Knee Osteoarthritis

I. Anatomy, Physiology and Kinesiology Background

Knee Joint
 The knee joint traditionally is classified as a modified hinge joint located between the
femur and the tibia. Actually, it is a complex ellipsoid joint that allows flexion,
extension, and a small amount of rotation of the leg.
 The tibiofemoral joint consists of the articulations between the large, convex femoral
condyles and the nearly flat and smaller tibial condyles
 It is considered to be a double condyloid (modified hinge) joint with 20 of freedom of
motion.
 Flexion and extension – sagittal plane around a coronal axis.
 ER and IR – transverse plane about a vertical axis.
 The large articular surface area of the femoral condyles permits extensive knee
motion in the sagittal plane for activities such as running, squatting, and climbing.
Joint stability is provided not by a tight bony fit, but by forces and physical
containment provided by muscles, ligaments, capsule, menisci, and body weight.
 Resting position: 25° flexion
 Close packed position: Full extension, lateral rotation of tibia
 Capsular pattern: Flexion, extension
 The knee region (L. regio genus) includes the prominences (condyles) of the distal
femur and proximal tibia, the head of the fibula, and the patella (knee cap, which lies
anterior to the distal end of the femur), as well as the joints between these bony
structures.
 The posterior region of the knee (L. poples) includes a well-defined, fat-filled
hollow, transmitting neurovascular structures, called the popliteal fossa.
 Seeley’s Anatomy
Moore Clinically Oriented
Netter’s Atlas Kinesiology of the Musculoskeletal System
Magee’s Orthopedic Physical Assessment 6th Ed.

II. Definition
 Osteoarthritis is also called as degenerative joint disease, is characterized by
degeneration of cartilage that results in structural and functional failure of
synovial joints.
 Most prevalent form of arthritis and is a leading cause of impaired mobility in
the elderly.
 OA can lead to loss of mobility, chronic pain, deformity, and loss of function.
 OA is present worldwide as a heterogeneous group of conditions that lead to
slow, progressive degeneration of joint structures with defective integrity of
articular cartilage in addition to related changes in the underlying bone at the
joint margins
 Can be divided into two classifications:
 Primary OA - a disorder of unknown cause, and the cascade of joint
degeneration events associated with it is thought to be related to a
defect in the articular cartilage.
 Secondary OA- has a known cause, which may be trauma, infection,
hemarthrosis, osteonecrosis, or some other condition.
References:
Robbins and Cotran Pathologic Basis of Disease, 9th Ed.
Lippincott’s Primary Care Orthopaedics
O’Sullivan Physical Rehabilitation, 6th Ed
Goodman 4th Pathology implications for Physical Therapy
III. Etiology

 Etiology of OA is multifactorial, including many components of biomechanics and

biochemistry.
 Injury before adulthood may start the remodeling of a bone that modifies joint
mechanics and nourishment in a way that winds up risky only later in life.
 Sports that involve high-intensity, acute, direct joint impact from contact with
different players do convey an increased risk of OA, particularly when repetitive
joint impact and twisting are combined.
 Labral tears can likewise disrupt the synovial seal that contains the synovial fluid
inside the joint. The resulting increase in joint friction can further harm the joint
and contribute to the advancement of osteoarthritic changes.
 Evidence is growing for the role of systemic factors such as genetics, nutrition
and weight control, estrogen deficiency (menopause), bone density, immune
system response, and local biomechanical factors (e.g., muscle weakness,
obesity, femoral dysmorphia, soft-tissue laxity, mechanical properties of the
cartilage and labrum, and loads and positions imposed on the joint by functional
activities)
 Smokers with knee OA sustain greater cartilage loss and have more severe knee
pain than those who do not smoke, suggesting a role for tobacco in cartilage
degeneration.
 Football players, soccer players, hockey players, and baseball pitchers are
especially at increased risk
 Women with this syndrome may develop OA earlier than the norm. Muscle
weakness in anyone can also cause joint changes leading to OA, such as occurs
with prolonged immobilization, polymyositis, multiple sclerosis, or any of the
myopathies
 Some studies show a link between patellar alignment and patellofemoral OA
manifested by a loss of cartilage thickness and knee pain and disability

References:
O’Sullivan Physical Rehabilitation, 6th Ed.
Goodman Pathology Implications for the Physical Therapist, 4th Ed.

IV. Epidemiology
 OA is the most well-known type of arthritis and is widespread among people
more than 40 years old.
 27 million adults age 25 or more of the U.S. populace have clinical OA of some
joint.
 As the normal age of the U.S. populace expands, an expected 67 million
Americans will gain some type of arthritis by the year 2030.
 Approximately 10% to 30% of those influenced with OA have significant pain and
disability.
 Understanding the risk factors related with OA can help in further clarifying the
disease process as well as helping to potentially slow down OA progression.
References:
O’Sullivan Physical Rehabilitation, 6th Ed.
 Frontera and De Lisa’s Physical Rehabilitation and Medicine, 5th Ed.

V. Pathophysiology
 An increase in water content is involved in OA, with the proteoglycans having
been swollen with water far beyond ordinary.
 Articular cartilage loses its compressive stiffness and elasticity which brings
about the transfer of compressive forces to underlying bone.
 The joint space narrows as the articular cartilage is destroyed.
 Portrayed by biosynthesis and repair as the chondrocytes attempt to recover the
damaged matrix while the later stage is degradative in nature as catabolic
enzyme activity digests the matrix and dissolves the cartilage.
 Fibrous, cartilaginous, and bony prominences, known as osteophytes, eventually
develop around the periphery of the joints, but can likewise develop along joint
capsule insertions or project from the degenerating joint surfaces.
 Mild fraying or “flaking” of superficial collagen fibers and deeper fraying or
“fibrillation” of the upper third of the cartilage follows and may advance to full-
thickness fissures.
 Fissuring and eburnation of the cartilage, which is portrayed as the diminishing
and loss of the articular cartilage, bringing about the exposure of the subchondral
bone, which becomes denser with the surface getting worn and polished, can
occur.
 Tissue changes in OA are the result of active joint remodeling processes
involving an imbalance between catabolic and anabolic repair activity.
 People with OA may have a general tendency toward increased bone metabolic
activity, especially in response to biomechanical or other stimuli such as occurs
with obesity and injury
 As OA develops, loss of cartilage, hypertrophic changes in neighboring bone and
joint capsule, mild synovial inflammation, and degenerative changes in the
menisci, ligaments, and tendons all contribute to pain and loss of joint function,
resulting in joint failure
 The role of inflammation in the pathophysiology and progression of early OA is
supported further by the observation that C-reactive protein levels are raised in
women with early knee OA and higher levels predict those whose disease will
progress.

References:
O’Sullivan Physical Rehabilitation, 6th Ed.
Goodman Pathology Implications for the Physical Therapist, 4th Ed.
Frontera and De Lisa’s Physical Rehabilitation and Medicine, 5th Ed.

VI. Clinical Manifestation

 The most common symptoms of OA include bony enlargement, limited range

of motion, crepitus on motion, tenderness on pressure, joint effusion,
malalignment, and joint deformity
 Inflammation is a prominent sign that plays a role in symptom generation.
Soft-tissue inflammation and edema are observed during acute exacerbations
  The most commonly involved joints associated with this disorder are the
weight-bearing joints, especially the hip and knee but also the shoulder,
lumbar and cervical spine and the first carpometacarpal and
metatarsophalangeal joints.
 Pain with activity is most likely caused by enthesopathy and mechanical
factors, whereas pain at rest may be caused by synovial inflammation.
 Night pain is a poor prognostic indicator and may occur as a result of
intraosseous hypertension, which stretches periosteal pain neurons
 Stiffness of relatively short duration (less than 30 minutes) can occur after
periods of inactivity, including sitting and sleeping. Morning stiffness usually
only lasts 5 to 10 minutes after awakening.
 Movement and activity dissipate this stiffness until the individual sits or rests
for a long period of time.
 Bony enlargement
 Crepitus on motion
 Tenderness on pressure
 Joint effusion (not always present)
 Malalignment
 Joint deformity
 quadriceps muscle atrophy
 Unsteadiness on uneven surfaces or stairs, varus or valgus deformity (knee)

References:
O’Sullivan Physical Rehabilitation, 6th Ed.
Goodman Pathology Implications for the Physical
Rehabilitation, 4th Ed.

VII. Sequelae
 Decrease ROM
 Chronic pain
 Loss of mobility
 Deformity
References:
O’Sullivan Physical Rehabilitation, 6th Ed.
Frontera and De Lisa’s Physical Rehabilitation and Medicine, 5th Ed.
Goodman Pathology Implications for the Physical
Rehabilitation, 4th Ed.

VIII. Prognosis
OA is a slow progressing disease that can be self-limiting or progress to advanced
joint and soft tissue damage leading to complete failure of that joint. In addition, it is a
chronic condition with unpredictable symptoms that often cause fluctuations in pain
and function, resulting to functional limitations and reduced independence, commonly
in adults older than 65 years of age. In such a case, joint surgery including
arthrodesis of some joints in the foot, or arthroplasty, for instance, of the knee is one
treatment option to help the patient regain function. Another option to consider is to
follow the guidelines for lifestyle changes, pain management, and self-management
incorporating exercise and weight loss that can help to substantially decrease the
pain and dysfunction for patients with OA.
 References:
O’Sullivan Physical Rehabilitation, 6th Ed.
Goodman Pathology Implications for the Physical
Rehabilitation, 4th Ed.

IX. Medical Assessment

MRI
MRI is becoming increasingly helpful in determining
OA pathology because of its ability to show the condition
of cartilage and the surrounding soft tissues.
MRI is used to identify the presence of bone marrow lesions, synovitis, and periarticular
inflammation that can the source of
chronic pain for patients with OA.

OSTEOARTHRITIS: RADIOGRAPHIC FINDINGS*

• Joint space widening (early evidence)
• Subchondral bone sclerosis
• Subchondral bone cysts
• Osteophytes
• Joint space narrowing

Osteoarthritis of the knee. Proliferative marginal osteophytes (larger

arrows), narrowing of the medial weight-bearing joint space, and ebur
nation (exposure of the subchondral bone, surface becomes smooth and
polished as it wears down) (smaller arrows)
 Goodman Pathology Implications for the Physical
Rehabilitation, 4th Ed.

X. Medical Treatment
 Acetaminophen
 Topical capsaicin and glucosamine/chondroitin
 NSAIDs
 corticosteroid injections
 Surgical operations
References:
Goodman Pathology Implications for the Physical
Rehabilitation, 4th Ed.
O’Sullivan Physical Rehabilitation, 6th Ed.
XI. PT Assessment
 Inspection & History taking
 Range of Motion
 Anthropometric Measurement
 MMT
 Special Test
 Functional Examination
 Mobility, Gait and Balance
 Psychological Status
 Environmental Factors
References:
O’Sullivan Physical Rehabilitation, 6th Ed.
Magee Orthopedic Physical Assessment, 6th Ed

XII. PT Treatment
 Modalities (HMP, Cryotherapy, TENS)
 Orthoses, Splints and Braces
 Range of Motion and Flexibility exercises
 Strengthening exercises
 Aquatic Therapy
 Gait and Balance training

References:
O’Sullivan Physical Rehabilitation, 6th Ed.
Goodman Pathology Implications for the Physical
Rehabilitation, 4th Ed.

Prepared by:
Delgado, Ela Jamina A.
Del Rosario, Dinson G.