Inflammation

    Inflammation is a normal response
    of the body to protect tissues from
    infection, injury or disease. The
    inflammatory response begins with
    the production and release of
    chemical agents by cells in the
    infected, injured or diseased
    tissue. These agents cause
    redness, swelling, pain, heat and
    loss of function. Inflamed tissues
    generate additional signals that
    recruit leukocytes to the site of
    inflammation. This inflammatory
    response usually promotes healing
    but, if uncontrolled, may become
    harmful.

    The inflammatory response can be
    either acute or chronic. Acute
    inflammation typically lasts only a
    few days. The treatment of acute
    inflammation, where therapy
    includes the administration of
    aspirin and other non-steroidal
    anti-inflammatory agents targeting
    the Cox – 2 enzyme, provides
    relief of pain and fever for patients.

In contrast, chronic inflammation lasts weeks, months or even indefinitely and causes
tissue damage.

CHRONIC INFLAMMATION   
In chronic inflammation, the inflammation becomes the problem rather than the
solution to infection, injury or disease. Chronically inflamed tissues continue to
generate signals that attract leukocytes from the bloodstream. When leukocytes
migrate from the bloodstream into the tissue they amplify the inflammatory response.
This chronic inflammatory response can break down healthy tissue in a misdirected
attempt at repair and healing.

Atherosclerosis is the leading cause of morbidity and mortality in Western societies,
claiming more lives each year than all forms of cancer combined. Coronary heart
disease (CHD) is the most common, and serious, consequence of this disease.

Atherosclerosis is a common and progressive disease of the arteries that results from
inflammation and the buildup of plaque under the inner lining of arteries and swells
into the hollow or lumen of the arteries. This accumulation takes place over years,
even decades, developing slowly and insidiously. Plaque formation begins as fatty
streaks on the inner arterial wall. Over time the fat deposits accumulate and grow,
narrowing the opening of the artery. Surrounding smooth muscle tissue also
proliferates to form larger plaques. The damage from atherosclerosis occurs when the
swelling, called a plaque, becomes large enough to reduce or completely block the
blood flow through the arteries. The artery wall becomes thickened and loses its
elasticity. Any tissue supplied by the blocked artery is in danger. Atherosclerosis,
depending on the location of the artery it affects, may result in heart attack, stroke or
amputation. Atherosclerosis of the blood vessels of the heart is called coronary artery
disease. There are no medications available for physicians to treat directly the
underlying chronic inflammation of atherosclerosis.

According to the American Heart Association, nearly 14 million Americans suffer from
CHD today. It is the single largest killer of American males and females. More than
one in five deaths are from CHD. It is estimated that the cost of CHD in the United
States for 2005 will be $142 billion.

Rheumatoid Arthritis is a common auto-immune disease which affects joints and
arterial blood vessels. Roughly 70% of patients with rheumatoid arthritis are young
and middle-aged women. We treat rheumatoid arthritis in a stepwise escalation,
starting with the occasional to regular use of anti-inflammatory agents such as
aspirin, ibuprofen and Cox – 2 Inhibitors, and proceed in resistant patients to
treatment with toxic drugs that affect the body's immune system, termed Disease
Modifying Anti-Rheumatic Drugs (DMARDS). New DMARDS target the modulation of
Tumor Necrosis Factor-alpha (TNFa), a protein that stimulates a broad range of
cellular activities implicated in the inflammation process, tissue repair and proliferation.

According to the Arthritis Foundation, there are 2.1 million people with rheumatoid
arthritis in the United States.  Rheumatoid arthritis and related diseases cost the U.S.
economy more than $65 billion annually in direct and indirect costs.

Asthma is a common chronic inflammatory disease of the bronchial tubes, which are
the airways in the lungs. Asthma is marked by episodic airway attacks that are
caused by many stresses, including allergy, cold air, ozone or exercise. Asthma
therapy has concentrated on the use of inhaled corticosteroids to reduce chronic
inflammation and bronchodilators to provide symptomatic relief. Asthmatic patients,
however, continue to experience flare-ups, or exacerbations, that are not prevented
or treated by these medicines.

We regularly use anti-inflammatory agents, such as anti-histamines, leukotriene
antagonists and corticosteroids, alone or in combination to treat this disease.
However, these diseases may suddenly flare due to either the tissue inflammation
that underlies them or bacteria that take advantage of the suppressed immune
response induced by present therapies.

Joint Inflammation
Repeated trauma or stress to the joint, incurred during everyday use, athletic
training, or performance, is often the initiating cause of joint inflammation. The
familiar symptoms -— pain, swelling, and heat —- are usually the result of
inflammation in the synovial membrane and joint capsule.  

The initial inflammation usually involves only the soft tissue structures of the joint
(synovial membrane/joint capsule), and cartilage damage is generally not present at
this early stage. The synovial membrane responds to injury by becoming inflamed, a
condition referred to as synovitis. This inflammation allows leukocytes, or white blood
cells, which are normally filtered out of the joint, to invade the joint space.
The inflamed synovial membrane and the leukocytes release destructive enzymes
such as free radicals, cytokines, and prostaglandins, all of which are potentially
damaging to the articular cartilage.

Left untreated, or allowed to recur repeatedly, these inflammatory mediators
produced by the inflamed joint have a degrading or damaging effect upon the
cartilage.
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