Medscape is available in 5 Language Editions – Choose your Edition here.



  • Author: Carlos J Lozada, MD; Chief Editor: Herbert S Diamond, MD  more...
Updated: Jul 18, 2016

Practice Essentials

Osteoarthritis (see the image below) is the most common type of joint disease, affecting more than 20 million individuals in the United States alone. It is the leading cause of chronic disability in those older than 70 years, costing the US greater than $100 billion annually.[1] It can be thought of as a degenerative disorder arising from the biochemical breakdown of articular (hyaline) cartilage in the synovial joints. However, the current view holds that osteoarthritis involves not only the articular cartilage but the entire joint organ, including the subchondral bone and synovium.

This radiograph demonstrates osteoarthritis of the This radiograph demonstrates osteoarthritis of the right hip, including the finding of sclerosis at the superior aspect of the acetabulum. Frequently, osteoarthritis at the hip is a bilateral finding, but it may occur unilaterally in an individual who has a previous history of hip trauma that was confined to that one side.

Signs and symptoms

Symptoms of osteoarthritis include the following:

  • Deep, achy joint pain exacerbated by extensive use - The disease’s primary symptom
  • Reduced range of motion and crepitus - Frequently present
  • Stiffness during rest (gelling) - May develop, with morning joint stiffness usually lasting for less than 30 minutes

Osteoarthritis of the hand

  • Distal interphalangeal (DIP) joints are most often affected
  • Proximal interphalangeal (PIP) joints and the joints at the base of the thumb are also typically involved
  • Heberden nodes, which represent palpable osteophytes in the DIP joints, are more characteristic in women than in men
  • Inflammatory changes are typically absent, less pronounced, or go unnoticed

See Clinical Presentation for more detail.


Osteoarthritis is typically diagnosed on the basis of clinical and radiographic evidence.[2, 3, 4, 5, 6] No specific laboratory abnormalities are associated with osteoarthritis.

Imaging studies

  • Plain radiography - The imaging method of choice because radiographs are cost-effective and can be readily and quickly obtained [4, 7] ; in the load-bearing areas, radiographs can depict joint-space loss, as well as subchondral bony sclerosis and cyst formation
  • Computed tomography (CT) scanning - Rarely used in the diagnosis of primary osteoarthritis; however, it may be used in the diagnosis of malalignment of the patellofemoral joint or of the foot and ankle joints
  • Magnetic resonance imaging (MRI) - Not necessary in most patients with osteoarthritis unless additional pathology amenable to surgical repair is suspected; unlike radiography, MRI can directly visualize articular cartilage and other joint tissues (eg, meniscus, tendon, muscle, or effusion)
  • Ultrasonography - No role in the routine clinical assessment of patients with osteoarthritis; however, it is being investigated as a tool for monitoring cartilage degeneration, and it can be used for guided injections of joints not easily accessed without imaging
  • Bone scanning - May be helpful in the early diagnosis of osteoarthritis of the hand [8] ; bone scans also can help differentiate osteoarthritis from osteomyelitis and bone metastases


The presence of noninflammatory joint fluid helps distinguish osteoarthritis from other causes of joint pain. Other synovial fluid findings that aid in the differentiation of osteoarthritis from other conditions are negative Gram stains and cultures, as well as the absence of crystals when fluid is viewed under a polarized microscope.

See Workup for more detail.


Nonpharmacologic interventions

The cornerstones of osteoarthritis therapy, nonpharmacologic interventions include the following:

  • Patient education
  • Heat and cold
  • Weight loss [9]
  • Exercise
  • Physical therapy
  • Occupational therapy
  • Unloading in certain joints (eg, knee and hip)

Pharmacologic therapy

For hand osteoarthritis, the American College of Rheumatology (ACR) conditionally recommends using one or more of the following:

  • Topical capsaicin
  • Topical nonsteroidal anti-inflammatory drugs (NSAIDs) - Including trolamine salicylate
  • Oral NSAIDs
  • Tramadol

For knee osteoarthritis, the ACR conditionally recommends using one of the following:

  • Acetaminophen
  • Oral NSAIDs
  • Topical NSAIDs
  • Tramadol
  • Intra-articular corticosteroid injections

For hip osteoarthritis, the ACR conditionally recommends using 1 or more of the following for initial management:

  • Acetaminophen
  • Oral NSAIDs
  • Tramadol
  • Intra-articular corticosteroid injections


A referral to an orthopedic surgeon may be necessary if the osteoarthritis fails to respond to a medical management plan. Surgical procedures for osteoarthritis include the following:

  • Arthroscopy
  • Osteotomy
  • Arthroplasty - Particularly with knee or hip osteoarthritis
  • Fusion

See Treatment and Medication for more detail.



Osteoarthritis is the most common type of joint disease, affecting more than 20 million individuals in the United States alone (see Epidemiology). It represents a heterogeneous group of conditions resulting in common histopathologic and radiologic changes. It has been thought of as a degenerative disorder arising from biochemical breakdown of articular (hyaline) cartilage in the synovial joints. However, the current view holds that osteoarthritis involves not only the articular cartilage but also the entire joint organ, including the subchondral bone and synovium.

Osteoarthritis predominantly involves the weight-bearing joints, including the knees, hips, cervical and lumbosacral spine, and feet. Other commonly affected joints include the distal interphalangeal (DIP), proximal interphalangeal (PIP), and carpometacarpal (CMC) joints. This article primarily focuses on osteoarthritis of the hand, knee, and hip joints (see Pathophysiology). For more information on arthritis in other joints, see Glenohumeral Arthritis and Wrist Arthritis.

Although osteoarthritis was previously thought to be caused largely by excessive wear and tear, increasing evidence points to the contributions of abnormal mechanics and inflammation. Therefore, the term degenerative joint disease is no longer appropriate in referring to osteoarthritis. (See Pathophysiology.)

Historically, osteoarthritis has been divided into primary and secondary forms, though this division is somewhat artificial. Secondary osteoarthritis is conceptually easier to understand: It refers to disease of the synovial joints that results from some predisposing condition that has adversely altered the joint tissues (eg, trauma to articular cartilage or subchondral bone). Secondary osteoarthritis can occur in relatively young individuals (see Etiology).[10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20]

The definition of primary osteoarthritis is more nebulous. Although this form of osteoarthritis is related to the aging process and typically occurs in older individuals, it is, in the broadest sense of the term, an idiopathic phenomenon, occurring in previously intact joints and having no apparent initiating factor.

Some clinicians limit the term primary osteoarthritis to the joints of the hands (specifically, the DIP and PIP joints and the joints at the base of the thumb). Others include the knees, hips, and spine (apophyseal articulations) as well.

As underlying causes of osteoarthritis are discovered, the term primary, or idiopathic, osteoarthritis may become obsolete. For instance, many investigators believe that most cases of primary osteoarthritis of the hip may, in fact, be due to subtle or even unrecognizable congenital or developmental defects.

No specific laboratory abnormalities are associated with osteoarthritis. Rather, it is typically diagnosed on the basis of clinical findings, with or without radiographic studies (see Workup).

The goals of osteoarthritis treatment include pain alleviation and improvement of functional status. Nonpharmacologic interventions are the cornerstones of osteoarthritis therapy and include the following:

  • Patient education
  • Application of heat and cold
  • Weight loss
  • Exercise
  • Physical therapy
  • Occupational therapy
  • Joint unloading, in certain joints (eg, knee and hip)

Intra-articular pharmacologic therapy includes corticosteroid injection and viscosupplementation, which may provide pain relief and have an anti-inflammatory effect on the affected joint. (See Treatment.) Oral pharmacologic therapy begins with acetaminophen for mild or moderate pain without apparent inflammation.

If the clinical response to acetaminophen is not satisfactory or the clinical presentation is inflammatory, consider nonsteroidal anti-inflammatory drugs (NSAIDs). (See Medication.) If all other modalities are ineffective and osteotomy is not viable, or if a patient cannot perform his or her daily activities despite maximal therapy, arthroplasty is indicated.

The high prevalence of osteoarthritis entails significant costs to society. Direct costs include clinician visits, medications, and surgical intervention. Indirect costs include such items as time lost from work.

Costs associated with osteoarthritis can be particularly significant for elderly persons, who face potential loss of independence and who may need help with daily living activities. As the populations of developed nations age over the coming decades, the need for better understanding of osteoarthritis and for improved therapeutic alternatives will continue to grow. (See Epidemiology.)



Joints can be classified in either functional or structural terms. A functional classification, based on movement, would categorize joints as follows:

  • Synarthroses (immovable)
  • Amphiarthroses (slightly moveable)
  • Diarthroses (freely moveable)

A structural classification would categorize joints as follows:

  • Synovial
  • Fibrous
  • Cartilaginous

Normal synovial joints allow a significant amount of motion along their extremely smooth articular surface. These joints are composed of the following:

  • Articular cartilage
  • Subchondral bone
  • Synovial membrane
  • Synovial fluid
  • Joint capsule

The normal articular surface of synovial joints consists of articular cartilage (composed of chondrocytes) surrounded by an extracellular matrix that includes various macromolecules, most importantly proteoglycans and collagen. The cartilage facilitates joint function and protects the underlying subchondral bone by distributing large loads, maintaining low contact stresses, and reducing friction at the joint.

Synovial fluid is formed through a serum ultrafiltration process by cells that form the synovial membrane (synoviocytes). Synovial cells also manufacture hyaluronic acid (HA, also known as hyaluronate), a glycosaminoglycan that is the major noncellular component of synovial fluid. Synovial fluid supplies nutrients to the avascular articular cartilage; it also provides the viscosity needed to absorb shock from slow movements, as well as the elasticity required to absorb shock from rapid movements.



Primary and secondary osteoarthritis are not separable on a pathologic basis, though bilateral symmetry is often seen in cases of primary osteoarthritis, particularly when the hands are affected.[2, 21] Traditionally, osteoarthritis was thought to affect primarily the articular cartilage of synovial joints; however, pathophysiologic changes are also known to occur in the synovial fluid, as well as in the underlying (subchondral) bone, the overlying joint capsule, and other joint tissues (see Workup).[22, 23, 24, 25]

Although osteoarthritis has been classified as a noninflammatory arthritis, increasing evidence has shown that inflammation occurs as cytokines and metalloproteinases are released into the joint. These agents are involved in the excessive matrix degradation that characterizes cartilage degeneration in osteoarthritis.[26] Therefore, it is no longer appropriate to use the term degenerative joint disease when referring to osteoarthritis.

While there is no cure for osteoarthritis, there is ongoing research into possible disease-modifying therapies, as in inflammatory arthritis. Recent studies of interleukin-17 (IL-17), a proinflammatory cytokine, have found increased IL-17 levels in the synovium of osteoarthritis joints, as is seen in inflammatory arthritis (ie, rheumatoid arthritis).[27]

In early osteoarthritis, swelling of the cartilage usually occurs, because of the increased synthesis of proteoglycans; this reflects an effort by the chondrocytes to repair cartilage damage. This stage may last for years or decades and is characterized by hypertrophic repair of the articular cartilage.

As osteoarthritis progresses, however, the level of proteoglycans eventually drops very low, causing the cartilage to soften and lose elasticity and thereby further compromising joint surface integrity. Microscopically, flaking and fibrillations (vertical clefts) develop along the normally smooth articular cartilage on the surface of an osteoarthritic joint. Over time, the loss of cartilage results in loss of joint space.

In major weight-bearing joints of persons with osteoarthritis, a greater loss of joint space occurs at those areas experiencing the highest loads. This effect contrasts with that of inflammatory arthritides, in which uniform joint-space narrowing is the rule.

In the osteoarthritic knee, for example, the greatest loss of joint space is commonly seen in the medial femorotibial compartment, though the lateral femorotibial compartment and patellofemoral compartment may also be affected. Collapse of the medial or lateral compartments may result in varus or valgus deformities, respectively.

Erosion of the damaged cartilage in an osteoarthritic joint progresses until the underlying bone is exposed. Bone denuded of its protective cartilage continues to articulate with the opposing surface. Eventually, the increasing stresses exceed the biomechanical yield strength of the bone. The subchondral bone responds with vascular invasion and increased cellularity, becoming thickened and dense (a process known as eburnation) at areas of pressure.[28]

The traumatized subchondral bone may also undergo cystic degeneration, which is attributable either to osseous necrosis secondary to chronic impaction or to the intrusion of synovial fluid. Osteoarthritic cysts are also referred to as subchondral cysts, pseudocysts, or geodes (the preferred European term) and may range from 2 to 20 mm in diameter. Osteoarthritic cysts in the acetabulum (see the image below) are termed Egger cysts.

This radiograph demonstrates osteoarthritis of the This radiograph demonstrates osteoarthritis of the right hip, including the finding of sclerosis at the superior aspect of the acetabulum. Frequently, osteoarthritis at the hip is a bilateral finding, but it may occur unilaterally in an individual who has a previous history of hip trauma that was confined to that one side.

At areas along the articular margin, vascularization of subchondral marrow, osseous metaplasia of synovial connective tissue, and ossifying cartilaginous protrusions lead to irregular outgrowth of new bone (osteophytes). Fragmentation of these osteophytes or of the articular cartilage itself results in the presence of intra-articular loose bodies (joint mice).

Along with joint damage, osteoarthritis may also lead to pathophysiologic changes in associated ligaments and the neuromuscular apparatus. For example, lateral collateral ligament complex abnormalities are common in knee osteoarthritis.

Pain mechanisms in osteoarthritis

Pain, the main presenting symptom of osteoarthritis, is presumed to arise from a combination of mechanisms, including the following:

  • Osteophytic periosteal elevation
  • Vascular congestion of subchondral bone, leading to increased intraosseous pressure
  • Synovitis with activation of synovial membrane nociceptors
  • Fatigue in muscles that cross the joint
  • Overall joint contracture
  • Joint effusion and stretching of the joint capsule
  • Torn menisci
  • Inflammation of periarticular bursae
  • Periarticular muscle spasm
  • Psychological factors
  • Crepitus (a rough or crunchy sensation)
  • Central pain sensitization

When the spine is involved in osteoarthritis, especially the lumbar spine, the associated changes are very commonly seen from L3 through L5. Symptoms include pain, stiffness, and occasional radicular pain from spinal stenosis. Foraminal narrowing is caused by facet arthritic changes that result in compression of the nerve roots. Acquired spondylolisthesis is a common complication of arthritis of the lumbar spine.



The daily stresses applied to the joints, especially the weight-bearing joints (eg, ankle, knee, and hip), play an important role in the development of osteoarthritis. Most investigators believe that degenerative alterations in osteoarthritis primarily begin in the articular cartilage, as a result of either excessive loading of a healthy joint or relatively normal loading of a previously disturbed joint. External forces accelerate the catabolic effects of the chondrocytes and further disrupt the cartilaginous matrix.[29, 30, 31, 32]

Risk factors for osteoarthritis include the following[33, 34, 35, 36] :

  • Age
  • Obesity [37, 38, 39]
  • Trauma
  • Genetics (significant family history)
  • Reduced levels of sex hormones
  • Muscle weakness [40]
  • Repetitive use (ie, jobs requiring heavy labor and bending) [41]
  • Infection
  • Crystal deposition
  • Acromegaly
  • Previous inflammatory arthritis (eg, burnt-out rheumatoid arthritis)
  • Heritable metabolic causes (eg, alkaptonuria, hemochromatosis, and Wilson disease)
  • Hemoglobinopathies (eg, sickle cell disease and thalassemia)
  • Neuropathic disorders leading to a Charcot joint (eg, syringomyelia, tabes dorsalis, and diabetes)
  • Underlying morphologic risk factors (eg, congenital hip dislocation and slipped femoral capital epiphysis)
  • Disorders of bone (eg, Paget disease and avascular necrosis)
  • Previous surgical procedures (eg, meniscectomy)
  • Diabetes mellitus [42]

Advancing age

With advancing age come reductions in cartilage volume, proteoglycan content, cartilage vascularization, and cartilage perfusion. These changes may result in certain characteristic radiologic features, including a narrowed joint space and marginal osteophytes. However, biochemical and pathophysiologic findings support the notion that age alone is an insufficient cause of osteoarthritis.


Obesity increases the mechanical stress in a weight-bearing joint. It has been strongly linked to osteoarthritis of the knees and, to a lesser extent, of the hips. A study that evaluated the associations between body mass index (BMI) over 14 years and knee pain at year 15 in 594 women found that a higher BMI at year 1 and a significant increase in BMI over 15 years were predictors of bilateral knee pain at year 15.[39] The association between BMI increase and knee pain was independent of radiographic changes.

In addition to its mechanical effects, obesity may be an inflammatory risk factor for osteoarthritis. Obesity is associated with increased levels (both systemic and intra-articular) of adipokines (cytokines derived from adipose tissue), which may promote chronic, low-grade inflammation in joints.[43]

Other causes

Trauma or surgery (including surgical repair of traumatic injury) involving the articular cartilage, ligaments, or menisci can lead to abnormal biomechanics in the joints and accelerate osteoarthritis. Although repairs of ligament and meniscal injuries usually restore joint function, osteoarthritis has been observed 5-15 years afterward in 50-60% of patients.[44]

Insults to the joints may occur even in the absence of obvious trauma. Microtrauma may also cause damage, especially in individuals whose occupation or lifestyle involves frequent squatting, stair-climbing, or kneeling.

Muscle dysfunction compromises the body’s neuromuscular protective mechanisms, leading to increased joint motion and ultimately resulting in osteoarthritis. This effect underscores the need for continued muscle toning exercises as a means of preventing muscle dysfunction.

Valgus malalignment at the knee has been shown to increase the incidence and risk of radiographic progression of knee osteoarthritis involving the lateral compartment.[45]


A hereditary component, particularly in osteoarthritis presentations involving multiple joints, has long been recognized.[46, 47, 48] Several genes have been directly associated with osteoarthritis,[49] and many more have been determined to be associated with contributing factors, such as excessive inflammation and obesity.

Osteoarthritis susceptibility genes (eg, ADAM12, CLIP, COL11A2, IL10, MMP3) have also been found to have differential methylation. Jefferies et al reports that hypomethylation of FURIN, which encodes a proprotein convertase, processes several ADAMTS molecules involved in osteoarthritic collagen degradation. Differential methylation among osteoarthritis susceptibility genes has been proposed as an alternative method for disruption of normal gene activity.

Additionally, Jefferies et al found evidence for hypermethylation and reduced expression of the type XI collagen gene COL11A2. Mutations involving COL11A2 have been associated with severe and early-onset osteoarthritis. Analysis by this goup has identified pathways enriched with "differentially methylated genes" that are effectors and upstream regulators seen in osteoarthritis linked with TGFB1 and ERG.[1]

Genes in the BMP (bone morphogenetic protein) and WNT (wingless-type) signaling cascades have been implicated in osteoarthritis. Two genes in particular, GDF5 (growth and differentiation factor 5) and FRZB (frizzled related protein), have been identified in the articular cartilage in animal studies and share a strong correlation with osteoarthritis.[50, 51, 52, 53]

Genome-wide association studies (GWAS) have identified an association between osteoarthritis of large joints and the MCF2L gene. This gene is key in neurotrophin-mediated regulation of peripheral nervous system cell motility.[54]

Genetic factors are also important in certain heritable developmental defects and skeletal anomalies that can cause congenital misalignment of joints. These may result in damage to cartilage and the structure of the joint.

Currently, clinical genetic testing is not offered to patients who have osteoarthritis unless they also have other anomalies that could be associated with a genetic condition. In the future, testing may allow individualization of therapeutics.



United States and international statistics

Osteoarthritis affects more than 20 million individuals in the United States, though statistical figures are influenced by how the condition is defined—that is, by self-report, by radiographic or symptomatic criteria, or by a combination of these.[55] On the basis of the radiographic criteria for osteoarthritis, more 50% of adults older than 65 years are affected by the disease.

Internationally, osteoarthritis is the most common articular disease. Estimates of its frequency vary across different populations.

Age-related demographics

Primary osteoarthritis is a common disorder of the elderly, and patients are often asymptomatic. Approximately 80-90% of individuals older than 65 years have evidence of radiographic primary osteoarthritis.[56]

Symptoms typically do not become noticeable until after the age of 50 years. The prevalence of the disease increases dramatically among persons older than 50 years, likely because of age-related alterations in collagen and proteoglycans that decrease the tensile strength of the joint cartilage and because of a diminished nutrient supply to the cartilage.[56]

Sex-related demographics

In individuals older than 55 years, the prevalence of osteoarthritis is higher among women than among men.[56] Women are especially susceptible to osteoarthritis in the DIP joints of the fingers. Women also have osteoarthritis of the knee joints more frequently than men do, with a female-to-male incidence ratio of 1.7:1. Women are also more prone to erosive osteoarthritis, with a female-to-male ratio of about 12:1.

Race-related demographics

Interethnic differences in the prevalence of osteoarthritis have been noted.[57] The disorder is more prevalent in Native Americans than in the general population. Disease of the hip is seen less frequently in Chinese patients from Hong Kong than in age-matched white populations. Symptomatic knee osteoarthritis is extremely common in China.[58]

In persons older than 65 years, osteoarthritis is more common in whites than in blacks. Knee osteoarthritis appears to be more common in black women than in other groups. Jordan et al found that in comparison with whites, African American men and women had a slightly higher prevalence of radiographic and symptomatic knee osteoarthritis but a significantly higher prevalence of severe radiographic knee osteoarthritis.[59]



The prognosis in patients with osteoarthritis depends on the joints involved and on the severity of the condition. No proven disease- or structure-modifying drugs for osteoarthritis are currently known; consequently, pharmacologic treatment is directed at symptom relief.

A systematic review found the following clinical features to be associated with more rapid progression of knee osteoarthritis[60] :

  • Older age
  • Higher BMI
  • Varus deformity
  • Multiple involved joints

Patients with osteoarthritis who have undergone joint replacement have a good prognosis, with success rates for hip and knee arthroplasty generally exceeding 90%. However, a joint prosthesis may have to be revised 10-15 years after its placement, depending on the patient’s activity level. Younger and more active patients are more likely to require revisions, whereas the majority of older patients will not. (See Treatment.)


Patient Education

Educate patients on the natural history of and management options for osteoarthritis, emphasizing the benefits of exercise and weight loss. Explain the differences between osteoarthritis and more rapidly progressive arthritides, such as rheumatoid arthritis.

Several Arthritis Foundation studies have demonstrated that education in osteoarthritis benefits the patient. Through education, patients can learn and implement strategies for reducing pain and improving joint function. Emphasize the need for physician follow-up visits.

For patient education information, see the Arthritis Center, as well as Osteoarthritis.

Contributor Information and Disclosures

Carlos J Lozada, MD Director of Rheumatology Fellowship Training Program, Professor of Clinical Medicine, Department of Medicine, Division of Rheumatology and Immunology, University of Miami, Leonard M Miller School of Medicine

Carlos J Lozada, MD is a member of the following medical societies: American College of Physicians, American College of Rheumatology

Disclosure: Received honoraria from Pfizer for consulting; Received grant/research funds from AbbVie for other; Received honoraria from Heel for consulting.


Schartess S Culpepper Pace, MD Assistant Professor of Medicine, Division of Rheumatology, University of Miami, Leonard M Miller School of Medicine

Schartess S Culpepper Pace, MD is a member of the following medical societies: American College of Rheumatology

Disclosure: Nothing to disclose.

Chief Editor

Herbert S Diamond, MD Visiting Professor of Medicine, Division of Rheumatology, State University of New York Downstate Medical Center; Chairman Emeritus, Department of Internal Medicine, Western Pennsylvania Hospital

Herbert S Diamond, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American College of Rheumatology, American Medical Association, Phi Beta Kappa

Disclosure: Nothing to disclose.


Samuel Agnew, MD, FACS Associate Professor, Departments of Orthopedic Surgery and Surgery, Chief of Orthopedic Trauma, University of Florida at Jacksonville College of Medicine; Consulting Surgeon, Department of Orthopedic Surgery, McLeod Regional Medical Center

Samuel Agnew, MD, FACS is a member of the following medical societies: American Association for the Surgery of Trauma, American College of Surgeons, Orthopaedic Trauma Association, and Southern Orthopaedic Association

Disclosure: Nothing to disclose.

Elliot Goldberg, MD Dean of the Western Pennsylvania Clinical Campus, Professor, Department of Medicine, Temple University School of Medicine

Elliot Goldberg, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, and American College of Rheumatology

Disclosure: Nothing to disclose.

Siriporn Janchai, MD Fellow, Department of Medicine, Section of Physical Medicine and Rehabilitation, Louisiana State University Health Science Center

Disclosure: Nothing to disclose.

James Monroe Laborde, MD, MS Clinical Assistant Professor, Department of Orthopedics, Louisiana State University Health Sciences Center and Tulane Medical School; Adjunct Assistant Professor, Department of Biomedical Engineering, Tulane University; Adjunct Assistant Professor, Department of Physical Medicine and Rehabilitation, Louisiana State University Medical School

James Monroe Laborde, MD, MS is a member of the following medical societies: American Academy of Orthopaedic Surgeons

Disclosure: Nothing to disclose.

Phillip J Marone, MD, MSPH Clinical Professor, Department of Orthopedic Surgery, Jefferson Medical College

Phillip J Marone, MD, MSPH is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American College of Surgeons, American Medical Association, American Orthopaedic Society for Sports Medicine, and Philadelphia County Medical Society

Disclosure: Nothing to disclose.

Furqan H Siddiqui, MD Assistant Professor of Medicine (Research), Louisiana State University Medical Center in New Orleans

Disclosure: Nothing to disclose.

Eli Steigelfest, MD Consulting Staff, Department of Rheumatology, The Consultant Group, PC

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

  1. Jeffries MA, Donica M, Baker LW, Stevenson ME, Annan AC, Humphrey MB. Genome-wide DNA methylation study identifies significant epigenomic changes in osteoarthritic cartilage. Arthritis Rheumatol. 2014 Oct. 66(10):2804-15. [Medline].

  2. Buckland-Wright C, Verbruggen G, Haraoui PB. Imaging: radiological assessment of hand osteoarthritis. Osteoarthritis Cartilage. 2000. 55-6.

  3. Jewell FM, Watt I, Doherty M. Plain radiographic features of osteoarthritis. Brandt KD, Doherty M, Lohmander LS, eds. Osteoarthritis. New York, NY: Oxford University Press; 1998. 217-37.

  4. Recht MP, Kramer J, Marcelis S, Pathria MN, Trudell D, Haghighi P, et al. Abnormalities of articular cartilage in the knee: analysis of available MR techniques. Radiology. 1993 May. 187(2):473-8. [Medline].

  5. Hunter DJ. Advanced imaging in osteoarthritis. Bull NYU Hosp Jt Dis. 2008. 66(3):251-60. [Medline].

  6. Keen HI, Wakefield RJ, Conaghan PG. A systematic review of ultrasonography in osteoarthritis. Ann Rheum Dis. 2009 May. 68(5):611-9. [Medline].

  7. Recht MP, Goodwin DW, Winalski CS, White LM. MRI of articular cartilage: revisiting current status and future directions. AJR Am J Roentgenol. 2005 Oct. 185(4):899-914. [Medline].

  8. Kraus VB, McDaniel G, Worrell TW, Feng S, Vail TP, Varju G, et al. Association of bone scintigraphic abnormalities with knee malalignment and pain. Ann Rheum Dis. 2009 Nov. 68(11):1673-9. [Medline].

  9. Felson DT, Zhang Y, Anthony JM, Naimark A, Anderson JJ. Weight loss reduces the risk for symptomatic knee osteoarthritis in women. The Framingham Study. Ann Intern Med. 1992 Apr 1. 116(7):535-9. [Medline].

  10. Kirkley A, Birmingham TB, Litchfield RB, Giffin JR, Willits KR, Wong CJ, et al. A randomized trial of arthroscopic surgery for osteoarthritis of the knee. N Engl J Med. 2008 Sep 11. 359(11):1097-107. [Medline].

  11. Kellgren JH. Osteoarthritis in patients and populations. Br Med J. 1961. Vol 2.:1-6.

  12. Loughlin J. The genetic epidemiology of human primary osteoarthritis: current status. Expert Rev Mol Med. 2005 May 24. 7(9):1-12. [Medline].

  13. Cheung EV, Adams R, Morrey BF. Primary osteoarthritis of the elbow: current treatment options. J Am Acad Orthop Surg. 2008 Feb. 16(2):77-87. [Medline].

  14. Dagenais S, Garbedian S, Wai EK. Systematic review of the prevalence of radiographic primary hip osteoarthritis. Clin Orthop Relat Res. 2009 Mar. 467(3):623-37. [Medline]. [Full Text].

  15. Lee P, Rooney PJ, Sturrock RD, Kennedy AC, Dick WC. The etiology and pathogenesis of osteoarthrosis: a review. Semin Arthritis Rheum. 1974 Spring. 3(3):189-218. [Medline].

  16. Murray RO. The aetiology of primary osteoarthritis of the hip. Br J Radiol. 1965 Nov. 38(455):810-24. [Medline].

  17. Radin ER, Paul IL, Rose RM. Pathogenesis of primary osteoarthritis. Lancet. 1972 Jun 24. 1(7765):1395-6. [Medline].

  18. Sharma L. Epidemiology of osteoarthritis. Moskowitz RW, Howell DS, Altman, RD, et al, eds. Osteoarthritis. 3rd ed. 2001. 3-27.

  19. Veys E, Verbruggen G. Evolution and prognosis of osteoarthritis. Reginster JY, Pelletier JP, Martel-Pelletier J, et al, eds. Osteoarthritis. 1999. 312-3.

  20. Valderrabano V, Horisberger M, Russell I, Dougall H, Hintermann B. Etiology of ankle osteoarthritis. Clin Orthop Relat Res. 2009 Jul. 467(7):1800-6. [Medline]. [Full Text].

  21. Jewell FM, Watt I, Doherty M. Plain radiographic features of osteoarthritis. Brandt KD, Doherty M, Lohmander LS, eds. Osteoarthritis. New York, NY: Oxford University Press; 1998. 217-37.

  22. Mankin HJ. The reaction of articular cartilage to injury and osteoarthritis (first of two parts). N Engl J Med. 1974 Dec 12. 291(24):1285-92. [Medline].

  23. Miller EJ, Van der Korst JK, Sokoloff L. Collagen of human articular and costal cartilage. Arthritis Rheum. 1969 Feb. 12(1):21-9. [Medline].

  24. Phadke K. Regulation of metabolism of the chondrocytes in articular cartilage--an hypothesis. J Rheumatol. 1983 Dec. 10(6):852-60. [Medline].

  25. Resnick D, Niwayama G. Degenerative disease of extraspinal locations. Resnick D, ed. Diagnosis of Bone and Joint Disorders. 3rd ed. 1995. 1263-1371.

  26. Poole AR. An introduction to the pathophysiology of osteoarthritis. Front Biosci. 1999 Oct 15. 4:D662-70. [Medline].

  27. van Baarsen LG, Lebre MC, van der Coelen D, Aarrass S, Tang MW, Ramwadhdoebe TH. Heterogeneous expression pattern of interleukin 17A (IL-17A), IL-17F and their receptors in synovium of rheumatoid arthritis, psoriatic arthritis and osteoarthritis: possible explanation for nonresponse to anti-IL-17 therapy?. Arthritis Res Ther. 2014. 16(4):426. [Medline].

  28. Radin EL, Paul IL. Response of joints to impact loading. I. In vitro wear. Arthritis Rheum. 1971 May-Jun. 14(3):356-62. [Medline].

  29. Burkitt HG, Stevens A, Lowe JS. Skeletal system. Basic Histopathology. 3rd ed. New York, NY: Churchill Livingstone; 1996. 260.

  30. Hamerman D. The biology of osteoarthritis. N Engl J Med. 1989 May 18. 320(20):1322-30. [Medline].

  31. Hartmann C, De Buyser J, Henry Y, Morère-Le Paven MC, Dyer TA, Rode A. Nuclear genes control changes in the organization of the mitochondrial genome in tissue cultures derived from immature embryos of wheat. Curr Genet. 1992 May. 21(6):515-20. [Medline].

  32. Howell DS. Pathogenesis of osteoarthritis. Am J Med. 1986 Apr 28. 80(4B):24-8. [Medline].

  33. Bullough PG. The geometry of diarthrodial joints, its physiologic maintenance, and the possible significance of age-related changes in geometry-to-load distribution and the development of osteoarthritis. Clin Orthop Relat Res. 1981 May. 61-6. [Medline].

  34. Aigner T, Rose J, Martin J, Buckwalter J. Aging theories of primary osteoarthritis: from epidemiology to molecular biology. Rejuvenation Res. 2004 Summer. 7(2):134-45. [Medline].

  35. OUTERBRIDGE RE. The etiology of chondromalacia patellae. J Bone Joint Surg Br. 1961 Nov. 43-B:752-7. [Medline].

  36. Zgoda M, Paczek L, Bartlomiejczyk I, Sieminska J, Chmielewski D, Górecki A. Age-related decrease in the activity of collagenase in the femoral head in patients with hip osteoarthritis. Clin Rheumatol. 2007 Feb. 26(2):240-1. [Medline].

  37. [Medline].

  38. Felson DT, Anderson JJ, Naimark A, Walker AM, Meenan RF. Obesity and knee osteoarthritis. The Framingham Study. Ann Intern Med. 1988 Jul 1. 109(1):18-24. [Medline].

  39. Goulston LM, Kiran A, Javaid MK, et al. Does obesity predict knee pain over fourteen years in women, independently of radiographic changes?. Arthritis Care Res (Hoboken). 2011 Oct. 63(10):1398-406. [Medline].

  40. Hurley MV. The role of muscle weakness in the pathogenesis of osteoarthritis. Rheum Dis Clin North Am. 1999 May. 25(2):283-98, vi. [Medline].

  41. Felson DT. Risk factors for osteoarthritis: understanding joint vulnerability. Clin Orthop Relat Res. 2004 Oct. S16-21. [Medline].

  42. Williams MF, London DA, Husni EM, Navaneethan S, Kashyap SR. Type 2 diabetes and osteoarthritis: a systematic review and meta-analysis. J Diabetes Complications. 2016 Jul. 30(5):944-50. [Medline].

  43. de Boer TN, van Spil WE, Huisman AM, Polak AA, Bijlsma JW, Lafeber FP, et al. Serum adipokines in osteoarthritis; comparison with controls and relationship with local parameters of synovial inflammation and cartilage damage. Osteoarthritis Cartilage. 2012 Aug. 20(8):846-53. [Medline].

  44. National Insititute of Arthritis and Musculoskeletal and Skin Diseases. Meeting on Post-Traumatic Osteoarthritis (PTOA). Available at Accessed: 28 Jun 2010.

  45. Felson DT, Niu J, Gross KD, Englund M, Sharma L, Cooke TD, et al. Valgus malalignment is a risk factor for lateral knee osteoarthritis incidence and progression: Findings from MOST and the osteoarthritis initiative. Arthritis Rheum. 2012 Nov 30. [Medline].

  46. Valdes AM, Spector TD. Genetic epidemiology of hip and knee osteoarthritis. Nat Rev Rheumatol. 2011 Jan. 7(1):23-32. [Medline].

  47. Felson DT. Developments in the clinical understanding of osteoarthritis. Arthritis Res Ther. 2009. 11(1):203. [Medline]. [Full Text].

  48. Pollard TC, Batra RN, Judge A, Watkins B, McNally EG, Gill HS, et al. Genetic predisposition to the presence and 5-year clinical progression of hip osteoarthritis. Osteoarthritis Cartilage. 2012 May. 20(5):368-75. [Medline].

  49. Valdes AM, Spector TD. The clinical relevance of genetic susceptibility to osteoarthritis. Best Pract Res Clin Rheumatol. 2010 Feb. 24(1):3-14. [Medline].

  50. Chang SC, Hoang B, Thomas JT, Vukicevic S, Luyten FP, Ryba NJ, et al. Cartilage-derived morphogenetic proteins. New members of the transforming growth factor-beta superfamily predominantly expressed in long bones during human embryonic development. J Biol Chem. 1994 Nov 11. 269(45):28227-34. [Medline].

  51. Lin K, Wang S, Julius MA, Kitajewski J, Moos M Jr, Luyten FP. The cysteine-rich frizzled domain of Frzb-1 is required and sufficient for modulation of Wnt signaling. Proc Natl Acad Sci U S A. 1997 Oct 14. 94(21):11196-200. [Medline]. [Full Text].

  52. Chapman K, Takahashi A, Meulenbelt I, Watson C, Rodriguez-Lopez J, Egli R, et al. A meta-analysis of European and Asian cohorts reveals a global role of a functional SNP in the 5' UTR of GDF5 with osteoarthritis susceptibility. Hum Mol Genet. 2008 May 15. 17(10):1497-504. [Medline].

  53. Bos SD, Slagboom PE, Meulenbelt I. New insights into osteoarthritis: early developmental features of an ageing-related disease. Curr Opin Rheumatol. 2008 Sep. 20(5):553-9. [Medline].

  54. Chapman K, Valdes AM. Genetic factors in OA pathogenesis. Bone. 2012 Aug. 51(2):258-64. [Medline].

  55. Pereira D, Peleteiro B, Araújo J, Branco J, Santos RA, Ramos E. The effect of osteoarthritis definition on prevalence and incidence estimates: a systematic review. Osteoarthritis Cartilage. 2011 Nov. 19(11):1270-85. [Medline].

  56. Roberts J, Burch TA. Osteoarthritis prevalence in adults by age, sex, race, and geographic area. Vital Health Stat 11. 1966 Jun. 1-27. [Medline].

  57. Hoaglund FT, Yau AC, Wong WL. Osteoarthritis of the hip and other joints in southern Chinese in Hong Kong. J Bone Joint Surg Am. 1973 Apr. 55(3):545-57. [Medline].

  58. Felson DT. Comparing the prevalence of rheumatic diseases in China with the rest of the world. Arthritis Res Ther. 2008. 10(1):106. [Medline]. [Full Text].

  59. Jordan JM, Helmick CG, Renner JB, Luta G, Dragomir AD, Woodard J, et al. Prevalence of knee symptoms and radiographic and symptomatic knee osteoarthritis in African Americans and Caucasians: the Johnston County Osteoarthritis Project. J Rheumatol. 2007 Jan. 34(1):172-80. [Medline].

  60. Chapple CM, Nicholson H, Baxter GD, Abbott JH. Patient characteristics that predict progression of knee osteoarthritis: A systematic review of prognostic studies. Arthritis Care Res (Hoboken). 2011 Aug. 63(8):1115-25. [Medline].

  61. [Guideline] Altman R, Alarcón G, Appelrouth D, Bloch D, Borenstein D, Brandt K, et al. The American College of Rheumatology criteria for the classification and reporting of osteoarthritis of the hand. Arthritis Rheum. 1990 Nov. 33(11):1601-10. [Medline].

  62. [Guideline] Altman R, Alarcón G, Appelrouth D, Bloch D, Borenstein D, Brandt K, et al. The American College of Rheumatology criteria for the classification and reporting of osteoarthritis of the hip. Arthritis Rheum. 1991 May. 34(5):505-14. [Medline].

  63. [Guideline] Altman R, Asch E, Bloch D, Bole G, Borenstein D, Brandt K, et al. Development of criteria for the classification and reporting of osteoarthritis. Classification of osteoarthritis of the knee. Diagnostic and Therapeutic Criteria Committee of the American Rheumatism Association. Arthritis Rheum. 1986 Aug. 29(8):1039-49. [Medline].

  64. Marshall M, Peat G, Nicholls E, van der Windt D, Myers H, Dziedzic K. Subsets of symptomatic hand osteoarthritis in community-dwelling older adults in the United Kingdom: prevalence, inter-relationships, risk factor profiles and clinical characteristics at baseline and 3-years. Osteoarthritis Cartilage. 2013 Nov. 21(11):1674-84. [Medline].

  65. Brandt KD. A pessimistic view of serologic markers for diagnosis and management of osteoarthritis. Biochemical, immunologic and clinicopathologic barriers. J Rheumatol Suppl. 1989 Aug. 18:39-42. [Medline].

  66. Patra D, Sandell LJ. Recent advances in biomarkers in osteoarthritis. Curr Opin Rheumatol. 2011 Sep. 23(5):465-70. [Medline].

  67. [Guideline] Zhang W, Moskowitz RW, Nuki G, Abramson S, Altman RD, Arden N, et al. OARSI recommendations for the management of hip and knee osteoarthritis, Part II: OARSI evidence-based, expert consensus guidelines. Osteoarthritis Cartilage. 2008 Feb. 16(2):137-62. [Medline].

  68. [Guideline] Zhang W, Moskowitz RW, Nuki G, Abramson S, Altman RD, Arden N, et al. 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. Osteoarthritis Cartilage. 2007 Sep. 15(9):981-1000. [Medline].

  69. American Academy of Orthopaedic Surgeons. Treatment of Osteoarthritis (OA) of the Knee. AAOS: American Academy of Orthopaedic Surgeons. Available at Accessed: July 8, 2013.

  70. Agency for Healthcare Research & Quality. Analgesics for Osteoarthritis: An Update of the 2006 Comparative Effectiveness Review. Available at Accessed: Oct 24, 2011.

  71. Citrome L, Weiss-Citrome A. A systematic review of duloxetine for osteoarthritic pain: what is the number needed to treat, number needed to harm, and likelihood to be helped or harmed?. Postgrad Med. 2012 Jan. 124(1):83-93. [Medline].

  72. Frakes EP, Risser RC, Ball TD, Hochberg MC, Wohlreich MM. Duloxetine added to oral nonsteroidal anti-inflammatory drugs for treatment of knee pain due to osteoarthritis: results of a randomized, double-blind, placebo-controlled trial. Curr Med Res Opin. 2011 Dec. 27(12):2361-72. [Medline].

  73. Neustadt DH. Intra-articular therapy. Moskowitz RW, Howell DS, Altman RD, et al, eds. Osteoarthritis. 3rd ed. 2001. 393-409.

  74. Lineker SC, Bell MJ, Boyle J, Badley EM, Flakstad L, Fleming J, et al. Implementing arthritis clinical practice guidelines in primary care. Med Teach. 2009 Mar. 31(3):230-7. [Medline].

  75. Godwin M, Dawes M. Intra-articular steroid injections for painful knees. Systematic review with meta-analysis. Can Fam Physician. 2004 Feb. 50:241-8. [Medline]. [Full Text].

  76. Lambert RG, Hutchings EJ, Grace MG, Jhangri GS, Conner-Spady B, Maksymowych WP. Steroid injection for osteoarthritis of the hip: a randomized, double-blind, placebo-controlled trial. Arthritis Rheum. 2007 Jul. 56(7):2278-87. [Medline].

  77. Stitik TP, Levy JA. Viscosupplementation (biosupplementation) for osteoarthritis. Am J Phys Med Rehabil. 2006 Nov. 85(11 Suppl):S32-50. [Medline].

  78. Bellamy N, Campbell J, Robinson V, Gee T, Bourne R, Wells G. Viscosupplementation for the treatment of osteoarthritis of the knee. Cochrane Database Syst Rev. 2006 Apr 19. CD005321. [Medline].

  79. Goldberg VM, Buckwalter JA. Hyaluronans in the treatment of osteoarthritis of the knee: evidence for disease-modifying activity. Osteoarthritis Cartilage. 2005 Mar. 13(3):216-24. [Medline].

  80. Altman RD, Moskowitz R. Intraarticular sodium hyaluronate (Hyalgan) in the treatment of patients with osteoarthritis of the knee: a randomized clinical trial. Hyalgan Study Group. J Rheumatol. 1998 Nov. 25(11):2203-12. [Medline].

  81. Stitik TP, Blacksin MF, Stiskal DM, Kim JH, Foye PM, Schoenherr L, et al. Efficacy and safety of hyaluronan treatment in combination therapy with home exercise for knee osteoarthritis pain. Arch Phys Med Rehabil. 2007 Feb. 88(2):135-41. [Medline].

  82. Waddell DD, Kolomytkin OV, Dunn S, Marino AA. Hyaluronan suppresses IL-1beta-induced metalloproteinase activity from synovial tissue. Clin Orthop Relat Res. 2007 Dec. 465:241-8. [Medline].

  83. Rabago D, Patterson JJ, Mundt M, Kijowski R, Grettie J, Segal NA, et al. Dextrose prolotherapy for knee osteoarthritis: a randomized controlled trial. Ann Fam Med. 2013 May-Jun. 11(3):229-37. [Medline]. [Full Text].

  84. Sawitzke AD, Shi H, Finco MF, Dunlop DD, Bingham CO 3rd, Harris CL, et al. The effect of glucosamine and/or chondroitin sulfate on the progression of knee osteoarthritis: a report from the glucosamine/chondroitin arthritis intervention trial. Arthritis Rheum. 2008 Oct. 58(10):3183-91. [Medline]. [Full Text].

  85. Clegg DO, Reda DJ, Harris CL, et al. Glucosamine, chondroitin sulfate, and the two in combination for painful knee osteoarthritis. N Engl J Med. 2006 Feb 23. 354(8):795-808. [Medline].

  86. Rutjes AW, Nüesch E, Reichenbach S, Jüni P. S-Adenosylmethionine for osteoarthritis of the knee or hip. Cochrane Database Syst Rev. 2009 Oct 7. CD007321. [Medline].

  87. Hathcock JN, Shao A. Risk assessment for glucosamine and chondroitin sulfate. Regul Toxicol Pharmacol. 2007 Feb. 47(1):78-83. [Medline].

  88. Gege C, Bao B, Bluhm H, Boer J, Gallagher BM, Korniski B, et al. Discovery and evaluation of a non-Zn chelating, selective matrix metalloproteinase 13 (MMP-13) inhibitor for potential intra-articular treatment of osteoarthritis. J Med Chem. 2012 Jan 26. 55(2):709-16. [Medline].

  89. Brown MT, Murphy FT, Radin DM, Davignon I, Smith MD, West CR. Tanezumab reduces osteoarthritic knee pain: results of a randomized, double-blind, placebo-controlled phase III trial. J Pain. 2012 Aug. 13(8):790-8. [Medline].

  90. Pierson R. Lilly Says New Type of Pain Drug Could Lessen Need for Opioids. Medscape Medical News. Available at May 25, 2016; Accessed: July 8, 2016.

  91. Roddy E, Doherty M. Changing life-styles and osteoarthritis: what is the evidence?. Best Pract Res Clin Rheumatol. 2006 Feb. 20(1):81-97. [Medline].

  92. Perrot S, Poiraudeau S, Kabir M, Bertin P, Sichere P, Serrie A, et al. Active or passive pain coping strategies in hip and knee osteoarthritis? Results of a national survey of 4,719 patients in a primary care setting. Arthritis Rheum. 2008 Nov 15. 59(11):1555-62. [Medline].

  93. Recommendations for the medical management of osteoarthritis of the hip and knee: 2000 update. American College of Rheumatology Subcommittee on Osteoarthritis Guidelines. Arthritis Rheum. 2000 Sep. 43(9):1905-15. [Medline].

  94. Bennell KL, Kyriakides M, Hodges PW, Hinman RS. Effects of two physiotherapy booster sessions on outcomes with home exercise in people with knee osteoarthritis: a randomized controlled trial. Arthritis Care Res (Hoboken). 2014 Nov. 66(11):1680-7. [Medline].

  95. Anandacoomarasamy A, Leibman S, Smith G, et al. Weight loss in obese people has structure-modifying effects on medial but not on lateral knee articular cartilage. Ann Rheum Dis. 2012 Jan. 71(1):26-32. [Medline].

  96. Messier SP. Obesity and osteoarthritis: disease genesis and nonpharmacologic weight management. Rheum Dis Clin North Am. 2008 Aug. 34(3):713-29. [Medline]. [Full Text].

  97. McCarthy GM, McCarty DJ. Effect of topical capsaicin in the therapy of painful osteoarthritis of the hands. J Rheumatol. 1992 Apr. 19(4):604-7. [Medline].

  98. Watt FE, Kennedy DL, Carlisle KE, Freidin AJ, Szydlo RM, Honeyfield L, et al. Night-time immobilization of the distal interphalangeal joint reduces pain and extension deformity in hand osteoarthritis. Rheumatology (Oxford). 2014 Feb 8. [Medline].

  99. Cohen R. Nighttime Finger Splints Can Ease Arthritis Pain. Medscape [serial online]. Available at Accessed: March 11, 2014.

  100. Juhl C, Christensen R, Roos EM, Zhang W, Lund H. 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 Rheumatol. 2014 Mar. 66(3):622-36. [Medline].

  101. Jan MH, Lin CH, Lin YF, Lin JJ, Lin DH. Effects of weight-bearing versus nonweight-bearing exercise on function, walking speed, and position sense in participants with knee osteoarthritis: a randomized controlled trial. Arch Phys Med Rehabil. 2009 Jun. 90(6):897-904. [Medline].

  102. Chaipinyo K, Karoonsupcharoen O. No difference between home-based strength training and home-based balance training on pain in patients with knee osteoarthritis: a randomised trial. Aust J Physiother. 2009. 55(1):25-30. [Medline].

  103. Marks R, Allegrante JP. Chronic osteoarthritis and adherence to exercise: a review of the literature. J Aging Phys Act. 2005 Oct. 13(4):434-60. [Medline].

  104. Wang C, Schmid CH, Hibberd PL, Kalish R, Roubenoff R, Rones R, et al. Tai Chi is effective in treating knee osteoarthritis: a randomized controlled trial. Arthritis Rheum. 2009 Nov 15. 61(11):1545-53. [Medline].

  105. Wang C, Schmid CH, Iversen MD, Harvey WF, Fielding RA, Driban JB, et al. Comparative Effectiveness of Tai Chi Versus Physical Therapy for Knee Osteoarthritis: A Randomized Trial. Ann Intern Med. 2016 May 17. [Medline].

  106. Kang JW, Lee MS, Posadzki P, Ernst E. T'ai chi for the treatment of osteoarthritis: a systematic review and meta-analysis. BMJ Open. 2011 Mar 28. 1(1):e000035. [Medline]. [Full Text].

  107. Goodman A. Knee Brace Reduces Damage, Pain in Osteoarthritis. Medscape Medical News. Available at Accessed: November 4, 2013.

  108. Hinman RS, Wrigley TV, Metcalf BR, Campbell PK, Paterson KL, Hunter DJ, et al. Unloading Shoes for Self-Management of Knee Osteoarthritis: A Randomized Trial. Ann Intern Med. 2016 Jul 12. [Medline].

  109. Liu H, Abbott J, Bee JA. Pulsed electromagnetic fields influence hyaline cartilage extracellular matrix composition without affecting molecular structure. Osteoarthritis Cartilage. 1996 Mar. 4(1):63-76. [Medline].

  110. Zizic TM, Hoffman KC, Holt PA, Hungerford DS, O'Dell JR, Jacobs MA, et al. The treatment of osteoarthritis of the knee with pulsed electrical stimulation. J Rheumatol. 1995 Sep. 22(9):1757-61. [Medline].

  111. Garland D, Holt P, Harrington JT, Caldwell J, Zizic T, Cholewczynski J. A 3-month, randomized, double-blind, placebo-controlled study to evaluate the safety and efficacy of a highly optimized, capacitively coupled, pulsed electrical stimulator in patients with osteoarthritis of the knee. Osteoarthritis Cartilage. 2007 Jun. 15(6):630-7. [Medline].

  112. Fukuda TY, Alves da Cunha R, Fukuda VO, et al. Pulsed shortwave treatment in women with knee osteoarthritis: a multicenter, randomized, placebo-controlled clinical trial. Phys Ther. 2011 Jul. 91(7):1009-17. [Medline].

  113. Ying KN, While A. Pain relief in osteoarthritis and rheumatoid arthritis: TENS. Br J Community Nurs. 2007 Aug. 12(8):364-71. [Medline].

  114. Pietrosimone BG, Saliba SA, Hart JM, Hertel J, Kerrigan DC, Ingersoll CD. Effects of transcutaneous electrical nerve stimulation and therapeutic exercise on quadriceps activation in people with tibiofemoral osteoarthritis. J Orthop Sports Phys Ther. 2011 Jan. 41(1):4-12. [Medline].

  115. Selfe TK, Taylor AG. Acupuncture and osteoarthritis of the knee: a review of randomized, controlled trials. Fam Community Health. 2008 Jul-Sep. 31(3):247-54. [Medline]. [Full Text].

  116. [Guideline] AAOS. American Academy of Orthopaedic Surgeons. Guideline on the Treatment of Osteoarthritis (OA) of the Knee. Available at Accessed: December 5, 2008.

  117. Marx RG. Arthroscopic Surgery for Osteoarthritis of the Knee?. New England Journal of Medicine. 2008. Vol. 359:1169-1170. [Full Text].

  118. Barclay L, Nghiem HT. Arthroscopic Surgery May Not Be Helpful for Knee Osteoarthritis. Medscape. Available at Accessed: September 29, 2010.

  119. Pagenstert G, Knupp M, Valderrabano V, Hintermann B. Realignment surgery for valgus ankle osteoarthritis. Oper Orthop Traumatol. 2009 Mar. 21(1):77-87. [Medline].

  120. Pipino G, Indelli PF, Tigani D, Maffei G, Vaccarisi D. Opening-wedge high tibial osteotomy: a seven - to twelve-year study. Joints. 2016 Jun 13. 4(1):6-11. [Medline].

  121. Daras M, Macaulay W. Total hip arthroplasty in young patients with osteoarthritis. Am J Orthop (Belle Mead NJ). 2009 Mar. 38(3):125-9. [Medline].

  122. Kuo A, Ezzet KA, Patil S, Colwell CW Jr. Total hip arthroplasty in rapidly destructive osteoarthritis of the hip: a case series. HSS J. 2009 Sep. 5(2):117-9. [Medline]. [Full Text].

  123. [Guideline] Weber KL, Jevsevar DS, McGrory BJ. AAOS Clinical Practice Guideline: Surgical Management of Osteoarthritis of the Knee: Evidence-based Guideline. J Am Acad Orthop Surg. 2016 Jun 28. [Medline]. [Full Text].

  124. Reichenbach S, Rutjes AW, Nüesch E, Trelle S, Jüni P. Joint lavage for osteoarthritis of the knee. Cochrane Database Syst Rev. 2010 May 12. CD007320. [Medline].

  125. Felson DT, Niu J, Clancy M, Aliabadi P, Sack B, Guermazi A, et al. Low levels of vitamin D and worsening of knee osteoarthritis: results of two longitudinal studies. Arthritis Rheum. 2007 Jan. 56(1):129-36. [Medline].

  126. Bergink AP, Uitterlinden AG, Van Leeuwen JP, Buurman CJ, Hofman A, Verhaar JA, et al. Vitamin D status, bone mineral density, and the development of radiographic osteoarthritis of the knee: The Rotterdam Study. J Clin Rheumatol. 2009 Aug. 15(5):230-7. [Medline].

  127. Canter PH, Wider B, Ernst E. The antioxidant vitamins A, C, E and selenium in the treatment of arthritis: a systematic review of randomized clinical trials. Rheumatology (Oxford). 2007 Aug. 46(8):1223-33. [Medline].

  128. Peregoy J, Wilder FV. The effects of vitamin C supplementation on incident and progressive knee osteoarthritis: a longitudinal study. Public Health Nutr. 2011 Apr. 14(4):709-15. [Medline].

  129. Brooks M. Topical Diclofenac 2% (Pennsaid) for Knee OA Pain Clears FDA. Medscape [serial online]. Available at Accessed: January 26, 2014.

  130. Gibofsky A, Hochberg MC, Jaros MJ, Young CL. Efficacy and safety of low-dose submicron diclofenac for the treatment of osteoarthritis pain: a 12 week, phase 3 study. Curr Med Res Opin. 2014 Aug 6. 1-11. [Medline].

  131. Miller M, Stürmer T, Azrael D, Levin R, Solomon DH. Opioid analgesics and the risk of fractures in older adults with arthritis. J Am Geriatr Soc. 2011 Mar. 59(3):430-8. [Medline].

This radiograph demonstrates osteoarthritis of the right hip, including the finding of sclerosis at the superior aspect of the acetabulum. Frequently, osteoarthritis at the hip is a bilateral finding, but it may occur unilaterally in an individual who has a previous history of hip trauma that was confined to that one side.
Osteoarthritis of the elbow is not commonly seen; however, it can occur with a history of previous trauma.
Osteoarthritis of the elbow is not commonly seen; however, it can occur with a history of previous trauma.
Osteoarthritis of the elbow is not commonly seen; however, it can occur with a history of previous trauma.
This radiograph demonstrates osteoarthritis of the right hip, including the finding of sclerosis at the superior aspect of the acetabulum. Frequently, osteoarthritis at the hip is a bilateral finding, but it may occur unilaterally in an individual who has a previous history of hip trauma that was confined to that one side.
Arthroscopic view of a torn meniscus before (top) and after (bottom) removal of loose meniscal fragments.
Arthroscopic view of an arthritic knee.
Arthroscopic view of a knee after the removal of loose fragments of articular and meniscal cartilage.
Arthroscopic view of the removal of cartilaginous loose body.
Anteroposterior radiograph shows knee replacement in 1 knee and arthritis in the other, with medial joint-space narrowing and subchondral sclerosis.
Anteroposterior radiograph of the pelvis and hips shows an arthritic hip not treated surgically and a total hip replacement.
Anteroposterior radiograph obtained after knee replacement.
Lateral radiograph obtained after knee replacement (same patient as in the above image).
Oblique projection demonstrates gradual narrowing and sclerosis of the facet joints as one progresses down the lumbar spine.
Standing radiograph of the knee reveals narrowing of the medial and lateral femorotibial compartments with marginal osteophytes.
H&E stain, high power magnification showing clusters of chondrocytes (center) that is a proliferation known as "chondrocyte cloning". Image courtesy of Francis Gannon, MD.
H&E stain, medium power magnification showing numerous vertical slits (upper left) in the articular surface cartilage known as "fibrillation" with increase in eosinophilia of the remaining cartilage due to loss of proteoglycans. Image courtesy of Francis Gannon, MD.
Gross photograph of external (top) and cut surface (bottom) showing areas of complete loss of articular cartilage with peripheral osteophytes formation. Image courtesy of Francis Gannon, MD.
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.