Osteoarthritis of Knee – Symptoms, Diagnosis, Treatment

Osteoarthritis of Knee
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Osteoarthritis of Knee (OA) which is also known as osteoarthrosis or degenerative joint disease (DJD), is a progressive disorder of the joints caused by gradual loss of cartilage and resulting in the development of bony spurs and cysts at the margins of the joints. The name osteoarthritis comes from three Greek words meaning bone, joint, and inflammation.

Osteoarthritis is a multifactorial process in which mechanical factors have a central role and is characterized by changes in structure and function of the whole joint. There is no cure, and current therapeutic strategies are primarily aimed at reducing pain and improving joint function. We searched Medline for relevant articles (1966 to January 2006) and the Cochrane library (to first quarter of 2006) and consulted experts in rheumatology to produce a narrative review with an update on management for primary care doctors. We concentrated on osteoarthritis of the knee as this is associated with the greatest public health burden.

Osteoarthritis (OA) a common disease of an aged population and one of the leading causes of disability. The incidence of knee OA is rising by increasing average age of the general population. Age, weight, trauma to joint due to repetitive movements, in particular, squatting and kneeling are common risk factors of knee OA. Several factors including cytokines, leptin, and mechanical forces are pathogenic factors of knee OA. In patients with knee pain attribution of pain to knee OA should be considered with caution. Since a proportion of knee OA is asymptomatic and in a number of patients identification of knee OA is not possible due to the low sensitivity of radiographic examination. In this review data presented in regard to prevalence, pathogenesis, risk factors.


osteoarthritis of knee

Epidemiology /Etiology of Osteoarthritis of knee

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.

Osteoarthritis is the most prevalent form of arthritis and occurs especially in the knee joint. It affects nearly 6% of all adults, but more women are affected than men.“According to a number of published reports, anywhere from 6% to over 13% of men, but between 7% and 19% of women, over 45 years of age are affected, resulting in a 45% less risk of incidence in men (Coleman, et al).

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

Causes of Osteoarthritis (OA) of Knee

Articular cartilage increased the water content

  • alterations in proteoglycans eventual decrease in the number of proteoglycans
  • collagen abnormalities organization and orientation are lost
  • binding of proteoglycans to hyaluronic acid

Synovium and capsule

An early phase of OA

  • mild inflammatory changes in synovium

The middle phase of OA

  • moderate inflammatory changes of the synovium
  • synovium becomes hypervascular

Late phases of OA

  • synovium becomes increasingly thick and vascular


Subchondral bone attempts to remodel

  • forming lytic lesion with sclerotic edges (different than bone cysts in RA)
  • bone cysts form in late stages

Cell biology

Proteolytic enzymes matrix metalloproteases (MMPs)

Responsible for cartilage matrix digestion

  • examples
  •  stromelysin
  •  plasmin
  • aggrecanase-1 (ADAM-TS-4)

Tissue inhibitors of MMPS (TIMPs)

  • control MMP activity preventing excessive degradation
  • the imbalance between MMPs and TIMPs has been demonstrated in OA tissues

Inflammatory cytokines

Secreted by synoviocytes and increase MMP synthesis, examples

  •  IL-1
  •  IL-6
  • TNF-alpha

Genetics >Inheritance

  • in-mendelian

Genes potentially linked to OA

  • vitamin D receptor
  • estrogen receptor 1
  • inflammatory cytokines
  •  IL-1
  • leads to the catabolic effect
  •  IL-4
  •  matrilin-3
  • BMP-2, BMP-5

Risk Factor

Age is not the only factor that plays a role in the evolution of OA. Other risk factors are

  • Obesity
  • Joint hypermobility or instability
  • Sports stress with high impact loading
  • Repetitive knee bending or heavy weight lifting
  • Specific occupations
  • Peripheral neuropathy
  • Injury to the joint
  • History of immobilization
  • Family history


  • 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
 How does a normal knee work?

Your knee joint is where your thigh bone (femur) and your shin bone (tibia) meet. It allows the bones to move freely but within limits.

Your knee is the largest joint in the body and also one of the most complicated. It needs to be strong enough to take our weight and must lock into position so we can stand upright. But it also has to act as a hinge so we can walk, and it must withstand extreme stresses, twists, and turns, such as when we run or play sports.

Osteoarthritis formation

When your knee has osteoarthritis its surfaces become damaged and it doesn’t move as well as it should do. The following happens:

  • The cartilage becomes rough and thin – this can happen over the main surface of your knee joint and in the cartilage underneath your kneecap.
  • The bone underneath the cartilage reacts by growing thicker and becoming broader.
  • All the tissues in your joint become more active than normal as if your body is trying to repair the damage.
  • The bone at the edge of your joint grows outwards, forming bony spurs called osteophytes.
  • The synovium may swell and produce extra fluid, causing the joint to swell – this is called an effusion or sometimes water on the knee.
  • The capsule and ligaments slowly thicken and contract.

These changes in and around your joint are partly the result of the inflammatory process and partly an attempt by your body to repair the damage. In many cases, your body’s repairs are quite successful and the changes inside your joint won’t cause much pain or, if there is the pain, it’ll be mild and may come and go.

However, in other cases, the repair doesn’t work as well and your knee is damaged. This leads to instability and more weight being put onto other parts of the joint. This can cause symptoms to become gradually worse and more persistent over time.

Risk factors

osteoarthritis of knee -follow chart

Risk Factors can be Classified into  Primary & secondary


A number of studies have shown that there is a greater prevalence of the disease among siblings and especially identical twins, indicating a hereditary basis. Although a single factor is not generally sufficient to cause the disease, about half of the variation in susceptibility has been assigned to genetic factors

As early human ancestors evolved into bipeds, changes occurred in the pelvis, hip joint, and spine which increased the risk of osteoarthritis. Additionally, genetic variations that increase the risk were likely not selected against because usually problems only occur after reproductive success.

The development of osteoarthritis is correlated with a history of previous joint injury and with obesity, especially with respect to knees. Since the correlation with obesity has been observed not only for knees but also for non-weight bearing joints and the loss of body fat is more closely related to symptom relief than the loss of body weight, it has been suggested that there may be a metabolic link to body fat as opposed to just mechanical loading.

Changes in sex hormone levels may play a role in the development of osteoarthritis as it is more prevalent among post-menopausal women than among men of the same age. A study of mice found natural female hormones to be protective while injections of the male hormone dihydrotestosterone reduced protection.


Secondary osteoarthritis (due to an old injury with fracture) of the ankle in a woman of 82 years old

This type of osteoarthritis is caused by other factors but the resulting pathology is the same as for primary osteoarthritis:

  • Older age. The risk of osteoarthritis increases with age.
  • Sex. Women are more likely to develop osteoarthritis, though it isn’t clear why.
  • Obesity. Carrying extra body weight contributes to osteoarthritis in several ways, and the more you weigh, the greater your risk. Increased weight puts added stress on weight-bearing joints, such as your hips and knees. In addition, fat tissue produces proteins that may cause harmful inflammation in and around your joints.
  • Joint injuries. Injuries, such as those that occur when playing sports or from an accident, may increase the risk of osteoarthritis. Even injuries that occurred many years ago and seemingly healed can increase your risk of osteoarthritis.
  • Certain occupations. If your job includes tasks that place repetitive stress on a particular joint, that joint may eventually develop osteoarthritis.
  • Genetics. Some people inherit a tendency to develop osteoarthritis.
  • Bone deformities. Some people are born with malformed joints or defective cartilage, which can increase the risk of osteoarthritis.
  • Alkaptonuria
  • Congenital disorders of joints
  • Diabetes doubles the risk of having a joint replacement due to osteoarthritis and people with diabetes have joint replacements at a younger age than those without diabetes.
  • Ehlers-Danlos Syndrome
  • Hemochromatosis and Wilson’s disease
  • Inflammatory diseases (such as Perthes’ disease), (Lyme disease), and all chronic forms of arthritis (e.g., costochondritis, gout, and rheumatoid arthritis). In gout, uric acid crystals cause the cartilage to degenerate at a faster pace.
  • Injury to joints or ligaments (such as the ACL), as a result of an accident or orthopedic operations.
  • Ligamentous deterioration or instability may be a factor.
  • Marfan syndrome
  • Joint infection

The symptom of Osteoarthritis (OA) of Knee

The main symptoms of osteoarthritis of the knee are:

  • Pain (particularly when you’re moving your knee or at the end of the day – this usually gets better when you rest)
  • Stiffness (especially after rest – this usually eases after a minute or so as you get moving)
  • Crepitus, a creaking, crunching, grinding sensation when you move the joint
  • Hard swellings (caused by osteophytes)
  • Soft swellings (caused by extra fluid in the joint).
  • Loss of flexibility – You may not be able to move your joint through its full range of motion.
  • Grating sensation – You may hear or feel a grating sensation when you use the joint.
  • Bone spurs – These extra bits of bone, which feel like hard lumps, may form around the affected joint.

Other symptoms can include:

  • your knee giving way because your muscles have become weak or the joint structure is less stable
  • your knee not moving as freely or as far as normal
  • your knees becoming bent and bowed
  • the muscles around your joint looking thin or wasted.

It’s unusual, but some people have pain in their knee that wakes them up at night. This generally only happens with severe osteoarthritis.

You’ll probably find that your pain will vary and that you have good days and bad days, sometimes depending on how active you’ve been but sometimes for no clear reason.

Some people find that changes in the weather (especially damp weather and low pressure) make their pain and stiffness worse. This may be because nerve fibers in the capsule of their knee are sensitive to changes in atmospheric pressure.

Diagnosis of Osteoarthritis (OA) of Knee

Physical Examination

osteoarthritis of knee -diagnosis

During the physical examination, your doctor will look for:

Grading Knee

osteoarthritis of knee -diagnosis/Grade+of+Osteoathritis

For the grading of osteoarthritis in the knee, the most reliable systems are the International Knee Documentation Committee (IKDC) system and the Ahlbäck system, which have been found to be superior to for example systems by Kellgren-Lawrence, Fairbank, Brandt, and Jäger-Wirth. These findings refer to posteroanterior weight-bearing projection radiographs made with the knee in 45° of flexion.

Ahlbäck classification
Grade Findings
I Joint space narrowing, with or without subchondral sclerosis. Joint space narrowing is defined by this system as a joint space less than 3 mm, or less than half of the space in the other compartment, or less than half of the space of the homologous compartment of the other knee.
II Obliteration of the joint space
III Bone defect/loss <5 mm
IV Bone defect/loss between 5 and 10 mm
V Bone defect/loss >10 mm, often with subluxation and arthritis of the other compartment

For the patellofemoral joint, a classification by Merchant 1974 uses a 45° “skyline” view of the patella

Stage Description
1 (mild) Patellofemoral joint space > 3mm
2 (moderate Joint space < 3 mm but no bony contact
3 (severe) Bony surfaces in contact over less than one-quarter of the joint surface
4 (very severe) Bony contact throughout the entire joint surface

Goldberg recommends the following as a common approach to the examination of all joints

  • Make sure the area is well exposed—no clothing covering either side. Patient gowns come in handy
  • Carefully inspect the joint or joints in question. Are there signs of inflammation or injury (swelling, redness, warmth)? Deformity? Because many joints are symmetrical, compare it with the opposite side
  • Understand normal functional anatomy. What does this joint normally do?
  • Observe the joint while the patient attempts to perform the normal activity. What can’t the patient do? What specifically limits him/her? Was there a discrete event (eg, trauma) that caused this? If so, what was the mechanism of injury?
  • Palpate the joint in question. Is there warmth? Point tenderness? If so, over what anatomic structures?
  • Assess the range of motion, both active (patient moves it) and passive (you move it). If the active range of motion is limited, determine causes of pain
  • Perform strength and neurovascular assessments
  • Perform specific provocative maneuvers related to pathology occurring in that joint (Goldbergpresents some for each joint)
  • In the setting of acute injury and pain, it is often very difficult to assess a joint because the patient “protects” the affected area, limiting movement and thus your examination. It helps to examine the unaffected side first. This will help to set the patient at ease and will help the physician to gain a sense of the patient’s normal range of motion.

Lab Diagnostic

Laboratory tests and x-rays are often used in addition to these criteria.

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Osteoarthritis of the hand can often be diagnosed on the basis of these criteria alone, and laboratory tests and x-rays may be unnecessary. But in some cases it needed.

A normal erythrocyte sedimentation rate (ESR)

The presence of bony outgrowths (osteophytes) on x-rays

The presence of joint space narrowing on x-rays, indicating a loss of cartilage

osteoarthritis of knee -Osteoathritis


Laboratory tests 

The number of characteristics associated with knee pain varies depending on whether a diagnosis is being made using clinical criteria only, using clinical and radiographic criteria, or using clinical and laboratory criteria, as follows

Clinical: Knee pain for most days of the prior month, in addition to at least 3 of the following:
  • crepitus on active joint motion
  • morning stiffness less than 30 minutes’ duration
  • age older than 50 years
  • bony enlargement of the knee on examination
  • bony tenderness of the knee on examination
  • no palpable warmth.
Clinical plus radiographic: Knee pain for most days of the prior month, plus radiographic evidence of osteophytes on joint margins in addition to 1 of the following:
  • crepitus on active motion
  • morning stiffness less than 30 minutes’ duration
  • age older than 50 years.
Clinical plus laboratory: Knee pain for most days of the prior month, in addition to at least 5 of the following:
  • crepitus on active joint motion
  • morning stiffness less than 30 minutes’ duration
  • age older than 50 years
  • bony tenderness to palpation
  • bony enlargement
  • no palpable warmth
  • erythrocyte sedimentation rate below 40 mm/h
  • a rheumatoid factor less than 1:40
  • synovial fluid consistent with OA (white blood cell count < 2000/μL).

Laboratory tests may be recommended to help diagnose OA by ruling out conditions with similar symptoms.

Imaging tests —

 X-rays are often helpful for tracking the status of OA over time, but x-rays may appear normal during the early stages.

Other types of imaging tests, such as ultrasound and magnetic resonance imaging (MRI), may be used to detect damage to cartilage, ligaments, and tendons, which cannot be known by the following an investigation


  • scars
  • trauma
  • erythema
  • Swelling
  • Muscle atrophy
  • normal quadriceps circumference >10 cm (VMO), 15 cm (quadriceps)
  • Asymmetry


  • antalgia
  • stride length
  • muscle weakness

Standing limb alignment

  • neutral, varus, valgus
  • Joint line tenderness

Tenderness over soft tissue structures

  • pes anserine bursae
  • patellar tendon
  • iliotibial band

Point of maximal tenderness

  • Effusion
  • patella balloting
  • milking

Active and passive

flexion/extension normal range

  • 10° extension (recurvatum) to 130° flexion

Rotation varies with flexion

  • in full extension, there is ma inimal rotation
  • at 90° flexion, 45° ER and 30° IR


  • in full extension, essentially 0°
  • at 30° flexion, a few degrees of passive motion possible


  • medial thigh – obturator
  • anterior thigh – femoral
  • posterolateral calf – sciatic
  • dorsal foot – peroneal
  • plantar foot – tibial


  • thigh adduction – obturator
  • knee extension – femoral
  • knee flexion – sciatic
  • toe extension – peroneal
  • toe flexion – tibial



  • popliteal
  • dorsalis pedis
  • posterior tibial

Ankle-brachial index

  • ABI < 0.9 is abnormal
  • Large hemarthrosis
  • Quadriceps avoidance gait (does not actively extend knee)

Pivot shift

  • extension to flexion: reduces at 20-30° of flexion
  • patient must be completely relaxed (easier to elicit under anesthesia)
  • mimics the actual giving way event


  • useful to quantify anterior laxity
  • measured with knee in slight flexion and 10-30° externally rotation

PCL Injury

Posterior sag sign

patient lies supine with hips and knees flexed to 90°, examiner supports ankles and observes for a posterior shift of the tibia as compared to the uninvolved knee

Posterior drawer (at 90° flexion)

With the knee at 90° of flexion, a posteriorly directed force is applied to the proximal tibia and posterior tibial translation is quantified

  • the medial tibial plateau of a normal knee at rest is ~1 cm anterior to the medial femoral condyle

Most accurate maneuver for diagnosing PCL injury

Quadriceps active test

  • attempt to extend a knee flexed at 90° to elicit quadriceps contraction
  • positive if anterior reduction of the tibia occurs relative to the femur

MCL Injury

Valgus instability = medial opening

  • 30° only – isolated MCL
  • 0° and 30° – combined MCL and ACL and/or PCL


  • Grade I: 0-5 mm opening
  • Grade II: 6-10 mm opening
  • Grade III: 11-15 mm opening

Anterior Drawer with tibia in external rotation

  • grade III MCL tears often associated with ACL and posteriomedial corner tears
  • pthe ostive test will indicate associated ligamentous injury

LCL Injury

Varus instability = lateral opening

  • 30° only – isolated LCL
  • 0° and 30° – combined LCL and ACL and/or PCL
  • Varus opening and increased external tibial rotatory instability at 30° – combined LCL and posterolateral corner

PLC Injury


Varus thrust or hyperextension thrust

Varus stress test

  • varus laxity at 0° indicates both LCL & cruciate (ACL or PCL) injury
  • varus laxity at 30° indicates LCL injury.

Dial test

  • > 10° ER asymmetry at 30° only consistent with isolated PLC injury
  • > 10° ER asymmetry at 30° & 90° consistent with PLC and PCL injury

Reversed pivot shift test

  • with the knee positioned at 90°, ER and valgus forces are applied to tibia
  • as the knee is extended, the tibia reduces with a palpable clunk
    • tibia reduces from a posterior subluxed position at ~20° of flexion to a reduced position in full extension (reduction force from IT band transitioning from a flexor to an extensor of the knee)

External rotation recurvatum test

  • positive when the leg falls into ER and recurvatum when the lower extremity is suspended by the toes in a supine patient
  • Peroneal nerve assessment injury present with altered sensation to foot dorsum and weak ankle dorsiflexion

Meniscus Injury

  • Joint line tenderness
  • Effusion

McMurray’s test

  • flex the knee and place a hand on the medial side of knee externally rotate the leg and bring the knee into extension
  • a palpable pop or click is a positive test and can correlate with a medial meniscus tear

Patella Pathology

Large Hemarthrosis

  • The absence of swelling supports ligamentous laxity and habitual dislocation mechanism
  • Medial-sided tenderness (over MPFL)
  • Increase in passive patellar translation
  • measured in quadrants of translation (midline of the patella is considered “0”) and should be compared to the contralateral side
  • normal motion is <2 quadrants of patellar translation
  • lateral translation of medial border of patella to lateral edge of trochlear groove is considered “2” quadrants and is an abnormal amount of translation
  • Patellar apprehension
  • Increased Q angle

J sign

  • excessive lateral translation in extension which “pops” into groove as the patella engages the trochlea early in flexion
  • associated with patella alta

American College of Rheumatology criteria for the diagnosis of knee osteoarthritis

Using history and clinical examination*
   Pain in the knee and three of the following
1-Age >50 years
2- Morning stiffness <30 minutes
3-Crepitus on active motions
4-Bony tenderness
5-Bony enlargement
6-No palpable warmth of synovium
Using history and clinical examination and radiographic findings
   Pain in the knee and one of the following
1-Age >50 years
2- Morning stiffness < 30 minutes
3-Crepitus on active motions and osteophyte
Using history and clinical examination and laboratory findings
   Pain in the knee and 5 of the following
1- Age >50 years
2- Morning stiffness <30 minutes
3-Crepitus on active motions
4-Bony enlargement
5-No palpable warmth of synovium
6-ESR <40 mm/h
7-Rhgeumatoid Factor <1/40
8-Synovial fluid signs of osteoarthritis

*Reference: Altman, R, et al.: Arthritis Rheum 29:1039, 1986.