OSTEOARTHRITIS V.

PATHOPHYSIOLOGY
 Begins with an increase in cartilaginous water
content
 This suggests that proteoglycans have
become swollen with water far beyond normal
GENERAL MEDICAL BACKGROUND
 This decreases stiffness of extracellular
matrix
I. DEFINITION
 Leading to further mechanical damage
 Proteoglycans are then later lost
- A chronic degenerative disorder primarily affecting
 This causes articular cartilage to lose its
the articular cartilage of synovial joints, with
compressive stiffness and elasticity
eventual bone remodeling and overgrowth at the
 Results into bone to bone forces
margins of the joint
 Articular cartilage is destroyed and joint
- There is also progression of synovial and capsular
space narrows
thickening and joint effusion
 Presence of new bone growths known as
- Primarily a non-inflammatory disorder, but
osteophytes
inflammation eventually occurs and is progressive
- Common in weight bearing joints (hips, knees,
and the lower back)
- “Degenerative joint disease”
- aka “Wear and Tear Arthritis”.
- Progressive loss of cartilage with remodeling of
subchondral bone and progressive deformity of
joint(s).
- A form of chronic arthritis found commonly in
middle-aged and elderly people.
- Affects especially the weight-bearing joint.
- The most common articular disorder

II. CLASSIFICATION

According to cause:
 Primary OA
- Idiopathic
 Secondary OA
- Repeated trauma
- Malalignment due to fractures
- Congenital subluxation of the hips
- Calcium deposits disease

According to joints affected: VI. CLINICAL MANIFESTATIONS

a. Localized ( 1 or 2 joints)  Commonly unilateral affectation
b. Generalized (3 or more)  Morning stiffness < 1 hour
 Crepitus
 Painful joints
III. EPIDEMIOLOGY  Pain worsens with motion
 Most common form of arthritis  Mostly seen in hands, hips, knees,
 >40 years old cervical spine, and lumbar spine
 Men > Women before age 50  Loss of motion
 Women > Men after age 50  Presence of nodes in the hand
 Estimated 2-3 % of the audit population has
symptomatic OA.

IV. ETIOLOGY

Systemic Factors:
 Age
 Gender
 Race
 Genetics  DIP = Heberden’s Nodes (most
 Metabolic/endocrine common)
 High bone density  PIP = Bouchard’s Nodes (least
 Nutritional status common)
 Congenital/developmental  Gait may be antalgic
 Obesity  Peri-articular muscle atrophy may be
noted
Local Factors:  Joint line tenderness
 Obesity  +/- effusion
 Major joint trauma
 Repetitive stress
 Muscle weakness
 Altered joint biomechanics
 Joint malalignment
 Proprioceptive impairments
OA CONDITIONS I. Epidemiology

1) GOUTY ARTHRITIS Sites of Predilection:

 Familial d/o of purine metabolism in which the a. Femoral head
uric acid is involved  20 - 30% of all femoral neck fractures
 Infancy to late adulthood
 Characterized by: Hyperuricemia &
 Men 30 – 60 years old
deposition of sodium urate in the tissues
 90% of patients with gouty arthritis are males
b. Carpal bones (Keinbock’s disease & Preiser’s
 Past age 30 disease)
 Rare in blacks  Uncommon
 Secondary gout: polycythemia, leukemia and  Usually affect adolescents & men, 20-40
myeloma  all of which are characterized by y.o.
overproduction of uric acid  Keinbock’s disease - Spontaneous
necrosis of the lunate bone
I. Clinical Picture:
 Preiser’s disease - Spontaneous
 Early: Recurring attacks of monarticular pain necrosis of the scaphoid bone
& inflammation
 Late: Chronic deforming articular changes c. Metatarsal head (Freiberg’s disease)
 Mostly in adolescents
**Attacks are precipitated by excessive intake  Commonly affecting 2nd metatarsal bone
of meats and other foods high in protein
st d. Tarsal navicular bone (Kohler’s disease)
 Joints most often involved: foot joints (1
 Uncommon
MTP), hand, wrist, knee and elbow  Usually bilateral
 Acute attacks: red, swollen, warm, tender and  Occurs in childhood 4 – 6 years old
extremely painful upon movement
e. Talus
**in x-ray films, appearance of uratic deposits f. Segmented fractures
at the near ends of the bones  A fragment from the shaft of a long bone
may be separated and undergo necrosis
II. Pathology
- Creamy or chalky deposits of SODIUM URATE g. Other locations (less common)
in the  Capitulum of the humerus
joint (aka tophi)
 Radial head
- Tophi may be found in the cartilage like in the
 Lateral femoral condyle
ear and
at subcutaneous tissue: fascia, kidneys, heart,
and
other viscera

III. Treatment:
- No cure but drugs may give relief: Colchicine
- Iburprofen, phenylbutazone, NSAIDS

IV. Chronic Management:

- Low-purine diet
- Avoid excess alcohol
-In late cases, excision of the tophi may be
necessary

2) CHONDROCALCINOSIS
 aka Pseudogout
 Aka Calcium pyrophosphate deposition
disease (CPPD)
 Idiopathic cause
 Deposition of crystals of CALCIUM II. Etiology
PYROPHOSPHATE within the articular
cartilage Any condition that cuts off blood supply to the bone:
 Patient may experience attacks of joint pain
also  Trauma
 May be assoc. with hyperthyroidism in the  Fractures
elderly  Dislocations
 Attacks may be precipitated by traumatic  Surgery
event like surgical operations  Excessive stripping of the periosteum
 MC affectation: Knee>Hip  Organ transplantation
 Remember, Uric acid levels are normal  Prolonged corticosteriod intake
 Management: Phenylbutazone  Radiation exposure

3) AVASCULAR NECROSIS Three Stages (Taking about 2 years)

 aka Osteonecrosis, Bone Infarction, Aseptic 1. Stage of Necrosis
Necrosis, Ischemic Bone Necrosis, and AVN. 2. Stage of Fragmentation
 Disease where there is cellular death  Dead bony trabeculae may fx by body weight.
(necrosis) of bone components due to  Epiphysis may become collapsed and
interruption of blood supply. fragmented.
 If Avascular Necrosis involves bones of a 3. Stage of Regeneration
joint, it often leads to destruction of the joint  New blood vessels enter the epiphysis and
articular surfaces. new bone is laid down on the dead
trabeculae.
 III. Pathophysiology
 Inadequate nutrition causes bone death.
 Bone death leads to changes in the normal
articulation causing abnormal motion.
 Bone death and abnormal articulation leads
to destruction of articular cartilages causes
disabling arthritis.
 If left untreated, bone collapses.
IV. Clinical Manifestations
 Possibly no SSx during early stages
 Joint pain with weight-bearing, progressing to
pain at rest.
 Pain and swelling that persist for several days
or weeks.
 Gradual development of aching pain takes
place, at first felt only on jarring or on exertion
but later persistent and severe.
 Joint stiffness.
 Limited ROM
 Osteoarthritis may develop.
VIII. Prognosis
 AVN healing is poor.
 Eventually, almost all patients develop
subchondral collapse, following which
progression to OA is inevitable.
 This means that the dead bone becomes
weak and breaks down.
 This causes the joint to become incongruous.
This causes OA.
IX. Med/Surg and other Rehab Mgt
 Must be referred for X-ray, MRI or CT-Scan
 Conservative Treatment
 Non-weight bearing; ROM exercises; e-stim for
bone growth; modification to treat pain.
 Limit necrosis.
 Reduce fatty substances, which react
with corticosteroids.
 Limit blood clot in the presence of
clotting disorders.

Stages of AVN ----- X end of OA conditions X -----

VII. COMPLICATIONS

If not treated early may lead to:

 Difficulty in performing ADLs
 Decreased proprioception and balance
 Muscle atrophy

VIII. DIAGNOSIS
 Radiographic changes such as joint
space narrowing

V. Complications
 Gout
 Traumatic arthritis
 Renal transplantation
 Sickle cell disease and other
hemoglobinopathies
 Caisson’s disease - decompression
sickness; “diver’s paralysis”

VI. Diagnosis

Best Imaging in EARLY STAGES

 MRI
 Detect chemical changes in the bone marrow.
 Allow visualization of affected area (CT to
determine extent of damage).
 Bone rebuilding process can be assessed.
 Radiographic changes visible relatively
Best Imaging in LATE STAGES late in the disease
 Plain Films  Subchondral Sclerosis
 Visualization of calcification.  Subchondral Cysts
 Visualization of new bone formation.  Osteophytes
 Visualization of microfractures.  Bone mineralization should be normal
 Subchondral bone has thickened
VII. Differential Diagnosis  Bony overgrowth
 Presence of nodes
HIP
AVASCULAR HIP HEMARTHROSIS IX. DIFFERENTIAL DIAGNOSIS
NECROSIS
Pain Pain in the Pain in the groin & thigh,
Location groin & thigh specifically over the
greater trochanter
Palpatio Tenderness Fullness in the hip joint
n over the hip both anterior to the groin
joint & over greater trochanter
LOM F-Ab-IR F-Ab-ER
Gait Antalgic

X. PROGNOSIS
 Slow progressing disease that can be self-
limiting or progress to advanced joint and soft
tissue damage leading to complete joint
failure.
 Joint surgeries may sometimes be the only
option to regain function
 Rapidly progressive joint damage is
uncommon
 Best treated early to prevent further
complications in the affected joints
 Symptoms usu. Exhibit a slowly progressive
and often intermittent course.
 Periods of improvement are frequent with
proper Tx.
 Mild – Mod: pt never severely incapacitated
(live with the dse.)
 Trauma may prolong and intensify the
symptoms.
 More disability follows involvement of spine,
hips, and knees > UE.
 If not treated earlier, OA may cause extreme
disability of one or more joints.
GENERAL HEALTHCARE MANAGEMENT
I. Medical, surgical, & pharmacologic
 No known drug that effects disease
progression
 Drugs mainly for pain relief
- Acetaminophen (oral analgesic) is usually
the drug of first choice
- NSAIDs
- Corticosteroid injections
 Surgical
- Arthroscopy
- Arthrodesis
 Arthroplasty
 Osteotomy
 Joint replacement
o If all other treatments are
ineffective, and pain is severe.
o Loss of joint motion
o Joints last 8 to 15 years without
complications
PHYSICAL THERAPY PROGNOSIS, PLAN OF
CARE & INTERVENTIONS
I. Plan of Care
1. Educate the patient
2. Decrease effects of stiffness
3. Decrease pain from mechanical stress
and prevent deforming stress
4. Increase ROM
5. Improve neuromuscular control,
strength, and muscle endurance
6. Improve balance
7. Improve physical conditioning
II. Intervention
1. Teach about deforming forces and
prevention; teach home exercise
program to reinforce interventions and
minimize symptoms
2. Active ROM; joint-play mobilization
techniques
3. Splinting or assistive equipment to
minimize stress or to correct faulty
biomechanics, strengthen supporting
muscles
4. Stretch muscle, joint, or soft tissue
restrictions with specific techniques
5. Low-intensity resistance exercises and
muscle repetitions
6. Balance training activities
7. Nonimpact or low-impact aerobic
exercise

II. Other healthcare management

 Physical Therapy
 Weight loss programs
 Patient education and disease self-
management programs
 Low impact aerobic exercises
 Joint protection and energy conservation

PHYSICAL THERAPY EXAMINATION,

EVALUATION, & DIAGNOSIS

I. Points of emphasis on examination

 Musculoskeletal examination (MMT, ROM)
 Neuromuscular examination
 Balance and tolerance examination
 Posture and gait examination
 Functional examination (ATDEP)

II. Problem list

 Pain with mechanical stress or excessive
activity
 Pain at rest in the advanced stages
 Stiffness after inactivity
 Limitation of motion
 Muscle weakness
 Decreased proprioception and balance
 Functional limitations in ADLs and IADLs

III. PT diagnosis