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Knee Osteoarthritis

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Last Update: June 26, 2023.

Continuing Education Activity

Knee osteoarthritis (OA), also known as degenerative joint disease of the knee, is typically the result of wear and tear and progressive loss of articular cartilage. It is most common in the elderly. Knee osteoarthritis can be divided into two types, primary and secondary. Primary osteoarthritis is articular degeneration without any apparent underlying reason. Secondary osteoarthritis is the consequence of either an abnormal concentration of force across the joint as with post-traumatic causes or abnormal articular cartilage, such as rheumatoid arthritis (RA). Osteoarthritis is typically a progressive disease that may eventually lead to disability. The intensity of the clinical symptoms may vary from each individual. However, they typically become more severe, more frequent, and more debilitating over time. The rate of progression also varies for each individual. Common clinical symptoms include knee pain that is gradual in onset and worse with activity, knee stiffness and swelling, pain after prolonged sitting or resting, and pain that worsens over time. Treatment for knee osteoarthritis begins with conservative methods and progresses to surgical treatment options when conservative treatment fails. While medications can help slow the progression of RA and other inflammatory conditions, no proven disease-modifying agents for the treatment of knee osteoarthritis currently exist. This activity highlights the role of the interprofessional team in caring for patients with this condition.


  • Identify the etiology of knee osteoarthritis.
  • Review the appropriate history, physical, and evaluation of knee osteoarthritis.
  • Outline the management options available for knee osteoarthritis.
  • Describe interprofessional team strategies for improving communication to advance medical care and improve outcomes for knee osteoarthritis.
Access free multiple choice questions on this topic.


Knee osteoarthritis (OA), also known as degenerative joint disease, is typically the result of wear and tear and progressive loss of articular cartilage. It is most common in the elderly. Knee osteoarthritis can be divided into two types, primary and secondary. Primary osteoarthritis is articular degeneration without any apparent underlying reason. Secondary osteoarthritis is the consequence of either an abnormal concentration of force across the joint as with post-traumatic causes or abnormal articular cartilage, such as rheumatoid arthritis (RA).

Osteoarthritis is typically a progressive disease that may eventually lead to disability. The intensity of the clinical symptoms may vary for each individual. However, they typically become more severe, more frequent, and more debilitating over time. The rate of progression also varies for each individual. Common clinical symptoms include knee pain that is gradual in onset and worse with activity, knee stiffness and swelling, pain after prolonged sitting or resting, and pain that worsens over time. Treatment for knee osteoarthritis begins with conservative methods and progresses to surgical treatment options when conservative treatment fails. While medications can help slow the progression of RA and other inflammatory conditions, no proven disease-modifying agents for the treatment of knee osteoarthritis currently exist.[1][2][3]


Knee osteoarthritis is classified as either primary or secondary, depending on its cause. Primary knee osteoarthritis is the result of articular cartilage degeneration without any known reason. This is typically thought of as degeneration due to age as well as wear and tear. Secondary knee osteoarthritis is the result of articular cartilage degeneration due to a known reason.[4][5]

Possible Causes of Secondary Knee OA

  • Posttraumatic
  • Postsurgical
  • Congenital or malformation of the limb
  • Malposition (varus/valgus)
  • Scoliosis
  • Rickets
  • Hemochromatosis
  • Chondrocalcinosis
  • Ochronosis
  • Wilson disease
  • Gout
  • Pseudogout
  • Acromegaly
  • Avascular necrosis
  • Rheumatoid arthritis
  • Infectious arthritis
  • Psoriatic arthritis
  • Hemophilia
  • Paget disease
  • Sickle cell disease

Risk Factors for Knee OA


  • Articular trauma
  • Occupation – prolonged standing and repetitive knee bending
  • Muscle weakness or imbalance
  • Weight
  • Health – metabolic syndrome


  • Gender - females more common than males
  • Age
  • Genetics
  • Race


Knee osteoarthritis is the most common type of arthritis diagnosed, and its prevalence will continue to increase as life expectancy and obesity rises. Depending on the source, roughly 13% of women and 10% of men 60 years and older have symptomatic knee osteoarthritis. Among those older than 70 years of age, the prevalence rises to as high as 40%. The prevalence of knee osteoarthritis in males is also lower than in females. Interestingly, not everyone who demonstrates radiographic findings of knee osteoarthritis will be symptomatic. One study found that only 15% of patients with radiographic findings of knee OA were symptomatic. Not factoring in age, the incidence of symptomatic knee osteoarthritis is roughly 240 cases per 100,000 people per year.[6][7]


Articular cartilage is composed primarily of type II collagen, proteoglycans, chondrocytes, and water. Healthy articular cartilage constantly maintains an equilibrium between each of the components so that any degradation of cartilage is matched by synthesis. Healthy articular cartilage is thus maintained. In the process of osteoarthritis, matrix metalloproteases (MMPs), or degradative enzymes, are overexpressed, disrupting the equilibrium and resulting in an overall loss of collagen and proteoglycans. In the early stages of osteoarthritis, chondrocytes secrete tissue inhibitors of MMPs (TIMPs) and attempt to increase the synthesis of proteoglycans to match the degradative process. However, this reparative process is not enough. The loss in equilibrium results in a decreased amount of proteoglycans despite increased synthesis, increased water content, the disorganized pattern of collagen, and ultimately loss of articular cartilage elasticity. Macroscopically these changes result in cracking and fissuring of the cartilage and ultimately erosion of the articular surface.[8]

Although knee osteoarthritis is closely correlated with aging, it is important to note that knee osteoarthritis is not simply a consequence of aging but rather its own disease. This is supported by the differences seen in cartilage with both osteoarthritis and aging. Furthermore, the enzymes responsible for cartilage degradation are expressed in higher amounts in knee osteoarthritis, whereas they are at normal levels in the normal aging cartilage.


Cartilage Changes in Aging [9]

  • Water content – decreased
  • Collagen – same
  • Proteoglycan content – decreased
  • Proteoglycan synthesis – same
  • Chondrocyte size – increased
  • Chondrocyte number – decreased
  • Modulus of elasticity – increased

Cartilage Changes in OA

  • Water content – increased
  • Collagen – disorganized
  • Proteoglycan content – decreased
  • Proteoglycan synthesis – increased
  • Chondrocyte size – same
  • Chondrocyte number – same
  • Modulus of elasticity – decreased

Matrix Metalloproteases

Responsible for cartilage matrix degradation

  • Stromelysin
  • Plasmin
  • Aggrecanase-1 (ADAMTS-4)
  • Collagenase
  • Gelatinase

Tissue Inhibitors of MMPs

Control MMP activity preventing excess degradation

  • TIMP-1
  • TIMP-2
  • Alpha-2-macroglobulin

History and Physical

Patients typically present to their healthcare provider with the chief complaint of knee pain. Therefore, it is essential to obtain a detailed history of their symptoms. Pay careful attention to the history as knee pain can be referred from the lumbar spine or the hip joint. It is equally important to obtain a detailed medical and surgical history to identify any risk factors associated with secondary knee OA.

The history of the present illness should include the following: 

  • Onset of symptoms
  • Specific location of pain
  • Duration of pain and symptoms
  • Characteristics of the pain
  • Alleviating and aggravating factors
  • Any radiation of pain
  • Specific timing of symptoms
  • Severity of symptoms
  • The patient's functional activity

Clinical Symptoms of Knee OA

Knee Pain

  • Typically of gradual onset
  • Worse with prolonged activity
  • Worse with repetitive bending or stairs
  • Worse with inactivity
  • Worsening over time
  • Better with rest
  • Better with ice or anti-inflammatory medication
  • Knee stiffness
  • Knee swelling
  • Decreased ambulatory capacity

Physical examination of the knee should begin with a visual inspection. With the patient standing, look for periarticular erythema and swelling, quadriceps muscle atrophy, and varus or valgus deformities. Observe gait for signs of pain or abnormal motion of the knee joint that can indicate ligamentous instability. Next, inspect the surrounding skin for the presence and location of any scars from previous surgical procedures, overlying evidence of trauma, or any soft tissue lesions.

Range of motion (ROM) testing is an essential aspect of the knee exam. Active and passive ROM with regard to flexion and extension should be assessed and documented.

Palpation along the bony and soft tissue structures is an essential part of any knee exam. The palpatory exam can be broken down into the medial, midline, and lateral structures of the knee.

Areas of Focus for the Medial Aspect of the Lnee

  • Vastus medialis obliquus
  • Superomedial pole patella
  • Medial facet of the patella
  • Origin of the medial collateral ligament (MCL)
  • Midsubstance of the MCL
  • Broad insertion of the MCL
  • Medial joint line
  • Medial meniscus
  • Pes anserine tendons and bursa

Areas of Focus for the Midline of the Knee

  • Quadricep tendon
  • Suprapatellar pouch
  • Superior pole patella
  • Patellar mobility
  • Prepatellar bursa
  • Patellar tendon
  • Tibial tubercle

Areas of Focus for the Lateral Aspect of the Knee

  • Iliotibial band
  • Lateral facet patella
  • Lateral collateral ligament (LCL)
  • Lateral joint line
  • Lateral meniscus
  • Gerdy’s tubercle

A thorough neurovascular exam should be performed and documented. It is important to assess the strength of the quadriceps and hamstring muscles as these often will become atrophied in the presence of knee pain. A sensory exam of the femoral, peroneal, and tibial nerve should be assessed as there may be concomitant neurogenic symptoms associated. Palpation of a popliteal, dorsalis pedis, and posterior tibial pulse is important as any abnormalities may raise the concern for vascular problems.

Other knee tests may be performed, depending on the clinical suspicion based on the history.

Special Knee Tests

  • Patella apprehension – patellar instability
  • J-sign – patellar maltracking
  • Patella compression/grind – chondromalacia or patellofemoral arthritis
  • Medial McMurray – a medial meniscus tear
  • Lateral McMurray – lateral meniscus tear
  • Thessaly test – a meniscus tear
  • Lachman – anterior cruciate ligament (ACL) injury
  • Anterior drawer – ACL injury
  • Pivot shift – ACL injury
  • Posterior drawer – posterior cruciate ligament (PCL) injury
  • Posterior sag – PCL injury
  • Quadriceps active test – PCL injury
  • Valgus stress test – MCL injury
  • Varus stress test – LCL injury


In addition to a thorough history and physical, radiographic imaging is required. The recommend views include standing anteroposterior (AP), standing lateral in extension, and a skyline view of the patella. A standing 45-degree posteroanterior (PA) view of the knee may be obtained, which gives a better assessment of the weight-bearing surface of the knee. Occasionally, long leg standing films will be obtained to view the degree of deformity and overall alignment of the lower extremity. It is important to understand that radiographs of the knee must be obtained with the patient standing. This gives an accurate representation of the joint space narrowing present. Often, films will be taken with the patient supine, which gives a false sense of joint space and alignment and should not be used to evaluate suspected knee OA.[10][11][12]

Radiographic Findings of OA

  • Joint space narrowing
  • Osteophyte formation
  • Subchondral sclerosis
  • Subchondral cysts

Treatment / Management

Treatment for knee osteoarthritis can be broken down into non-surgical and surgical management. Initial treatment begins with non-surgical modalities and moves to surgical treatment once the non-surgical methods are no longer effective. A wide range of non-surgical modalities is available for the treatment of knee osteoarthritis. These interventions do not alter the underlying disease process, but they may substantially diminish pain and disability.[9][13][12]

Non-Surgical Treatment Options [10]

  • Patient education
  • Activity modification
  • Physical therapy
  • Weight loss
  • Knee bracing
  • Acetaminophen
  • Nonsteroidal anti-inflammatory drugs (NSAIDs)
  • COX-2 inhibitors
  • Glucosamine and chondroitin sulfate
  • Corticosteroid injections
  • Hyaluronic acid (HA)

The first-line treatment for all patients with symptomatic knee osteoarthritis includes patient education and physical therapy. A combination of supervised exercises and a home exercise program have been shown to have the best results. These benefits are lost after 6 months if the exercises are stopped. The American Academy of Orthopedic Surgeons (AAOS) recommends this treatment.

Weight loss is valuable in all stages of knee osteoarthritis. It is indicated in patients with symptomatic arthritis with a body mass index greater than 25. The best recommendation to achieve weight loss is diet control and low-impact aerobic exercise. There is moderate evidence for weight loss based on the AAOS guidelines.

Knee bracing in osteoarthritis includes unloader-type braces that shift the load away from the involved knee compartment. This may be useful in the setting where either the lateral or medial compartment of the knee is involved, such as in a valgus or varus deformity.

Drug therapy is also the first-line treatment for patients with symptomatic osteoarthritis. A wide variety of NSAIDs are available, and the choice should be based on physician preference, patient acceptability, and cost. The duration of treatment with NSAIDs should be based on effectiveness, adverse effects, and past medical history. There is strong evidence for NSAID use based on the AAOS guidelines.

Glucosamine and chondroitin sulfate are available as dietary supplements. They are structural components of articular cartilage, and the thought is that a supplement will aid in the health of articular cartilage. No strong evidence exists that these supplements are beneficial in knee OA; in fact, there is strong evidence against the use according to the AAOS guidelines. There are no major downsides to taking the supplement. If the patient understands the evidence behind these supplements and is willing to try the supplement, it is a relatively safe option. Any benefit gained from supplementation is likely due to a placebo effect.

Intra-articular corticosteroid injections may be useful for symptomatic knee osteoarthritis, especially where there is a considerable inflammatory component. The delivery of the corticosteroid directly into the knee may reduce local inflammation associated with osteoarthritis and minimize the systemic effects of the steroid.

Intra-articular hyaluronic acid injections (HA) injections are another injectable option for knee osteoarthritis. HA is a glycosaminoglycan found throughout the human body and is an important component of synovial fluid and articular cartilage. HA breaks down during the process of osteoarthritis and contributes to the loss of articular cartilage as well as stiffness and pain. Local delivery of HA into the joint acts as a lubricant and may help increase the natural production of HA in the joint. Depending on the brand of HA, it can either be produced from avian cells or bacterial cells in the laboratory and therefore must be used with caution in those with avian allergies. While this is a prevalent treatment option, it is not highly supported in the literature, and there is strong evidence against its use based on the AAOS guidelines. 

Surgical Treatment Options [13]

  • Osteotomy
  • Unicompartmental knee arthroplasty (UKA)
  • Total knee arthroplasty (TKA)

A high tibial osteotomy (HTO) may be indicated for unicompartmental knee osteoarthritis associated with malalignment. Typically an HTO is done for varus deformities where the medial compartment of the knee is worn and arthritic. The ideal patient for an HTO would be a young, active patient in whom arthroplasty would fail due to excessive component wear. An HTO preserves the actual knee joint, including the cruciate ligaments, and allows the patient to return to high-impact activities once healed. It does require additional healing time compared to an arthroplasty, is more prone to complications, depends on bone and fracture healing, is less reliable for pain relief, and ultimately does not replace cartilage that is already lost or repair any remaining cartilage. An osteotomy will delay the need for arthroplasty for up to 10 years.

Indications for HTO

  • Young (less than 50 years old), active patient
  • Healthy patient with good vascular status
  • Non-obese patients
  • Pain and disability interfering with daily life
  • Only one knee compartment is affected
  • A compliant patient who will be able to follow postoperative protocol

Contraindications for HTO

  • Inflammatory arthritis
  • Obese patients
  • Knee flexion contracture greater than 15 degrees
  • Knee flexion less than 90 degrees
  • If the procedure will need greater than 20 degrees of deformity correction
  • Patellofemoral arthritis
  • Ligamentous instability

A UKA also is indicated in unicompartmental knee osteoarthritis. It is an alternative to an HTO and a TKA. It is indicated for older patients, typically 60 years or older, and relatively thin patients, although, with newer surgical techniques, the indications are being pushed.

Indications for UKA

  • Older (60 years or older), lower demand patients
  • Relatively thin patients

Contraindications for UKA

  • Inflammatory arthritis
  • ACL deficiency
  • Fixed varus deformity greater than 10 degrees
  • Fixed valgus deformity greater than 5 degrees
  • Arc of motion less than 90 degrees
  • Flexion contracture greater than 10 degrees
  • Arthritis in more than one compartment
  • Younger, higher activity patients or heavy laborers
  • Patellofemoral arthritis 

A TKA is the surgical treatment option for patients failing conservative management and those with osteoarthritis in more than one compartment. It is regarded as a valuable intervention for patients who have severe daily pain along with radiographic evidence of knee osteoarthritis.

Indications for TKA

  • Symptomatic knee OA in more than one compartment
  • Failed non-surgical treatment options

Contraindications for TKA


  • Active or latent knee infection
  • Presence of active infection elsewhere in the body
  • Incompetent quadriceps muscle or extensor mechanism


  • Neuropathic arthropathy
  • Poor soft-tissue coverage
  • Morbid obesity
  • Noncompliance due to major psychiatric disorder or alcohol or drug abuse
  • Insufficient bone stock for reconstruction
  • Poor health or presence of comorbidities that make the patient an unsuitable candidate for major surgery and anesthesia
  • Patient’s poor motivation or unrealistic expectations
  • Severe peripheral vascular disease

Advantages of UKA vs. TKA

  • Faster rehabilitation and quicker recovery
  • Less blood loss
  • Less morbidity
  • Less expensive
  • Preservation of normal kinematics
  • Smaller incision
  • Less post-surgical pain and shorter hospital stay

Advantages of UKA vs. HTO

  • Faster rehabilitation and quicker recovery
  • Improved cosmesis
  • Higher initial success rate
  • Fewer short-term complications
  • Lasts longer
  • Easier to convert to TKA

Differential Diagnosis

Any potential cause of local or diffuse knee pain should be considered in the differential diagnosis of knee osteoarthritis.

  • Hip arthritis
  • Low back pain
  • Spinal stenosis
  • Patellofemoral syndrome
  • Meniscal tear
  • Pes anserine bursitis
  • Infections arthritis
  • Gout
  • Pseudogout
  • Iliotibial band syndrome
  • Collateral or cruciate ligament injury


Strong evidence shows that age, ethnicity, BMI, the number of co-morbidities, MRI-detected infrapatellar synovitis, joint effusion, and both radiographic and the baseline of OA severity are predictive for clinical progression of knee osteoarthritis.[14] The most severe cases will result in total knee arthroplasty.[15]


Complications associated with non-surgical treatment are largely associated with NSAID use.

Common Adverse Effects of NSAID Use

  • Stomach pain and heartburn
  • Stomach ulcers
  • A tendency to bleed, especially while taking aspirin
  • Kidney problems

Common Adverse Effects of Intra-Articular Corticosteroid Injection

  • Pain and swelling (cortisone flare)
  • Skin discoloration at the site of injection
  • Elevated blood sugar
  • Infection
  • Allergic reaction

Common Adverse Effects of Intra-Articular HA Injection

  • Injection site pain
  • Muscle pain
  • Trouble walking
  • Fever
  • Chills
  • Headache

Complications Associated with HTO

  • Recurrence of deformity
  • Loss of posterior tibial slope
  • Patella baja
  • Compartment syndrome
  • Peroneal nerve palsy
  • Malunion or nonunion
  • Infection
  • Persistent pain
  • Blood clot

Complications Associated with UKA

  • Stress fracture of the tibia
  • Tibial component collapse
  • Infection
  • Osteolysis
  • Persistent pain
  • Neurovascular injury
  • Blood clot

Complications Associated with TKA

  • Infection
  • Instability
  • Osteolysis
  • Neurovascular injury
  • Fracture
  • Extensor mechanism rupture
  • Patellar maltracking
  • Patellar clunk syndrome
  • Stiffness
  • Peroneal nerve palsy
  • Wound complications
  • Heterotopic ossification
  • Blood clot

Postoperative and Rehabilitation Care

Postoperative and rehabilitation care after a TKA is aimed at restoring the highest possible range of mobility in and full muscular control of the operated knee. Adequate rehabilitation is an important requirement for successful TKA.[9] The specific rehabilitation program following a TKA is somewhat controversial and varies from surgeon to surgeon. Bed mobility, transfer training, and bedside exercises begin the same day as surgery. Full weight-bearing, typically with a walker, under the supervision of a therapist, is also allowed. Active range of motion (ROM), terminal knee extensions, straight leg raises, and muscle strengthening exercises begin postoperative day one. Gait training and transfers continue as well. In general, the patient must demonstrate safe ambulation with an assistive walking device on flat ground and stairs, the ability to safely transfer from bed to seated and standing positions, and adequate pain control prior to being discharged from the hospital. Patients are typically discharged to home or a skilled nursing facility. This is based on individual needs in consultation with social work. Discharge to home is greatly preferred if possible.

The typical hospital stays for a TKA is 1 to 2 nights, depending on the patient. The first postoperative visit is at the two-week mark, where a wound check is performed, and surgical staples are removed if present. Outpatient physical therapy will begin at this time if not begun already. The patient increases their ambulation, independence in their activities of daily living, works on their ROM and works on their quadriceps strength. Patients can resume driving when they can operate the pedals safely and rapidly. This usually takes 4 to 6 weeks. Return to work usually takes 4 to 10 weeks, depending on the work obligations. Patient follow-up is routinely at 6 weeks, 3 months, and one year after surgery. Once strength, mobility, and balance are regained, patients can resume low-impact sporting activities. High-impact activities are discouraged.

Deterrence and Patient Education

Patient education centers around non-medication and medication-based approaches. Non-medication approaches include weight loss, orthoses/bracing to correct joint alignment, exercise and physical therapy, and support groups. Medication compliance needs to be emphasized; sometimes, patient compliance wanes as symptomatic control from the drug occurs. Patients need to understand the disease has no cure and the likely progression that can take place, particularly with non-compliance to the therapeutic recommendations.

Pearls and Other Issues

The best predictor of final postoperative ROM following TKA is preoperative ROM, and patients should be aware of this before TKA.

Enhancing Healthcare Team Outcomes

Knee osteoarthritis (OA) is best managed by an interprofessional team that consists of an orthopedic surgeon, rheumatologist, physical therapist, dietitian, pain specialist, internist, nursing staff, physical therapist, and pharmacist. The disorder has no cure, and thus attempts should be made to prevent the progression of the disorder. The patient should be referred to a dietitian for weight loss and physical therapy to regain joint function and muscle strength. Treatment for knee osteoarthritis begins with conservative methods and progresses to surgical treatment options when conservative treatment fails. The pharmacist should look at the patient's medications to ensure there are no interactions and that the dosing and indications are all correct. While medications can help slow the progression of RA and other inflammatory conditions, no proven disease-modifying agents for the treatment of knee osteoarthritis currently exist. [Level 2]

Employing interprofessional collaboration and information sharing regarding the patient's case will drive better outcomes and increase the chances of avoiding TKA. [Level 5]

Review Questions


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Disclosure: Hunter Hsu declares no relevant financial relationships with ineligible companies.

Disclosure: Ryan Siwiec declares no relevant financial relationships with ineligible companies.

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