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Expert Definition

Understanding This Symptom

Medical Definition

Subject Matter Expert Verified

Osteoarthritis (OA), also known as degenerative joint disease (DJD), is the most common form of arthritis, characterized by progressive breakdown of articular cartilage, changes in subchondral bone, and joint dysfunction.

It primarily affects weight-bearing joints such as the knees, hips, hands, and spine, causing joint pain, stiffness, crepitus, and reduced range of motion.

Unlike rheumatoid arthritis, OA is not an autoimmune condition but rather a mechanical and metabolic disorder of joint aging and wear.

Quick Facts

Expert-reviewed by medical professionals
Based on current medical research
Updated for 2026 standards

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Healthy State

What Optimal Health Looks Like

Understanding how your body functions when healthy helps identify dysfunction

In a healthy joint, the articular cartilage is a smooth, resilient connective tissue that covers the ends of bones, providing a low-friction surface for joint movement and absorbing shock during weight-bearing activities.

This cartilage is composed of chondrocytes embedded in a dense extracellular matrix of type II collagen, proteoglycans (especially aggrecan), and water.

The subchondral bone beneath the cartilage provides structural support and acts as a shock absorber.

The synovial membrane produces viscous synovial fluid that lubricates the joint and nourishes the cartilage through diffusion.

Healthy Function

Your body is designed to maintain balance and self-regulate

Optimal Range
Development Process

How This Develops

1

Cartilage degradation - Chondrocytes produce increased inflammatory cytokines (IL-

2

Chondrocyte senescence - Aging chondrocytes undergo cellular senescence, losing their ability to repair and regenerate matrix components

3

Subchondral bone changes - Increased bone turnover leads to subchondral sclerosis (hardening), cyst formation, and osteophyte (bone spur) development at joint margins

4

Joint space narrowing - Progressive cartilage loss reduces the joint space visible on X-ray, a key diagnostic marker

5

Synovial inflammation - Secondary synovitis develops from cartilage debris, causing additional pain and swelling

6

Altered biomechanics - Ligament laxity, muscle weakness, and joint malalignment increase mechanical stress on compromised cartilage, accelerating degeneration

7

Metabolic factors - Obesity, diabetes, and metabolic syndrome increase systemic inflammation and adipokine production, worsening cartilage damage

Understanding the mechanism helps us target the root cause rather than just treating symptoms.

Cost of Waiting

What Happens If Left Untreated

Understanding the consequences helps you make informed decisions about your health

Short-Term Consequences

Days to weeks

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Time Matters

Don't wait for symptoms to worsen. Early intervention leads to better outcomes.

Common Questions

Frequently Asked Questions

Expertise Behind This Guide

Evidence-Based Information

Dr. Hafeel Afsar, DHA Licensed Integrative Medicine Specialization: Musculoskeletal disorders, joint health, regenerative medicine, anti-aging medicine Qualifications: Board-certified in Integrative Medicine, Advanced Training in Orthobiologics and Joint Preservation Experience: 15+ years treating osteoarthritis with integrative protocols combining conventional pain management, physical therapy, lifestyle modification, and regenerative therapies

References & Further Reading

Zhang Y, Jordan JM. Epidemiology of Osteoarthritis. Clin Geriatr Med. 2010;26(3):355-369. PMID: 20699159 - Comprehensive review of OA epidemiology, risk factors, and burden of disease.
Kolasinski SL, Neogi T, Hochberg MC, et al. 2019 American College of Rheumatology Guideline for the Management of Osteoarthritis of the Hand, Hip, and Knee. Arthritis Care Res (Hoboken). 2020;72(2):149-162. PMID: 31908149 - Evidence-based clinical guidelines for OA treatment.
Martel-Pelletier J, Barr AJ, Cicuttini FM, et al. Osteoarthritis. Nat Rev Dis Primers. 2016;2:16072. PMID: 27734805 - Authoritative review of OA pathophysiology and novel therapeutic approaches.

This information is for educational purposes and not a substitute for professional medical advice.