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Osteoarthritis: Pathophysiology, Manifestations, and Management

Pathophysiology

  • Osteoarthritis (OA) is a degenerative joint disease characterized by damage to articular cartilage at the ends of bones and changes within the synovial joint structures (joint capsule, synovium, and synovial fluid).

  • Commonly affected joints: fingers, wrists, knees (knees are the most common due to bearing body weight and constant movement).

  • Etiology: OA is often described as wear-and-tear or overuse. It may be idiopathic when no specific cause is identified, but the majority of cases have an underlying identifiable factor (overuse, prior injury, or trauma).

  • Joint anatomy overview (as described in the transcript): cartilage at the joint end of bones, synovial membrane lining the joint capsule, inner synovial fluid, and the joint space between bones.

  • Progressive structural changes with wear:

    • Joint space narrows; bones can grind against each other (bone-on-bone contact).

    • Cartilage erosion with progressive loss can lead to exposure of subchondral bone.

    • Formation of clefts/fibrillations within cartilage that extend toward the bone and may lead to denuding of the bone (loss of cartilage coverage).

    • Subchondral bone responds with sclerosis (hardening) and possible cyst formation.

  • Cartilage and cellular biology:

    • Cartilage is produced by chondrocytes, the cartilage cells.

    • In OA, inflammatory mediators (cytokines) contribute to destruction of collagen in the extracellular matrix of cartilage.

    • Pro-inflammatory factors rise relative to anti-inflammatory factors, leading to degeneration.

    • Chondrocyte apoptosis (death) and reduced proliferation lead to decreased cartilage production (collagen and proteoglycans).

    • Resulting degeneration includes cartilage thinning, fibrillations, and eventual loss of cartilage.

  • Consequences of joint damage:

    • Loose cartilage fragments can float in the joint space.

    • Fibrillations and bone clefts can allow synovial fluid to enter subchondral bone, forming cysts.

    • Osteophytes (bone spurs) form at joint margins and can press on the synovial membrane.

    • Osteophytes and cartilage fragments contribute to joint irritation and pain.

    • Osteophytes may damage surrounding tissues (e.g., ligaments) and promote inflammation in the joint.

  • Terminology and key concepts:

    • Osteophyte = bone spur.

    • Joint mice = small fragments of bone/cartilage floating in the joint.

    • Crepitus = crackling or grating sound or feel when moving a joint (often heard in OA).

  • Inflammatory involvement in OA pathology:

    • There is an imbalance between pro-inflammatory and anti-inflammatory factors within the joint.

    • Nitric oxide production increases and can contribute to chondrocyte death.

    • Increased intraosseous pressure due to vascular changes can occur in the subchondral bone.

  • Pathophysiology flow (as a simplified sequence):

    • Stressor or initial insult → inflammatory response within the joint → cytokines degrade cartilage extracellular matrix → reduced chondrocyte proliferation and ECM synthesis (collagen, proteoglycans) → cartilage degeneration and thinning → fibrillations/clefts → denuding of subchondral bone → sclerosis and cyst formation → osteophyte development → synovial irritation and pain → potential loose bodies (joint mice).

  • Visual summary reference from the transcript: a flow-like representation of risk factors impacting structural cartilage damage and subsequent joint changes.

Risk factors

  • Age and obesity contribute to increased joint load and wear on cartilage.

  • Malalignment of joints increases abnormal stress on the cartilage (e.g., knee valgus/varus malalignment).

  • Gender differences: OA, particularly knee OA, is more common in females. Reasons discussed include hip anatomy differences that influence knee loading angles and subsequent joint stress.

  • Sports and trauma:

    • Knee injuries from sports (e.g., football, rugby, soccer) can predispose to OA later in life due to prior joint damage.

    • Any trauma such as sprains, strains, or fractures can contribute to OA development.

  • Genetic predisposition: some individuals have inherent structural predispositions that increase cartilage damage risk even without major trauma; more likely relevant to idiopathic/primary OA.

  • Other contributing factors (less central to the unit but noted): neurological, hematological, and endocrine disorders can influence OA risk.

  • The transcript emphasizes a schematic flow where age, obesity, malalignment, and joint injury feed into structural damage and OA progression, with genetic influences modulating susceptibility.

Clinical manifestations

  • Pain in affected joints (primary symptom).

  • Stiffness and reduced range of motion in the involved joint.

  • Crepitus (audible or palpable crackling/crunching with joint movement).

  • Joint swelling and possible effusion.

  • Tenderness around the joint and feeling of instability or weakness.

  • Deformity and functional impairment with progressive disease.

  • Pain sources can be multifactorial: cartilage fragments, cartilage breakdown, bone-on-bone contact, cysts in subchondral bone, inflammation of the synovium due to osteophytes, and joint effusions.

Diagnostics

  • X-ray: primary imaging to assess bone changes, joint space narrowing, osteophytes, and subchondral sclerosis.

  • MRI: used to assess extent of damage, cartilage quality, and involvement of soft tissues; can reveal cartilage defects not visible on X-ray.

  • CT: can help evaluate bone structures and related issues (e.g., bone spurs altering tendon function) but is less informative for cartilage integrity.

  • Arthroscopy: direct visualization of the joint; can be used diagnostically and therapeutically (e.g., removal of loose bodies or damaged cartilage, possible repair depending on joint status).

  • Diagnosis is typically clinical + imaging; progression assessment may involve MRI/CT as needed.

Management and treatment

  • General goal: manage pain, maintain function, and slow progression; OA is not usually curable with current therapies.

  • Non-pharmacologic management:

    • Weight management to reduce joint load (especially for knee/hip OA).

    • Exercise and physical therapy focusing on low-impact, non-weight-bearing or minimally loading activities (e.g., pool exercises, walking in water, swimming) to maintain joint mobility and muscle strength.

    • Offloading devices or braces may be used to reduce stress on the affected joint.

    • Activity modification to minimize repetitive stress on the joint.

  • Pharmacologic management:

    • NSAIDs (e.g., ibuprofen) for pain and inflammation.

    • Acetaminophen (paracetamol) for pain relief.

    • Topical capsaicin cream for pain relief (note: capsaicin is chili-based; caution advised to avoid transferring capsaicin to other areas such as the eyes or face, particularly if applying to hands).

  • Intra-articular treatments:

    • Corticosteroid injections for intra-articular inflammation when significant pain is present.

    • Arthroscopic debridement or lavage in selected cases (may remove loose cartilage fragments and may provide symptomatic relief depending on joint and extent of disease).

  • Surgical options:

    • Joint replacement (arthroplasty) is common for severe OA of the knee or hip when conservative management fails to control pain and restore function.

  • Supplements (as discussed in the lecture):

    • Glucosamine vs. chondroitin:

    • The instructor notes that glucosamine alone is ineffective for OA outcomes.

    • Chondroitin is suggested as the component that can help cartilage; however, in scientific literature, evidence for significant clinical benefit is mixed and not universally accepted. The lecture emphasizes chondroitin as the active component for cartilage support.

    • Important clarification: cartilage cells are not themselves chondroitin; chondroitin sulfate is a major proteoglycan component of cartilage ECM, contributing to resilience and hydration.

  • Important practical notes from the lecture:

    • Capsaicin caution to avoid contact with eyes or face after application if hands are used on hands that will touch the face.

    • Diagnosis often relies on imaging; MRI can reveal extent and associated tissue involvement beyond what X-ray shows.

  • The overall emphasis of management is symptom control, functional improvement, and joint preservation, with the choice of interventions tailored to the specific joint involved and the severity of disease.

Key concepts recap (quick reference)

  • OA pathophysiology involves cartilage degradation, chondrocyte dysfunction/apoptosis, subchondral bone changes, osteophyte formation, and synovial inflammation.

  • Pain etiologies are multifactorial: mechanical bone-on-bone contact, loose cartilage fragments, cysts, and inflammatory processes.

  • Risk factors include age, obesity, malalignment, injury, gender-specific anatomy, and genetic predisposition.

  • Diagnosis combines clinical evaluation with imaging (X-ray, MRI; CT for related structures; arthroscopy for direct assessment).

  • Management focuses on non-surgical pain relief and functional improvement, reserving surgery (joint replacement) for severe, refractory cases.

  • Supplements: evidence for glucosamine and chondroitin is variable; lecture emphasizes chondroitin as the cartilage-supporting component, with a scientific caveat about cartilage biology (cartilage is produced by chondrocytes, not by chondroitin itself).

Practical scenarios and tips

  • If a patient reports knee pain with crepitus and reduced mobility, consider OA in the differential; imaging with X-ray is a first step, followed by MRI if needed to assess cartilage and soft tissues.

  • For patients with obesity and knee OA, discuss weight-loss strategies and pool-based exercises to reduce joint load and improve function.

  • If there are inflammatory features or significant effusion, intra-articular corticosteroid injections can be considered for transient relief.

  • For advanced OA with functional limitation unresponsive to conservative therapy, knee or hip replacement may be considered after evaluation by an orthopedic surgeon.

If you have any questions on a specific section or need this organized for a study deck, I can tailor the notes further (e.g., more concise flashcards or a detailed diagram outline).