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Can Gout Cause Joint Damage

Who Is Affected By Gout

Gout | Treating Severe Joint Pain | What Patients Should Know

Gout can affect anyone. It usually occurs earlier in men than women. It generally occurs after menopause in women. Men can be three times more likely than women to get it because they have higher levels of uric acid most of their lives. Women reach these uric acid levels after menopause.

People are more likely to get gout if they have:

  • Obesity, or a lot of extra weight.

You are also more likely to develop gout if you:

  • Consume a diet high in animal proteins
  • Consume a significant amount of alcohol
  • Are on water pills .

What Increases Your Chances For Gout

The following make it more likely that you will develop hyperuricemia, which causes gout:

  • Being male
  • Using certain medications, such as diuretics .
  • Drinking alcohol. The risk of gout is greater as alcohol intake goes up.
  • Eating or drinking food and drinks high in fructose .
  • Having a diet high in purines, which the body breaks down into uric acid. Purine-rich foods include red meat, organ meat, and some kinds of seafood, such as anchovies, sardines, mussels, scallops, trout, and tuna.
  • The Role Of Uric Acid

    Uric acid is produced when your body breaks down purines, which are substances naturally found in your body, as well as in protein-rich foods. At normal levels in your blood, uric acid is a powerful antioxidant and does not cause any damage. The body keeps uric acid at a set level by excreting it through the kidneys and in urine.

    It is possible to have hyperuricemia and not develop gout. About two-thirds of people with elevated uric acid levels never have gout attacks. It is not known why some people do not react to abnormally high levels of uric acid.

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    What Can Trigger A Gout Attack

    Several things can cause the crystals to shake loose into your joint cavity, triggering an attack. These include:

    • a knock or injury to the joint
    • an illness that may make you feverish
    • having an operation
    • having an unusually large meal, especially a fatty meal
    • drinking too much alcohol
    • dehydration
    • starting urate lowering therapy, especially at a high dose, or not taking your treatment regularly each day.

    Mechanisms Of New Bone Formation

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    Although bone erosion is the most pronounced feature observed in joints from patients with chronic gout, pathological new bone formation is also frequently observed. The mechanisms behind new bone formation in gout are unknown. The features of new bone formation in gout have recently been described using plain radiography and CT. The most common specific features of new bone formation in gout were bone sclerosis and bony spurs. Periosteal new bone formation was less common and ankylosis was rare. Osteophytes were also frequently observed. Joints with bone erosion and/or intraosseous tophi were more likely to have features of new bone formation, suggesting that there is a connection between bone erosion, the presence of tophi, and new bone formation during bone remodeling in gout.

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    Cellular Mechanisms Of Bone Erosion

    Bone damage in chronic gout is closely associated with sites of MSU crystal deposition, with histologic and advanced imaging studies showing that crystals are often located adjacent to or within erosive lesions . MSU crystal deposits have been observed in histologic samples of subchondral bone in patients with gout, indicating that bone cells, such as osteoclasts and osteoblasts, are in direct contact with MSU crystals following tophus infiltration into the bone.

    Gout And Oawhats The Connection

    A swollen, stiff knee might immediately lead you to suspect you have osteoarthritis , but the culprit could also be gout. Like many close relatives, the two conditions share common features. And because they often occur together, you might wonder which one is causing your symptoms.

    Its definitely possible for people to have both conditions at the same time. Theyre the two most common types of arthritis, says Svetlana Krasnokutsky, MD, assistant professor of medicine in the Division of Rheumatology at NYU Langone Health. They can affect the same joints.

    OA is a degenerative disease that gradually breaks down the cartilage that cushions bones. It causes pain, swelling, and stiffness in joints like the knees, hips, fingers, lower back, and neck. In gout, uric acid crystals build up in the joints. Gout often affects the big toe joint, but the ankles, knees, hands, and wrists can also be involved.

    Knowing which condition you haveor whether youve got both gout and osteoarthritis can help your doctor fine-tune your treatment.

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    Psychological And Emotional Problems

    Chronic gout causes chronic and sometimes constant pain. Gout may affect your ability to walk, work, and carry out normal tasks. Living with pain can be emotionally distressing. Talk to your doctor about the impact gout has on your emotional health, and ask for suggestions about ways to cope with it.

    Educational content made possible by Horizon Therapeutics.

    Gout And Mental Health

    Gout , Pseudogout & Joint Pain – Everything You Need To Know – Dr. Nabil Ebraheim

    The chronic pain associated with repeated gout attacks can lead to stress, anxiety, and depression. Gout can cause severe pain that can make it tough for you to get around, go to work, and complete daily tasks. That impact on your daily life can impacts patients mental, social, and physical well-being.

    Its not just about functionality and disability, but also how patients view themselves, says Dr. Khanna. I talk to patients about the fact that gout is treatable, and its possible to stay completely flare-free if they take their medications.

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    The Four Stages Of Gout

    Gout is best understood by seeing it as having four phases or stages :

    Stage 1: High uric acid

    Elevated uric acid without gout or kidney stone, this stage has no symptoms and is generally not treated.

    Stage 2: Acute flares

    This stage is marked by acute gout attacks causing pain and inflammation in one or more joints.

    Stage 3: Intercritical periods

    These are periods of time between acute attacks, during which a person feels normal but is at risk for recurrence of acute attacks.

    Stage 4: Advanced gout

    This is a stage of chronic gouty arthritis, in which there are lumps of uric acid, or tophi , frequent attacks of acute gout, and often a degree of pain even between attacks .

    Figure 1: Stages of Gout

    Figure 2: Illustration of Toe Joint with Gouty Tophus. normal toe joint Urate crystals, shown in white, at the “bunion joint,” represent a gouty tophus.)

    Figure 3: Progression of Gout

    Can Damage To My Joints Caused By Gout Be Reversed

    Unfortunately, damage to your joints cannot be reversed. However, with treatment, any additional damage to the joints can be prevented. In some cases, surgery may be used to remove large deposits of tophi from under the skin. If you believe you have symptoms of gout, talk to your doctor right away.

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    The Relationship Between Gout Numbness And Tingling

    Inflammation and the painful feeling of burning sensation are always a given to an individual with gout. These two symptoms of gout are sometimes being accompanied by the feeling of numbness and tingling. Isnt it an annoying set of painful symptoms? But, arent you curious about the relationship of gout with the feeling of numbness and tingling? In case you do, then take note of the things you will learn with the succeeding paragraphs.

    This article explains the relationship between gout, numbness and tingling. Keep reading and be well informed.

    Get More Information About The Current State Of Gout Research

    How To Naturally Remove Uric Acid Crystallization In ...
    • Dalbeth N, et al. Ann Rheum Dis. 2009 68:1290-1295.
    • Schett G, et al. RMD Open. 2015 Aug 15 1:e000046.
    • McQueen FM, et al. Rheumatology . 2014 53:95-103.
    • Dalbeth N, et al. Ann Rheum Dis. 2015 74:1030-1036.
    • Doghramji PP, et al. Postgrad Med. 2012 124:98-109.
    • Yu KH, et al. Rheumatology . 2004 43:191-194.
    • McQueen FM, et al. Rheumatology . 2014 53:95-103.
    • Desai MA, et al. RadioGraphics. 2011 31:1365-1375.
    • Popovich I, et al. Skeletal Radiol. 2014 43:917-924.

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    The Role Of Osteoclasts

    As with other erosive arthropathies, such as rheumatoid arthritis and psoriatic arthritis, the osteoclast has been identified as a key cellular mediator of localized bone loss in gout. Osteoclasts are multinucleated cells derived from hematopoietic stem cells their main function is to resorb mineralized bone, helping to preserve a normal bone mass during physiological bone remodeling. The differentiation of osteoclasts, or osteoclastogenesis, is a highly regulated process involving the interaction of receptor activator of nuclear factor-B , expressed on osteoclast precursor cells, with receptor activator of nuclear factor-B ligand , which is expressed or secreted by mature osteoblasts and activated T lymphocytes. Osteoprotegerin is a soluble decoy receptor for RANK secreted by osteoblasts and is a negative regulator of osteoclastogenesis. Therefore, during bone remodeling, stromal cells have an important role in controlling osteoclastogenesis and subsequent bone resorption by determining the number of osteoclasts formed.

    The Link Between Oa And Gout

    A key unanswered question in gout pathogenesis is why MSU crystals preferentially form and deposit in certain joints. The first metatarsophalangeal joint is often the first and most common joint to suffer from a gouty attack. Other than the known factors that contribute to the formation of MSU crystals, such as local temperature and pH, there is growing evidence to suggest that the presence of OA is related to MSU crystal formation and deposition. It is now well recognized that there is an association between gout and OA and that this relationship is likely to influence which joints are affected by gout.

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    The Role Of Osteoblasts

    Osteoblasts are responsible for new bone formation and are derived from mesenchymal stem cells. Osteoblasts may contribute to bone erosion in gout by promoting osteoclast formation. Human osteoblasts stimulated with MSU crystals and IL-1 showed upregulated expression of osteoclastogenesis promoters, such as prostaglandin E 2 and IL-6. MSU crystals have also been shown to inhibit OPG gene and protein expression in an osteoblastic cell line, without significantly altering RANKL gene expression. In addition, a recent study reported increased protein expression of RANKL in tophus samples from patients with gout, whereas OPG expression was largely absent.

    To summarize, the available data suggest that osteoblasts contribute to bone loss in gout in 2 ways. Firstly, by modulating the RANKL/OPG axis to promote osteoclastogenesis and bone resorption and, secondly, through the reduction of viability, differentiation, and function of osteoblasts following exposure to MSU crystals, leading to impaired mineralization and bone formation in joints affected by MSU crystal deposition.

    Other Mediators Of Bone Erosion In Gout

    Gout – causes, symptoms, diagnosis, treatment, pathology

    Other cell types are also likely to contribute to the joint damage observed in gout as the tophus contains numerous immune and stromal cells that produce a variety of soluble factors. Cell-cell interactions between these various immune and stromal cells may contribute to joint damage in gout. An in vitro study investigating the interactions between neutrophils and osteoblasts cultured on calcified matrix demonstrated that neutrophils were able to induce osteoblast retraction in the presence of MSU crystals, which allowed osteoclast-like cells to resorb the newly exposed matrix surface below. MSU crystals in the presence of IL-1 stimulated Ptgs2 gene expression and the release of PGE 2 protein from chondrocytes and synovial fibroblasts, which could enhance osteoclastogenesis.

    Other innate and adaptive immune cells present within the tophus, such as mononucleated and multinucleated macrophages and T and B lymphocytes that come into contact with MSU crystals, are also likely to promote osteoclastogenesis through increased expression of RANKL, IL-1, IL-6, tumor necrosis factor- , and PGE 2 . T lymphocytes have been shown to be especially important, as osteoclast formation from synovial fluid mononuclear cells derived from patients with chronic gout was inhibited in T-cell depleted cultures.

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    Altered Bone Remodeling In Gout

    From the data that are currently available on the role of bone cells in mediating bone erosion in gouty joints, the authors suggest that physiological bone remodeling is altered at the tophus-bone interface. In vitro and histological analyses have confirmed that there is excessive osteoclast formation and activity as well as reduced osteoblast viability and function at sites of MSU crystal deposition, overall resulting in localized bone loss . The balance of bone resorption and bone formation at these sites is further disrupted because the inhibition of osteoblast differentiation from mesenchymal stem cells in the presence of MSU crystals leads to a decreased population of cells needed to replace and repair these erosive lesions with new bone. This model focuses entirely on the mechanism of bone loss in response to MSU crystals. As discussed later, the mechanisms of new bone formation in joints affected by chronic gout require further study.

    How Can A Gout Attack Be Prevented

    Diet plays a key role diet in gout prevention: Since foods can directly set off gout attacks, patients with gout should receive counseling as to which foods are more likely to induce attacks. Losing weight is often also helpful. However, as important as diet is in gout, for most people with gout diet, and even weight loss, are not enough, and medications will be needed to get to their uric acid goal.

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    How Is Gout Treated

    Gout can be effectively treated and managed with medical treatment and self-management strategies. Your health care provider may recommend a medical treatment plan to

    • Manage the pain of a flare. Treatment for flares consists of nonsteroidal anti-inflammatory drugs like ibuprofen, steroids, and the anti-inflammatory drug colchicine.
    • Prevent future flares. Making changes to your diet and lifestyle, such as losing weight, limiting alcohol, eating less purine-rich food , may help prevent future attacks. Changing or stopping medications associated with hyperuricemia may also help.
    • Prevent tophi and kidney stones from forming as a result of chronic high levels of uric acid. Tophi are hard, uric acid deposits under the skin. For people with frequent acute flares or chronic gout, doctors may recommend preventive therapy to lower uric acid levels in the blood using drugs like allopurinol, febuxostat, and pegloticase.

    In addition to medical treatment, you can manage your gout with self-management strategies. Self-management is what you do day to day to manage your condition and stay healthy, like making healthy lifestyle choices. The self-management strategies described below are proven to reduce pain and disability, so you can pursue the activities important to you.

    Therapeutic Strategies For Prevention And Treatment Of Structural Joint Damage In Gout

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    Since the discovery that IL-1 is critical for initiation of MSU crystal-induced acute inflammation, several clinical trials have demonstrated reduced inflammation and fewer gouty flares in patients with gout following treatment with inhibitors of IL-1 signaling, such as canakinumab, rilonacept, and anakinra. As described earlier, IL-1 is also expressed within the tophus, and this cytokine has potent catabolic effects on bone and cartilage. Longer-term studies are needed to determine whether IL-1 inhibitors are effective in preventing development or progression of joint damage in people with gout.

    Finally, given that osteoclast-mediated bone resorption is responsible for the focal bone erosions observed in gouty joints, therapies that aim to inhibit osteoclast activity may also be useful for preventing bone erosion in gouty joints. Bisphosphonates are widely available agents that have potent anti-osteoclast activity. Studies that assess the effects of bisphosphonates in the prevention of bone erosion in gout will be of interest.

    The authors have nothing to disclose.

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    Chronic Untreated Gout Can Lead To Joint Damage And Deformity

    W.D. Auer/Alamy

    For some people, gout can be chronic, which means multiple, severe gout attacks several times a year.

    Chronic gout, sometimes called gouty arthritis, can lead to a number of serious complications if left untreated.

    Complications of gout include:

    • Loss of mobility or range of motion
    • Bone loss
    • Chronic kidney disease

    Get An Accurate Diagnosis And Treatment

    While gout attack symptoms do resolve on their own, people are advised to seek medical treatment. If left untreated, gout can become chronic and cause lasting joint damage.

    Diagnosis begins with a clinical exam and interview. Patients are encouraged to be honest with their health care providers about their eating, drinking, and other lifestyle habits. This honesty can be helpful both for diagnosing gout and creating a treatment plan. Diagnosis may also involve blood tests, urine tests, and medical imaging, such as x-rays and ultrasound.

    See Gout Diagnosis

    Treatment typically involves advice to avoid alcohol and certain foods known to trigger gout, such as foods and drink high in sugar, seafood, red meat, and organ meats.19 Medications to lower urate levels in the bloodâwhich can lead to gout attacksâare often recommended. Losing excess weight is another effective way to reduce the risk of a gout attack and chronic gout.20

    See Gout Treatment

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    Cell Damage Due To Acidosis

    Unlike the central nervous system, the peripheral nervous system is very vulnerable to chemical and mechanical stress. This means that acids will easily damage the nerves hence causing numbness and tingling. They will be more exposed to the corroding power of the free radicals. In fact, even the central nervous system can be a victim if you suffer from extreme acidosis. These acids are supposed to have no effect against the brain, but with too many acids the blood-brain barrier, composed of mostly endothelial cells, can be breached. Needless to say, this can be fatal.

    Furthermore, continuous damage of cells will also result in more damaged insulin receptors. This makes the cells reject glucose which forces the blood to absorb more sugar. The high level of sugar in the blood makes it thick and this can cause a greater blood supply shortage and may result in diabetes.

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