrocyte apoptosis. It appears that chondroitin sulfate also has the potential to treat OA through the mitochondrial pathway.
Quercetin inhibited the accumulation of nitric oxide (NO), matrix metalloproteinase 3 (MMP-3) produced by inflammation through AMPK/SIRT1 signaling, playing a key role in inhibiting extracellular matrix degeneration. Quercetin also decreased chondrocyte apoptosis by inhibiting the caspase signaling pathway. Therefore, quercetin is a potential therapeutic drug for OA that acts through the mitochondrial pathway. More phytochemicals in the link
https://www.frontiersin.org/articles/10.3389/fmed.2020.581402/full (2022).--