Osteoarthritis of Knee

See also: Total Knee Arthroplasty (TKA)

See also: Knee Biomechanics

INTRODUCTION

ETIOLOGY AND INCITING FACTORS

PATHOlOGY

CLINICAL FEATURES

DIAGNOSIS

TREATMENT OPTIONS

SPECIFIC JOINTS

Osteoarthritis is a chronic joint disorder in which there is progressive softening and disintegration of articular cartilage accompanied by the new growth of cartilage and bone at the joint margins (osteophytes) and capsular fibrosis.

The term Osteoarthritis was originally coined by John Spender

The current working definition of osteoarthritis states that the disease consists of morphologic, biochemical, molecular, and biomechanical changes of both cells& matrix leading to softening, fibrillation, ulceration & loss of articular cartilage, sclerosis, and eburnation of subchondral bone, osteophytes, subchondral cysts.

Osteoarthritis is a dynamic phenomenon-it that shows features of both destruction and repair.

Although any synovial joint is susceptible to OA,  The interphalangeal joints &MCP joint of the hand, first metatarsophalangeal joint, facet joints of the spine, hip joint, and knee joint are involved more.

Joint and Articular cartilage

Articular cartilage- is specialized connective tissue has to gel like matrix consisting of a proteoglycan ground substance

in which are embedded an architecturally structured collagen network and a relatively sparse scattering of specialized cells, the chondrocytes,

It is more slippery than any man-made material, offering very little frictional resistance to movement and surface gliding.

It decreases friction and distributes loads and is classically described as avascular, aneural, and alymphatic.

Composition

a)Water-65-80% of wet wt.-is exchangeable with synovial fluids. Shifts in and out of the cartilage to allow deformation of the cartilage surface in response to stress.

b)Collagen-10-20% of wet wt. Type II collagen accounts for 90-95% of the total collagen content of articular cartilage and provides a cartilaginous framework and tensile strength.

c)Proteoglycans- 10-15% of wet wt.-provide compressive strength.     

a)Chondrocytes-5% of wet wt.-active in protein synthesis.

Articular cartilage layers

a.Gliding Zone (superficial)

b.Transitional Zone (middle)

c.Radial zone (deep zone)

d.Tide mark

e.Calcified zone      

The Matrix

Contains

Collagen

Proteoglycans and

65 to 80% water

PROTEOGLYCANS

Proteoglycans are large molecules of high molecular weight consisting of a central protein core with radially attached carbohydrate side chain (glycosaminoglycans) –  that is keratin sulphate and chondroitin sulphate which are Hydrophilic – water attracting.

ARTICULAR CARTILAGE – Nutrition

Chondrocytes receive nutrition through fluid pulsing through channels in the cartilage connecting the fluid space deep to the subchondral bone to the synovial fluid.

The outer 2/3^rd is supplied by synovial fluid pulsing into these channels.

The inner 1/3^rd by oxygen-rich fluid diffusing from under the subchondral bone.

Prevalence

OA is the most commonest of all joint diseases. It is a truly universal disorder, affecting both sexes and all races

Autopsy studies show OA changes in everyone over the age of 65 years.

OA of the finger joints is particularly common in elderly women, affecting more than 70%of those over 70 years

Men and women are equally likely to develop OA.

OSTEOARTHRITIS

PRIMARY

The excessive load placed on normal
joint tissue

The reasonable load applied on
inferior joint tissue

OSTEOARTHRITIS

SECONDARY

Trauma

Laxity

Infection

Metabolic disorder(Gout)

Obesity -twice in obese people mainly affecting weight-bearing joints

Occupation -OA of the knee is more common in workers engaged in knee bending activities while OA in the upper limbs occurs in people working with heavy vibrating tools 

Inciting factors

Inflammatory processes -such as rheumatoid disease

Metabolic disorders-Gouty deposits of urate, Alkaptonuric, Onchrosis, Wilsons ds

Biomechanical factors- Cartilage is fatigue prone, cyclical loading produces # of collagen fibers and also produces proteoglycan depletion. Structure abnormalities may be a result of  -Articular # dislocation  -Acetabular dysplasia              -Slipped epiphysis  -Osteonecrosis              -malalignment of a joint                                                                

Hormonal- Diabetics are uniquely susceptible to OA  -Acromegaly

Repeated Intra synovial Hemorrhage- In patients with defective clotting factors, repeated hemorrhages can lead to severe damage to articular cartilage as well as to subchondral bone structures

PATHOGENESIS

Articular cartilage is composed of chondrocytes surrounded by a matrix of water, proteoglycans & collagen. The chondrocyte regulates the content & structure of the surrounding matrix.

Earliest change (cartilage is still morphologically intact)increase in water content of cartilage and easier extractability of the matrix proteoglycans

Later stage -loss of proteoglycans &defects appear in the cartilage

– As the cartilage becomes less stiff, secondary damage to chondrocytes causes the release of cell enzymes & further matrix breakdown     

PATHOLOGY

Cardinal Features are   -progressive cartilage destruction  -Subarticular cyst formation   -sclerosis of the surrounding bone  -osteophyte formation  -capsular fibrosis

Histologically  -early-stage- cartilage shows small irregularities or splits in the surface. 

          -late stage -clefts become more extensive

And in some areas cartilage is lost to the point that the underlying bone is completely denuded 

Clinical features

PAIN

    -is the usual presenting symptom   

    -may be widespread 

    -maybe referred to a distant site                  -starts insiduosly & increases over months to years  

    -aggravated by exertion and relieved by rest 

Clinical Features

Middle-aged pt.—Pain is presenting symptom, widespread, insidious, and increases slowly over months or years.

It is aggravated by exertion and relieved by rest. In the late stages, pt may have pain in bed at night.

Possible causes of pain:

-Capsular fibrosis

-Pain from stretching the shrunken capsule

-Muscular fatigue

-Bone pressure due to vascular congestion and intraosseous hypertension.

Stiffness occurs after a period of inactivity.

Swelling-intermittent or continuous

Deformity

Loss of function

üMovement is always restricted but is often painless within the permitted range. it may be accompanied by crepitus.

STIFFNESS

SWELLING-Intermittent (Effusion)                  

-Continuous (Capsular thickening, osteophyte formation)

DEFORMITY – Capsular contracture – Joint instability

LOSS OF FUNCTION

LOCAL TENDERNESS IS PRESENT

MUSCLE WASTING

RESTRICTION OF MOVEMENT

CREPITUS

JOINT INSTABILITY 

IMAGING

PLAIN RADIOGRAPH  -In the early stages X-Ray Appearance is   normal 

-Narrowing of the joint space  -Sclerosis of the subchondral bone  -Cysts close to the articular surface  -Osteophytes at the margins  -In the late stage displacement of  the joint and bone destruction

RADIONUCLIDE SCANNING WITH Tc99 SCAN- shows increased activity during the bone phase in the subchondral region

ARTHROSCOPIC EVALUATION-is more sensitive than MRI or Radiograph in assessing defects of articular cartilage

CLINICAL VARIANTS

MONOARTICULAR & PAUCIARTICULAR OA

POLYARTICULAR OA

OA IN UNUSUAL SITES

ENDEMIC OA

KASHIN BECK DISEASE

MSELENI JT. DISEASE

Differential diagnosis

Avascular necrosis – idiopathic necrosis causes joint pain &local effusion differentiating feature in AVN joint space is preserved in face of progressive bone collapse &deformity

Inflammatory arthropathies-Rheumatoid                   -Ankylosing Spondylosis  >History is short            >X-Rays show atrophic & erosive changes             >systemic features present

Chronic infections

Patello femoral Ds 

TREATMENT

CONSERVATIVE

Prevent weight bearing.

Immobilize the knee.

Corticosteroids injection.

Quadriceps exercises.

Management of osteoarthritis

Nonpharmacological

Patient education.

Weight loss.

Temperature modalities.

Exercise

Orthotic and dressing.

Cane

Modification in activities of daily living.

Systemic agents

Non-narcotic analgesic

   Acetaminophen(pcm):initial systemic intervention. 4 gm/day equivalent to ibuprofen 1200-2400mg/day.

NSAIDS : ibuprofen,naproxen,diclofenac and others.

  to reduce potential GI events misoprostol can be added in a dose of 200 mcg qid.

Cox-2 inhibitors

Reduce GI adverse events.

Three such agents are available: celecoxib, rofecoxib,and valdecoxib.

Inhibits endothelial prostacyclins.

But does not affect platelets thromboxane.

Cardiovascular safety remains an area of investigation.

Narcotic analgesic

Codeine and propoxifen.

TRAMADOL: inhibits the uptake of norepinephrine and serotonin. No addictive tendencies.

    seizure and allergic reactions are potential side effects.

Intra-articular agents

Corticosteroids: reduce cellular infiltrates in joints and subsequent inflammation. effective in effusion and inflammation or both.

Hyaluronic acid derivatives are administered intraarticularly one week apart from two agents hyalgan and synvis.

    MOA= unknown. Anti-inflammatory effect ,short term lubricant effect,analgesic effect.

INDICATIONS OF INTRAARTICULAR STEROID:-

1.No response to systemic therapy.

2. Provide pain relief.

3. Help in rehabilitative & physical therapy.

●

CONTRAINDICATIONS

1. Local or systemic infections.

2. Uncontrolled DM.

3. Anticoagulant therapy.

4. Hemorrhagic effusions.

5.Severe joint destruction.

SURGICAL MANAGEMENT

ARTHROSCOPIC DEBRIDEMENT

REALIGNMENT OSTEOTOMY

UNICOMPARTMENTAL ARTHROPLASTY

TOTAL JT.  ARTHROPLASTY

REALIGNMENT OSTEOTOMIES

•OBJECTIVE- to transfer weight-bearing forces from the arthritic portion to the healthier portion.

•

•IDEAL CANDIDATE

1. Thin, active individual in the 5^th – 6^th decade.

2. Localized, activity-related unicompartmental knee pain.

3.No patellofemoral symptoms.

4. Stable knee.

5. Full knee extension & flexion of 90 degrees.

•

UNICOMPARTMENTAL ARTHROPLASTY

INDICATIONS

●

1. Unicompartmental arthritis.

2. Sedentary life style.

3. Older then 60 yrs.

4.No ligamentous laxity.

5. Mild/moderate angular deformity.

•

OA OF KNEE

CAUSES

Injury

Loads.

Infection.

CNS disease.

RA, Gouty arthritis.

ACR radiologic and clinical criteria for knee and hip osteoarthritis

Knee osteoarthritis.Set of criteria:

    knee pain and one of the following features

        Age >50 years ,morning stiffness<30 min ,crepitus AND radiological osteophytes

Performances:

    sensitivity = 91%, specificity = 86%.

CLINICAL PICTURE

Painful creaking and granting on active motion.

Tenderness.

Floating patella

Muscle spasm.

Muscle atrophy.

Later flexion deformity.

Locking.

SURGERY

Debridement.

Proximal tibial osteotomy.

    indication:

1. Pain and disability.

        2. Varus or valgus deformity due to degenerative arthritis.

        3. The ability of the patient to use crutches.

        4. Good vascular status.

  contraindication

Narrowing of lateral compartment cartilaginous spaces.

Lateral tibial subluxation.

Medial compartment tibial bone loss is more than 2 or 3 mm.

Flexion contracture is more than 15 degrees.

Knee flexion is less than 90 degrees.

More than 20 degrees of correction is needed.

Distal femoral osteotomy:

    if the valgus deformity is more than 12 to 15 degrees, the plain of the knee joint deviates from the horizontal by more than 10 degrees.

Poor outcome: RA, the inadequate motion of the knee before osteotomy.

Total  knee arthroplasty

Arthrodesis: severe disability especially in young active patients.

Especially benefited when the knee is in varus or valgus deformity.

Patellectomy: should be preserved whenever possible.

Total knee arthroplasty for patellofemoral arthritis.

TOTAL KNEE ARTHROPLASTY

•Treatment of choice for end-stage arthritis.

•Best suited for

• > 50 yrs of age. 

•Willing to forgo high-impact activities.

•INDICATIONS

1. Relief of pain

2. Correction of deformity

3. Improvement of stability

•

References

•Canale, Campbell’s Operative orthopedics 12^th edition

•Solomon, Apley’s system of orthopedics and fractures

•Turek SL, Textbook of Orthopaedics, 4^th