Osteoarthritis
From Wikipedia, the free encyclopedia
| ICD-10 | M15-M19, M47 |
|---|---|
| ICD-9 | 715 |
| OMIM | 165720 |
| DiseasesDB | 9313 |
| MedlinePlus | 000423 |
| eMedicine | med/1682 orthoped/427 pmr/93 radio/492 |
Osteoarthritis (OA, also known as degenerative arthritis or degenerative joint disease, and sometimes referred to as "arthrosis" or "osteoarthrosis" or in more colloquial terms "wear and tear"), is a condition in which low-grade inflammation results in pain in the joints, caused by wearing of the cartilage that covers and acts as a cushion inside joints. As the bone surfaces become less well protected by cartilage, the patient 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. The word 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.
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 (Green 2001). Treatment is with NSAIDs, local injections of glucocorticoid or hyaluronan, and in severe cases, with joint replacement surgery. There has been no cure for OA, as cartilage has not been induced to regenerate. However, if OA is caused by cartilage damage (for example as a result of an injury) Autologous Chondrocyte Implantation may be a possible treatment.[1] Clinical trials employing tissue-engineering methods have demonstrated regeneration of cartilage in damaged knees, including those that had progressed to osteoarthritis.[2] Further, in January 2007, Johns Hopkins University was offering to license a technology of this kind, [3] listing several clinical competitors in its market analysis.
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[edit] Signs and symptoms
The main symptom is chronic pain, causing loss of mobility and often stiffness. "Pain" is generally described as a sharp ache, or a burning sensation in the associated muscles and tendons. OA can cause a crackling noise (called "crepitus") when the affected joint is moved or touched, and patients may experience muscle spasm and contractions in the tendons. Occasionally, the joints may also be filled with fluid. Humid weather increases the pain in many patients.
OA commonly affects the hand, feet, spine, and the large weight-bearing joints, such as the hips and knees, although in theory, any joint in the body can be affected. As OA progresses, the affected joints appear larger, are stiff and painful, and usually feel worse, the more they are used throughout the day, thus distinguishing it from rheumatoid arthritis.
In smaller joints, such as at the fingers, hard bony enlargements, called Heberden's nodes (on the distal interphalangeal joints) and/or Bouchard's nodes (on the proximal interphalangeal joints), may form, and though they are not necessarily painful, they do limit the movement of the fingers significantly. OA at the toes leads to the formation of bunions, rendering them red or swollen.
[edit] Causes
Osteoarthritis often affects multiple members of the same family, suggesting that there is hereditary susceptiblity to this condition. A number of studies have shown that there is a greater prevalence of the disease between siblings and especially identical twins, indicating a hereditary basis[citation needed]. Up to 60% of OA cases are thought to result from genetic factors. Researchers are also investigating the possibility of allergies, infections, or fungi as a cause. There is some evidence that allergies, whether fungal, infectious or systemically induced, may be a significant contributing factor to the appearance of osteoarthritis in a synovial sac.
[edit] Two types
[edit] 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.
[edit] Secondary
This type of OA is caused by other factors or diseases but the resulting pathology is the same as for primary OA:
- Congenital disorders, such as:
- Congenital hip luxation
- People with abnormally-formed joints (e.g. hip dysplasia) 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—the evidence is weak at best that this has any connection to arthritis [1].
- 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.
- Hormonal disorders.
- Ligamentous deterioration or instability may be a factor.
- Obesity. Obesity puts added weight on the joints, especially the knees.
- Osteopetrosis (High bone density).
- Sports injuries, from exercise, athletic activity, or work. For example, certain sports, such as weightlifting, running, or even football, put undue pressure on the knee joints. Injuries resulting in broken ligaments can lead to instability of the joint and over time wear of the cartilage and eventually osteoarthritis.
- Surgery to the joint structures.
[edit] Diagnosis
Diagnosis is normally done through x-rays. This is possible because loss of cartilage, subchondral ("below cartilage") sclerosis, subchondral cysts, the narrowing of the joint space between adjacent bones, and bone spur formation (osteophytes) show up clearly in x-rays. Plain films, however, often do not correlate with the findings of a 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.
In 1990, the American College of Rheumatology developed a set of criteria for the diagnosis of hand osteoarthritis based on hard tissue enlargement and swelling of certain joints using data from a multi-center study. These criteria were found to be 92% sensitive and 98% specific for hand osteoarthritis versus other entities such as rheumatoid arthritis and spondyloarthropities [4].
As yet, there are no methods available to detect OA in its early and potentially treatable stages.
[edit] 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.
[edit] Coping skills and lifestyle changes
No matter what the severity, or where the OA lies, conservative measures, such as weight control, appropriate rest and exercise, and the use of mechanical support devices are usually beneficial to sufferers. In the case of OA of the knees, knee braces, a cane, or a walker can be a helpful aid for walking and support. Regular exercise, if possible, in the form of walking or swimming, is encouraged. Applying local heat before, and cold packs after exercise, can help relieve pain and inflammation, as can relaxation techniques. Weight loss can relieve joint stress and may delay progression[citation needed]. Proper advice and guidance by a health care provider 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 excercises (JPE). Grip strength, the primary outcome parameter, increased by 25% in the excericse group versus no improvement in the control group. Global hand function improved by 65% for those undertaking JPE [5]. Dealing with chronic pain can be difficult and result in depression. Communicating with other patients and carers can be helpful, as can maintaining a positive attitude. People who take control of their treatment, communicate with their health care provider, and actively manage their arthritis experience can reduce pain and improve function.[citation needed]
[edit] Dietary
Supplements which may be useful for treating OA include:
- Antioxidants, including vitamins C and E in both foods and supplements, provide pain relief from OA. (McAlindon TE, et al, 1996).
- Chondroitin sulphate improves symptoms of OA, and delays its progression (Poolsup N et al, 2005).
- Hydrolyzed collagen (hydrolysate) (a gelatin product) may also prove beneficial in the relief of OA symptoms, as substantiated in a German study by Beuker F. et. al. and Seeligmuller et. al. In their 6-month placebo-controlled study of 100 elderly patients, the verum group showed significant improvement in joint mobility.
- Ginger (rhizome) extract - has improved knee symptoms moderately (Altman RD, 1991).
- Glucosamine: A molecule derived from glucosamine is used by the body to make some of the components of cartilage and synovial fluid. Supplemental glucosamine may improve symptoms of OA and delay its progression (Poolsup N et al, 2005). However, a recent large study suggests that glucosamine is not effective in treating OA of the knee (McAlindon et al 2004).
- Methylsulfonylmethane (MSM): A small study by Kim et al. suggested that MSM significantly reduced pain and improved physical functioning in OA patients without major adverse events (Kim et al). The authors cautioned that although this short pilot study did not address the long-term safety and usefulness of MSM, they suggest that physicians should consider its use for certain osteoarthritis patients.
- S-adenosyl methionine: small scale studies have shown it to be as effective as NSAIDs in reducing pain, although it takes about four weeks for the effect to take place.
- Selenium deficiency has been correlated with a higher risk and severity of OA, therefore selenium supplementation may reduce this risk [2].
- vitamins B9 (folate) and B12 (cobalamin) taken in large doses significantly reduced OA hand pain, presumbably by reducing systemic inflammation (Flynn MA 1994).
- Vitamin D deficiency has been reported in patients with OA, and supplementation with Vitamin D3 is recommended for pain relief (Arabelovic, 2005).
Other nutritional changes shown to aid in the treatment of OA include decreasing saturated fat intake (Wilhelmi G, 1993) and using a low energy diet to decrease body fat (Christensen R, 2005). Lifestyle change may be needed for effective symptomatic relief, especially for knee OA (De Filippis L, 2004). Reducing sugar, processed foods, fatty foods and nightshade vegetables have helped many. According to Dr. John McDougall, a low fat vegetarian diet can reduce arthritis symptoms. A macrobiotic diet has been known to reduce symptoms as well.
[edit] Systemic treatment
Included in the medication regime for most cases, a mild pain reliever may be sufficiently efficacious. In more severe cases, NSAIDs are usually prescribed which can reduce both the pain and inflammation quite effectively. These include medications such as diclofenac, ibuprofen and naproxen. High doses are often required. All NSAIDs act by inhibiting the formation of prostaglandins, which play a central role in inflammation and pain. However, these drugs are rather taxing on the gastrointestinal tract, and may cause stomach upset, cramping diarrhoea, and peptic ulcer.
Another type of NSAID, COX-2 selective inhibitors (such as celecoxib, and the withdrawn rofecoxib and valdecoxib) reduce this risk substantially. These latter NSAIDs carry an elevated risk for cardiovascular disease, and some have now been withdrawn from the market. Another medication, acetaminophen (tylenol/paracetamol), is commonly used to treat the pain from OA, although unlike NSAIDs, acetaminophen does not treat the inflammation. Application of heat — often moist heat — eases inflammation and swelling in the joints, and can help improve circulation, which has a healing effect on the local area.
Most doctors nowadays are loath to use steroids in the treatment of OA as their effect is modest and the adverse effects may outweigh the benefits. For severe pain, narcotic pain relievers such as tramadol, and eventually opioids (hydrocodone, oxycodone or morphine) may be necessary; these should be reserved for very severe cases, and are rarely medically necessary for chronic pain.
[edit] Topical
"Topical treatments" are treatments designed for local application and action. Some NSAIDs are available for topical use (e.g. ibuprofen and diclofenac) and may improve symptoms without having systemic side-effects.
Creams and lotions, containing capsaicin, are effective in treating pain associated with OA if they are applied with sufficient frequency.
Severe pain in specific joints can be treated with local lidocaine injections or similar local anaesthetics, and glucocorticoids (such as hydrocortisone). Corticosteroids (cortisone and similar agents) may temporarily reduce the pain.
[edit] Surgery
If the above management is ineffective, joint replacement surgery may be required. Individuals with very painful OA joints may require surgery such as fragment removal, repositioning bones, or fusing bone to increase stability and reduce pain.
[edit] Other approaches
There are various other modalities in use for osteoarthritis:
- Low level laser therapy ; this is a light wave based treatment that may reduce pain. The treatment is painless, inexpensive and without risks or side effects. Unfortunately, it may not actually have any real benefits.[3].
- Prolotherapy (proliferative therapy); this is the injection of an irritant substance (such as dextrose) to create an acute inflammatory reaction. It is claimed to strengthen and heal damaged tissues including ligaments, tendons and cartilage as part of this reaction. The injection is painful (like corticosteroids or hyaluronic acid) and may cause an increase in pain for a few days afterwards. The only other significant risk is the rare possibility of infection.
- Radiosynoviorthesis: A radioactive isotope (a beta-ray emitter with a brief half-life) is injected into the joint to soften the tissue. Due to the involvement of radioactive material, this is an elaborate and costly procedure, but it has a success rate of around 80%.
[edit] Prognosis
The most common course of OA is an intermittent, progressive worsening of symptoms over time, although in some patients the disease stabilizes. Prognosis also varies depending on which joint is involved.
Factors associated with progression of OA:
- Knees: High body mass index, varus or valgus knee deformity.
- Hips: Night pain, presence of femoral osteophytes, and subchondral sclerosis in females.
- Hands: Older age.
[edit] References
- Altman RD, Marcussen KC. Arthritis Rheum. 2001 Nov; 44(11):2531-8
- Arabelovic S, McAlindon TE. Curr Rheumatol Rep. 2005 Mar; 7(1):29-35.
- Christensen R. Osteoarthritis Cartilage. 2005 Jan; 13(1):20-7.
- De Filippis L et al. Reumatismo. 2004 Jul-Sep; 56(3):169-84.
- Flynn MA, Irvin W, Krause G. J Am Coll Nutr. 1994 Aug; 13(4):351-6.
- Green GA. Understanding NSAIDS: from aspirin to COX-2. Clin Cornerstone 2001; 3:50-59. PMID 11464731.
- McAlindon T, Formica M, LaValley M, Lehmer M, Kabbara K. Effectiveness of glucosamine for symptoms of knee osteoarthritis: Results from an internet-based randomized double-blind controlled trial. Am J Med 2004; 117:643-9. PMID 15501201.
- McAlindon TE, Jacques P, Zhang Y, et al. Do antioxidant micronutrients protect against the development and progression of knee osteoarthritis? Arthritis Rheum 1996; 39:648-656
- Mooney V. Spinal arthritis complete treatment guide Spine-health.com May 25, 2005.
- Theososdakis, Jason: The Arthritis Cure. Publisher: Saint Martin's Press 2004 ISBN : 0312990634
- Wilhelmi G. Z Rheumatol. 1993 May-Jun; 52(3):174-9.
[edit] See Also
[edit] External links
- WebMDHealth: Osteoarthritis Basics
- MedicineNet.com: Osteoarthritis
- MedlinePlus: Osteoarthritis
- Osteoarthritis Clinical Trials Resource
- University of Maryland
- Spine-health.com: Understanding Osteoarthritis of the Spine
- ArthritisMD (Physician submitted articles) - research based arthritis articles by physicians
- Understanding osteoarthritis
- Focuses on living with arthritis with links to support groups in 16 different countries
- ABC Salutaris: Arthrosis
