Bones Diseases

Chapter 12

DISEASES OF BONES AND JOINTS

Introduction to Human Skeleton 

• The human skeleton is the internal framework of the body. It is composed of 270 bones at birth. This total decreases to 206 bones by adulthood after some bones have fused together. The bone mass in the skeleton reaches maximum density around age 30. The human skeleton can be divided into the axial skeleton and the appendicular skeleton. The axial skeleton is formed by the vertebral column, the rib cage and the skull. The appendicular skeleton, which is attached to the axial skeleton, is formed by the pectoral girdles, the pelvic and the bones of the upper and lower limbs. The individual bones are attached in such a way that a large variety of co-ordinate movements are made possible in different parts of the body. These movements are made possible by skeletal muscles, the fact that the bones act as levers, cartilage which reduces friction and ligaments which prevent dislocation and the presence of movable joints. The site or place where two or more bones of the skeleton are attached to each other is called a joint or place of articulation.

Structure Function of Joints 

• A joint is formed where two or more bones come in close contact in the body and are attached to each other by ligaments or cartilage.

Types of Joints:

•  Joints can be classified according to the degree and type of movement they allow. The following types of joints can be recognized:

• a) Fibrous (or immovable) Joints: These joints are firmly held together by a thin layer of strong connective tissue. There is no movement between the bones such as the sutures of the skull and the teeth in their sockets. 

•  b) Cartilaginous Joints: Cartilaginous joints are joints where the articular surfaces of the bones forming the joints are attached to each other by means of white fibro cartilaginous discs and ligaments which allow only a limited degree of movement. Examples are the cartilaginous joint between the vertebrae, the cartilage in the symphysis which binds the pubic bones together at the front of the pelvic girdle, and the cartilage in the joint between the sacrum and the hip bone.

• c) Synovial Joints: Synovial joints are freely movable joints and shows free movement including flexion (bending), extension (straightening or bending), abduction (away from the middle of the body), adduction (towards the midline), rotation, supination (turning the palm up, inversion (turning the sole of the foot inward) and eversion (turning the sole of the foot outward).

• There articular surfaces are covered with hyaline cartilage. This articular cartilage is avascular, non-nervous and elastic. Lubricated with synovial fluid, the cartilage forms slippery surfaces for free movements. 

• Between the articular surfaces there is a joint cavity filled with synovial fluid. The cavity may be partially or completely subdivided by an articular disc known as meniscus.

Functions of the Skeleton 

• 1. Support: The skeleton is the framework of the body, it supports the softer tissues and provides points of attachment for most skeletal muscles.

• 2. Protection: The skeleton provides mechanical protection for many of the body’s internal organs, reducing risk of injury to them. For example, cranial bones protect the brain, vertebrae protect the spinal cord, and the ribcage protects the heart and lungs.

• 3. Assisting in Movement: Skeletal muscles are attached to bones, therefore when the associated muscles contract they cause bones to move.

• 4. Storage of Minerals: Bone tissues store several minerals, including calcium (Ca) and phosphorus (P). When required, bone releases minerals into the blood, facilitating the balance of minerals in the body.

• 5. Production of Blood Cells: The red bone marrow inside some larger bones produce blood cells (RBC, WBC and Platelets)

• 6. Storage of Chemical Energy: With increasing age some bone marrow changes from ‘red bone marrow’ to ‘yellow bone marrow’. Yellow bone marrow consists mainly of adipose cells, and a few blood cells. It is an important chemical energy reserve.  

Bone Structure 

• Each bone in the skeleton contains two forms of tissue: compact (dense) bone that is relatively solid and spongy (cancellous) bone that forms an open network of struts and plates. Compact bone is found on the external surface of the bone. Spongy bone is located inside the bone. The proportion of compact and spongy bone varies with the shape of the bone. Compact bone is thickest where stresses arrive from a limited range of directions. Spongy bone is located where bones are not heavily stressed or where stresses arrive from many directions. Spongy bone is much lighter than compact bone which helps to reduce the weight of the skeleton and makes it easier for muscles to move the bones. Tendons: These attach muscle to bone.

• Ligaments: These attach bone to bone.

• Skeletal muscles:

• These muscles contract to pull on tendons and move the bones of the skeleton. In addition to producing skeletal movement, muscles also maintain posture and body position, support soft tissues, guard entrances and exits to the digestive and urinary tracts, and maintain body temperature.

• Cartilage: This is a type of connective tissue. It is a firm gel-like substance. The body contains three major types of cartilage: hyaline cartilage, elastic cartilage and fibrocartilage.

• Hyaline cartilage:

• It is the most common type of cartilage. This type of cartilage provides stiff but somewhat flexible support. Examples in adults include the tips of ribs (where they meet the sternum) and part of the nasal septum. Another example is articular cartilage, which is cartilage that covers the ends of bones within a joint. The surfaces of articular cartilage are slick and smooth, which reduces friction during joint movement.

• Elastic cartilage:

• It provides support but can tolerate distortion without damage and return to its original shape. The external flap of the ear is one place where elastic cartilage can be found. Fibrocartilage resists: Fibrocartilage resists compression, prevents bone-to-bone contact, and limits relative movement. Fibrocartilage can be found within the knee joint, between the pubic bones of the pelvis, and between the spinal vertebrae.

• Disease of Bones and Joints:

• Rheumatoid arthritis

• Osteoporosis

• Gout

Rheumatoid Arthritis

• Rheumatoid arthritis (RA) is an autoimmune disease that results in a chronic, systemic inflammatory disorder that may affect many tissues and organs, but principally attacks flexible (synovial) joints. It can be a disabling and painful condition, which can lead to substantial loss of functioning and mobility if not adequately treated. The hallmark feature of this condition is persistent symmetric polyarthritis (synovitis) that affects the hands and feet, though any joint lined by a synovial membrane may be involved. Extra-articular involvement of organs such as the skin, heart, blood vessels, lungs and eyes can be significant. Although rheumatoid arthritis affects approximately 1% of world population. It can occur at any age, usually begins after age 40 (Peak incidence is between 4th and 6th decade). The disorder is much more common in women than in men. Genetic and autoimmune factors are mainly responsible for the initiation of disease process.

Juvenile Rheumatoid Arthritis (JRA) 

• Juvenile rheumatoid arthritis causes joint inflammation and stiffness for more than six weeks in a child aged 16 or younger. Even though infectious agents such as viruses, bacteria, and fungi have long been suspected, the cause of rheumatoid arthritis is unknown. Treatment focuses on controlling symptoms and preventing joint damage.

Epidemiology

• Worldwide, the annual incidence of RA is approximately 3 cases per 10,000 populations, and the prevalence rate is approximately 1%, increasing with age and peaking between the ages of 35 and 50 years. In 2010, it resulted in about 49,000 deaths globally. About 1.5 million people in the United State have RA. Nearly three times as many women have the disease as men. In women, RA most commonly begins between ages 30 and 60. In men, it often occurs later in life. RA is a chronic disease, and although rarely, a spontaneous remission may occur. The natural course is almost invariably one of persistent symptoms, waxing and waning in intensity, and a progressive deterioration of joint structures leading to deformations and disability.

Etiology 

• The cause of RA is unknown. Genetic, environmental, hormonal, immunologic and infectious factors may play significant roles. Socioeconomic, psychological, and lifestyle factors (e.g., tobacco use, the main environmental risk) may influence disease outcome.

• Immunologic factors:

• Rheumatoid arthritis occurs when immune system attacks the synovium, the lining of the membranes that surround joints. All of the major immunologic elements play fundamental roles in the initiation, propagation and maintenance of the autoimmune process of RA.

• Genetic factors:

• Half of the risk for RA is believed to be genetic. It is strongly associated with the inherited tissue type major histocompatibility complex (MHC) antigen HLA-DR4 (most specifically DR0401 and 0404), and the genes PTPN 22 and PAD I4, hence family history is an important risk factor. Inheriting the PTPN22 gene has been shown to double a person’s susceptibility to RA. PADI4 has been identified as a major risk factor in people of Asian descent, but not in those of European descent. First-degree relatives' prevalence rate is 2–3% and disease genetic concordance in monozygotic twins is approximately 15–20%.

•  Infectious agents: 

• For many decades, numerous infectious agents have been suggested as potential causes of RA, including Mycoplasma organisms, Epstein Barr virus (EBV), and rubella virus.

• Hormonal factors: 

• Sex hormones may play a role in RA, as evidenced by the disproportionate number of females with this disease, its amelioration during pregnancy, its recurrence in the early postpartum period, and its reduced incidence in women using oral contraceptives. Hyperprolactinemia may be a risk factor for RA.

• Other factors: 

• Smoking is the most significant non-genetic risk with RA being up to three times more common in smokers than non-smokers, particularly in men. Vitamin D deficiency is more common in patients with rheumatoid arthritis than in the general population.

Pathophysiology 

• The pathogenesis of RA is not completely understood. An external trigger (e.g., cigarette smoking, infection, or trauma) that triggers an autoimmune reaction, leading to synovial hypertrophy and chronic joint inflammation along with the potential for extra-articular manifestations, is theorized to occur in genetically susceptible individuals.
• Synovial cell hyperplasia and endothelial cell activation are early events in the pathologic process that progresses to uncontrolled inflammation and consequent cartilage and bone destruction. Genetic factors and immune system abnormalities contribute to disease propagation.

• Rheumatoid Arthritis and Joint Inflammation:

• Joint inflammation is a hallmark of rheumatoid arthritis. That includes:

• Stiffness:

• The joint is harder to use and might have a limited range of motion. “Morning stiffness” is one of the hallmark symptoms of rheumatoid arthritis. While many people with other forms of arthritis have stiff joints in the morning. People with rheumatoid arthritis take more than an hour (sometimes several hours) before their joints feel loose.

• Swelling:

• Fluid enters into the joint and it becomes puffy; this also contributes to stiffness.

• Pain:

• Inflammation inside a joint makes it sensitive and tender. Prolonged inflammation causes damage that also contributes to pain.

• Redness and warmth:

• The joints may be somewhat warmer and more pink or red than neighboring skin. Other symptoms: RA can affect many areas of the body. These effects all result from the general process of inflammation.

Complications 

• Rheumatoid Arthritis Skin Problems:

•  Rheumatoid arthritis (RA) is primarily a disease of the joints. But the disease and many of the medications used to treat it can also affect the skin, causing problems as diverse as sun sensitivity, rash, and firm lumps of tissue called nodules. 

• Lung involvement, due to either damage to the lungs or inflammation of the lining around the lungs, is common but sometimes causes no symptoms. If shortness of breath develops, it can be treated with drugs that reduce inflammation in the lungs.

• Rheumatoid arthritis can even affect a joint in voice box or larynx (cricoarytenoid joint), causing hoarseness. Rheumatoid arthritis can cause inflammation in the lining around the heart, but it usually has no symptoms. If symptoms do develop, it may cause shortness of breath or chest pain. In addition, people with rheumatoid arthritis are more likely to develop clogged arteries in their heart, which can lead to chest pain and heart attacks.

• The eyes are affected in less than 5% of people with rheumatoid arthritis. When the eyes are affected, symptoms can include red, painful eyes or possibly dry eyes. Early rheumatoid arthritis tends to affect smaller joints first, particularly the joints that attach fingers to hands and toes to feet. As the disease progresses, symptoms often spread to the knees, ankles, elbows, hips and shoulders. In most cases, symptoms occur in the same joints on both sides of body. 

Tests and Diagnosis

• Rheumatoid arthritis can be difficult to diagnose in its early stages because the early signs and symptoms mimic those of many other diseases. There is no one blood test or physical finding to confirm the diagnosis. 

•  Physical exam:

•  To check joints for swelling, redness, warmth and also check reflexes and muscle strength. 

•  Laboratory studies:

•  Routine viral screening by serologic testing neither significantly facilitate the diagnosis of RA in patients with early RA, nor it is helpful as a potential identifier of disease progression. 

• • Erythrocyte sedimentation rate (ESR)

• C-reactive protein (CRP) level

• Complete blood count (CBC)

• Rheumatoid factor (RF) assay 

• Antinuclear antibody (ANA) assay

• Markers of inflammation: 

• The ESR and the CRP level are associated with disease activity.  

• Hematologic parameters:

•  People with rheumatoid arthritis tend to have an elevated erythrocyte sedimentation rate (ESR), which indicates the presence of an inflammatory process in the body. Creactive protein (CRP) levels are an even better indication than ESR of the amount of inflammation present. In people with rheumatoid arthritis, if the CRP is high, it suggests that there is significant inflammation or injury in the body.

Treatments and Drugs 

• There is no cure for rheumatoid arthritis. Medications can reduce inflammation in joints in order to relieve pain and prevent or slow joint damage. Occupational and physical therapy helps how to protect joints. If joints are severely damaged by rheumatoid arthritis, surgery may be necessary. 

•  Medications:

•  Many drugs used to treat rheumatoid arthritis have potentially serious side effects.

• NSAIDs:

•  NSAIDs can relieve pain and reduce inflammation. (e.g. Aspirin, Fenoprofen, Piroxicam, Indomethacin etc.)

•  Steroids: 

• Corticosteroid medications, such as prednisone, reduce inflammation and pain and slow joint damage. Side effects may include thinning of bones, cataracts, weight gain and diabetes. Corticosteroids are used to relieve acute symptoms, with the goal of gradually tapering off the medication. 

• Disease modifying antirheumatic drugs (DMARDs): 

• These drugs can slow the progression of rheumatoid arthritis and save the joints and other tissues from permanent damage. Common DMARDs include Gold, d-penicillamine, chloroquine or hydroxychloroquine, sulfasalazine, leflunomide etc. Side effects vary but may include liver damage, bone marrow suppression and severe lung infections.

• Immunosuppressants: 

• These medications act to suppress immune system, which is out of control in rheumatoid arthritis. Examples include cyclosporine, azathioprine, methotrexate. These medications can increase susceptibility to infection.

• TNF-inhibitors:

• Tumor necrosis factor-alpha (TNF-α) is an inflammatory substance produced by body. TN inhibitors can help to reduce pain, morning stiffness and tender or swollen joints. Examples include etanercept, infliximab, adalimumab, golimumab and certolizumab. Potential side effects include nausea, diarrhea, hair loss and an increased risk of serious infections. 

• Other drugs: 

• Several other rheumatoid arthritis drugs target a variety of processes involved with inflammation in body. These drugs include anakinra, abatacept, rituximab, tocilizumab and tofacitinib. Side effects vary but may include itching, abdominal pain, headache, runny nose or sore throat.

• Surgery: 

• If medications fail to prevent or slow joint damage, surgery requires repairing damaged joints. Surgery may help restore ability to use joint. It can also reduce pain and correct deformities. Rheumatoid arthritis surgery may involve one or more of the following procedures: 

• Total joint replacement

• Tendon repair

• Joint fusion 

Osteoarthritis 

• Osteoarthritis (OA) is the most common form of arthritis, affecting millions of people around the world. It can be thought of as a degenerative disorder arising from the biochemical breakdown of articular (hyaline) cartilage in the synovial joints. However, the current view holds that osteoarthritis involves not only the articular cartilage but also the entire joint organ, including hands, neck, lower back, knees and hips.

• There are two types of osteoarthritis: 

•  Primary osteoarthritis: 

•  It is mostly related to aging. With aging, the water content of the cartilage increases, and the protein makeup of cartilage degenerates. 

•  Secondary osteoarthritis: 

•  Secondary osteoarthritis is caused by another disease or condition. Conditions that can lead to secondary osteoarthritis include obesity, repeated trauma or surgery to the joint structures, abnormal joints at birth (congenital abnormalities), gout, diabetes, and other hormone disorders. 

Epidemiology

• Globally approximately 250 million people have osteoarthritis of the knee (3.6% of the population). Osteoarthritis affects nearly 27 million people in the United States. It is estimated that 80% of the population have radiographic evidence of osteoarthritis by age 65, although only 60% of those will have symptoms. Osteoarthritis globally causes moderate to severe disability in 43.4 million people. 

Causes 

• Osteoarthritis occurs when the cartilage that cushions the ends of bones in joints deteriorates over time. Cartilage is a firm, slippery tissue that permits nearly frictionless joint motion. In osteoarthritis, the slick surface of the cartilage becomes rough. The daily stresses applied to the joints, especially the weight-bearing joints (e.g., ankle, knee and hip), play an important role in the development of osteoarthritis. Most investigators believe that degenerative or alterations in osteoarthritis primarily begin in the articular cartilage, as a result of either excessive loading of a healthy joint or relatively normal loading of a previously disturbed joint. External forces accelerate the catabolic effects of the chondrocytes and further disrupt the cartilaginous matrix. 

• Older age: 

• The risk of osteoarthritis increases with age.

•  Sex: 

• Women are more likely to develop osteoarthritis, though the reason is unknown.

• Obesity: 

• Carrying more body weight puts added stress on weight-bearing joints, such as knees.

• Joint injuries: Injuries, such as those that occur when playing sports or from an accident, may increase the risk of osteoarthritis.

• Genetics (significant family history)

•  Reduced levels of sex hormones 

•  Muscle weakness 

•  Repetitive use (jobs requiring heavy Laboure and bending) 

•  Infection 

•  Crystal deposition

•  Acromegaly 

•  Previous inflammatory arthritis (e.g., burnt-out rheumatoid arthritis) 

Pathophysiology 

• Osteoarthritis is a degenerative joint disease that may cause gross cartilage loss and morphological damage to other joint tissues, more subtle biochemical changes occur in the earliest stages of osteoarthritis progression. The water content of healthy cartilage is finely balanced by compressive force driving water out and swelling pressure drawing water in. Collagen fibers exert the compressive force, whereas the Gibbs–Donna effect and cartilage proteoglycans create osmotic pressure which tends to draw water in.

• However during onset of osteoarthritis, the collagen matrix becomes more disorganized and there is a decrease in proteoglycan content within cartilage. The breakdown of collagen fibers results in a net increase in water content.

Symptoms

• Osteoarthritis symptoms often develop slowly and worsen over time. 

• Signs and symptoms of osteoarthritis include: 

•  Pain: 

• Joint may hurt during or after movement. 

•  Tenderness: 

• Joint may feel tender, if light pressure is applied on it. 

•  Stiffness: 

• Joint stiffness may be most noticeable when wake up in the morning or after a period of inactivity.

•  Loss of flexibility: 

• The joints are not able to move through its full range of motion. Grating sensation: May hear or feel a grating sensation when use the joint. 

•  Bone spurs:

•  These extra bits of bone, which feel like hard lumps, may form around the affected joint. 

Tests and Diagnosis 

• Physical exam:

• Physical examination of affected joint includes, checking for tenderness, swelling or redness.

Imaging tests:

• Pictures of the affected joint can be obtained during imaging tests.

• Examples include:

X-rays:

• An X-ray may also show bone spurs around a joint. Many people have Xray evidence of osteoarthritis before they experience any symptoms.

Magnetic resonance imaging (MRI):

• MRI can be helpful in determining what exactly is causing pain.

Lab tests:

• Analyzing blood or joint fluid can help to pinpoint the diagnosis.

Blood tests:

• Blood tests may help to rule out other causes of joint pain, such as rheumatoid arthritis.

Joint fluid analysis:

• Draw fluid out of the affected joint for inflammation and pain is caused by gout or an infection

Treatments and Drugs 

• There is no known cure for osteoarthritis, but treatments can help to reduce pain and maintain joint movement.

Medications:

• Osteoarthritis symptoms can be relieved by a variety of medications, including: Acetaminophen:

• Acetaminophen can relieve pain, but it does not reduce inflammation.

NSAIDs:

• NSAIDs may reduce inflammation and relieve pain. NSAIDs include Ibuprofen, Indomethacin, Diclofenac sodium, Adelfina and Naproxen.

Narcotics:

• Narcotics like codeine and may provide relief from more severe osteoarthritis pain. Lifestyle and home remedies: Lifestyle changes and home treatments also can help to reduce osteoarthritis symptoms.

Rest:

• Experiencing pain or inflammation in joint, rest it for 12 to 24 hours.

Exercise:

• Exercise can increase endurance and strengthen the muscles around joint, making joint more stable.

Lose weight:

• Being overweight or obese increases the stress on weight-bearing joints, such as knees and hips. Even a small amount of weight loss can relieve some pressure and reduce pain.

Use heat and cold to manage pain:

• Both heat and cold can relieve pain in joint. Heat also relieves stiffness, and cold can relieve muscle spasms and pain.

Osteoporosis

• Osteoporosis is a condition that weakens bones, making them fragile and more likely to break (Latin “porous bones”). The inside of a healthy bone has small spaces, like a honeycomb. Osteoporosis increases the size of these spaces, causing the bone to lose strength and density. In addition, the outside of the bone grows weaker and thinner. Osteoporosis can occur in people of any age, but it is more common in older adults, especially women. People with osteoporosis are at a high risk of fractures, or bone breaks, while doing routine activities such as standing or walking.

Causes 

• Losing bone is a normal part of the ageing process, but some people lose bone density much faster than normal. This can lead to osteoporosis and an increased risk of fractures. Women also lose bone rapidly in the first few years after the menopause. Women are more at risk of osteoporosis than men, particularly if the menopause begins early (before the age of 45). 

• Many other factors can also increase the risk of developing osteoporosis, including Long-term use of high-dose oral corticosteroids 

• Other medical conditions – such as inflammatory conditions, hormone related conditions, or malabsorption problems. 

• Family history of osteoporosis – particularly history of a hip fracture in a parent.

• Other conditions that may lead to osteoporosis include overuse of corticosteroids (Cushing syndrome), thyroid problem, lack of muscle use, bone cancer, certain genetic disorders, use of certain medications, and problems such as low calcium in the diet. 

Symptoms 

• Early in the course of the disease, osteoporosis may cause no symptoms or warning signs. Later, it may cause height loss or dull pain in the bones or muscles, particularly low back pain or neck pain. If symptoms do appear, some of the earlier ones may include:

• Receding gums

• Weakened grip strength

• Weak and brittle nails

• Severe Osteoporosis 

• Later in the course of the disease, sharp pains may come on suddenly. The pain may not radiate (spread to other areas); it may be made worse by activity that puts weight on the area, may be accompanied by tenderness, and generally begins to subside in one week. Pain may linger more than three months.

Diagnosis 

• Diagnosis of osteoporosis begins with a careful family history of osteoporosis or a history of previous broken bones.

• Blood tests are used to measure calcium, phosphorus, vitamin D, testosterone, and thyroid and kidney function.

• Based on a medical examination, a specialized test called a bone mineral density test that can measure bone density in various sites of the body. The diagnosis of osteoporosis or osteopenia can be made based on the results of these tests.

Treatment

• There is no cure for osteoporosis, but proper treatment can help to protect an strengthen bones. These treatments can help slow the breakdown of bone in body, and some treatments can spur the growth of new bone. The lifestyle changes can include increasing intake of calcium and vitamin D, as well as getting appropriate exercise. 

• Diet:

• Young adults should be encouraged to achieve normal peak bone mass by getting enough calcium (1,000 mg daily) in their diet (drinking milk or calcium-fortified orange juice and eating foods high in calcium such as salmon), performing weightbearing exercise such as walking or aerobics (swimming is aerobic but not weight-bearing), and maintaining normal body weight.

• Exercise:

• Lifestyle modification should also be incorporated into treatment. Regular exercise can reduce the likelihood of bone fractures associated with osteoporosis.

Medications 

• The most common drugs used to treat osteoporosis are called bisphosphonates which are used to prevent the loss of bone mass. They may be taken orally or by injection include:

• Alendronate

• Ibandronate

• Zoledronic acid other medications may be used to prevent bone loss or stimulate bone growth.

• They include:

• Testosterone:

• In men testosterone therapy may help to increase bone density.

• Hormone therapy:

• For women, estrogen used during and after menopause can help to stop bone density loss.

• Raloxifene: This medication has been found to provide the benefits of estrogen without many of the risks, although there is still an increased risk of blood clots.

• Denosumab: This drug is taken by injection and may prove even more promising than bisphosphonates at reducing bone loss.

• Teriparatide: This drug is also taken by injection and stimulates bone growth. Calcitonin salmon: This drug is taken as a nasal spray and reduces bone reabsorption. 

Gout 

• Gout is a metabolic disorder characterized by elevated serum uric acid levels and deposits of urate crystals in synovial fluids and surrounding tissues in joints. It is a type of arthritis that is characterized by sudden, severe attacks of joint pain with redness, warmth, and swelling in the affected area. It usually attacks only one joint at a time. It most often strikes the joint of the big toe, where it is also known as podagra, but other toes can also be involved.

Epidemiology

• Gout affects around 1–2% of the Western population at some point in their lifetimes and is becoming more common. Rates of gout have approximately doubled between 1990 and 2010. This rise is believed due to increasing life expectancy, changes in diet, and an increase in diseases associated   with gout, such as metabolic syndrome and high blood pressure. A number of factors have been found to influence rates of gout, including age, race, and the season of the year. In men over the age of 30 and women over the age of 50, prevalence is 2%. Some studies have found that attacks of gout occur more frequently in the spring. This has been attributed to seasonal changes in diet, alcohol consumption, physical activity and temperature.

Causes 

• Gout is caused initially by an excess of uric acid in the blood (hyperuricemia). Uric acid is produced in the body through the breakdown of purines specific chemical compounds that are found in certain foods such as meat, poultry and seafood.

• Age and gender:

• Men produce more uric acid than women. But after menopause, the uric acid level in women is equal to men.

• Genetics:

• A family history of gout increases the likelihood of the condition developing. Lifestyle Factors:

• Alcohol consumption interferes with the removal of uric acid from the body. Eating a high-purine diet also increases the amount of uric acid in the body.

• Lead exposure: 

• Chronic lead exposure has been linked in some cases to gout. 

• Medications: 

• Certain medications can increase the levels of uric acid in the body, such as diuretics and drugs containing salicylate, Niacin etc. Weight: Being overweight increases the risk as there is more tissue in the body for turnover or breakdown, leading to the production of excess uric acid.

• Other health problems:

• If the kidneys are unable to eliminate waste products adequately (renal insufficiency) then uric acid levels can remain high. Other conditions that can contribute are high blood pressure (hypertension), diabetes and hypothyroidism.

Pathophysiology

• Gout is a disorder of purine metabolism, and occurs when its final metabolite, uric acid, crystallizes in the form of monosodium urate, precipitating in joints, on tendons, and in the surrounding tissues. These crystals then trigger a local immune mediated inflammatory reaction, with one of the key proteins in the inflammatory cascade being interleukin. An evolutionary loss of uricase, which breaks down uric acid, in humans and higher primates has made this condition common. 

Clinical Manifestations

• The signs and symptoms of gout are almost always acute, occurring suddenly often at night and without warning.

•  Intense joint pain: 

• Gout usually affects the large joint of big toe, but it can occur in feet, ankles, knees, hands and wrists. The pain is likely to be most severe within the first 12 to 24 hours after it begins.

•  Lingering discomfort: 

• After the most severe pain subsides, some joint discomfort may last from a few days to a few weeks. Later attacks are likely to last longer and affect more joints. Inflammation and redness: 

• The affected joint or joints become swollen, tender and red. 

Complications

• People with gout can develop more severe conditions, such as:

• Recurrent gout: Some people may never experience gout signs and symptoms again. But others may experience gout several times each year.

• Advanced gout:

• Untreated gout may cause deposits of urate crystals to form under the skin in nodules called tophi. Tophi can develop in several areas such as fingers, hands, feet, elbows or Achilles tendons along the back of ankle. Tophi usually are not painful, but they can become swollen and tender during gout attacks.

• Kidney stones:

• Urate crystals may collect in the urinary tract of people with gout, causing kidney stones.

Symptoms 

• Symptoms of gout include sever pain, bone erosion, redness and swelling in joints, often the big toe. 

Diagnosis 

• Joint fluid test: 

• Joint fluid test (arthrocentesis) is useful to see whether uric acid crystals are present. This is the only test for diagnosis of gout. 

•  Blood test: 

• To measure the uric acid level in blood. Blood test results can be misleading, though some people have high uric acid levels, but never experience gout.

• Urine Test: 

• A test to measure levels of uric acid in urine. 

•  X-ray: 

• X-rays of extremities (hands and feet) are sometimes useful in the late stages of the disease; X-rays are not usually helpful in the early diagnosis. Pain often causes people to seek medical attention before any long-term changes can be seen on an X-ray. But X-rays may help to rule out other causes of arthritis. 

Treatment 

• The goals of treatment for gout are fast pain relief and prevention of future gout attacks and long-term complications, such as joint destruction and kidney damage. NSAIDs:

• NSAIDs may control inflammation and pain in people with gout. NSAIDs include indomethacin, ibuprofen, naproxen, and etoricoxib.

• Colchicine:

• A type of pain reliever that effectively reduces gout pain, especially when started soon after symptoms appears.

• Corticosteroids:

• Corticosteroid medications, such as the drug prednisone, may control gout inflammation and pain. Corticosteroids may be administered in pill form, or they can be injected into joint. Corticosteroids are generally reserved for people who cannot take either NSAIDs or colchicine.

• Medications that block uric acid production:

• Xanthine oxidase inhibitors, including allopurinol and febuxostat, limit the amount of uric acid that body makes.

• Medication that improves uric acid removal:

• Probenecid improves kidney’s ability to remove uric acid from body. This may lower uric acid levels and reduce risk of gout, but the level of uric acid in urine is increased.

• Politicize:

• This medicine is for gout that has lasted a long time and has not responded to other treatment.

Prevention 

During symptom free periods, these dietary guidelines may help protect against future gout attacks. Drink 8 to 16 cups (about 2 to 4 liters) of fluid each day, with at least half being water. Eat a moderate amount of protein, preferably from healthy sources, such as low-fat or fat-free dairy, eggs, and nut butters.