What is Osteoarthritis (OA)?
Of the more than 100 forms of arthritis, osteoarthritis (OA) is the most common, and one of the most pervasive of all chronic pain conditions. Also known as degenerative arthritis or degenerative joint disease, OA is an active inflammatory process, both mechanical and biological, that destabilizes the normal process of breakdown and regeneration of cartilage cells. This destabilization can be initiated by many factors, including genetic, developmental, metabolic and traumatic events. One thing is clear: OA causes degeneration that involves all the joint tissues (cartilage, bone, synovial cavity, ligaments and muscle), eventually wearing away all protective materials and resulting in joint failure.

Misleadingly coined the “wear and tear” disease, OA has been shown to be much more complex. In fact, exercise actually strengthens cartilage by promoting balance between the natural process of synthesizing new cartilage cells and breaking down old ones and is a first line treatment for those with OA. Not only do metabolic imbalances play a role in the developments of OA, but aberrations in other parts of the joint are clearly part of the processes that lead to progressive joint degeneration. In addition, active tissue within the cartilage itself makes destructive enzymes and inflammatory molecules during the OA disease process.

OA affects nearly 27 million people in the US, accounting for 25 percent of primary care visits and half of all nonsteroidal anti-inflammatory drug (NSAID) prescriptions. An estimated 80 percent of the population will have radiographic evidence of OA by age 65, although on 60 percent of those will have symptoms.
Osteoarthritis was the second-most expensive condition seen in US hospital stays in 2011, costing in aggregate $14.8 billion for approximately 964,000 hospitalizations. By payer, it was the second-most costly condition billed to Medicare and private insurance.

What causes OA?
Risk factors for OA such as age, gender, trauma, overuse, genetics and obesity can each make contributions to the process of injury in different compartments of the joint. These factors are promote abnormal biochemical processes involving the cartilage, bone and synovium, which over a period of years result in the characteristic features of OA: degradation of articular cartilage, osteophyte formation, subchondral sclerosis, meniscal degeneration, bone marrow lesions and synovial proliferation. These risk factors themselves vary according to the affected joint—hand, neck, hip, knee or spine.


Age is the risk factor most commonly correlated with OA. Age-related mechanical stress on joints can arise because of altered gait, muscle weakening, changes in the body’s ability to sense movement within joints and joint position (propriocieption), and weight changes. In addition, changes may occur due to a declining ability of the cartilage’s healthy cells (chondrocytes) to maintain and repair cartilage tissue. Chondrocytes also have a long life, so they repair and regenerate themselves much less often than other cells. The lack of turnover in cartilage cells makes them especially susceptible to the damaging effects of reactive oxygen species, known as free radicals.


The occurrence of hip OA is slightly higher in men, though after the age of 50 there is a marked increase in prevalence in women, specifically in the knee. This is understood to be a result of diminishing estrogen levels. This correlates with the increased incidence of osteoporosis in women after menopause, when estrogen levels recede. Though hormone replacement therapy has been a successful adjunct therapy in some, HRT carries its own health risks.


A serious jolt to a joint can predispose a person to OA. Research shows that 10 to 20 years after a serious injury to the knee about 50 percent of patients will develop OA. Twelve percent of end-stage OA, where there is little or no cartilage left, severe pain and loss of function in the hip, knee and ankle is due to injury. Severe trauma can set in motion a complex biological and chemical reaction wherein cartilage cells begin to die and various proteins released cause altered cell regulation, inflammation and increased bone cell turnover, which can cause bone thinning or bone spurs.


There is a genetic predisposition to OA, though it is difficult to measure since OA is so prevalent in the general population. There are multiple genetic factors that can contribute to development of OA, but they differ according to the specific joint affected (hand, neck, hip, knee or spine), and are also influenced by gender and race. Several specific genes have been identified in tracking disease risk, and several chromosomes have been found to be likely to harbor these genes. Specifically, genes for proteins that regulate inflammation are associated with susceptibility to OA in some joints. Many of these discoveries have pointed to the role of inflammatory pathways, particularly in the pathology of knee OA. Though no interventions are currently available for those found to be at risk from genetic predisposition, it is hoped that further research will produce new treatments and risk predictions based on genetic profiles.


An increase in pressure across weight-bearing joints in people who are obese is the primary factor leading to joint degeneration, especially because obese people tend to have misaligned joints, also caused by carrying extra weight. However, fat cells also produce hormones, such as leptin and cytokines, and other chemicals that have been show to narrow joint space in the hip and produce inflammation. Another hormone produced by fat cells is adiponectin. Obesity causes the fat cells to produce less adiponectic, which plays a protective role in the joints. So the abnormalities produced by the fat cells of the obese do as much harm as the extra carrying of weight. This explains why overweight and obese people also have a higher risk for OA in non-weight-bearing joints, such as those of the hand.


Pain: Persistent joint pain may occur during or after movement. As the disease progresses, pain can become constant with no stimuli. It can also become severe. Effective pain relief may require using a number of analgesics or pain-relieving strategies together. The complexity of multiple pain pathways and processes often means that two or more treatments may have and additive effect on the different components of the pain response. This technique is known as balanced or multimodal analgesia.
By tackling pain early and effectively it is hoped that the development of chronic pain can be stopped. Timing of analgesia is important. Regular analgesia will be appropriate if the pain is constant. Taking the analgesia before exercise can help pain with exertion. Some patients will need palliative care for their joint pain. For these individuals long-term opioids may be appropriate.

Referred pain:
An arthritic joint can cause pain to radiate to other regions of the body, e.g., an arthritic hip joint can cause pain to be felt in the buttocks, groin, thigh or knee. Spinal arthritis can cause pain to radiate to the neck or limbs.

The joint may feel tender with the application of even light pressure.

Stiffness, joint deformity:
Joint stiffness may be most noticeable upon waking in the morning or after a period of inactivity. This phenomenon is known as gelling. Joints may change in shape as the disease progresses.

The joint may swell as the body’s own attempt to prevent further joint use.

The joint may feel warm to the touch. This is due to the body’s inflammatory response.

Loss of flexibility:
Movement may be impossible, or range of motion may be limited.

Grating, grinding sensation:
A sensation of grating or grinding may be felt or heard.

The joint may feel loos or unstable due to missing cartilage or damaged ligaments. The joint is losing its support structure.

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

When the disease becomes severe, bones rub on bones and create rough edges that catch on one another. Joint locking can also be caused by loose material in the knee like cartilage or bone fragments.

Radiological evidence:
Joint space loss, osteophyte formation, subchondral bone thickening or cyst formation.

Spotlight: Osteoarthritis of the hand and fingers

OA of the hands is not only painful, but it can be particularly disabling. When the cartilage in a finger joint degenerates, the bone next to it becomes inflamed and is stimulated to produce new bone. This new bone many times comes in the form of a calcified bony protrusion called a bone spur. At the smallest joint on the end of the fingers it is called a Hegerden’s node. When a node occurs at the middle joint it is called a Bouchard’s node, both deformities named for the doctors who first identified them. Though not necessarily painful themselves, their presence and the swelling they produce can make it almost impossible to bend and move the fingers. They can also cause pain, numbness, tenderness and weakness in the surrounding tissue. The pain can feel dull or burning, and presents upon increased joint use, sometimes hours later. Small mucous cysts may develop on the end joints of the fingers, causing ridges or dents in the nail plates.


Diagnosis of osteoarthritis can be made by a primary care physician or rheumatologist and may include:

  • Medical history and physical
  • Joint pain index
  • Traumatic injuries report
  • Checking for swelling, redness or heat, tender points and rashes
  • Checking for nodes and all other visible or reported symptoms
  • Imaging

X-rays will confirm a diagnosis of arthritis, but to distinguish a case of osteoarthritis the physician will be looking for:

  • Narrowing between joints (joint space), due to loss of cartilage
  • Bone spurs
  • Distribution of irregularities on one side (one knee or one side of the hip)
  • Cysts in the bone beneath the joint surface
  • Imaging of the hand can be especially helpful in diagnosing OA
  • Laboratory Testing

If the physician is unsure of the nature of joint swelling, a joint aspiration may be performed. A needle is inserted into the join to withdraw synovial fluid from the joint. The fluid is tested for chemistry, viscosity, blood cell count, appearance and microorganisms (to rule out infection).
In an OA patient the fluid is clear; in an RA patient it will be cloudy because of a high number of white blood cells. The fluid is tested for crystals to rule out a diagnosis of gout, another type of arthritis that is caused by high levels of uric acid in the blood. Blood and urine tests may also be ordered to rule out gout.

Treatment options
There are currently no treatments for OA that modify disease progression. Treatment is palliative and preventative at present.

An exercise/physical activity program
tailored to the individual should be a core treatment for people with OA regardless of age, comorbidity, pain severity and disability. Exercise should include local muscle strengthening, stretching and general aerobic fitness. Strengthening the muscles around the affected joint helps make the joint more stable and reduces the likelihood of further degeneration. Keeping the joint moving might be painful at first, but after loosening and warming up, movement facilitates the rebuilding of cartilage and also keeps muscles from atrophying. In addition, isometric exercise—tensing the muscles for a period of time without actually moving them—will increase muscle size and strength. Exercises that put pressure on or may jolt the joints, like jogging, playing tennis or anything that involves jumping, are not for the person with OA. Swimming in a heated pool and walking in a flat area—gentle movement—are best.

Weight loss
will lessen pain and reduce stress on weight-bearing joints. It will also help correct body chemistry that goes awry in obese patients and causes additional joint damage, inflammation and pain. Weight loss also increases self-esteem and reduces the anxiety and depression that many times comes with a chronic pain condition.

Heat therapy
works best with a moderate temperature and used over the muscles adjacent to the joint. Never apply heat for more than 20 minutes.

  • Heating pads
  • Hot packs
  • Moist heat: warm towels, warm showers or bathes, a heated whirlpool

Cold therapy works by numbing the local tissue. Ice and cold packs should never be placed directly onto the skin. Do not use cold therapy for more than 20 minutes, and be careful not to make the joint overly cold, as making the joint numb increases the risk of overusing it.

Analgesics, anti-inflammatory drugs and injections

As with all pain relievers, there are risks involved. A physician should monitor even the use of over-the-counter medications.

  • Acetaminophen (Tylenol) is generally considered safe, though it can pose some risk to kidneys or to the liver in some people with liver disease
  • Aspirin, a mild form of nonsteroidal anti-inflammatory drug (NSAID)
  • Prescription NSAIDs can have some side effects that must be dealt with, such as GI problems. Sometimes, taking them with food or using antacids can help with these side effects.
  • Topical NSAIDS
  • Muscle relaxants
  • OTC topical creams and sprays (do not use with heat or cold therapy)
  • Opioids for severe pain
  • Joint injections of corticosteroids
  • Injectable hyaluronic acid

Transcutaneous electrical nerve stimulation sends small electrical pulses to painful areas.
Physical therapy: A physical therapist can teach people with OA how to move in a way that prevents further damage to the joints, help create a strengthening exercise program and perform therapeutic massage and movement therapy.
Occupational therapy: An occupational therapist can assess the home environment and recommend physical changes that can make it safer, more comfortable and easier to move through.
Psychotherapy: Psychiatrists, psychologists and social workers can help people with OA cope with stress. They can also work with families and caregivers to help them understand and appreciate what their loved one is going through and how best to help.
Surgery: Surgery is considered a last, but many times appropriate, resort for people who have severe, intractable pain, marked joint instability and significant disability making it difficult or impossible to take care of their own daily needs.

Adjunctive and Complementary Therapy

Aids and devices

  • Footwear, bracing, joint support and walking aids
  • Splinting for those with hand osteoarthritis
  • Jar, door knob and faucet turners
  • Cervical collars
  • Orthopedic pillows
  • Foot stools
  • Reclining chairs
  • Reaching devices
  • Bathroom aids such as raised toilets and handrails

Integrative therapies

  • Meditation
  • Mindfulness training
  • Cognitive-behavioral therapy emphasizing pain management
  • Dealing with depression
  • Deep abdominal breathing
  • Progressive muscle relaxation
  • Visualization and guided imagery
  • Tai chi
  • Acupuncture
  • Biofeedback

The use of glucosamine or chondroitin products is not recommended for the treatment of osteoarthritis.

Joint protection

Further damage to the joints can be avoided by:

  • Resting inflamed joints by reducing loading, time in use and repetitions.
  • Using the largest muscles and joints that can do the job, like standing up from a
    chair using hips and knees rather than pushing up with hands.
  • Using proper movement techniques for lifting, sitting, standing, bending and reaching.
  • Using appliances, gadgets and modifications for home equipment to minimize stress on joints. Examples include raising the height of a chair to make standing and sitting easier, using a smaller kettle with less water, boiling potatoes in a sieve to facilitate removal when cooked.
  • Planning the week ahead to anticipate difficulties.
  • Using biomechanics and ergonomics to best effect. This includes good posture, aligning joints correctly, taking frequent breaks from sitting at a computer and avoiding staying in one position for an extended period of time.
  • Balancing activity with rest and organizing the day to pace activities.
  • Simplifying tasks.
  • Recruiting others to help.
  • Making exercise a part of everyday life including exercises that improve joint range of motion, stamina and strength. Exercise should also be used for cardiovascular fitness and to maintain or improve balance.

Future treatment possibilities
Scientists and researchers are working on a class of medications know as disease-modifying osteoarthritis drugs (DMOADs). There are several clinical trials testing these chemicals designed to block the effects of inflammatory cytokines. However, the slow progression of OA makes measurement of symptoms difficult over the short periods of time typically allotted to clinical trials.
A new MRI technique called delayed gadolinium-enhanced MRI of cartilage (dGEMRIC) is helping with early detection. In addition, new ways of rebuilding cartilage, including the use of stem cells and fat-derived cartilage are being studied.

Osteoarthritis is more common in older age groups and therefore it is more likely that other conditions will coexist: this raises several issues.

  • A patient’s ability to adhere to an exercise program if, for example, angina, chronic obstructive pulmonary disease, previous stroke or obesity is present.
  • Polypharmacy issues. Drugs taken for other conditions can influence the choice of drug treatments for osteoarthritis.
  • Other medical conditions can influence the choice of treatments for osteoarthritis, such as a history of duodenal ulcer, chronic kidney impairment, heart failure and liver problems.
  • The risk of falls increases with polypharmacy, increasing age, osteoarthritis and other medical conditions.
  • The presence of severe comorbid conditions may influence the decision to perform joint replacement surgery.
  • Prognosis of osteoarthritis disability is worse in the presence of two or more comorbidities.
  • Quality of sleep can be adversely affected by osteoarthritis and other comorbid conditions.
  • Depression can accompany any chronic or long-term condition. Screening should be undertaken in primary care and general hospital settings for depression in high-risk groups, for example, those with significant physical illnesses causing disability.

Best Nutrition
As with all forms of arthritis, reducing inflammation is key. A diet rich in omega-3 fatty acids and low in inflammation-producing foods is recommended. Think smaller portions and more green leafy vegetables, less sugar, fewer processed foods and less fat. If overweight, your physician or a dietician can help you create a weight-loss plan that includes lowering caloric intake coupled with exercise.

Best Exercise Regime

  • Moderate, gentle physical exercise
  • Stretching
  • Physical therapy
  • Strength training for joint support
  • Weight control

Support and Resources
The Arthritis Foundation
Arthritis Foundation Online Community