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The disease pathology of knee osteoarthritis (OA) is characterized by degeneration of articular cartilage and associated subchondral bone.1 It is traditionally classified as a non-inflammatory arthritis, although inflammatory processes are present in certain stages of the disease.


Primary knee OA is thought to be caused by repetitive mechanical stress, which initiates and perpetuates degeneration.2 Secondary OA is initiated by prior trauma, sepsis, or inflammatory conditions with resultant joint instability, incongruity of the articular surface, and/or altered cartilage metabolism and matrix composition.3

Epidemiology including risk factors and primary prevention

OA is the leading cause of musculoskeletal debility in the world and 11th highest contributor to global disability.4 Approximately 19-28% of Americans over the age of 45 have knee OA.5 Prevalence of knee OA peaks around the age of 50, with an average of 30 years of disease burden.4,6 Since the mid-20th century, prevalence of knee OA has doubled, even when controlling for age and BMI.7

Multiple local and systemic risk factors have been identified. Advanced age is the risk factor most associated with OA, with incidence rates increasing significantly over the age of 50.8 Obesity is another strong risk factor linked to knee OA, associated with significant rates of incidence and progression.9,10 Other risk factors include female sex, hormonal status, osteoporosis, ethnicity, genetic predisposition, dietary intake, muscle weakness, altered biomechanics, joint laxity/deformity, occupational factors, certain competitive sports, and previous trauma.11

The evidence for effective primary prevention of knee OA is somewhat limited; however, risk may be reduced through weight loss, regular exercise, prevention and management of osteoporosis.6,12,13,14


Initiation and progression of knee OA is a consequence of one or more factors including loss of cartilage matrix, alteration of the extracellular matrix, and chondrocyte injury. The disease may also involve focal macroscopic chondral or subchondral injury. Cartilage edema may develop secondary to increased chondrocyte activity in response to such injury. Over time and with repetitive injury, disruption of matrix equilibrium leads to a catabolic shift; the cartilage thus begins to lose structural integrity, resulting in progressive surface fibrillations and erosions. Resultant breakdown products stimulate synovial inflammation, immune cell activity, and high levels of proinflammatory cytokines as the disease progresses. The role of inflammation in symptom and disease progression in knee OA is unclear, but evidence indicates these factors exacerbate cartilage erosion.15 Inflammatory factors such as interleukins, tumor necrosis factor, and prostaglandin E2 have been linked to further matrix-degrading enzyme reproduction, oxidation of molecules, and decreased matrix synthesis. These factors may also play a significant role in pain produced by nociceptors located throughout the joint capsule.16

Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)

Knee OA is characterized by an insidious onset of pain and progressive limited range of motion. Symptoms worsen over time, typically in a stepwise fashion. Patients note symptoms with ambulation, transfers, and ascending stairs. Knee stiffness or “locking” secondary to the formation of loose bodies, degenerative meniscal tears, and osteophyte formation may occur.17 These can significantly increase pain severity, hinder activities of daily living, and reduce quality of life.

Specific secondary or associated conditions or complications

OA has been linked to deformities of the knee joint, most often a varus deformity.18 Secondary altered biomechanics during functional tasks may lead to the development of pes anserine and/or trochanteric bursitis. Knee OA has also been associated with greater prevalence and increased risk of developing frailty in the elderly.19 Knee OA may alter gait patterns, aberrantly loading the contralateral joint during ambulation, which may result in secondary OA in the opposite hip and knee. Associated health effects such as weight gain and reduced cardiovascular health may arise from decreased activity levels.20,21 Increasing evidence has found that knee OA with pain, especially in females, Caucasians, < 65 years of age, and BMI > 30, is associated with a significant increase in premature all-cause mortality.10



The classic clinical criteria to diagnose knee OA from the American College of Rheumatology (ACR)22 (sensitivity 95%, specificity 69%), includes knee pain, and at least 3 of the following:

  1. Greater than 50 years of age
    2. Morning stiffness for less than 30 minutes
    3. Crepitus on active motion of the knee
    4. Bony tenderness near the knee joint line
    5. Bony enlargement about the knee joint
    6. No palpable warmth

Of note, the ACR is set to release updated OA guidelines later in 2019.

The European League Against Rheumatism (EULAR) evidence-based recommendations for the clinical symptoms associated with the presence of radiographic knee OA include the following:

  1. Persistent knee pain
  2. Morning stiffness
  3. Impaired function of knee
  4. Crepitus on exam
  5. Restricted range of movement
  6. Bony enlargement

Estimated probability of radiographic knee OA increases with increasing numbers of positive features, reaching 99% estimated probability with the presence of all 6 features.23

Physical Exam

Inspection: Assess for joint hypertrophy, varus/valgus deformity, effusion, and skin changes.

Palpation: Tenderness to palpation may be present. This is most commonly present at the medial joint line or patellofemoral articulation. An effusion may be palpable at the suprapatellar bursa with associated ballottement of the patella.

Range of motion (ROM): Active and passive ROM may induce pain. ROM may be limited in flexion early in the course of disease with limitations in extension typically occurring in later stages.

Strength: Manual muscle testing may be limited secondary to pain. Muscle atrophy and weakness may be seen over time secondary to avoidance of painful activities. This is typically seen initially and most prominently in the quadriceps (in particular the distal vastus medialus obliqus) and associated hip musculature, but may also involve the hamstrings.24

Special Tests: Instability may be noted on valgus and/or varus stress testing. Special tests have not been well-correlated to functional measures or self-reported pain outcomes.24

Clinical Functional Assessment

Pain and stiffness from knee OA may cause difficulty with functional weight-bearing activities, such as ambulation, stair climbing, and transitioning from sit to stand. The times to complete load-bearing activities such as walk tests, timed-up-and go tests, chair rise, and stair climb are slower in people with OA compared with people who do not. These functional assays are useful as research measures to characterize progression of knee OA. The Osteoarthritis Research Society International (OARSI) recommends the use of a set of five performance-based tests of physical function in people with knee OA:

  1. Thirty Second Chair-Stand Test
  2. Forty Meter Fast-Paced Walk Test
  3. A Stair-Climb Test (e.g. Single Step-Down Test or Step-Up Test; no specific test recommendation)
  4. Timed Up-and-Go Test
  5. Six Minute Walk Test

A description of the tests, copies of scoring sheets, and clinimetric data may be found here.25

Patient reported outcome (PRO) measures have also been developed and validated for use in the assessment of OA severity and treatment outcomes. Examples include the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC), which is a 24-item assessment of a patient’s pain, stiffness, and physical function and the Knee injury and Osteoarthritis Outcome Score (KOOS), which is an assessment of pain, symptoms, activities of daily living, sports/recreation, and knee-related quality of life using a 42-item questionnaire.

Laboratory Studies

When laboratory findings are added to the above ACR’s classic clinical criteria,22 sensitivity and specificity for the diagnosis of OA are 92% and 75%, respectively, when at least 5 of the 9 total features are present.

  • Erythrocyte Sedimentation Rate < 40 mm/hr
  • Rheumatoid Factor Titer < 1:40
  • Synovial Fluid with Clear Color, Normal Viscosity, and White Blood Cell Count < 2000

There is no definitive biochemical marker for knee OA, although markers of cartilage degradation such as CTXII and COMP urine assays have been associated with clinical and radiographic findings of OA.26


Plain radiography continues to be the gold standard in imaging of knee OA, due to convenience and low cost. Weight-bearing radiographs can further aide evaluation. Anterior-posterior, lateral, notch, and Merchant views are recommended. Radiographic findings include joint space narrowing, subchondral bony sclerosis, osteophytes, subchondral cysts, and loose bodies as well as varus/valgus alignment and osteopenia.

Kellgren-Lawrence Radiographic Grading Scale for OA1:

  • Grade 0: No radiographic findings of OA
  • Grade 1: Doubtful narrowing of joint space and possible osteophytic lipping
  • Grade 2: Definite osteophytes with possible narrowed joint space
  • Grade 3: Definite osteophytes with moderate joint space narrowing and some sclerosis
  • Grade 4: Definite osteophytes with severe joint space narrowing, subchondral sclerosis, and definite deformity of bony contour

Clinically significant changes in radiographic scores can often take one to two years to manifest, with more subtle changes only detectable on supplemental assessments (i.e. MRI).27

When radiographic evidence of osteophytes is added to the ACR’s classic clinical criteria22, the criteria has a sensitivity of 91% and specificity 86% for diagnosis of knee OA.

Supplemental Assessment Tools

MRI may be considered for diagnostic purposes very early in the course of knee OA as MR pathology can be detected before radiographic or morphologic changes become apparent.18 MRI may also be considered to help evaluate or rule out other knee conditions, which may be present in the differential diagnosis for a given patient.

Ultrasound imaging may allow for assessment of knee OA features such as synovial pathology and may be considered by sufficiently skilled operators when radiographs are inconclusive; however, ultrasound is limited by its inability to assess deeper articular structures and subchondral bone.28

Early Predictions of Outcomes

Baseline rates of incidence and progression of knee OA have been estimated to be 2.5% and 3.6% per year, respectively.9 Predictors of disease progression include age, obesity, the presence of OA in other joints, previous knee injury, history of regular sports progression, and varus deformity of the knee.9,29 Radiographic features of disease, including Kellgren-Lawrence scale severity, presence of chondrocalcinosis, and osteophyte score, are also predictive of progression29. Increased physical activity (of any intensity level) and increased quadriceps muscle strength is associated with decreased progression of disability in adults with knee OA.30,31


Aquatic exercise is a viable option for those patients experiencing significant pain with land-based exercise. Access to resistance exercise equipment and safe walking routes or treadmills can help patients remain strong and active31-33. Ground floor habitation or living in buildings with elevator access can help improve patient access and mobility.

Social Role and Support System

It is important to determine if the patient’s stiffness, pain, or decreased ROM is interfering with his or her ability for self-care. Having someone who can provide assistance, or regular positive social interaction (be it a family member or paid caregiver), can ultimately affect the patient’s outcomes in dealing with OA.34 There has been evidence that normal mood at baseline in patients with knee OA, characterized by self-efficacy with pain and improved satisfaction with life, predict improved function. Increased pain catastrophizing and fear of movement (kinesophobia) predicts poor function.35

Therapists and care teams can provide psychosocial support to patients by helping them understand that OA pain is a symptom that can be managed. This is very important in helping individuals overcome the kinesophobia due to OA pain. This may help patients fully engage in safe exercise, even when some knee pain is present. This process can help patients improve muscle strength and reduce the pain severity.

Professional Issues



Available or Current Treatment Guidelines

Guidelines for the treatment of OA of the knee have been published by the American College of Rheumatology (link), the American Academy of Orthopedic Surgeons (AAOS) (link), and the Osteoarthritis Research Society International (link).33,36,37

While differences exist among these three sets of recommendations, there is agreement in the following non-surgical management strategies:


  • Low-impact land-based exercise
  • Aquatic exercise
  • Strength training and neuromuscular education
  • Education and self-management
  • Weight loss in obese patients

Conditionally recommended:

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

Three items are of particular note. First, in patients > 75 years of age, a topical NSAID is recommended as oral NSAIDs increase the risk of serious gastrointestinal adverse outcome, including bleeding, ulcer, or perforation. Second, the use of intra-articular hyaluronic acid injections is notably absent from the above list despite its common use in clinical practice. Recommendations between the societies ranged from a strong “cannot recommend” its use by the AAOS, to “no recommendation regarding its use” by the ACR, to “uncertain” by the OARSI. Additional study is clearly needed to more firmly establish the efficacy of this treatment. Finally, several braces (e.g. off-loader braces), orthotics (e.g. medial and lateral wedges), and assistive devices (e.g. canes) have been used in the treatment of knee OA. These items received inconsistent levels of review among the three societies with differing levels of recommendation when discussed by more than one society.

At Different Disease Stages

Early management of OA should focus on decreasing pain level, increasing function, and attempting to slow the disease progression. Physical therapy for low-impact land-based exercise, aquatic exercise, and strength training and neuromuscular education should be considered as the foundation of the treatment plan for any stage of OA. Strength training should focus on improving quadriceps, hamstrings, calf, and hip muscle strength. Structured weight-loss programs should be implemented in patients who are overweight or obese. Oral analgesics, intra-articular injections, therapeutic modalities, and bracing/orthotics are additional treatment options that should be considered within the context of an individual patient and their co-morbidities.

Hyaluronic acid injections are a possible treatment in patients who fail initial conservative measures, although current evidentiary support is uncertain as reflected in the different levels of recommendations of use by the ACR, AAOS, and OARSI. Intra-articular corticosteroid injections may be helpful in patients who have moderate to severe OA of the knee to target decreasing inflammation to reduce pain. However, like hyaluronic acid injections, there is not substantial evidence to support its benefits, and repeated use of intra-articular corticosteroids could potentially cause thinning of cartilage.38

Arthroscopic debridement should not be considered as a means of intervention in patients with a primary diagnosis of knee OA as there are very high levels of evidence that do no support its use.39 However, younger non-obese patients with symptom duration of < 6 months stemming from a primary diagnosis of meniscal tear, loose body, or other mechanical derangement with a concomitant diagnosis of incidental mild (Kellgren-Lawrence scale grade 1) OA of the knee may benefit in the event of failure of conservative measures.40

In later stages of the disease, some patients may fail conservative management and require surgical intervention in the form of joint arthroplasty.

Coordination of Care

OA is multifaceted and may require the input from several healthcare professionals. Direct communication among the care team members (physical therapists, physicians, and family) is important to understanding the patient’s progress and helping to achieve optimal outcomes. When treating an elderly patient, communication with the primary care provider can help address medical issues that may be a barrier to therapy or other treatments. Care may also be coordinated with the primary care provider to help an obese patient enroll in a structured weight-loss program and obtain the help of a nutritionist or a bariatric surgeon.

Patient and Family Education

It is important to educate patients and family members about modifiable risk factors for the development and progression of OA, so they may target specific risk factors and make appropriate lifestyle changes to reduce the disease risk and manage OA symptoms.

Measurement of Treatment Outcomes

Multiple survey-based and objective functional measures of mobility and function have been developed as previously described in the Clinical Functional Measures section.

Translation into Practice

The use of both objective functional (e.g. Thirty Second Chair-Stand Test, Forty Meter Fast-Paced Walk Test) and PRO (e.g. WOMAC, KOOS) measures have use for both tracking clinical course and response to treatments as well as providing measures of patient outcomes for quality of care reporting.


Cutting Edge/Emerging and Unique Concepts and Practice

Regenerative biologic medicine techniques include intra-articular injection of mesenchymal stem cells or platelet-rich plasma (PRP). Meta-analysis and review of studies to date have shown that PRP injections generally appear to be more effective at reducing pain than placebo and hyaluronic acid injections, though there was also an increase in non-specific adverse events.41,42 Systematic review also reveals that amnion-derived mesenchymal stem cells have been demonstrated to improve pain and function while decreasing radiologic evidence of OA, while adipose-derived mesenchymal stem cells revealed improved clinical outcomes without radiologic improvement. Bone marrow-derived mesenchymal stem cells effects were short-lived, but generally had good clinical improvement ratios.43 Limited evidence indicates prolotherapy may be useful in improving knee pain, function, and stiffness compared to baseline.44


Gaps in the Evidence Based Knowledge

Additional research is needed in determining factors that help predict which subgroups of patients may benefit from specific interventions, and combined interventions such as bracing or hyaluronic acid injections and exercise. Research is also needed to provide evidence-based recommendations on lifestyle modifications for primary prevention as well as guidance on shaping public policy and population health initiatives.

The optimal exercise prescription for OA symptom management remains unclear.

Better knowledge regarding OA prevention strategies and interventions that can alter the course of OA progression, particularly in the post-traumatic injury knee, is needed.

Research is needed to determine whether there are OA pain phenotypes that are better responders to specific interventions.

Larger and higher-quality human studies of biologic therapies are needed to confirm beneficial findings from smaller studies.


  1. Cifu DX. Braddom’s Physical Medicine and Rehabilitation. 5th Edition. Philadelphia, PA: Elsevier. 2016: 666-668.
  2. Rosenthal BP. Knee Osteoarthritis. In: Scott WN. Insall & Scott Surgery of the Knee. 5th Edition. Philadelphia, PA: Churchill Livingstone; 2012: 718-722.
  3. Buckwalter JA, Martin JA. Sports and osteoarthritis. Curr Opin Rheumatol. 2014 Sep; 16(5): 634-639.
  4. Cross M, Smith E, Hoy D, et al. The global burden of hip and knee osteoarthritis: estimates from the global burden of disease 2010 study. Ann Rheum Dis. 2014;73(7):1323-1330.
  5. Lawrence RC, Felson DT, Helmick CG, Arnold LM, Choi H, Deyo RA, Gabriel S, Hirsch R, Hochberg MC, Hunder GG, Jordan JM, Katz JN, Kremers HM, Wolfe F; National Arthritis Data Workgroup. Estimates of the prevalence of arthritis and other rheumatic conditions in the United States Part II. Arthritis Rheum. 2008 Jan; 58(1): 26-35.
  6. Charlesworth J, Fitzpatrick J, Perera NKP, Orchard J. Osteoarthritis- a systematic review of long-term safety implications for osteoarthritis of the knee. BMC Musculoskelet Disord. 2019;20(1):151
  7. Wallace IJ, Worthington S, Felson DT, et al. Knee osteoarthritis has doubled in prevalence since the mid-20th century. Proc Natl Acad Sci U S A. 2017;114(35):9332-9336.
  8. Oliveria SA, Felson DT, Reed JI, Cirillo PA, Walker AM. Incidence of symptomatic hand, hip, and knee osteoarthritis among patients in a health maintenance organization. Arthritis Rheum. 1995 Aug; 38(8): 1134-1141.
  9. Cooper C, Snow S, McAlindon TE, et al. Risk factors for the incidence and progression of radiographic knee osteoarthritis. 2000;43(5):995-1000.
  10. Cleveland RJ, Alvarez C, Schwartz T, et al. The impact of painful knee osteoarthritis on mortality: a community-based cohort study with over 24 years of follow-up. 2019;27(4):593-602.
  11. Felson DT, Lawrence RC, Dieppe PA, Hirsch R, Helmick CG, Jordan JM, Kington RS, Lane NE, Nevitt MC, Zhang Y, Sowers M, McAlindon T, Spector TD, Poole AR, Yanovski SZ, Ateshian G, Sharma L, Buckwalter JA, Brandt KD, Fries JF. Osteoarthritis: new insights. Part 1: the disease and its risk factors. Ann Intern Med. 2000 Oct 17; 133(8): 635-646.
  12. Neogi T, Zhang Y. Osteoarthritis prevention. Curr Opin Rheumatol. 2011 Mar; 23(2): 185-191.
  13. Bliddal H, Christensen R. The treatment and prevention of knee osteoarthritis: a tool for clinical decision-making. Expert Opin Pharmacother. 2009 Aug; 10(11): 1793-804.
  14. Vincent HK, Heywood K, Connelly J, Hurley RW. Obesity and weight loss in the treatment and prevention of osteoarthritis. PM&R. 2012 May ;4(5 Suppl): S59-67.
  15. de Lange-Brokaar BJ, Ioan-Facsinay A, van Osch GJ, Zuurmond AM, Schoones J, Toes RE, Huizinga TW, Kloppenburg M. Synovial inflammation, immune cells and their cytokines in osteoarthritis: a review. Osteoarthritis Cartilage. 2012 Dec; 20(12): 1484-1499.
  16. Lee AS, Ellman MB, Yan D, et al. A current review of molecular mechanisms regarding osteoarthritis and pain. Gene. 2013;527(2):440-447
  17. Nelson AE, Jordan JM. Clinical Features of Osteoarthritis. In: Firestein GS, Budd RC, Gabriel SE, McInnesand IB, O’Dell JR. Kelley’s Textbook of Rheumatology. 9th ed. Saunders; 2013: 1636-1645.
  18. Manske RC, Ningini CM, Broztman SB. The Arthritic Lower Extremity. In: Brotzman SB. Clinical Orthopaedic Rehabilitation: An Evidence-Based Approach. 3rd Philadelphia, PA: Mosby, Inc; 2011: 380-389.
  19. Misra D, Felson DT, Silliman RA, Nevitt M, Lewis CE, Torner J, Neogi T. Knee osteoarthritis and frailty: findings from the multicenter osteoarthritis study and osteoarthritis initiative. J. Gerontol. 2015 March; 70(3); 337-342.
  20. Hawker GA, Croxford R, Bierman AS, Harvey PJ, Ravi B, Stanaitis I, Lipscombe LL. All-cause mortality and serious cardiovascular events in people with hip and knee osteoarthritis: a population based cohort study. PLoS One. 2014 Mar 7;9(3):e91286.
  21. Sohn MW, Manheim LM, Chang RW, Greenland P, Hochberg MC, Nevitt MC, Semanik PA, Dunlop DD. Sedentary behavior and blood pressure control among osteoarthritis initiative participants. Osteoarthritis Cartilage. 2014 Sep;22(9):1234-40.
  22. Kalunian KC. Diagnosis and classification of osteoarthritis. UpToDate. 2015.
  23. Zhang W, Doherty M, Peat G, et al. EULAR evidence-based recommendations for the diagnosis of knee osteoarthritis. Ann Rheum Dis. 2010;69(3):483-489.
  24. Iversen MD, Price LL, von Heideken J, Harvey WF, Wang C. Physical examination findings and their relationship with performance-based function in adults with knee osteoarthritis. BMC Musculoskelet Disord. 2016;17:273.
  25. Dobson F, Hinman RS, Roos EM, et al. OARSI recommended performance-based tests to assess physical function in people diagnosed with hip or knee osteoarthritis. 2013;21(8):1042-1052.
  26. Bijlsma JW, Berenbaum F, Lafeber FPJTL. Osteoarthritis: an update with relevance for clinical practice. 2011;377(9783):2115-2126.
  27. Boegård T, Rudling O, Petersson I, Jonsson KJO, cartilage. Joint space width of the tibiofemoral and of the patellofemoral joint in chronic knee pain with or without radiographic osteoarthritis: a 2-year follow-up. 2003;11(5):370-376.
  28. Roemer FW, Eckstein F, Hayashi D, Guermazi A. The role of imaging in osteoarthritis. Best Pract Res Clin Rheumatol. 2014 Feb;28(1):31-6.
  29. 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): 1115-1125.
  30. Dunlop D. Relation of physical activity time to incident disability in community dwelling adults with or at risk of knee arthritis: prospective cohort study. British Medical Journal. 2014; 348: 2472.
  31. Mikesky AE, Mazzuca SA, Brandt KD, Perkins SM, Damush T, Lane KA. Effects of strength training on the incidence and progression of knee osteoarthritis. Arthritis Rheum. 2006 Oct 15; 55(5): 690-699.
  32. Alnahdi AH, Zeni JA, Snyder-Mackler L. Muscle impairments in patients with knee osteoarthritis. Sports Health. 2012 Jul;4(4):284-92.
  33. Hochberg MC, Altman RD, April KT, Benkhalti M, Guyatt G, McGowan J, Towheed T, Welch V, Wells G, Tugwell P. American College of Rheumatology 2012 recommendations for the use of nonpharmacologic and pharmacologic therapies in osteoarthritis of the hand, hip and knee. Arthritis Care & Research. 2012 April; 64(4): 465-474.
  34. Rivera NV, Parmelee PA, Smith DM. The impact of social interactions and pain on daily positive and negative affect in adults with osteoarthritis of the knee. Aging Ment Health. 2018:1-7.
  35. Helminen EE, Sinikallio SH, Valjakka AL, Vaisanen-Rouvali RH, Arokoski JP. Determinants of pain and functioning in knee osteoarthritis: a one-year prospective study. Clin Rehabil. 2016;30(9):890-900.
  36. 36. McAlindon TE, et. al. OARSI guidelines for the non-surgical management of knee osteoarthritis. Osteoarthritis Cartilage. 2014 Mar;22(3):363-88.
  37. Jevsevar DS. Treatment of osteoarthritis of the knee: evidence-based guideline, 2nd edition. J Am Acad Orthop Surg. 2013 Sep;21(9):571-6.
  38. McAlindon TE, LaValley MP, Harvey WF, Price LL, Driban JB, Zhang M, Ward RJ. Effect of Intra-articular Triamcinolone vs Saline on Knee Cartilage Volume and Pain in Patients With Knee Osteoarthritis: A Randomized Clinical Trial. JAMA. 2017 May 16;317(19):1967-1975. doi: 10.1001/jama.2017.5283. PMID: 28510679.
  39. Felson DT. Arthroscopy as a treatment for knee osteoarthritis. Best Pract Res Clin Rheumatol. 2010 Feb;24(1):47-50.
  40. Shin CS, Lee JH. Arthroscopic treatment for osteoarthritic knee. Knee Surg Relat Res. 2012 Dec;24(4):187-92.
  41. Khoshbin A, Leroux T, Wasserstein D, et al. The Efficacy of Platelet-Rich Plasma in the Treatment of Symptomatic Knee Osteoarthritis: A Systematic Review With Quantitative Synthesis. Arthroscopy : the journal of arthroscopic & related surgery: official publication of the Arthroscopy Association of North America and the International Arthroscopy Association. 2013. 29:2037-48. 10.1016/j.arthro.2013.09.006.
  42. Shen L, Yuan T, Chen S, et al. The temporal effect of platelet-rich plasma on pain and physical function in the treatment of knee osteoarthritis: Systematic review and meta-analysis of randomized controlled trials. Journal of Orthopaedic Surgery and Research. 2017. 12. 10.1186/s13018-017-0521-3.
  43. Delanois R, Etcheson J, Sodhi N, et al. Biologic Therapies for the Treatment of Knee Osteoarthritis. The Journal of Arthroplasty. 2018. 34. 10.1016/j.arth.2018.12.001.
  44. Rabago D, Patterson JJ, Mundt M, Zgierska A, Fortney L, Grettie J, Kijowski R. Dextrose and morrhuate sodium injections (prolotherapy) for knee osteoarthritis: a prospective open-label trial. J Altern Complement Med. 2014 May; 20(5): 383-391.

Original Version of the Topic

Daniel C. Herman, MD, Ashley D. Zapf, MD, Heather K. Vincent, PhD, Kevin R Vincent, MD PhD. Knee Osteoarthritis. 10/6/2015.

Author Disclosure

Kevin Vu, BA
Nothing to Disclose

William Lian, MD
Nothing to Disclose

Donald Kasitinon, MD
Nothing to Disclose

Thiru Annaswamy, MD MA
Nothing to Disclose