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Treatments for Arthritis Overview Arthritis (Rheumatoid
Arthritis, Osteoarthritis) is a progressive, chronic condition
classified as an inflammatory disease and autoimmune disorder that
affects about 1.3 million Americans. For some of these people, arthritis
may emerge after a specific injury or repetitive use of one or more
joints. For others, arthritis results from the immune system incorrectly
attacking the synovium, or the thin layer of tissue that lines the
joints. In any case, arthritis is never simply a part of normal aging. In Rheumatoid Arthritis
(RA), the joints of the hands, wrists, elbows, knees and ankles are
commonly affected by inflammation. RA also tends to occur symmetrically,
meaning that if one hand has damage to the joints, then the opposite
hand will also be affected. However, RA is also a systemic condition and
can affect other organs, including the heart, lungs and even the skin.
Conversely, osteoarthritis (OA), also known as ‘degenerative
arthritis,’ is localized to the affected joint and the impact on the
synovium remains targeted to the site. Researchers believe that
the mechanism of both RA and OA is basically the same and involves
impaired collagen synthesis and dysfunctional proteoglycans, the
specialized proteins that make up cartilage that surrounds each joint.
In the absence of arthritis, the cartilage absorbs shock from the joint
by releasing water to create a protective barrier. Meanwhile, the
synovial tissue secretes a special fluid to lubricate the cartilage and
keep it smooth. However, when this normal process is interrupted in the
early stages of OA, the cartilage retains water, becomes inflamed and
slowly deteriorates. Eventually, the very bone the cartilage was
designed to protect will form cavities and calcium overgrowths known as
osteophytes, resulting in pain with movement. In the later stages, OA
may progress to the point that pain is experienced even when at rest. Currently, there is no
cure for arthritis. However, it is imperative that aggressive treatments
begin at the first sign of symptoms to help avoid serious complications
later, including disability or deformity. In addition, simple blood
tests will determine if you are at specific risk for becoming
susceptible to an advanced form of the disease by checking for the
presence of antibodies to rheumatoid factor (RF) or cyclic citrullinated
proteins (anti-CCP). Patients diagnosed with RA, whether they test
positive for antibodies or not, are generally at increased risk for
developing other autoimmune disorders, as well as cardiovascular and
kidney disease. Symptoms and Diagnosis
of Arthritis The symptoms may be
different from one person to another and depends on whether the
inflammatory condition is due to OA or RA, but the typical signs of
arthritis include: - Swelling, redness or
tenderness of the joints - Decreased range of
motion - General stiffness - Fatigue - Muscle aches - Fever While blood tests may
reveal the presence of RA antibodies, not everyone that tests positive
develops RA. Furthermore, there are no standard lab tests that can rule
out arthritis over other joint diseases. Therefore, diagnosis is made
based on a physical examination, a review of medical history, and an
account of the symptoms experienced. However, there are certain blood
tests that can help confirm the physician’s findings in addition to
testing for antibodies, such as: - A blood test for
c-reactive protein, which measures the degree of inflammation present. - An ESR test (also known
as the Biernacki Reaction),
which determines erythrocyte sedimentation rate, or the rate at which
red blood cells precipitate
and form sediment in the bottom of a test tube in the span of one hour.
An elevated rate indicates a high level of fibrogen, a protein that
causes blood cells to stick together to form clots. content and a
greater degree of inflammation. In addition, X-rays or
magnetic resonance imaging (MRI) may be used to help determine the
degree of damage to the synovium and inflammation in the joints. Conventional Therapies Conventional treatment
for arthritis usually involves the use of medications that can be broken
down into three main types: NSAIDS:
Nonsteroidal anti-inflammatory drugs to reduce inflammation. This
includes over-the-counter medications, such as aspirin or ibuprofen.
Some prescription medications in this class, however, have recently been
found to increase the risk of heart attack or stroke and have been
removed from the market. Corticosteroids: Corticosteroid
medications (i.e., prednisone) may be prescribed in order to
quickly reduce inflammation. However, many of the drugs in this class
can produce serious side effects and, for this reason, are usually given
for a short duration. DMARDs: Disease-modifying antirheumatic drugs attempt to slow the progression of the disease by suppressing the immune system.
Complimentary
Therapies Massage: Many Western
physicians are beginning to suggest massage therapy for their arthritis
patients. Studies have shown that massage therapy can relieve muscle
ache and joint pain, while reducing stress hormones. Massage also
promotes an increased production of endorphins, the body’s natural
painkillers. Acupuncture: This therapy
is based on belief in Traditional Chinese Medicine (TCM) that disease is
the result of an imbalance of energy in the body. In acupuncture,
needles are used to stimulate the 14 meridian points, which are seen as
the channels in which energy travels in the body. As with massage,
research has shown that this form of therapy also increases endorphin
release, as well as other pain-relieving neurotransmitters. Acupressure: Also known
as Shiatsu, this form of therapy
is also based on the TCM system of meridian points referenced in
acupuncture. However, rather than using needles to stimulate these
points, the practitioner using pressure techniques with the thumb,
forefinger and palm of the hands. Recommended
Supplements in the Treatment of Arthritis Even Western allopathic
physicians recognize the importance of diet and nutrition to combat the
oxidative damage and progressive degeneration associated with arthritis.
In addition, unlike NSAID therapy, nutritional therapy strives to
address the underlying cause of this disease by providing natural
antioxidants and anti-inflammatory agents that minimize the action of
inflammatory cytokines and promote collagen synthesis. Omega-3 The
result of more than 20 years of research has established that omega-3
fatty acids are of excellent benefit for arthritis sufferers. Of
particular benefit are the fatty acids eicosapentaenoic
acid (EPA) and docosahexaenoic acid (DHA), which improve overall
metabolic functioning while decreasing levels of inflammation-producing
cytokines. S-adenosylmethionine
(SAM-e) SAM-e is the active form
of the amino acid methionine, which is manufactured by the body from
adenosine triphosphate and methionine before being converted into
cysteine. Studies have shown that SAM-e protects the synovium by
blocking certain enzymes responsible for cartilage breakdown. In
addition, research indicates that SAM-e may help to restore joint
cartilage and lining since it stimulates cell growth and the production
of specialized proteins known as proteoglycans. SAM-e also seems to be
better tolerated than either naproxen or piroxicam. However, since SAM-e
is not generally well absorbed, the enteric-coated tablets are
recommended. Helpful Herbs in the
Treatment of Arthritis Borage Borage seed oil is a rich
source of gamma-linoleic acid (GLA), which possess anti-inflammatory
qualities. Specifically, GLA goes to work by blocking the action of
arachidonic acid, which is found in animal proteins. Otherwise, this
acid would be converted in the body into leukotrienes and other
prostaglandins, which mediate inflammation. GLA also blocks the action
of another inflammatory mediator known as tumor necrosis factor-alpha by
synthesizing into the prostaglandin precursor dihomo-gama-linolenic acid
(DGLA). Evening Primrose Oil Evening primrose oil is
also high in GLA content. In fact, this botanical offers one of the best
modes of bioavailability of GLA. As such, it delivers similar benefits
to that which borage seed oil provides. Ashwagandha Ashwagandha is well known
in Ayurvedic medicine as a potent treatment for rheumatoid arthritis
because the extract obtained from the root and berry of the plant
possess anti-inflammatory, antioxidant and immunomodulatory properties.
Studies have shown that the active constituents of this herb seem to
target and inhibit cyclooxygenase, as well as being compared to
hydrocortisone sodium succinate in efficacy. Curcumin The
active component of turmeric, curcumin
has demonstrated an ability to inhibit several inflammatory mediators,
including cytokines, lipoxygenase enzyme, and COX-2. Curcumin also
blocks the action of collagenase, hyaluronidase, and elastase, which
play a role in cartilage deterioration. Capsaicin Commonly known as cayenne
or chili pepper, capsaicin is formulated into a topical application to
be absorbed via the skin. This substance is valued for its pain-reducing
effect by inhibiting the action of an agent called substance P, a
neurotransmitter that signals pain to the brain. Nettle
References
Mori TA, Beilin LJ. Omega-3 fatty acids and inflammation. Curr Atheroscler Rep. 2004 Nov;6(6):461-7. Zak A, Tyrzicka E, et al. Pathophysiology of and clinical significance of polyunsaturated fatty acids n-3 family [in Czech]. Cas Lek Cesk. 2005;144(suppl 1):6-18. Caruso
I, et al. Italian double blind multicenter study comparing S-adenosylmethionine,
naproxen and placebo in the treatment of degenerative joint disease. Am
J Med 1987;83:66-71. Maccagno A. Double-blind controlled clinical trial of oral S-adenosylmethionine versus piroxicam in knee osteoarthritis. Am J Med 1987;83:72-7. Osteoarthritis: the clinical picture, pathogenesis, and management with studies on a new therapeutic agent, S-adenosylmethionine. Proceedings of a symposium. Am J Med 1987;83:1-110. di Padova C. S-adenosylmethionine in the treatment of osteoarthritis. Review of the clinical studies. Am J Med 1987;83:95-103. Bradley JD, et al. A randomized, double blind, placebo controlled trial of intravenous loading with S-adenosylmethionine (SAM) followed by oral SAM therapy in patients with knee osteoarthritis. J Rheumatol 1994;21:905-11. Leventhal LJ, et al. Treatment of rheumatoid arthritis with gamma-linolenic acid. Ann Intern Med 1993;119:867-73. Zurier RB, et al. Gamma-linolenic acid treatment of rheumatoid arthritis. A randomized, placebo-controlled trial. Arthritis Rheum 1996;39:1808-17. Kast RE. Borage oil reduction of rheumatoid arthritis activity may be medicated by increased cAMP that suppresses tumor necrosis factor-alpha. International Immunopharmacol 2001;2197-99. Belch JJ, Hill A. Evening primrose oil and borage oil in rheumatologic conditions. Am J Clin Nutr 2000;71:352S-6S. Kulkarni RR, Patki PS, Jog VP, et al. Treatment of osteoarthritis with a herbomineral formulation: a double-blind, placebo-controlled, cross-over study. J Ethnopharmacol. 1991;33:91-5. Plummer SM, Holloway KA, et al. Inhibition of cyclo-oxygenase 2 expression in colon cells by the chemopreventive agent curcumin involves inhibition of NF-kappaB activation via the NIK/IKK signalling complex. Oncogene. 1999 Oct 28;18(44):6013-20. Banerjee M, Tripathi LM, et al. Modulation of inflammatory mediators by ibuprofen and curcumin treatment during chronic inflammation in rat. Immunopharmacol Immunotoxicol. 2003 May;25(2):213-24. Joe B, Lokesh BR. Effect of curcumin and capsaicin on arachidonic acid metabolism and lysosomal enzyme secretion by rat peritoneal macrophages. Lipids. 1997 Dec;32(11):1173-80. McCarthy GM, et al. Effect of topical capsaicin in the therapy of painful osteoarthritis of the hands. J Rheumatol 1992;19:604-7. Obertreis B, Ruttkowski T, et al. Ex-vivo in-vitro inhibition of lipopolysaccharide stimulated tumor necrosis factor-alpha and interleukin-1 beta secretion in human whole blood by extractum urticae dioicae foliorum. Arzneimittelforschung. 1996 Apr;46(4):389-94. Schulze-Tanzil G, de SP, et al. Effects of the antirheumatic remedy hox alpha—a new stinging nettle leaf extract—on matrix metalloproteinases in human chondrocytes in vitro. Histol Histopathol. 2002 Apr;17(2):477-85. |
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