DEGENERATIVE ARTHROPATHIES

OSTEOARTHRITIS

Ostoearthrosis, Degenerative Joint Disease (DJD), Hypertrophic Arthritis, Degenerative Disc Disease ( DDD, in the Spine), Generalized Osteoarthritis ( Kellegrens Syndrome)

I. Definition:

A slowly progressive musculoskeletal disorder

Affects the joints of the hands ( those involved with a pinch grip), spine and weight bearing jts ( hip, knee) of LE

The most common articular disorder

II. Epidemiology:

Associated with increased age

More common in women than men

Radiographic evidence in > 50-80% of those 65 y/o.

Estimated 2-3 % of the audit population has symptomatic OA.

III. Risk Factors for OA:

Obesity

Heredity ( esp. OA of the DIP jts)

Age

Previous Joint Trauma

Abnormal Joint Mechanics ( Excessive knee varus or valgus )

Smoking ( may contribute to de degenerative joint dse)

IV. Pathologic Features of OA

A. EARLY:

Swelling

Loosening of collagen framework structure restraint

Chondrocytes increase proteoglycan synthesis but also realease more degradative enzymes.

Increase Cartilage Water Content

B. LATER

Degredative Enzymes break down protooglycans faster than it can be produced by chondrocytes, resulting in diminished proteoglycan content in the cartilage.

Articular Cartilage thins and softens ( jt-space narrowing will be seen eventually)

Fissuring and cracking of cartilage. Repair attempted but inadequate

Underlying bone is exposed, allowing synovial fluid to be forced by the presence of wt into the bone. This shows up as cyst or geodes on radiograhs

Remodelling and hypertrophy of the subchondral sclerosis and osteophytes (spurs) formation

V. CLASSIFICATION OF OSTEOARTHRITIS:

A. PRIMARY OR INDIOPATHIC OA:

1. LOCALIZED:

Hands ( Heberdens and Bouchards, First CMC)

Hands ( Erosive, Inflammatory)

Feet ( first MTP)

Hip

Knee

Spine

2. GENERALIZED ( KELLEGRENS SYNDROME)

B. SECONDDARY OA:

1. Pain in involved joints

2. Pain worse activity, better with rest

3. Morning stiffness ( if present) < 30 mins

4. Stiffness after a period of immobility ( gelling)

5. Joint enlargement

6. Joint Instability

7. Limitation of joint mobility

8. Perlarticular Mm atrophy

9. Crepitus

VI. JOINTS TYPICALLY INVOLVED IN PRIMARY ( IDIOPATHIC) OA:

1. DIP jts of hands

2. Pip jts hands

3. First CMC jts of thumb

4. Acromioclavicular jt

5. Hip

6. Knee

7. First NTP jts of the feet

VII. RADIOGRAPHIC FEATURES:

A- No ankylosis

Alignment may be abnormal

B- Bone Mineralization

Bony Subchondral sclerosis

Bony Spurs ( Osteophytes )

C- No Calcification in cartilage

Cartilage space narrowing which is non-uniform (occurs in area of maximal stress in wt bearing jts.)

D- Deformities of Heberdens Bouchards Nodes

E- No erasions

Gull wing Sign in Erosive Arthritis

S- Slowly progression over years

No specific nail in degenerative Disc Disease ( a collection of nitrogen in a degerated disc space)

VIII. Laboratory Findings:

ESR normal

RF Negative

ANA not present

Synovial Fluid

High Viscosity with good string sign

Color is yellow and clear

WBC counts typically < 1000-2000/ mm3

No crystals and negative cultures

IX.Differential Dx of OA and RA

OA

RA

1. non systemic

systemic

2. non-inflammatory

assoc. with cutaneous and

inflammatory changes

3. affects wt. bearing jts

small jts.

4. (-) RF

(+) RF but not all

5. (-) subcutaneous

(+) subcutaneous nodes

6. Normal ESR and Serologic testinc. ESR; Leukocytosis with

eosinophilia

7. clear synovial fluid; high viscositysynovial fluid is turbid; low viscosity

and few cellswith many polymorphonuclear cells

8. (+) osteophytes

(-) osteophytes

9. DIP affectation

terminal jts not usually affected

( ex. DIP)

10. involve fewer jts

involves many jts at particular time

OA is sometimes difficult to differentiate with RA because sometimes the two may co exist.

OA maybe stipulated by gouty, neuropathic or tuberculous jt dse.

CLASS:

a.Primary OA

affects DIP, PIP, 1st CMC, hip, knee, MTP, cervical and lumbar jt.

b.Secondary OA

See ETIOLOGY

X.MEDICAL MANAGEMENT

General Measures:

a. reassurance

b. rest/ modification of activity

DRUGS:

a. Aspirin-drug of choice

b. NSAIDS

c. Corticosteroid

LOCAL TREATMENT:

a. Splints/ braces

b. Massage

c. Exercise

XI.SURGERY - last resort

Indications:

a. Severe pain

b. Loss of function

c. Progression of deformity

SOFT TISSUE PROCEDURES

a. Synovectomy

b. Soft tissue release

c. Tendon transfer

BONE AND JOINT PROCEDURES

a. Arthrodesis

to relieve pain, result to a very stable joint but sacrifices freedom of motion

b. Osteotomy

improve jt alignment

c. Arthoplasty

jt replacement to relieve pain and restore fxn

CERVICAL SPONDYLOSIS

I.DEFINITION:

Spondylosis is described as the degenerative changes which occur to the intervertebral disc and vertebral bodies.

II.EPIDEMIOLOGY:

Common in advancing age ( esp. in the cervical spine)

Less than 40 y.o ( asymptomatic), 25% have DJD, 4% have foraminal stenosis.

More than 70 yo: 70% have degenerative spine changes.

III.ETIOLOGY

No specific cause

Factors contributing to degenerative changes of the spine:

a. Aging

b. Trauma

c. Work activities

d. Genetics

IV.PATHOPHYSIOLOGY

1. IV disc loose hydration with age, leading to cracks and fissures.

2. Disc subsequently collapses owing to biomechanical incompetence causing annulus to bulge outwards

3. Surrounding ligaments also loose their elastic properties and develop taction spurs.

4. Uncovertebral spurring occurs as a result of the degenerative process in which the facet jts. loose cartilage, becomes sclerotic and develop osteophytes.

5. Stenonis due to spur formation, disc protrusion, ligamentum hypertrophy.

V.CLINICAL MANIFESTATION

a. Morning neck pain

b. Stiffness

c. Neck fatigue late in the day

d. Loss of neck ROM

e. Pain at the extremes of ROM extension ROM is affected first

f. Sometimes crystallization

VI.COMPLICATIONS

a. Neurological deficits

b. Vertebral artery injury- ( due to facet osteophyte formation)

c. Myelopathy- ( if arthritis is combined with disc degeneration or post disc herniation)

d. Cervical spinal stenosis

VII.DIAGNOSIS:

1. Plain films- later radiograph

2. CT scan- ( to R/O fx)

3. MRI- Most sensitive

VIII.MEDICAL MANAGEMENT

1. Long hot shower for morning stiffness

2. soft cervical collar

3. NSAIDS

4. Acetaminophen- NSAIDS posses unacceptable medical risk for complication.

PT EVALUATION AND MANAGEMENT OF OSTEOARTHRITIS AND CERVICAL SPONDYLOSIS

PT EVALUATION

A. Objectives of Rehabilitation

a. To improve function

b. To prevent /remedy musculoskeletal impairment

B. Assesment

1. HPI

2. ROM

3. Strength

4. Endurance

5. Jt stability

a. Ligamentous laxity

b. Ligamentous instability

6. Functional Assesement ATDEP

7. Functional mobility and gait analysis

PT MANAGEMENT

A. Gen Guidelines:

1. Problems

a. Jt stiffness

b. Pair due to stress/excessive activity

c. LOM due to progression of condition

d. If present, pain at rest

e. Deformities

2. Goals and Plans of Care

GOAL

Plan of Care

a. dec. jt stiffness

PROM progressing to AROM; jt

play techniques; Pt education

b. dec. pain from mechanical

strengthening ex., modification of

stresses

activities with intermittent rest pd.

Stretching exercise

c. Inc. ROM

grade 1 & 2 oscillation and modalities

d. prevent deformities

braces, pt education

Specific Jt. Problems

1. Hip pain- usually felt around greater trochanter

may radiate to the groin but often experienced in L3 dermatone

Mx: use of assistive devices to decrease mechanical stresses in ambulation

2. Tredelenburg Gait- due to abductor weakness

Mx: Isometric exercise to gluteus medius; use o assistive devices

3. Limitation of hip extension- leads to backache due to attempted extension

Mx: maintenance of Hip ext by lying prone position ( McKenzie #1) for 30-40 min. bid.

4. Inc. Leg length of the affected side- associated with unilateral hip ossification

Mx: Shoe modification

5. Knee pain- causes LOM

Mx: Modalities with rest, elastic wrap or splint; grade 1 oscillation.

6. Knee jt effusion inhibits voluntary contraction of the squads

Mx: ROM exercise

7. Restricted ROM due to contractures of the knee jt capsules and hamstrings

Mx: Stretching exercise

8. Genu Varum

Mx: shoe modification

9. Hallux Valgus with Bunions

10. Hallux Rigidus

11. Abrasions at soles/ dorsum of toes

12. Metatarsal head calluses

Mx: Use of proper footwear/ shoe modification

13. CMC Jt pain

Mx. use a functional thumb post splint to relieve pain and allow functional activities

14. Inc tension in the Spine

Mx. Relaxation techniques; traction to inc. IV foramen diameter

AVASCULAR NECROSIS OF THE BONE

I. Definition

Bone death resulting from blood supply deprivation in the absence of pyogenic and tuberculous infection

Osteonecrosis is the term currently used recognizing the fact that bone may die because of reasons other than loss of circulation

II. Epidemiology

Sites of Predilection:

A. Femoral head

20 - 30% of all femoral neck fractures

Infancy to late adulthood

Men 30 60 years old

B. Carpal bones (Keinbocks disease & Preisers disease)

Uncommon

Usually affect adolescents & men, 20-40 y.o.

i. Keinbocks disease

Spontaneous necrosis of the lunate bone

ii. Preisers disease

Spontaneous necrosis of the scaphoid bone

C. Metatarsal head (Freibergs disease)

Mostly in adolescents

Commonly affecting 2nd metatarsal bone

D. Tarsal navicular bone (Kohlers disease)

Uncommon

Usually bilateral

Occurs in childhood 4 6 years old

E. Talus

F. Segmented fractures

A fragment from the shaft of a long bone may be separated and undergo necrosis

G. Other locations (less common)

Capitulum of the humerus

Radial head

Lateral femoral condyle

III. Etiology

Any condition that cuts off blood supply to the bone:

A. Trauma

B. Fractures

C. Dislocations

D. Surgery

Excessive stripping of the periosteum

E. Organ transplantation

F. Prolonged corticosteriod intake

G. Radiation exposure

IV. Pathophysiology

Infarction

Death of marrow elements & cancellous bone

*Degeneration & disappearance of osteocytes from lacunae

Necrosis

Marked hyperemia of tissues adjacent to infarct

Invasion of young tissue & new blood vessels

Osteoclastic resorptionOsteoblastic repair

(either may predominate)

Reparative tissue reaches articular cartilage at the periphery of the necrotic zone

Epiphyseal cartilage undergoes osteoarthritic changes

V. Clinical Manifestations

General:

A. Local swelling

B. Tenderness

C. Thickening over affected bone

D. Limited ROM

E. Muscle atrophy

Specific:

F. Carpal bone osteonecrosis

LOM of wrist extension

G. Hip avascular necrosis

Pain in groin & thigh

Tenderness over hip joint

LOM in F-Ab-IR

Antalgic gait

X-ray shows Crescent Sign

VI. Complications

Gout

Traumatic arthritis

Renal transplantation

Sickle cell disease and other hemoglobinopathies

Caissons disease - decompression sickness; divers paralysis

VII. Diagnosis

X-ray

A. Thin radioluscent line beneath joint surface

Crescent Sign in hip avascular necrosis)

B. Denser area

C. Fragmentation

D. Thickening over fragmented area

Scintigraphy using radioactive technetium diphosphate

E. Cold initially

F. With time & revascularization becomes hot

VIII. Differential Diagnosis

HIP AVASCULAR NECROSISHIP HEMARTHROSIS

Pain LocationPain in the groin & thighPain in the groin & thigh, specifically over the greater trochanter

PalpationTenderness over the hip jointFullness in the hip joint both anterior to the groin & over greater trochanter

LOMF-Ab-IRF-Ab-ER

GaitAntalgic

IX. Prognosis

May progress into osteoarthritis

Kohlers disease good prognosis; little or no permanent disability

X. Medical / Surgical Management

Femoral head

A. Medical Management: (children)

Conservative protection of hip joint in abduction for prolonged period until reconstitution of femoral head is complete

B. Surgical Management: (older patients)

Intramedullary or muscle-pedicle bone grafting

Osteotomy

Interposition or replacement arthroplasty

Arthrodesis

Total hip replacement

For older patients and other patients with activity restrictions

Carpal bones (Keinbocks disease & Preisers disease)

C. Medical Management:

Wrist immobilization in short dorsiflexion splint

D. Surgical Management:

Reserved only if immobilization gives unsatisfactory healing

i. Simple excision

ii. Total bone replacement

iii. Arthrodesis

Metatarsal head (Freibergs disease)

E. Medical Management:

Immobilization in a plaster boot or anterior arch pad

F. Surgical Management:

Reserved only in late painful cases

i. Simple excision with use of anterior arch support post-op

Tarsal navicular bone (Kohlers disease)

G. Medical Management:

Use of longitudinal arch support & restriction of activity

Immobilization with foot in slight inversion by plaster cast for 6 8 weeks

If much pain upon weight-bearing

H. Surgical Management:

Usually not applicable

XI. PT Evaluation

History

Physical Examination

Note for:i. Swelling

ii. Tenderness

iii. LOM

iv. Functional deficits

XII. PT Management

Hot packs

ROM exercises

Immobilization through splinting

Patient education

LEGG-CALVE-PERTHES DISEASE

XIII. Definition

An idiopathic form of osteonecrosis of the femoral head occurring in children

Similar to avascular necrosis of adulthood

Also called COXA PLANA because it frequently results in flattening of the femoral head

XIV. Epidemiology

Occurs between 2-12 y.o. (Usually 5-7 y.o.)

Affects boys > girls (4:1)

Rare in blacks; oriental = whites

(L) = (R)

Unilateral (85%) > bilateral (15%)

Familial predisposition in 1/5 - of all cases

Correlated with low birth weight & growth delay

XV. Etiology

Unknown

Possible causes:

A. Endocrine disturbance

B. Trauma

C. Inflammation

D. Inadequate nutrition

E. Genetic factors

Most popular theory:

Occlusion of the arterial supply to the epiphysis with multiple episodes of infarction

Although vascular occlusion does not explain many of the observations reported

Blood Supply to Femoral Head:

F. Artery to the Ligamentum Teres

From Obturator Artery

Major blood supply to femoral head in children

G. Medial Femoral Circumflex Artery

From Femoral Artery

Major blood supply to femoral head in adults

H. Lateral Femoral Circumflex Artery

From Deep Femoral Artery

XVI. Pathophysiology

Necrotic Stage

Vascular damage

X-ray findings:

A. Small capital epiphysis

B. Increased radiodensity of the femoral head

C. Appearance of an osteopathic area in the medial aspect of the proximal femoral neck

Fragmentation / Resorption Stage

Fibrous tissue invades the region & gradually resorbs necrotic bone

X-ray findings:

D. Enlargement of femoral neck

Revascularization / Reossification Stage

Begins after all necrotic tissue has been resorbed & completed when the joint reossified

Remodeling Stage

Some resultant deformity may resolve as the joint is subjected to weight bearing & normal forces

Healed Stage

Represents the final outcome of the disease process

Bony tissue is once again viable & further resolution of deformity is minimal

XVII. Clinical Manifestation

Early:

A. Hip pain & stiffness

Most common symptom

Gradual insidious onset

Aggravated by strenuous exercise

An aching sensation rather than a sharp pain located in the groin area radiating down to the

Anteromedial area of the thigh

B. Irritable Hip Syndrome

Toxic synovitis of the hip

Adductor spasm & quads atrophy

C. Antalgic gait

D. LOM in F-Ab-IR

E. Muscle atrophy in thigh & buttock area

Late:

F. Hip pain

G. Functional activity limitation

H. Limp

Can be: antalgic, stiff-hip, short-leg, or Trendelenburg type

XVIII. Complications

Enlarged femoral head

Alteration of the femoral neck angle

LLD

Gross incongruence of articular cartilages

XIX. Diagnosis

Diagnosis is usually through X-rays

Characteristic deformities upon X-ray:

i. Crescent sign

ii. Coxa plana

Caterall Classification

Group I

iii. 25% of the femoral head in the anterior central region is involved

iv. No metaphyseal reaction

v. No subchondral fracture line or sequestrum

Group II

vi. Nearly 50% of the femoral head in the anterolateral region is involved

vii. Viable bone over growth plate

viii. (+) Sequestrum & subchondral fracture

Group III

ix. Approximately 75% of the femoral head is involved

x. Diffuse metaphyseal reactions

xi. Extension of the subchondral fracture to the posterior half of the epiphysis

Group IV

xii. Entire femoral head is involved; widespread collapse of the epiphysis

Salter-Thompson Classification

Group A

xiii. Subchondral fracture involving approximately of the femoral head

Group B

xiv. No evidence of an intact viable margin is seen on the A-P radiographs

XX. Prognosis

Recovery more likely when signs & symptoms of disease develop before the age of 5 or 6 years

Poor prognosis: patients older than 9 years; demonstrating lateral subluxation of the femoral head; premature closure of the physis; & loss of ROM

XXI. Medical / Surgical Management

Medical Management

A. Placing patient in NWB position

Pharmacological Management

B. NSAIDS

Surgical Management

C. Innominate osteotomy

Anterolateral coverage of femoral head

D. Varus derotational osteotomy of the proximal femur

Done when majority of the femoral head is uncovered & the angle of Wiberg is decreased; if there is significant femoral anteversion

E. Trochanteric advancement

Transfer of the greater trochanter distally

F. Chiani osteotomy

Salvage procedure to accomplish coverage of the flattened femoral head in an older child when head is subluxating and painful

XXII. PT Evaluation

Gait analysis

Limp is usually antalgic therefore the pelvis dips in the involved side & the stride is short

Leg-roll test

Shows generally decreased IR of involved hip

Thomas test

Shows mild flexion contracture; limited hip abduction

Muscle atrophy

Some degree usually observed in the thigh & buttocks area

XXIII. PT Management

Goals:

A. Decrease joint stiffness

B. Increase ROM

C. Containment of the femoral head in the acetabulum

D. Relief of pain and stress at the hip joint

E. Prevent further deformities

Conservative treatment:

F. Traction

G. Bracing

Through plaster cast

i. Maintaining abduction at 10 & slight IR

ii. Removed after 6-8 weeks

Abduction orthosis

iii. After cast is removed, it will be replaced by an orthosis

iv. Splint is usually worn for 24 hrs a day

v. Total conservative treatment may last approximately for 24 months

Types of orthosis used for LCP:

vi. Toronto abduction Orthosis

Maintains hip at 45, abduction 18, IR yet allows ambulation and hip & knee flexion. A 90 is maintained at all times between the two legs

vii. Scottish Rite Brace

With a pelvic band, the hip is maintained in abduction

viii. Newington Childrens Hospital Ambulatory Brace

Demonstrates the abduction, IR principle provides covering of the femoral head while protecting the knee against valgus thrust; not an ischial weight-bearing brace

In children aged 4 years with signs of joint problems:

ix. Brace should be worn on the involved hip at 70-80 abduction and some IR

x. Normal hip should be placed in 30 abduction

In children between 5 to 10 years:

xi. Abduction devices should be worn day and night

xii. Active program in partial or FWB should be conducted during this time

H. Exercises

NWB is stressed

i. NWB ROM exercises with the orthosis

ii. ROM exercises in whirlpool or therapeutic pool

The exercises should target:

iii. Hip abductors

iv. Internal rotators

v. Knee flexors

Specific muscles:

vi. Gluteus medius

vii. Gluteus maximus

viii. Quadriceps femoris