Osteoarthritis

Cartilage
Tough but flexible connective tissue
Cushions bones at joints between bones, the rib cage, and the intervertebral discs
Gives shape and support to other parts of the body. such as the ears, nose and windpipe
Not as hard and rigid as bone, but, is stiffer and less flexible than muscle
Composed of specialized cells called chondrocytes that produce a large amount of
extracellular matrix composed of collagen fibers, abundant ground substance rich in
proteoglycan, and elastin fibers.
Does not contain blood vessels
The chondrocytes are supplied by diffusion and the pumping action generated by
compression of the articular cartilage or flexion of the elastic cartilage. Thus, cartilage
grows and repairs more slowly.

Types of Cartilage:
* Three types:

1. Hyaline cartilage
* low-friction and wear-resistant tissue
* present within joints
* designed to bear and distribute weight
* strong, rubbery, flexible tissue but has a
poor regenerative capacity

2. ELASTIC CARTILAGE
* more flexible that hyaline cartilage
* present in the ear, larynx and epiglottis

3. FIBROCARTILAGE
* tough and inflexible form of cartilage
* found in the knee and between vertebrae Fibrocartilage

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 Osteoarthritis (OA)
is a condition affect synovial joints that represents failed repair of joint damage that results
from stresses that may be initiated by an abnormality in any of the synovial joint tissues.

1 OA may be localized to 1 joint, to a few joints, or be generalized.

Osteoarthritis (OA) is by far the most common form of arthritis and is a major cause of pain
and disability in older people
The prevalence rises progressively with age and it has been estimated that 45% of all people
develop knee OA and 25% hip OA at some point during life.
Types of Osteoarthritis
* 2 main types of osteoarthritis - different causes:
idiopathic osteoarthritis
® No identifiable cause
® May be localized (confined to one or two joints) or generalized ( present in three or more
joints)
Secondary osteoarthritis
* Caused by an underlying condition: joint injury, accumulation of calcium inside the joint,
other bone and joint conditions (eg, rheumatoid arthritis), or a medical condition, such as
diabetes

Table 1 Principal manifestations of OA

Symptoms
Joint pain Usually affects 1 to few joints at a time
Insidious onset: slow progression over months to years
Variable intensity throughout the day and the week
May be intermittent and relapsing
Increased by joint use and impact
Relieved by rest
Night pain may occur in severe OA
Stiffness Short-lived (<30 min) early morning stiffness
Short-lived inactivity-related stiffness (gelling)
Swelling Some (eg, nodal OA) patients present with swelling and/or deformity

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Age >40 y a
Constitutional symptoms (eg, Absent
weight loss, sweats, fever)
Signs
Appearance Swelling (usually bony ± fluid/soft tissue)
Resting position (attitude)
Deformity
Muscle wasting (global: all muscles acting over the joint)
Feel Absence of warmth
Swelling: bony or effusion
Effusion if present is usually small and cool
Joint-line tenderness
Periarticular tenderness (especially knee, hip)
Movement Coarse crepitus b
Reduced range of movement
Weak local muscles

26.37 Symptoms and signs of osteoarthritis

Pain
Insidious onset over months or years
Variable or intermittent nature over time (‘good days, bad days’)
Mainly related to movement and weight-bearing, relieved by rest
Mild morning stiffness (< 15 mins) and inactivity gelling (< 5 mins) after rest
Usually only one or a few joints painful
Clinical signs
Restricted movement due to capsular thickening or blocking by osteophyte
Palpable, sometimes audible, coarse crepitus due to rough articular surfaces
Bony swelling around joint margins
Deformity, usually without instability
Joint-line or periarticular tenderness
Muscle weakness and wasting ‫من المصدر لالطالع‬
Mild or absent synovitis

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Table 2 Stages of pain in OA

Stage 1 (Early) Predictable sharp pain, usually brought on by a mechanical insult that
eventually limits high-impact activities. There may only be a minimal
effect on function.

Stage 2 (Mild- Pain becomes a more regular feature, and begins to affect daily activities.
moderate) There may be unpredictable episodes of stiffness.

Stage 3 Constant dull/aching pain, punctuated by short episodes of often

(Advanced) unpredictable intense, exhausting pain that results in severe functional
limitations.

Diagnosis
Diagnosis is made with reasonable certainty based on
history and clinical examination
No single test can diagnose osteoarthritis
Most doctors use methods that include medical history,
a physical exam, x-rays, or lab tests
Different types of arthritis need different treatments

The diagnosis of osteoarthritis includes 3 major stages:

1. Patient history analysis
2 Physical examination
3. Imaging and Laboratory tests
Patient history analysis
The diagnosis begins with medical history, or information about :

Patient's health background

conditions running in the family as some disorder are inherited.
Symptoms that prompts a patient to seck medical attention

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Physical Examination
®* Based on the symptoms and the physical signs found when examining joints. The doctor
checks for:

joint tenderness
creaking or grating (crepitus) sounds
bony swelling
excess fluid
reduced movement
joint instability
muscle thinning

Imaging and Laboratory Tests

Imaging Tests:
* X-ray
* Magnetic Resonance Imaging (MRI)
* Arthroscopy
Laboratory tests :
® Blood tests :
® Joint Fluid Analysis/Joint aspiration

Imaging Tests
X-ray
Most useful test to confirm osteoarthritis
Cartilage doesn't show up on X-ray images
Cartilage loss is revealed by a narrowing of the space between the bones in your joint
Bone spurs may be observed around a joint.
Patients may have X-ray evidence of osteoarthritis before experiencing any symptoms
Detect calcium settling in joints

MRI
Uses radio waves and a strong magnetic field to produce detailed images of bone and soft
tissues, including cartilage

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 Not commonly needed for diagnosis, but, may help provide more information in complex
cases
Expensive than X-ray
Does not involve radiation risk 7
Provides 2-D view resulting in better images | |/

Arthroscopy
Minimally invasive surgical procedure
An Arthroscope is inserted into the joint
area through small incisions to find or
even repair damage done to the joint
Reduced recovery time
High success rate due to less damage done
to connective issue
Less scarring
Advantageous to athletes

Laboratory Tests
Blood test
No blood test for osteoarthritis as such
Suggested to rule out other types of arthritis e.g. rheumatoid arthritis

Joint Fluid Analysis/Joint aspiration

A needle is used to draw fluid out of the affected joint after the administration of
anesthesia
Examination and testing of the fluid to determine presence of inflammation ; crystals or
joint deterioration

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BOX Simplified clinical approach to identifying OA subsets
1. Number of joints involved
o a. Localized: 1–2 joint regions involved only (specify location)
o b. GOA: ≥3 joint regions involved, with spine/hands being one of the regions
affected (nodal GOA if nodes present)
2. Classic or atypical OA (atypical OA: unusual distribution, young age of onset
[<45 years], rapid progression)
Causes of atypical OA include:
o a. Prior trauma (common): mainly monoarticular or oligoarticular OA, young
onset, often with a clear history of injury
o b. Dysplasia:
 i. Localized (eg, hip): childhood or young adult onset
 ii. Polyarticular (eg, spondyloepiphysial dysplasia): young onset, short
stature, morphologic features, and a positive family history may be
present
o c. Childhood arthropathy or derangement: eg, juvenile idiopathic arthritis,
Perthes disease and slipped femoral epiphysis of hip, septic arthritis
o d. Metabolic or endocrine diseases: eg, hemochromatosis, which mainly
targets metacarpophalangeal joints (MCPJs), wrists, hips, and may be of
young onset, mainly in men; acromegaly, which has typical signs of OA with
little restriction in movements, hypermobility
o e. Late avascular necrosis: predominantly hips, shoulders, and knees, more
rapid progression, risk factors present (eg, steroid use)
o f. Neuropathic joints: rapid clinical progression, marked joint disorganization
 i. Hindfoot, midfoot: diabetes mellitus
 ii. Shoulders, elbows, wrists: syringomyelia
o g. Apatite-associated destructive arthritis: old age, rapid progression; targets
hips, knees, and shoulders
3. Clinical joint inflammation: usually absent; if present, consider:
o a. Crystal deposition: CPPD and gout (OA encourages deposition of both
crystal types)
o b. Coexistent inflammatory arthritis: eg, RA, seronegative spondyloarthropathy
o c. Erosive OA: targets hand IPJs

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Table \ Common periarticular lesions that coexist with knee OA
Soft Tissue Disorder Signs and Symptoms

Anserine bursitis Inferomedial knee pain, localized soft tissue swelling

(rarely), tenderness over the upper medial tibia

Semimembranosus- Medial knee pain, tenderness closer to the joint line than in anserine
tibial collateral bursitis
ligament bursitis
Medial collateral Medial knee pain, localized tenderness, and pain on stressing the
ligament (inferior medial ligament (valgus strain with knee unlocked)
insertion) enthesopathy
Tender medial fat pad Medial knee pain, tenderness over either the inferior or superior fat
pad below or above the joint line

lliotibial tract (band) Lateral distal thigh and knee pain, and tenderness maximal over the
syndrome lateral femoral condyle

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Treatment and Management
® Osteoarthritis often gradually worsens, and no cure exists Se
® Staying active, maintaining a healthy weight and other treatments may slow
progression of the disease and help improve pain and joint function

Experts like:

A physiatrist may help in formulating a non-pharmacologic management plan

for the patient with osteoarthritis, and
A nutritionist may help the patient to lose weight
Orthopedic surgeon may be necessary if the osteoarthritis fails to respond to a medical
management plan
Surgical procedures for osteoarthritis include arthroscopy, osteotomy, and ( particularly
with knee or hip osteoarthritis) arthroplasty

Recommendation 1
* Education and training in ergonomic principles, pacing of activity, and use of assistive devices, should be offered to every patient

» Formerly included in the recommendations under the term ‘joint protection’

» Intensive programs not shown to be more (cost-effective than more simple strategies

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