OSTEOARTHRITISAnd Crystal Induced

Arthropathies

Dr Humaira Achakzai

DEFINITIONOsteoarthritis OA is a degenerative disease of (synovial) joints, characterized by Breakdown of articular cartilage Proliferative changes of surrounding

bones

EPIDEMIOLOGY

Osteoarthritis(OA) is the most common joint diseaseOA of the knee joint is found in 70% of the population over 60 years of ageRadiological evidence of OA can be found in over 90 % of the population

LIMITED FUNCTION

OA may cause functional loss (Activites of daily living)Most important cause of disability in old ageMajor indication for joint replacement surgery

CHARACTERISTICS OF OA

OA is a chronic disease of the musculoskeletal system, without systemic involvement OA is mainly a noninflammatory disease of synovial joints No joint ankylosis is observed in the course of the disease

CLASSIFICATION OF OA

Primary OA Secondary OA

Etiology is unknown Etiology is known

RISK FACTORS FOR PRIMARY OA

Age SexObesityGeneticsTrauma (daily)

SECONDARY OSTOARTHRITIS☛Results from problems that can cause cartilage damage1.Physical trauma (external, internal, biomechanical derangements,2.Inflammatory disorders

a. inflammatory arthritis (e.g. rheumatoid arthritis)b. joint infectionc. gout, pseudogout

3. Metabolic disordersa. hemochromatosis (excess iron)b. Wilson’s Disease (excess copper)

4. Endocrine disordersa.Diabetes b.acromegaly

Pathophysiology☛The earliest and most characteristic feature of OA is Cartilage Damage1-Cartilage

a. Covers the ends of articulated bones, b. Provides a low-friction interface greatly capable of absorbing shock, c. Physical characteristics result from collagenfibers (50% of the dry weight of cartilage) intermingled with proteoglycans

2-. Collagen Hyaline (joint) cartilage -Type II collagen.

Gives cartilage tensile strength and allows it to resist shear forces during motion under loadAltered cartilage in OA contains increased amounts of Type collagen (normally found in skin, bones, tendons)Constrains the negatively charged, highly hydrated proteoglycans. This produces a large swelling pressure and gives cartilage its elasticity and resistance to compression. Under high-load conditions, proteoglycans release water and lubricate the cartilage surface (hydrostatic lubrication)3-Proteoglycansa. Complex macromolecules than bind a large number of water molecules in cartilageb. Markedly diminished in osteoarthritic cartilagec. Enzymatic damage by matrix metalloproteases is an important cause of osteoarthritis and early damage significantly impacts proteoglycansd. Immobilization causes decreased proteoglycan synthesis and aggregation, further diminishing normal cartilage function

Pathophysiology….Contd

4-BONEa. Bony degeneration is also a universal b. Includes localized increases in bone density (scelorisis) and

new bone formation osteophytes Unknown whether cartilage abnormalities cause bone

degeneration

Morphology of Primary OA

Primary Generalized OA

LABORATORY FINDINGS OF OA

There are no pathognomonic laboratory findings for OA

Laboratory analysis is performed for differential diagnosis

RADIOLOGIC FINDINGS OF OA

Narrowing of joint space (due to loss of cartilage)

Osteophytes

Subchondral (paraarticular) sclerosis

Bone cysts

RADIOLOGIC GRADE OF OA

G1 NormalG2 MildG3 ModerateG4 Severe

Kellgren Lawrence Classification

DIAGNOSIS OF OA

CLINICAL FINDINGS Joint pain + RADIOLOGIC FINDINGS Osteophytes

SIGNS AND SYMPTOMS

Joint pain - degenerative Stiffness following inactivity – 30 min Limitation of ROM – later stages Deformity – restricition of ADL

OA OF KNEE JOINT (GONARTHROSIS)

More common in obese females over 50 years of ageJoint stiffness (<30 minutes)Mechanical painPhysical examination findings: CrepitusPain on pressurePainful ROM and functional limitationLimitation of ROM in later stages of OA (first extension)Laboratory analysis within normal limits

GENU VALGUM - ORTHOSIS

OA OF HIP JOINT

More common in males over 40 years of ageJoint stiffnessPain of hip, gluteal and groin areas radiating to the knee (N obturatorius)Mechanical painLimited walking function

X-RAY OF HIP OA

Peripheral JointsHands Feet

Treatment Concepts1. Patient education2. Reinforce importance of exercise to maintain strength and ROM

Exercises - Swimming - Walking - Strengthening

3. Physical modalities: a. Decrease of joint loading

- Weight control - Splinting - Walking sticks

b. muscle strengthening

4.Analgesicsa. acetaminophenb. non-steroidal anti-inflammatory drugs

5.Corticosteroid injections6. Joint replacement surgery for end stage disease 7. On the horizon:

a. autologous cartilage graftsb. stem cells to grow new cartilage

STRUCTURE MODIFYING TREATMENT

Hyaluronic acid injection (HA)

Glycose amino glycans (GAG)

PRIMARY PREVENTION OF OA ??

Regular exercises

Weight control

Prevention of trauma

HAND OA - RESTING SPLINT

INDICATIONS OF SURGICAL INTERVENTION

Severe joint pain, resistant to conservative treatment methodsLimitation of daily living activitiesDeformity, angular deviations, instability

CRYSTALLINE-INDUCED INFLAMMATORY ARTHRITIS

A. Gout (acute gouty arthropathy)☛Gout is a disease of hyperuricemia1. Clinical Features

a. Generally affects men over age 30 b. Presents as an acute attack of highly inflammatory monoarticular arthritis

c. Most commonly involved joint is the great toe i. 50% first attack ii. 90% eventually

d. Other common joints (in order of frequency): ankle, knee, wrist, finger, elbowe. 50% recurrence within the first year (90-95% by 10 years)f. Risk of clinical gout increases with serum urate level

Differential Diagnosis

a. Infection! acute gout often looks like cellulitis b. Inflamed bunion (bursitis) c. Trauma d. Psoriatic arthritis e.Reactive arthritis f. Pseudogout

3. Etiologya. Acute inflammation is caused by monosodium urate (MSU) crystalsb. Saturation of urate at 37°C is 7.0mg/dl –close to normal serum levelc. Most patients with gout are under excretors rather than overproducers of urated. Serum urate levels rise in males at puberty and in females at menopausee. Causes of hyperuricemia

i. Overproduction - increased purine biosynthesis - inherited enzyme defects - increased nucleic acid turnover •myeloproliferative diseases •hemolytic anemias •psoriasis (increased skin turnover) •increased breakdown of adenosine triphosphate (ATP

Causes of hyperuricemiai. Overproduction

- increased purine biosynthesis - inherited enzyme defects - increased nucleic acid turnover

myeloproliferative diseases •hemolytic anemias •psoriasis (increased skin turnover) increased breakdown of adenosine triphosphate (ATP severe illness strenuous exercise excessive ethanol consumption

ii. Underexcretion (decreased renal clearance)- intrinsic renal disease (decreased filtration, decreased secretion, or both)

•renal insufficiency•gout•lead nephropathy•endocrinopathy(hypothyroidism, hyper- andhypoparathyroidism)

- competition for excretion by organic acids•drugs (e.g. thiazides, nicotinic acid, low-dose salicylates)•lactic acid (e.g. lactic acidosis, heavy ethanol use)•ketosis•glycogen storage disease

Diagnosisa. Aspiration of synovial fluidb. Demonstration of needle-shaped crystalswith negative birefringence (frequently insidepolymorphonuclear WBCs) on polarizedmicroscopy

Treatment Conceptsa. Don’t treat asymptomatic hyperuricemia.b. For acute attacks:

i. Non-steroidal anti-inflammatory drugs (NSAIDS) or corticosteroids (systemic or intra-articular) ii. High-dose colchicine is an outdated treatment approach

c. For prevention of acute attacks: i. Urate-lowering agents are available that increase urinary excretion of uric acid or inhibit metabolic

production of uric acid

B. Pseudogout1. Clinical

PseudogoutClinical featuresa. Acute, inflammatory, gout-like attacks that occur secondary to calcium pyrophosphate dihydrate (CPPD) crystals.b. Patients are typically older (60’s-70’s)c. Male/Female incidence is about 1:1d. Knee is to pseudogout as big toe is to gout (wrist is also common)e. Trauma (e.g. surgery) is a common trigger Laboratory Data

a. Serum calcium level usually normal. b. Inflammatory synovial fluid; usually containing rhomboid shaped crystals with positive birefringence c. Radiographs typically show linear deposition of CPPD in hyaline cartilage or fibrocartilage “chondrocalcinosis”

.Associated Conditions a. Hyperparathyroidism b. Hemochromatosis c. Hypothyroidism d. Gout e. Hypomagnesemia f. Hypophosphatasia

Treatment conceptsa. NSAIDb. intra-articular steroidsc. low-dose colchicine may help preventsattacks

Diagnosis of Crystalline Arthropathy

1. Birefringent Crystals a. Refraction (bending) of light by an optically active structure yields two perpendicular rays (one fast

and one slow) → “birefringence” b. The optical orientation (sign) of the fast and slow wave of a birefringent crystal isdetermined by

using a first order redretardation plate (compensator)

2. “Positive” birefrigence a. Crystal appears blue when its longitudinal axis is parallel to the direction of slow vibration of light in

the compensator (the direction of slow vibration is marked on the compensator) b. Crystal appears yellow when it is perpendicular to the compensator's slow ray c. Calcium pyrophosphate dihydrate has weakly positive birefringence

3. "Negative” birefrigence a. Crystal appears yellow when its longitudinal axis is parallel to the compensator's slow ray b. Crystal is blue when perpendicular to the compensator's slow ray c. Monosodium urate has strong negative birefringence

QUESTIONS?