Tuesday, July 5, 2011

What is osteoarthritis?


Causes and Symptoms

There are several causes of osteoarthritis (OA), including traumatic injuries,
joint overuse or repetitive movement of a joint, obesity, congenital bone
deformities, and genetic or metabolic diseases such as diabetes or
Paget's
disease of the bone. Other risk factors include old age and
female gender. The most commonly affected joints are in the hands, hips, knees,
and spine. An inherited genetic defect in the production of collagen leads to
defective cartilage and to more rapid joint deterioration. OA in the
hands or hips may be hereditary. OA in the knees and hips is linked to excess
weight, which puts added stress on these joints. Muscle weakness can also
predispose one to OA; thigh strengthening exercises can reduce one's risk of
developing OA in the knees.



In healthy joints, cartilage containing synovial fluid and elastic tissue reduces
friction as joints move. Osteoarthritis develops when the cartilage wears away and
bone rubs against bone. The most prominent symptom of osteoarthritis is joint
pain. Other symptoms include morning stiffness or stiffness after long periods of
immobility. Early in the disease, individuals may experience joint pain after
strenuous exercise. As the disease progresses, joints stiffen and diminished joint
mobility is experienced even with slight activity. As joint mobility decreases,
the muscles surrounding the joint weaken, thereby increasing the likelihood of
further injury to the joint. As the cartilage wears away, crepitus can often be
heard and a grating sensation can be felt as bone moves against bone. The
development of Heberden’s nodes on the distal interphalangeal joints and
Bouchard’s nodes on the proximal interphalangeal joints of the hands is not
uncommon.


Confirmation of osteoarthritis is based on a history of joint pain and physical
findings that indicate arthritic changes in the joints. In a physical examination,
a doctor may check for swelling and joint tenderness under pressure, as well as a
loss of the joint's range of mobility. An X-ray can show a loss of joint space,
osteophytes, bone cysts, and sclerosis of subchondrial bone. Sometimes, a
computed
tomography (CT) scan or magnetic resonance imaging (MRI) may
be helpful in confirming the presence of osteoarthritis and can show the loss of
cartilage.




Treatment and Therapy

The goal of treatment for OA is to preserve physical function and reduce pain.
Education, physical therapy, and occupational
therapy are instrumental in maintaining independence and
improving muscle strength around affected joints. Pacing activities to avoid
overexertion of the affected joints is an effective means to prevent further pain
and injury. Heat therapies such as warm soaks, paraffin, and mud treatments may
help to lessen the discomfort in tender joints. Moderate exercise such as walking,
swimming, strength training, and stretching all may help to maintain mobility in
arthritic joints and to improve posture and balance. Relaxation techniques, stress
reduction activities, and biofeedback may also be helpful.


Over-the-counter topical analgesic ointments may help to reduce joint swelling and
pain. Acetaminophen is very effective for controlling OA pain. However, persons
who take blood-thinning medicines, have liver disease, or consume large amounts of
alcohol should use acetaminophen with caution. Nonsteroidal anti-inflammatory
drugs (NSAIDs) such as ibuprofen and naproxen are also
effective for pain relief, but they may cause gastrointestinal bleeding. This
class of drugs selectively blocks the enzyme COX-2, thus controlling the
production of prostaglandins, natural chemicals that contribute to body
inflammation and cause the pain and swelling of arthritis.
Since they do not block the COX-1 enzyme cyclooxygenase-1, which is present in the
stomach and inflammation sites, the natural mucous linings of the stomach and
intestine are protected, thereby reducing the incidence of upset, ulceration, or
bleeding; however, COX-2 selective inhibitors increase the rate of cardiovascular
events such as heart attacks and stroke. Any medication used to treat OA should be
taken under the direction of a health care provider.


Glucosamine and chondroitin naturally occur in the body. Both have been promoted for the treatment of OA. Glucosamine may promote the formation and repair of cartilage, while chondroitin may promote water retention and elasticity in cartilage and prevent cartilage breakdown. However, recent studies indicate that taking glucosamine for arthritis may increase a patient's risk of developing glaucoma.


When interventions to relieve symptoms of OA no longer work, an orthopedic surgeon
may inject cortisone or hyaluronic acid into joint spaces. Hyaluronic acid is used
to replace the synovial fluid that a joint has lost in order to maintain knee
movement without pain. Cortisone may be injected into affected joint spaces to
provide temporary relief of joint pain. Surgical intervention to trim torn and
damaged cartilage from joint spaces, to partially or totally replace severely
damaged joints in the knees and hips, or to fuse bones together are effective
treatments in the most severe, debilitating stages of OA. Realignment of a joint
(osteotomy) and joint replacement surgery other possible procedures.




Perspective and Prospects

Arthritis comprises more than one hundred diseases and conditions and is the major
cause of disability in the United States. The incidence of OA increases with age,
but it can affect individuals as young as eighteen. According to the Arthritis
Foundation, approximately twenty-seven million people in the United States have
OA, and it is the most common form of arthritis. OA affects nearly 14 percent of
US adults over the age of twenty-five and more than 33 percent of adults over the
age of sixty-five, according to the US Centers for Disease Control and Prevention.
In 2010, hip and knee OA ranked as the eleventh highest contributor to global
disability. OA is three times more common among women, although before forty-five
years of age, it is more common in men. There is no cure for OA, but a healthy
diet, regular exercise and physical therapy, weight control, and the use of
medications are measures that can slow its progress and maintain joint function.




Bibliography


Ali, Naheed.
Arthritis and You: A Comprehensive Digest for Patients and
Caregivers
. Lanham: Rowman, 2013. Print.



Brower, Anne C.
Arthritis in Black and White. Philadelphia: Elsevier
Saunders, 2012. Print.



Cross, Marita, et al. "The Global Burden of
Hip and Knee Osteoarthritis: Estimates from the Global Burden of Disease
2010 Study." Annals of the Rheumatic Diseases 73.7 (2014):
1323–30. Print.



Foltz-Gray, Dorothy.
The Arthritis Foundation’s Guide to Good Living with
Osteoarthritis
. 2nd ed. Atlanta: Arthritis Foundation, 2004.
Print.



Juhl, C., et al. "Impact of Exercise Type and
Dose on Pain and Disability in Knee Osteoarthritis: A Systematic Review and
Meta-Regression Analysis of Randomized Controlled Trials." Arthritis
and Rheumatology
66.3 (2014): 622–36. Print.



Lane, Nancy E., and
Daniel J. Wallace. All about Osteoarthritis: The Definitive Resource
for Arthritis Patients and Their Families
. New York: Oxford UP,
2002. Print.



Firestein, Gary S., et al.
Kelley's Textbook of Rheumatology. 9th ed. Philadelphia:
Elsevier, 2013. Print.



Nelson, Miriam E., et
al. Strong Women and Men Beat Arthritis. New York:
Putnam’s, 2002. Print.



Sayce, Valerie, and
Ian Fraser. Exercise Beats Arthritis: An Easy to Follow Program of
Exercises
. Palo Alto: Bull, 1998. Print.



Sutton, Amy L., ed.
Arthritis Sourcebook: Basic Consumer Health Information About
Osteoarthritis, Rheumatoid Arthritis, Other Rheumatic Disorders,
Infectious Forms of Arthritis, and Diseases with Symptoms Linked to
Arthritis
. 2nd ed. Detroit: Omnigraphics, 2004.
Print.



Yelin, E. “The
Economics of Osteoarthritis.” Osteoarthritis. Ed. K.
Brandt, M. Doherty, and L. Lohmander. New York: Oxford UP, 1998.
Print.

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