Rheumatoid arthritis (RA) is a chronic inflammatory disease mediated by immune mechanisms and affects multiple organs & tissues in the body although generally manifests with joint involvement as its major presentation.

It is considered to be an autoimmune disease where the body’s immune structures due to certain faulty system attack some organs & tissues instead of defending them.

Frequency & distribution

This disease occurs all over the world and affects all races & both sexes although women are affected more than men. The disease characteristically presents during middle age and most of the cases present between 35 and 50.

What cases RA?

RA is an immune mediated inflammatory disease and it appears that a combination of genetic & environmental factors is responsible for the development of this disease.

Genetic factors are thought to explain abut 60% of the disease susceptibility to RA. Some of the frequent genetic makers include;

* HLA-DRB1
* HLA-DR4
* HLA-DR1 etc.

Since the genetic susceptibility alone cannot account for the incidence of RA environmental factors are incriminated too and few such factors include;

* Urbanization & climatic changes
* Smoking (HLA-?1 susceptibility)
* ? Infectious causes etc.

The earliest miscoscopical lesions seen in RA include micro vascular injury & increase in the number of synovial lining cells. As this process continues the synovial tissue becomes edematous and protrudes into the joint cavity as villous projections.

The RA lesions are with activated macrophages, lymphocytes & fibroblasts and they secrete chemical substances called as cytokines & chemokines. These agents are thoughtd to induce the synovial, cartilage & bone damage also the systemic manifestations of RA.

Clinical manifestations

RA symptoms and signs can be grouped under two categories including;

* Joint manifestations & related
* Systemic manifestations (non-joint)

The joint manifestations include;

Multi-joint involvement usually symmetrical is characteristic feature of RA. Both small and/or large joints may be involved although the involvement small hand joint is very characteristic. Affected joist are swollen, painful and stiff. This stiffness is characteristically seen in the morning. Joint involvement is associated with generalized weakness, low grade fever, sick feeling (malaise), loss of appetite & weight etc.

The Systemic manifestations of RA include;

* Rheumatoid nodules
* Vasculitis
* Lung & pleural involvement
* Heart & pericardial involvement
* Peripheral neuropathy/ mononeuritis multiplex
* Cervical spine (atlanto-axial joint damage)
* Eye involvement
* Felty’s syndrome
* Osteoporosis (bone thinning)
* Tumor development (lymphoma) etc.

Rheumatoid nodules occur in about 20 to 30% of RA patients and geerally occur near joints and extensor surfaces. Rheumatic vasculitis affects the blood vessels and can affect virtually any organ and patient’s manifestation would depend upon the type of organ involved (e.g. heart involvement can induce heart attack). Lung & heart involvement may be secondary to vascilitis ir due to nodular development. The nerve damage is either bilaterally symmetrical peripheral neuropathy or in the form mononeuritis multiplex.

Felty’s syndrome comprises;

* Chronic RA
* Enlarged spleen
* Decreased White & red blood cells and platelets.

Osteoporosis occurrence is common to RA and this can be aggravated by glucocorticoid usage. RA patients rarely may develop B cell lymphomas.

Diagnosis

The following investigations are performed including;

* Blood tests
* Radiological studies

X-ray studies
CT or MRI
Bone scanning etc.

* Synovial fluid analysis
* Synovial biopsy etc.

The following blood tests are usually considered to detect and/or assess the prognosis of RA;

* RA factor
* Anti-CCP
* ESR or CRP
* Complete blood count (CBC)

RA (rheumatoid) factor is one of the most commonly employed blood test (serological test) in this regard although there are some indication that anti-CCP may be a better test for this purpose. This antibody is detected in more than 60% of RA patients. But it is not specific for RA as about 5% of general population may harbor this antibody in their blood and also may be seen in patients having their disorders like lupus (SLE), Tuberculosis, syphilis etc.

Anti-CCP, antibodies to CCP, has sensitivity similar to TA factor and more specific for RA so now-a-days there is some recommendation to use this test instead of RA factor. But again anti-CCP is not totally diagnostic for RA and its sensitivity is only comparable with RA factor that means many patients who indeed have RA may not be detected by these two blood tests. Also they are not specific means these tests come abnormal even if somebody do not have RA.

ESR (sed rate) and CRP (reactive protein) are examples for acute-phase reactants and they are elevated in varieties of acute inflammatory conditions and are not specific for RA. However these agents are frequently ordered as hey serve as a supporting evidence for underlying the inflammation and also give some clue as the activity of the disease, in the sense a high blood value of sed rate or CRP generally correlate with an on going active inflammation rather than controlled chronic disease.

A CBC may reveal normo-chromic, normocytic type anemia and increased platelets and these two findings generally correlate with disease activity.

Radiological tests are frequently used for RA diagnosis and management. Simple plain x-rays are generally more than sufficient. None of the radiological findings are diagnostic of RA. They reveal findings including

* Fluid in the joints
* Synovial thickening
* Loss of joint cartilage
* Bone erosions etc.

The symmetric involvement especially the smaller joints of the hands are highly characteristic for RA although yet not diagnostic.

Other imaging studies like MRI, CT, bone scan etc may be able to detect minor pathologies missed by x-rays especially in the early stages of the disease although most often they are not necessary as the combination of clinical features, blood abnormalities and plain x-ray findings are more than sufficient for arriving at the diagnosis.

Synovial fluid analysis may be performed to confirm the inflammatory nature of the joint swelling and fluid accumulation. The typical findings include turbid fluid with reduced viscosity, elevated protein count, normal or slightly decreased glucose, increased WBCs (white blood cells) especially the neutrophills. C3, C4, total hemolytic components are characteristically decreased in RA.

There are certain criteria put forward for the diagnosis of RA and this system uses both clinical features & investigational findings as below

1) Morning stiffness in and around the joints
2) Arthritis of three or more joint areas
3) Arthritis of hand joints
4) Symmetric arthritis
5) Subcutaneous nodules (rheumatoid nodules)
6) Serum rheumatoid factor
7) Typical radiographic changes

Out of these seven at least four criteria should be positive to consider a patient is having RA. This system of identifying RA has a sensitivity of abut 91 to 94% and specificity of around 89%.

Management

RA has no curative treatment so far and the purpose of the treatment is to provide symptomatic relief, reduce joint inflammation, and slow down or suppress any chronic joint destruction a

In general the therapeutic approaches to RA may discussed under seven headings

1) NSAIDs (non steroidal anti-inflammatory drugs)
2) Steroids (glucocorticoids)
3)  DMARDs (disease modifying anti rheumatic drugs)
4)  Biologic agents
5)  Immunosuppressive therapies
6)  Surgical therapies
7) General measures

NSAIDs are useful when patients present with acute severe pain & inflammation of joints. Although they help symptomatically they do not have any impact on the course of the illness.

Examples for traditional or non specific NSAIDs include;

* Ibuprofen
* Indomethacin
* Piroxicam
* Paracetamol etc.

Examples for the newer COX -2 inhibitors include;

* Celecoxib

The selective COX-2 inhibitors are considered to be safer for the stomach compared to the on selective COX inhibitors however the cardiovascular complications like heart attack, stroke are a concern with these agents.

A low dose oral steroid like prednisolone usage is generally recommended. In addition to alleviate pain & inflammatory manifestations it may slow down the onset of bone erosion as well. Although small doses of steroids are not as notorious as the large dose steroids to produce serious side effects but still the following side effects are possible including;

* Gastro intestinal ulcers
* Diabetes mellitus
* High blood pressure
* Osteoporosis (thinning of bones)
* Infections etc.

DMARDs like methotrexate are routinely used on long term basis to slow down or control the course of RA. Studies have revealed that DMARDs do not induce remission but rather suppress the symptoms.  The side effects of chronic usage of methotrexate include;

* Oral ulcers
* Gastrointestinal upset
* Liver damage
* Lung damage etc.

Biologic agents are a recent addition to the therapeutic intervention for RA and few of these available agents include;

* Infliximab
* Rituximab
* Abatacept
* Etanercept
* Adalimumab
* Anakinra etc.

These are TNF (tumor necrosis factor) neutralizing agents or IL-1 receptor antagonists and help in controlling the clinical manifestations of RA. They may be used with agents like methotrexate or alone. In addition to ameliorating the symptoms they also slow down the disease process and joint damage. However some of these gents are associated with serious complications on long term usage including;

* TB (tuberculosis) reactivation
* Lymphoma tumor development
* Lupus like disease development etc.

Immunosuppressive therapy with drugs like

* Azathioprine
* Cyclosporine
* Leflunomide
* Cyclophosphamide etc.

Their effectiveness and side effects are in general comparable with DMARDs although methotrexate in general is favored by physicians than other agents.

Surgery I required if major joint damage has taken place and some commonly performed procedures include joint replacement, synoviectomy etc.

The general management includes;

* Exercise and activities as tolerated
* Some rest during severe symptoms
* Splinting the severely inflamed joints
* Assistive & orthotic devices etc.

Low back pain or lower back pain (also described as lumbago) is an aching discomfort that occus in the lumbar portion of the spine. It is one of the most common health problems, and is the reason most often given for taking time off work.

Low back pain may be the result of excessive strain on the lower back due to a poor posture, being overweight, or having to do a lot of carrying or lifting of heavy loads. For a few people, persistent back pain may be due to arthritis.

What causes low back pain?

Back pain is usually caused by a mechanical disorder of one of the structures in or around the spine. The pain may be the result of damage to a ligament or muscle, or to one of the joints between adjacent vertebrae bones of the spine. Occasionally the pain is due to a disc prolapse, a condition in which the spongy material between the vertebrae, bulges through its surrounding ligament and presses on adjacent spinal nerves. This nerve pressure causes pain in the back and also pain running down the back of the legs sciatica.

Other causes of back pain include arthritis, ankylosing spondylitis a disease of the joints and, rarely a tumour in the spinal column. It may also be caused by abdominal problems such as peptic ulcer, pancreatitis inflammation of the pancreas, or aortic aneurism localized widening of the aorta.

In most cases, back pain goes away within a few days. It often improves before the doctor has arranged any tests, so the exact cause may not be confirmed. If the pain persists or keeps coming back, tests will be done to establish a diagnosis.

How is low back pain diagnosed and treated?

Most episodes of low back pain can be resolved by resting the back for a few days. However, if the condition is persistent or recurrent, the doctor’s diagnosis can usually be made by means of a physical examination. This includes testing neurological nervous system responses and muscle function.

Other diagnostic studies may include a CT computed tomography scan an x-ray procedure which produces a detailed crossectional image of a particular part of the body, or a myelogram an x-ray of the back taken after an injection of a dye into the spine.

Bed rest for at least a few days is often recommended. Painkillers, anti-inflammatory drugs and muscle relaxants can help relieve muscle spasm.

Manipulation of the back by a doctor, physiotherapist or osteopath can be very effective, helping to relieve the pain and spasms in some cases.

What can I do myself?

Avoid prolonged sitting and keep the back mobile. Take regular exercise aimed at strengthening abdominal and back muscles. Swimming is excellent exercise for back pain. Using a back rub can also help control minor bouts of back pain. Some people find relief from cold treatment with an ice pack.

For persistent backache, a gradual lost os excess weight will help reduce the weight-bearing load on the spine. Sleeping on a firm mattress and, for severe, chronic back pain, wearing a corset-like back brace can also help to ease the situation.

Reducing emotional stress if at all possible can help, as many people unconsciously tighten their back muscles when they are worried or tense.

What will the doctor do?

Your doctor will examine your posture and the movements of your back when you are standing. You will then be asked to lie down so your back can be checked for areas of tenderness and muscle spasm. The nerve and muscle function in both legs will also be checked, as pressure on the spinal nerve can cause numbness or weakness.

Is low back pain dangerous?

Low back pain is rarely dangerous. However, if the pain is accompanied by leg weakness, a feeling of numbness, or bladder or bowel problems, this indicates that there is pressure on one or more of the spinal nerves.

If the pain is caused by a disc prolapse or tumour, prolonged pressure on a spinal nerve will require surgery, as permanent nerve damage can result. You must see a doctor if the pain is persistent.

SYMPTOMS

• Pain that radiates from the back into a leg sciatica.
• Numbness or tingling sensations which occur in one or both legs.
• Weakness in a leg.
• Loss of control over bladder or bowel.
• Muscle spasm.

WARNING
Anyone with severe back pain caused by an injury or fall, or who is unable to move, should be taken by ambulance to the nearest hospital.

Do not move the injured person as this should only be done by trained staff.

How can I avoid low back pain?

• Maintain your ideal weight.
• Practise back and abdominal exercises.
• Wear flat or low shoes.
• Sleep on a firm mattress.
• When lifting, squat down in a knee-bend, pick up the object and hold it close. Keep your back upright, but not unnaturally straight. Slowly straighten your legs as you rise.

ALTERNATIVE  TREATMENTS
Many people with recurrent back pain have found relief by studying and following the Alexander Technique. This is a system of posture adjustment and training for the correct movement of the spine, neck and limbs. The technique is taught in individual classes.

Osteoporosis is the thinning of bones which can cause them to become porous and fragile. It is linked with aging, progresses more rapidly after menopause and women are more affected compared to men. It is estimated that 1 in 3 women and 1 in 12 men over the age of 50 worldwide have osteoporosis. However, the good news is that this disease is preventable and can be treated.

Osteoporosis is often called the silent disease as most people don’t know they have osteoporosis until the disease has progressed – often up to the point of fracture, sometimes in the hip, wrist and even spine.

Undiagnosed osteoporosis often results in a vertebral fracture, but the pain is frequently dismissed as just general back pain. The lack of awareness on this can lead to serious illness, deformity and sometimes death. But osteoporosis alone may not cause back pain. It is possible that it might weaken the spine to where it can no longer withstand normal stress or bumps, resulting in vertebral fracture. So in fact, it is the fracture that causes pain.

There is a sub-condition of osteoporosis, called Osteopenia. Osteopenia is a condition where the bone mineral density is found to be lower than normal, but now low enough to be classified as osteoporosis. While this may seem like a progressive sign towards developing osteoporosis, not everyone with osteopenia will develop osteoposis. Osteopenia occurs more frequently in post-menopausal women as a result of the loss of estrogen. As the conclusive diagnosis of osteopenia puts one at greater risk for osteoporis, patients should seek advice for implementing preventive measure from their physicians.

What causes Osteoporosis and what are its risk factors?

The human bones are made of complex and constantly changing living tissues. They are somehow able to grow and heal, and are affected by dietary changes, body chemistry and exercise levels as well.

In the early life, our body grows more bone than its removal. Most people achieve peak bone mass by around the age of 30 and after that age, more bone is lost than is being replaced. So large amounts of bone loss over time will lead to osteoporosis.
There are 2 primary types of osteoporosis that are far more common in women than in men:

1. Postmenopausal osteoporosis – this generally develops after menopause, when estrogen levels drop abruptly, leading to bone loss. Mostly happens in the trabecular bone which is inside the hard cortical bone.
2. Senile osteoporosis – more likely to happen after age 70 which involves the thinning both bone types, trabecular and cortical.

Additionally, certain medications and health conditions can cause damage to the bone and lead what is known as “secondary osteoporosis”. At any point in time, patients being treated or found with any of the following conditions should discuss the risk of osteoporosis with their physicians:

1. Gastrointestinal disorders
2. Marrow disorders
3. Endocrine disorders
4. Seizure disorders
5. Collagen disorders
6. Eating disorders (such as anorexia or bulimia)

As treatment for osteoporosis is often different, it is important to differentiate between the primary and secondary causes of osteoporosis. To find out its cause, a complete or thorough medical history, physical examination and appropriate diagnostic tests must be conducted by the physician.
Let’s see the key risk factors for developing osteoporosis:

1. Advance in age – normally symptoms appear after age 65
2. Gender – a study has shown that women are four times more likely to develop osteoporis than men
3. Heredity – family history of osteoporosis or fracture on the mother’s side
4. Personal history – any type of fracture after age 45
5. Race – Caucasian and asian women are at greater risk
6. Body type – women with smaller bones who weighs less than 127 pounds
7. Menstrual history – normal menopause increases the risk of osteoporosis and early menopause can aggravate this risk
8. Lifestyle – lacking in calcium and/or vitamin D, little or no exercise (especially weight-bearing exercise), abuse of alcohol, smoking, too much cola/soda drinks.
9. Testosterone deficiency (hypgonadism) – found in men

Are women at greater risk for developing osteoporosis?

The answer is yes. In women, estrogen plays a very crucial role in maintaining bone strength. Starting at about age 30 through onset of menopause, women lose a small amount of bone every year as a natural part of the aging process.  When women reach menopause, estrogen levels decrease significantly, causing the rate of bone loss to increase around 8 to 10 years before it can return to premenopausal rates.

What are the symptoms of Osteoporosis?

Osteoporosis normally goes undetected for years and the first outward sign is fracture itself. Advanced osteoporosis is capable of getting one disabled and often leading to one or more of the following:

1. Chronic or severe pain
2. Fractures in the spine, wrist or hip
3. Deformation of the spine (hunched back, lost of height)
4. Limited function and reduced mobility
5. Loss of independence
6. Decreased lung capacity
7. Difficulty in sleeping

Osteoporosis is the leading cause of spine fractures, especially in women over the age of 50, but only about one third of all spine fractures can be diagnosed.
Vertebral compression fractures  – Most osteoporosis spine fractures start with an acute back pain, usually after routine activity, such as lifting or bending, that slightly strains the back or spine. After a month or two, this acute pain is usually replaced by an achy pain.

How to Prevent Osteoporosis?

Type I osteoporosis or Postmenopausal osteoporosis can be considerably influenced by normal preventive measures. Most of these behaviours are up to the individual and should be practised in life as early as possible. For those genetically predisposed to osteoporosis, the following practices are even more important:

1. Regular exercise – weight-baring exercises or exercises that work one’s bones and muscles against gravity are essential and can help in maintaining bone health
2. Ensure of adequate Calcium & Vitamin D intake – Calcium can keep bones strong. Vitamin D helps in ensuring the absorption and retention of Calcium in the bones. The requirements for Calcium and Vitamin D may vary depending on age and gender.
3. Eat a balanced and healthy diet – While certain foods provide excellent sources of calcium, diets high in protein and/or sodium can increase the loss of calcium in the body
4. Avoid or quit smoking – smoking has a detrimental effect on bone density, leading to greater risk of injury and longer recovery times.
5. Reduce or limit alcohol consumption – too much alcohol in the body has been proven to accelerate bone loss
6. Reduce or limit intake of colas/sodas – excess of cola or soda can increase the risk of osteoporosis
7. Undergo a bone density testing – If you are postmenopausal, over the age of 65 or have other risk factors, one should do that every 1 or 2 years. Bone mineral density tests can indicate normal, low or osteoporotic bone density levels, as well as any increased risks of bone fracture.

What are the available treatments for Osteoporosis?

Once a patient has been diagnosed for osteoporosis, the patient and physician should cooperate together to develop a treatment plan where the goal is to slow any further bone loss and prevent fractures from happening. Treatments for osteoporosis today may include

1. Dietary or Nutritional Education
2. Exercise (if no fracture found) – help in maintaining bone density and reduce the risk of falls
3. Medication – to slow bone loss and prevent fractures. Osteoporosis medications can fall into 2 categories:
   a) medications that slow or stop bone resorption rate
   b) medications that help increase bone formation
4. Treatment for vertebral fractures which may include:
   a) rest, though long-term rest accelerates bone loss
   b) rigid back braces for supporting the spine
   c) ice or heat and pain medications
   d)surgery such as kyphoplasty or vertebroplasty, which may be necessary in certain conditions where the patient’s fracture is causing severe pain and/or deformity, or the patient has failed to respond to three months of non-surgical treatment

The good news is that even once osteoporosis has been diagnosed, it is still possible to slow bone loss, build bone density and prevent fractures. However, continually advancing osteoporosis and related fractures are not an avoidable outcome after being diagnosed with this disease.