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Introduction
Continuing Education Activity Go to:
Etiology
Knee osteoarthritis (OA), also known as degenerative joint disease of the knee, is typically the result of
Epidemiology
wear and tear and progressive loss of articular cartilage. It is most common in the elderly. Knee
Pathophysiology
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 Histopathology
either an abnormal concentration of force across the joint as with post-traumatic causes or abnormal History and Physical
articular cartilage, such as rheumatoid arthritis (RA). Osteoarthritis is typically a progressive disease
Evaluation
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 Treatment / Management
time. The rate of progression also varies for each individual. Common clinical symptoms include knee Differential Diagnosis
pain that is gradual in onset and worse with activity, knee stiffness and swelling, pain after prolonged Prognosis
sitting or resting, and pain that worsens over time. Treatment for knee osteoarthritis begins with
Complications
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 Postoperative and Rehabilitation Care
disease-modifying agents for the treatment of knee osteoarthritis currently exist. This activity Deterrence and Patient Education
highlights the role of the interprofessional team in caring for patients with this condition.
Pearls and Other Issues
Objectives: Enhancing Healthcare Team Outcomes
References
Review the appropriate history, physical, and evaluation of knee osteoarthritis.
Etiology Go to:
Recent Activity
Knee osteoarthritis is classified as either primary or secondary, depending on its cause. Primary Turn Off Clear
knee osteoarthritis is the result of articular cartilage degeneration without any known reason. This is Knee Osteoarthritis - StatPearls
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] Osteoarthritis - StatPearls
Congenital or malformation of the limb Cell Viability Assays - Assay Guidance Manual
Malposition (varus/valgus)
See more...
Scoliosis
Rickets
Hemochromatosis
Chondrocalcinosis
Ochronosis
Wilson disease
Gout
Pseudogout
Acromegaly
Avascular necrosis
Rheumatoid arthritis
Infectious arthritis
Psoriatic arthritis
Hemophilia
Paget disease
Modifiable
Articular trauma
Weight
Non-modifiable
Age
Genetics
Race
Epidemiology Go to:
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]
Pathophysiology Go to:
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.
Histopathology Go to:
Collagen – same
Cartilage Changes in OA
Collagen – disorganized
Matrix Metalloproteases
Stromelysin
Plasmin
Aggrecanase-1 (ADAMTS-4)
Collagenase
Gelatinase
TIMP-1
TIMP-2
Alpha-2-macroglobulin
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.
Onset of symptoms
Severity of symptoms
Knee Pain
Knee stiffness
Knee swelling
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.
Medial meniscus
Quadricep tendon
Suprapatellar pouch
Patellar mobility
Prepatellar bursa
Patellar tendon
Tibial tubercle
Iliotibial band
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.
Evaluation Go to:
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
Osteophyte formation
Subchondral sclerosis
Subchondral cysts
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]
Patient education
Activity modification
Physical therapy
Weight loss
Knee bracing
Acetaminophen
COX-2 inhibitors
Corticosteroid injections
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.
Osteotomy
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.
Non-obese patients
Inflammatory arthritis
Obese patients
Patellofemoral arthritis
Ligamentous instability
Inflammatory arthritis
ACL deficiency
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.
Absolute
Relative
Neuropathic arthropathy
Morbid obesity
Poor health or presence of comorbidities that make the patient an unsuitable candidate for major
surgery and anesthesia
Less morbidity
Less expensive
Smaller incision
Improved cosmesis
Lasts longer
Any potential cause of local or diffuse knee pain should be considered in the differential diagnosis of
knee osteoarthritis.
Hip arthritis
Spinal stenosis
Patellofemoral syndrome
Meniscal tear
Infections arthritis
Gout
Pseudogout
Prognosis Go to:
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 Go to:
Complications associated with non-surgical treatment are largely associated with NSAID use.
Stomach ulcers
Kidney problems
Infection
Allergic reaction
Muscle pain
Trouble walking
Fever
Chills
Headache
Recurrence of deformity
Patella baja
Compartment syndrome
Malunion or nonunion
Infection
Persistent pain
Blood clot
Infection
Osteolysis
Persistent pain
Neurovascular injury
Blood clot
Infection
Instability
Osteolysis
Neurovascular injury
Fracture
Patellar maltracking
Stiffness
Wound complications
Heterotopic ossification
Blood clot
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.
The best predictor of final postoperative ROM following TKA is preoperative ROM, and patients
should be aware of this before TKA.
Employing interprofessional collaboration and information sharing regarding the patient's case will
drive better outcomes and increase the chances of avoiding TKA. [Level 5]
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