Osteoarthritis (OA) also known as degenerative arthritis or degenerative joint disease or osteoarthrosis, is a group of mechanical abnormalities involving degradation of joints, including articular cartilage and subchondral bone. Symptoms may include joint pain, tenderness, stiffness, locking, and sometimes an effusion. A variety of causes—hereditary, developmental, metabolic, and mechanical deficits—may initiate processes leading to loss of cartilage. When bone surfaces become less well protected by cartilage, bone may be exposed and damaged. As a result of decreased movement secondary to pain, regional muscles may atrophy, and ligaments may become more lax.
Treatment generally involves a combination of exercise, lifestyle modification, and analgesics. If pain becomes debilitating, joint replacement surgery may be used to improve the quality of life. OA is the most common form of arthritis, and the leading cause of chronic disability in the United States. It affects about 1.9 million people in Australia, 8 million people in the United Kingdom and nearly 27 million people in the United States.
The main symptom is pain, causing loss of ability 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 people may experience muscle spasms and contractions in the tendons. Occasionally, the joints may also be filled with fluid. Some people report increased pain associated with cold temperature, high humidity, and/or a drop in barometric pressure, but studies have had mixed results.
OA commonly affects the hands, 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 better with gentle use but worse with excessive or prolonged use, 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. Some people notice these physical changes before they experience any pain.
Damage from mechanical stress with insufficient self repair by joints is believed to be the primary cause of osteoarthritis. Sources of this stress may include: misalignments of bones caused by congenital or pathogenic causes; mechanical injury; excess body weight; loss of strength in the muscles supporting a joint; and impairment of peripheral nerves, leading to sudden or uncoordinated movements. However exercise, including running in the absence of injury, has not been found to increase the risk. Nor has cracking one's knuckles been found to play a role.
Primary osteoarthritis of the left knee. Note the osteophytes, narrowing of the joint space (arrow), and increased subchondral bone density (arrow).
A number of studies have shown that there is a greater prevalence of the disease among siblings and especially identical twins, indicating a hereditary basis. Although a single factor is not generally sufficient to cause the disease, about half of the variation in susceptibility has been assigned to genetic factors.
As early human ancestors evolved into bipeds, changes occurred in the pelvis, hip joint and spine which increased the risk of osteoarthritis. Additionally genetic variations that increase the risk were likely not selected against because usually problems only occur after reproductive success.
The development of OA is correlated with a history of previous joint injury and with obesity, especially with respect to knees. Since the correlation with obesity has been observed not only for knees but also for non-weight bearing joints and the loss of body fat is more closely related to symptom relief than the loss of body weight, it has been suggested that there may be a metabolic link to body fat as opposed to just mechanical loading.
Changes in sex hormone levels may play a role in the development of OA as it is more prevalent among post-menopausal women than among men of the same age. A study of mice found natural female hormones to be protective while injections of the male hormone dihydrotestosterone reduced protection.
This type of OA is caused by other factors but the resulting pathology is the same as for primary OA:
Primary 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[better source needed] as a result of a reduced proteoglycan content, thus causing the cartilage to be less resilient. The water content of healthy cartilage is finely balanced by compressive force driving water out & swelling pressure drawing water in. Collagen fibres exert the compressive force, whereas the Gibbs-Donnan effect & cartilage proteoglycans create osmotic pressure which tends to draw water in. However during onset of OA there is an increase in cartilage water content. This increase occurs because whilst there is an overall loss of proteoglycans, it is outweighed by a loss of collagen. 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 what 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.
Diagnosis is made with reasonable certainty based on history and clinical examination.X-rays may confirm the diagnosis. The typical changes seen on X-ray include: joint space narrowing, subchondral sclerosis (increased bone formation around the joint), subchondral cyst formation, and osteophytes. Plain films may not correlate with the findings on physical examination or with the degree of pain. Usually other imaging techniques are not necessary to clinically diagnose OA.
Related pathologies whose names may be confused with OA 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 OA which is a degenerative pathology affecting a high incidence of distal phalangeal joints of female patients. A polished ivory-like appearance may also develop on the bones of the affected joints, reflecting a change called eburnation.
Histopathology of osteoarthrosis of a knee joint in an elderly female.
Histopathology of osteoarthrosis of a knee joint in an elderly female.
Severe osteoarthritis and osteopenia of the carpal joint and 1st carpometacarpel joint.
OA can be classified into either primary or secondary depending on whether or not there is an identifiable underlying cause.
Both primary generalized nodal OA and erosive OA (EOA, also called inflammatory OA) are sub-sets of primary OA. EOA is a much less common, and more aggressive inflammatory form of OA which often affects the distal interphalangeal joints of the hand and has characteristic articular erosive changes on x-ray.
Lifestyle modification (such as weight loss and exercise) and analgesics are the mainstay of treatment. Acetaminophen ( also known as paracetamol) is recommended first line with NSAIDs being used as add on therapy only if pain relief is not sufficient. This is due to the relative greater safety of acetaminophen.
For overweight people, weight loss may be an important factor. Patient education has been shown to be helpful in the self-management of arthritis. It decreases pain, improves function, reduces stiffness and fatigue, and reduces medical usage. Patient education can provide on average 20% more pain relief when compared to NSAIDs alone in patients with hip OA.
Moderate exercise is beneficial with respect to pain and function in those with osteoathritis of the knee and possibly hip. While some evidence supports certain physical therapies evidence for a combined program is limited. There is not enough evidence to determine the effectiveness of massage therapy.
The use of orthoses (which include splints, braces or insoles) have been studied. Lateral wedge insoles do not appear to be useful in osteoarthritis of the knee. Knee braces may be useful.
The evidence for manual therapy is inconclusive. Functional, gait, and balance training has been recommended to address impairments of position sense, balance, and strength in individuals with lower extremity arthritis as these can contribute to higher falls in older individuals.
Injection of glucocorticoids (such as hydrocortisone) leads to short term pain relief that may last between a few weeks and a few months.Joint injections of hyaluronic acid have not been found to lead to significant improvement. Hyaluronic acid injects have been associated with significant harm. Nevertheless another study about hyaluronic acid injections says efficacy on pain and function, and no adverse effect when compared to saline injections.
If disability is significant and more conservative management is ineffective, joint replacement surgery or resurfacing may be recommended. Evidence supports joint replacement for both knees and hips. For the knee it improves both pain and functioning.Arthroscopic surgical intervention for OA of the knee however has been found to be no better than placebo at relieving symptoms.
There is little evidence supporting benefits for some supplements, including: the Ayurvedic herbal preparations with brand names Articulin F and Eazmov, collagen, devil’s claw, Duhuo Jisheng Wan (a Chinese herbal preparation), fish liver oil, ginger, the herbal preparation Gitadyl, glucosamine, hyaluronic acid, omega-3 fatty acids, the brand-name product Reumalax, stinging nettle, turmeric, vitamins A, C, and E in combination, vitamin E alone, vitamin K and willow bark. There is insufficient evidence to make a recommendation about the safety and efficacy of these treatments.Chondroitin is not recommended as a treatment for OA.
While acupuncture leads to a statistically significant improvement in pain relief, this improvement is small and may be of questionable clinical significance. Waiting list-controlled trials for peripheral joint osteoarthritis do show clinically relevant benefits, but these may be due to placebo effects. Acupuncture does not seem to produce long-term benefits. While electrostimulation techniques such as TENS have been used for twenty years to treat osteoarthritis in the knee, there is no conclusive evidence to show that it reduces pain or disability.
Globally approximately 250 million people have osteoarthritis of the knee (3.6% of the population). OA affects nearly 27 million people in the United States, accounting for 25% of visits to primary care physicians, and half of all NSAID prescriptions. It is estimated that 80% of the population have radiographic evidence of OA by age 65, although only 60% of those will have symptoms. In the United States, hospitalizations for OA increased from 322,000 in 1993 to 735,000 in 2006.
Globally OA causes moderate to severe disability in 43.4 million people as of 2004.
In the United States, there were approximately 964,000 hospitalizations for osteoarthritis in 2011, a rate of 31 stays per 10,000 population. With an aggregate cost of $14.8 billion, it was the second-most expensive condition seen in U.S. hospital stays in 2011. By payer, it was the second-most costly condition billed to Medicare and private insurance.
OA is derived from the Greek word part osteo-, meaning "of the bone", combined with arthritis: arthr-, meaning "joint", and -itis, the meaning of which has come to be associated with inflammation. The -itis of OA could be considered misleading as inflammation is not a conspicuous feature. Some clinicians refer to this condition as osteoarthosis to signify the lack of inflammatory response.
Evidence for OA found in the fossil record is studied by paleopathologists, specialists in ancient disease and injury. OA has been reported in fossils of the large carnivorous dinosaur Allosaurus fragilis.
There are ongoing efforts to determine if there are agents that modify outcomes in OA. Sprifermin is one candidate drug. There is also tentative evidence that strontium ranelate may decrease degeneration in OA and improve outcomes.
^Centers for Disease Control and Prevention (CDC) (February 2001). "Prevalence of disabilities and associated health conditions among adults--United States, 1999". MMWR Morb. Mortal. Wkly. Rep.50 (7): 120–5. PMID11393491.Cite uses deprecated parameters (help)
^Elsternwick (2013). "A problem worth solving.". Arthritis and Osteoporosis Victoria.
^Van Manen MD, Nace J, Mont MA (November 2012). "Management of primary knee osteoarthritis and indications for total knee arthroplasty for general practitioners". J Am Osteopath Assoc112 (11): 709–15. PMID23139341.Cite uses deprecated parameters (help)
^de Figueiredo EC, Figueiredo GC, Dantas RT (December 2011). "Influência de elementos meteorológicos na dor de pacientes com osteoartrite: Revisão da literatura" [Influence of meteorological elements on osteoarthritis pain: a review of the literature]. Rev Bras Reumatol (in Portuguese) 51 (6): 622–8. doi:10.1590/S0482-50042011000600008. PMID22124595.Cite uses deprecated parameters (help)
^Hogervorst, T; Bouma, HW; de Vos, J (August 2009). "Evolution of the hip and pelvis.". Acta orthopaedica. Supplementum80 (336): 1–39. PMID19919389.Cite uses deprecated parameters (help)
^van der Kraan, PM; van den Berg, WB (April 2008). "Osteoarthritis in the context of ageing and evolution. Loss of chondrocyte differentiation block during ageing.". Ageing research reviews7 (2): 106–13. PMID18054526.Cite uses deprecated parameters (help)
^Coggon D, Reading I, Croft P, McLaren M, Barrett D, Cooper C (May 2001). "Knee osteoarthritis and obesity". Int. J. Obes. Relat. Metab. Disord.25 (5): 622–7. doi:10.1038/sj.ijo.0801585. PMID11360143.Cite uses deprecated parameters (help)
^ abcMaroudas AI (April 1976). "Balance between swelling pressure and collagen tension in normal and degenerate cartilage". Nature260 (5554): 808–9. doi:10.1038/260808a0. PMID1264261.Cite uses deprecated parameters (help)
^ abBrocklehurst R, Bayliss MT, Maroudas A, Coysh HL, Freeman MA, Revell PA, Ali SY (January 1984). "The composition of normal and osteoarthritic articular cartilage from human knee joints. With special reference to unicompartmental replacement and osteotomy of the knee". J Bone Joint Surg Am66 (1): 95–106. PMID6690447.Cite uses deprecated parameters (help)
^Chou MC, Tsai PH, Huang GS, Lee HS, Lee CH, Lin MH, Lin CY, Chung HW (April 2009). "Correlation between the MR T2 value at 4.7 T and relative water content in articular cartilage in experimental osteoarthritis induced by ACL transection". Osteoarthr. Cartil.17 (4): 441–7. doi:10.1016/j.joca.2008.09.009. PMID18990590.Cite uses deprecated parameters (help)
^Grushko G, Schneiderman R, Maroudas A (1989). "Some biochemical and biophysical parameters for the study of the pathogenesis of osteoarthritis: a comparison between the processes of ageing and degeneration in human hip cartilage". Connect. Tissue Res.19 (2–4): 149–76. doi:10.3109/03008208909043895. PMID2805680.
^Mankin HJ, Thrasher AZ (January 1975). "Water content and binding in normal and osteoarthritic human cartilage". J Bone Joint Surg Am57 (1): 76–80. PMID1123375.Cite uses deprecated parameters (help)
^Zhang W, Doherty M, Peat G, Bierma-Zeinstra MA, Arden NK, Bresnihan B, Herrero-Beaumont G, Kirschner S, Leeb BF, Lohmander LS, Mazières B, Pavelka K, Punzi L, So AK, Tuncer T, Watt I, Bijlsma JW (March 2010). "EULAR evidence-based recommendations for the diagnosis of knee osteoarthritis". Ann. Rheum. Dis.69 (3): 483–9. doi:10.1136/ard.2009.113100. PMID19762361.Cite uses deprecated parameters (help)
^Bierma-Zeinstra SM, Oster JD, Bernsen RM, Verhaar JA, Ginai AZ, Bohnen AM (August 2002). "Joint space narrowing and relationship with symptoms and signs in adults consulting for hip pain in primary care". J. Rheumatol.29 (8): 1713–8. PMID12180735.Cite uses deprecated parameters (help)
^Altman R, Alarcón G, Appelrouth D, Bloch D, Borenstein D, Brandt K, Brown C, Cooke TD, Daniel W, Gray R (November 1990). "The American College of Rheumatology criteria for the classification and reporting of osteoarthritis of the hand". Arthritis Rheum.33 (11): 1601–10. doi:10.1002/art.1780331101. PMID2242058.Cite uses deprecated parameters (help)
^ abCibulka MT, White DM, Woehrle J, et al. (April 2009). "Hip pain and mobility deficits—hip osteoarthritis: clinical practice guidelines linked to the international classification of functioning, disability, and health from the orthopaedic section of the American Physical Therapy Association". J Orthop Sports Phys Ther39 (4): A1–25. doi:10.2519/jospt.2009.0301. PMID19352008.Cite uses deprecated parameters (help)
^Penny P, Geere J, Smith TO (October 2013). "A systematic review investigating the efficacy of laterally wedged insoles for medial knee osteoarthritis". Rheumatol. Int.33 (10): 2529–38. doi:10.1007/s00296-013-2760-x. PMID23612781.Cite uses deprecated parameters (help)
^Parkes MJ, Maricar N, Lunt M, LaValley MP, Jones RK, Segal NA, Takahashi-Narita K, Felson DT (August 2013). "Lateral wedge insoles as a conservative treatment for pain in patients with medial knee osteoarthritis: a meta-analysis". JAMA310 (7): 722–30. doi:10.1001/jama.2013.243229. PMID23989797.Cite uses deprecated parameters (help)
^Sturnieks DL, Tiedemann A, Chapman K, Munro B, Murray SM, Lord SR (November 2004). "Physiological risk factors for falls in older people with lower limb arthritis". J. Rheumatol.31 (11): 2272–9. PMID15517643.Cite uses deprecated parameters (help)
^Zhang W, Moskowitz RW, Nuki G, Abramson S, Altman RD, Arden N, Bierma-Zeinstra S, Brandt KD, Croft P, Doherty M, Dougados M, Hochberg M, Hunter DJ, Kwoh K, Lohmander LS, Tugwell P (September 2007). "OARSI recommendations for the management of hip and knee osteoarthritis, part I: critical appraisal of existing treatment guidelines and systematic review of current research evidence". Osteoarthr. Cartil.15 (9): 981–1000. doi:10.1016/j.joca.2007.06.014. PMID17719803.Cite uses deprecated parameters (help)
^Chen YF, Jobanputra P, Barton P, Bryan S, Fry-Smith A, Harris G, Taylor RS (April 2008). "Cyclooxygenase-2 selective non-steroidal anti-inflammatory drugs (etodolac, meloxicam, celecoxib, rofecoxib, etoricoxib, valdecoxib and lumiracoxib) for osteoarthritis and rheumatoid arthritis: a systematic review and economic evaluation". Health Technol Assess12 (11): 1–278, iii. PMID18405470.Cite uses deprecated parameters (help)
^Nüesch E, Rutjes AW, Husni E, Welch V, Jüni P (2009). "Oral or transdermal opioids for osteoarthritis of the knee or hip". In Nüesch, Eveline. Cochrane Database of Systematic Reviews (4): CD003115. doi:10.1002/14651858.CD003115.pub3. PMID19821302.
^ abcdeDe Silva V, El-Metwally A, Ernst E, Lewith G, Macfarlane GJ (May 2011). "Evidence for the efficacy of complementary and alternative medicines in the management of osteoarthritis: a systematic review". Rheumatology (Oxford)50 (5): 911–20. doi:10.1093/rheumatology/keq379. PMID21169345.Cite uses deprecated parameters (help)
^ abcCameron M, Gagnier JJ, Little CV, Parsons TJ, Blümle A, Chrubasik S (November 2009). "Evidence of effectiveness of herbal medicinal products in the treatment of arthritis. Part I: Osteoarthritis". Phytother Res23 (11): 1497–515. doi:10.1002/ptr.3007. PMID19856319.Cite uses deprecated parameters (help)
^Moseley JB, O'Malley K, Petersen NJ, Menke TJ, Brody BA, Kuykendall DH, Hollingsworth JC, Ashton CM, Wray NP (July 2002). "A controlled trial of arthroscopic surgery for osteoarthritis of the knee". N. Engl. J. Med.347 (2): 81–8. doi:10.1056/NEJMoa013259. PMID12110735.Cite uses deprecated parameters (help)
^Lopez, HL (May 2012). "Nutritional interventions to prevent and treat osteoarthritis. Part II: focus on micronutrients and supportive nutraceuticals". PM & R : the journal of injury, function, and rehabilitation4 (5 Suppl): S155–68. doi:10.1016/j.pmrj.2012.02.023. PMID22632695.
^ abRosenbaum CC, O'Mathúna DP, Chavez M, Shields K (2010). "Antioxidants and antiinflammatory dietary supplements for osteoarthritis and rheumatoid arthritis". Altern Ther Health Med16 (2): 32–40. PMID20232616.
^Pirotta M (September 2010). "Arthritis disease - the use of complementary therapies". Aust Fam Physician39 (9): 638–40. PMID20877766.Cite uses deprecated parameters (help)
^Abdel-Tawab M, Werz O, Schubert-Zsilavecz M (June 2011). "Boswellia serrata: an overall assessment of in vitro, preclinical, pharmacokinetic and clinical data". Clin Pharmacokinet50 (6): 349–69. doi:10.2165/11586800-000000000-00000. PMID21553931.Cite uses deprecated parameters (help)
^Burdett N, McNeil JD (September 2012). "Difficulties with assessing the benefit of glucosamine sulphate as a treatment for osteoarthritis". Int J Evid Based Healthc10 (3): 222–6. doi:10.1111/j.1744-1609.2012.00279.x. PMID22925619.Cite uses deprecated parameters (help)
^Wu D, Huang Y, Gu Y, Fan W (June 2013). "Efficacies of different preparations of glucosamine for the treatment of osteoarthritis: a meta-analysis of randomised, double-blind, placebo-controlled trials". Int. J. Clin. Pract.67 (6): 585–94. doi:10.1111/ijcp.12115. PMID23679910.Cite uses deprecated parameters (help)
^Miller KL, Clegg DO (February 2011). "Glucosamine and chondroitin sulfate". Rheum. Dis. Clin. North Am.37 (1): 103–18. doi:10.1016/j.rdc.2010.11.007. PMID21220090. "The best current evidence suggests that the effect of these supplements, alone or in combination, on OA pain, function, and radiographic change is marginal at best."Cite uses deprecated parameters (help)
^Reichenbach S, Sterchi R, Scherer M, Trelle S, Bürgi E, Bürgi U, Dieppe PA, Jüni P (April 2007). "Meta-analysis: chondroitin for osteoarthritis of the knee or hip". Annals of Internal Medicine146 (8): 580–90. doi:10.7326/0003-4819-146-8-200704170-00009. PMID17438317.Cite uses deprecated parameters (help)
^Rutjes AW, Nüesch E, Sterchi R, Kalichman L, Hendriks E, Osiri M, Brosseau L, Reichenbach S, Jüni P (2009). "Transcutaneous electrostimulation for osteoarthritis of the knee". In Rutjes, Anne WS. Cochrane Database of Systematic Reviews (4): CD002823. doi:10.1002/14651858.CD002823.pub2. PMID19821296.
^Vos T, Flaxman AD, Naghavi M, Lozano R, Michaud C, Ezzati M, Shibuya K, Salomon JA, Abdalla S, Aboyans V, et al. (December 2012). "Years lived with disability (YLDs) for 1160 sequelae of 289 diseases and injuries 1990-2010: a systematic analysis for the Global Burden of Disease Study 2010". Lancet380 (9859): 2163–96. doi:10.1016/S0140-6736(12)61729-2. PMID23245607.Cite uses deprecated parameters (help)
Treatment Guidelines. Osteoarthritis Research Society International. Recommendations for the management of hip and knee osteoarthritis. Part II OARSI Recommendations for Management of Hip & Knee OA 2007. Part III Changes in Evidence 2010.