Crystalline Arthritis

Crystalline arthritis refers to a group of joint disorders caused by the deposition of microscopic crystals in the joints and soft tissues. These conditions are a common cause of musculoskeletal pain, particularly in primary care settings. The condition can be acute, chronic, or even asymptomatic, with inflammation triggered by the body’s response to crystal accumulation.

 

Types of Crystalline Arthritis

Crystalline arthritis is classified based on the type of crystal involved:

1. Gout

• It is caused by the deposition of monosodium urate (MSU) crystals.
• Often presents as acute, intensely painful attacks.

2. Calcium Pyrophosphate Deposition Disease (CPPD)

• Also known as pseudogout or chondrocalcinosis.
• Caused by calcium pyrophosphate dihydrate (CPPD) crystals.
• Mimics gout but usually affects different joints and has different crystal characteristics.

3. Hydroxyapatite Deposition Disease (HADD)

• Involves calcium hydroxyapatite (CHA) crystals.
• It is also termed basic calcium phosphate (BCP) crystal deposition disease.
• Can cause conditions such as calcific tendinitis and hydroxyapatite-induced arthritis.

 

Clinically Relevant Anatomy

Joints Commonly Affected

• First Metatarsophalangeal Joint (Big Toe) - most commonly affected in gout (known as podagra).
• Knees - frequently involved in both gout and CPPD.
• Ankles - commonly affected in gout attacks.
• Shoulders - especially in elderly women with Milwaukee shoulder syndrome (linked to HADD).
• Wrists - involvement common in CPPD; less so in gout.
• Elbows - olecranon bursitis may occur in gout.
• Digits - interphalangeal joints and wrists often affected in CPPD.

 Soft Tissues and Cartilage Involvement

• Synovium - inflammation due to direct crystal deposition.
• Tendons and Sheaths - chronic gout can lead to tophi formation here.
• Bursae - commonly the olecranon and prepatellar bursae are affected, especially in gout.

 

Etiology

General Factors

Crystalline arthritis is multifactorial. Contributing factors include:

• Genetic predisposition
• Metabolic and comorbid medical conditions
• Dietary factors, such as high purine intake
• In some rare cases, inherited metabolic disorders

CPPD-Specific Causes

• Results from an imbalance between pyrophosphate production and pyrophosphatase activity in cartilage.
• Excess pyrophosphate binds calcium to form CPP crystals, appearing as snowball-like clumps under a microscope.

Conditions Associated with CPPD Crystals

• Found in - calcific tendinitis, calcific periarthritis, systemic sclerosis and dermatomyositis
• Often present in patients with advanced osteoarthritis.

 

Pathology

Crystal Characteristics

1. MSU Crystals (Gout) - needle-shaped and negatively birefringent under polarized light.
2. Crystals (Pseudogout) - rhomboid-shaped and weakly positively birefringent.
3. CHA Crystals (HADD) - not birefringent; detected via electron microscopy or special stains.
4. Crystals may be intra- or extracellular and can incite an inflammatory response similar to infection.

 

Clinical Presentation

 

Diagnosing Crystalline Arthritis

Differential Diagnosis

• Septic arthritis
• Rheumatoid arthritis
• Osteoarthritis
• Psoriatic arthritis
• Reactive arthritis
• Ankylosing spondylitis
• Hemochromatosis-related arthropathy
• Hyperparathyroidism-related arthropathy
• Sarcoidosis
• Spondyloarthropathies
• Tuberculous arthritis
• Systemic lupus erythematosus (SLE)
• Hemophilic arthropathy
• Amyloid arthropathy

Physiotherapy Management and Interventions for Crystalline Arthritis

Goals of Treatment

1. Alleviate pain and inflammation
2. Preserve joint function
3. Minimize recurrences
4. Educate patients for self-management

 

Non-Pharmacological Approaches

1. Immobilization

• Essential during acute attacks.
• Use of splints, crutches, or temporary rest.

2. Aspiration and Injection

• Joint aspiration reduces intra-articular pressure and confirms diagnosis.
• Corticosteroid injections provide targeted inflammation control.

3. Heat and Cold Therapy**

• Ice packs for acute flares.
• Warm compress during subacute/chronic stages.

4. Physical Therapy

Physical therapy is usually initiated after the acute inflammation subsides. Starting too early can worsen symptoms, but delaying too long may lead to chronic limitations.

Common Interventions

• Stretching and ROM Exercises
• Resistance training with bands or weights
• Manual therapy (if needed)
• Functional training (e.g., walking, stair climbing)
• Patient education on joint protection techniques

 

Pharmacological Treatment

1. NSAIDs

• First-line for acute attacks.
• Short-term use until symptoms resolve.

2. Colchicine

• Effective in both acute attacks and prophylaxis.
• Must be dosed carefully to avoid GI side effects.

3. Oral Glucocorticoids

• An alternative when NSAIDs or colchicine are contraindicated.

4. Biologics / Immunomodulators

• Used in refractory or severe cases, examples include, Anakinra (IL-1 receptor blocker) and Canakinumab (IL-1β monoclonal antibody)

 

Lifestyle and Education

• Hydration - delps prevent crystal formation.
• Dietary Changes:

         > For gout - avoid purine-rich foods for example, red meat, seafood, and alcohol.

         > For CPPD - ensure appropriate calcium and magnesium intake.

• Weight Management - reduces mechanical load on joints.
• Smoking Cessation and Regular Exercise during remission periods.

 

Surgical Intervention

• Reserved for chronic, unmanageable cases with calcific deposits.
• Options include arthroscopic debridement, image-guided aspiration, or surgical excision.

Crystalline arthritis encompasses several distinct but overlapping conditions characterized by the deposition of crystals in and around joints. Proper identification of the crystal type, along with individualized management strategies—ranging from conservative treatment to advanced pharmacotherapy—are essential for reducing pain, improving function, and preventing recurrences. A multidisciplinary approach involving rheumatologists, physiotherapists, and patient education is key to optimizing outcomes.