Is a group of diseases and mechanical abnormalities entailing degradation of joints,  including articular cartilage and the subchondral bone next to it. Clinical symptoms of OA may include joint pain, tenderness, stiffness, inflammation, creaking, and locking of joints. In OA, a variety of potential forces — hereditary, developmental, metabolic, and mechanical — may initiate processes leading to loss of cartilage — a strong protein matrix that lubricates and cushions the joints. As the body struggles to contain ongoing damage, immune and regrowth process can accelerate damage. When bone surfaces become less well protected by cartilage, subchondral bone may be exposed and damaged, with regrowth leading to a proliferation of ivory-like, dense, reactive bone in central areas of cartilage loss, a process called eburnation. The patient increasingly experiences pain upon weight bearing, including walking and standing. Due to decreased movement because of the pain, regional muscles may atrophy, and ligaments may become more lax.  OA is the most common form of arthritis, and the leading cause of chronic disability in the United States.

“Osteoarthritis” is derived from the Greek word “osteo“, meaning “of the bone”, “arthro“, meaning “joint”, and “itis“, meaning inflammation, although many sufferers have little or no inflammation. A common misconception is that OA is due solely to wear and tear, since OA typically is not present in younger people. However, while age is correlated with OA incidence, this correlation merely illustrates that OA is a process that takes time to develop. There is usually an underlying cause for OA, in which case it is described as secondary OA. If no underlying cause can be identified it is described as primary OA. “Degenerative arthritis” is often used as a synonym for OA, but the latter involves both degenerative and regenerative changes.

OA affects nearly 27 million people in the United States, accounting for 25% of visits to primary care physicians, and half of all NSAID (Non-Steroidal Anti-Inflammatory Drugs) prescriptions. It is estimated that 80% of the population will have radiographic evidence of OA by age 65, although only 60% of those will show symptoms. In the United States, hospitalizations for osteoarthritis soared from about 322,000 in 1993 to 735,000 in 2006.

OA affects nearly 21 million people in the United States, accounting for 25% of visits to primary care physicians, and half of all NSAID (Non-Steroidal Anti-Inflammatory Drugs) prescriptions. It is estimated that 80% of the population will have radiographic evidence of OA by age 65, although only 60% of those will be symptomatic. Some investigators believe that mechanical stress on joints underlies all osteoarthritis, with many and varied sources of mechanical stress, including misallignments of bones due to congenital or pathogenic causes; mechanical injury; being overweight; loss of strength in muscles supporting joints; and impairment of peripheral nerves, leading to sudden or uncoordinated movements that overstress joints.

Primary

This type of OA is a chronic degenerative disorder related to but not caused by aging, as there are people well into their nineties who have no clinical or functional signs of the disease. As a person ages, the water content of the cartilage decreases due to a reduced proteoglycan content, thus causing the cartilage to be less resilient. Without the protective effects of the proteoglycans, the collagen fibers of the cartilage can become susceptible to degradation and thus exacerbate the degeneration. Inflammation of the surrounding joint capsule can also occur, though often mild (compared to that which occurs in rheumatoid arthritis). This can happen as breakdown products from the cartilage are released into the synovial space, and the cells lining the joint attempt to remove them. New bone outgrowths, called “spurs” or osteophytes, can form on the margins of the joints, possibly in an attempt to improve the congruence of the articular cartilage surfaces. These bone changes, together with the inflammation, can be both painful and debilitating.

Secondary

This type of OA is caused by other factors but the resulting pathology is the same as for primary OA:

• Congenital disorders, such as:the chronica; disease
  • Congenital hip luxation
  • People with abnormally-formed joints (e.g. hip dysplasia (human)) are more vulnerable to OA, as added stress is specifically placed on the joints whenever they move. [However, recent studies have shown that double-jointedness may actually protect the fingers and hand from osteoarthritis.]
• Cracking joints
• Diabetes.
• Inflammatory diseases (such as Perthes’ disease), (Lyme disease), and all chronic forms of arthritis (e.g. costochondritis, gout, and rheumatoid arthritis). In gout, uric acid crystals cause the cartilage to degenerate at a faster pace.
• Injury to joints, as a result of an accident.
• A joint infection, e.g. from an injury.
• Hormonal disorders.
• Ligamentous deterioration or instability may be a factor.
• Obesity. Obesity puts added weight on the joints, especially the knees.
• Sports injuries, or similar injuries from exercise or work. Certain sports, such as running or football, put undue pressure on the knee joints. Injuries resulting in broken ligaments can lead to instability of the joint and over time to wear on the cartilage and eventually osteoarthritis.
• Pregnancy
• Alkaptonuria
• Hemochromatosis and Wilson’s disease

Diagnosis

Diagnosis is normally done through x-rays. This is possible because loss of cartilage, subchondral (”below cartilage”) sclerosis, subchondral cysts from synovial fluid entering small microfractures under pressure, narrowing of the joint space between the articulating bones, and bone spur formation (osteophytes) – from increased bone turnover in this condition, show up clearly on x-rays. Plain films, however, often do not correlate well with the findings of physical examination of the affected joints.

With or without other techniques, such as MRI (magnetic resonance imaging), arthrocentesis and arthroscopy, diagnosis can be made by a careful study of the duration, location, the character of the joint symptoms, and the appearance of the joints themselves. As yet, there are no methods available to detect OA in its early and potentially treatable stages.

In 1990, the College of Rheumatology, using data from a multi-center study, developed a set of criteria for the diagnosis of hand osteoarthritis based on hard tissue enlargement and swelling of certain joints. These criteria were found to be 92% sensitive and 98% specific for hand osteoarthritis versus other entities such as rheumatoid arthritis and spondyloarthropities

Related pathologies whose names may be confused with osteoarthritis include pseudo-arthrosis. This is derived from the Greek words pseudo, meaning “false”, and arthrosis, meaning “joint.” Radiographic diagnosis results in diagnosis of a fracture within a joint, which is not to be confused with osteoarthritis which is a degenerative pathology affecting a high incidence of distal phalangeal joints of female patients.

Treatment

Generally speaking, the process of clinically detectable osteoarthritis is irreversible, and typical treatment consists of medication or other interventions that can reduce the pain of OA and thereby improve the function of the joint.

Conservative care

No matter the severity or location of OA, conservative measures such as weight control, appropriate rest and exercise, and the use of mechanical support devices are usually beneficial. In OA of the knees a knee braces can be helpful. A cane, or a walker can reduce pressure on involved leg joints which can be helpful for walking and support. Regular exercise, if possible, in the form of walking or swimming, or other low impact activities are encouraged. Applying local heat before, and cold packs after exercise, can help relieve pain and inflammation, as can relaxation techniques. Heat — often moist heat may improve circulation, which has a healing effect on the local area before activity, but should be followed by cryo-therapy (cold packs should not be used on any injury or area of swelling for more than 10-12 minutes at a time, waiting 20 minutes to reapply) to reduce the inflammation. Weight loss can relieve joint stress and may delay progression (Prevention suggestion cited here). Proper advice and guidance by health care providers such as physical therapists, occupational therapists, and medical doctors is important in OA management, enabling people with this condition to improve their quality of life.

In 2002, a randomized, blinded assessor trial was published showing a positive effect on hand function with patients who practiced home joint protection exercises (JPE). Grip strength, the primary outcome parameter, increased by 25% in the exercise group versus no improvement in the control group. Global hand function improved by 65% for those undertaking JPE. 

Medical treatment

Implantation may be a possible treatment. Clinical trials currently employ tissue that is strong and able to lubricate joints. The chondrocytes are implanted into an area of damaged cartilage, and must be protected as they integrate into the joint, typically in a strong, biocompatible, biodegradeable scaffolding that allows for growth factors to stimulate cartilage production. As new cartilage is produced, the scaffolding is absorbed. 

Dietary

Supplements which may be useful for treating OA include:

Glucosamine

There is still controversy about glucosamine’s effectiveness for OA of the knee. A 2005 review concluded that glucosamine may improve symptoms of OA and delay its progression. However, a subsequent large study suggests that glucosamine is not effective in treating OA of the knee, and a 2007 meta-analysis that included this trial states that glucosamine hydrochloride is not effective.

Chondroitin

Along with glucosamine, chondroitin sulfate has become a widely used dietary supplement for treatment of osteoarthritis. A meta-analysis of randomized controlled trials found no benefit from chondroitin. However, the Osteoarthritis Research Society International is in support of the use of chondroitin sulfate for OA