Osteoarthritis

Populations and Risk Factors

• Most common after age 40; prevalence increases sharply with age — affects approximately 30 million Americans and roughly one-third of adults over 65
• Men and women affected equally before age 55; women have significantly higher rates after menopause (2–3 times higher for hand and knee OA), likely due to estrogen's protective effect on cartilage metabolism
• Obesity is the strongest modifiable risk factor — every pound of body weight translates to approximately 3–4 pounds of compressive force across the knee during walking, accelerating cartilage degradation in weight-bearing joints
• History of joint injury (fracture, ligament tear, meniscal injury) increases risk 3–6 times due to altered joint mechanics and accelerated focal loading
• Occupational risk: repetitive heavy lifting, kneeling, squatting (construction workers, farmers, carpet layers); athletes with high-impact sport histories (soccer, football, running)
• Genetic predisposition, especially for hand OA (Heberden and Bouchard nodes) and hip OA — first-degree relatives have approximately double the risk
• Sedentary lifestyle: immobilization deprives cartilage of synovial fluid nutrition (cartilage is avascular — it relies entirely on compression-decompression cycles to imbibe nutrients from synovial fluid)
• Joint malalignment (genu varum, genu valgum) concentrates load on one compartment, accelerating focal degeneration

Causes and Pathophysiology

Cartilage Degeneration Sequence

• Healthy cartilage function: Articular (hyaline) cartilage is avascular, aneural, and alymphatic — it receives all nutrition from synovial fluid through a compression-decompression pumping mechanism during joint loading. Chondrocytes maintain the extracellular matrix by synthesizing type II collagen and proteoglycans (aggrecan), which trap water and give cartilage its shock-absorbing resilience.
• Initiation: Aging reduces chondrocyte metabolic activity and cartilage water content, making the matrix drier, stiffer, and more brittle. Simultaneously, cumulative mechanical stress (obesity, repetitive loading, prior injury) exceeds the cartilage's ability to repair microdamage. The balance tips from synthesis toward degradation.
• Matrix breakdown: Proteolytic enzymes (matrix metalloproteinases — MMPs) released by chondrocytes and synoviocytes degrade the collagen and proteoglycan network faster than it can be replaced. Water content paradoxically increases initially as the proteoglycan network loses its ability to organize water binding, causing cartilage swelling and softening (chondromalacia) — this is why early OA can show cartilage that is edematous before it thins. The surface develops fibrillation (fraying), then fissuring, then progressive thinning.
• Why this matters clinically: The softened, fibrillated cartilage surface produces crepitus on palpation and movement — the grinding or grating felt during passive joint motion. The loss of shock absorption transfers mechanical stress to the subchondral bone, triggering the remodeling cascade below.

Subchondral Bone Remodeling

• As cartilage thins, the subchondral bone absorbs increasing mechanical load. The bone responds with sclerosis (thickening and hardening) to resist the increased stress. However, sclerotic bone is less compliant than normal bone, further reducing shock absorption and accelerating cartilage destruction — a self-reinforcing cycle.
• Subchondral bone cysts (geodes) may form in areas of maximal stress as fluid is forced into microfractures under the sclerotic surface.
• Osteophytes (bone spurs) form along joint margins where the capsule attaches to bone, representing the body's attempt to redistribute load by increasing the joint surface area. Osteophytes restrict ROM by creating a mechanical block — this is the pathological basis for the bony (hard) end-feel found on PROM in advanced OA. In the spine, osteophytes may narrow the foramen and compress nerve roots (spondylosis).

Joint Capsule and Synovial Changes

• The joint capsule thickens and fibroses over time, contributing to the capsular pattern of restriction. Capsular fibrosis explains why PROM shows a characteristic pattern: in the hip, IR is lost first and most, followed by flexion and abduction; in the knee, flexion is lost more than extension.
• Intermittent low-grade synovitis occurs when cartilage fragments ("joint mice") are shed into the synovial fluid, provoking an inflammatory response. This explains episodic warmth and effusion in a joint that is otherwise "non-inflammatory." The cartilage fragments also cause clicking and mechanical locking.
• Synovial fluid becomes thinner and less viscous (reduced hyaluronic acid concentration), further diminishing its lubricating and nutritive capacity.

Muscular Consequences

• Arthrogenic inhibition: Joint swelling and pain reflexively inhibit the surrounding musculature (particularly quadriceps in knee OA, gluteus medius in hip OA) via the arthrogenic muscle inhibition reflex. This weakness precedes and accelerates joint instability.
• Compensatory hypertonicity: Muscles crossing the joint develop protective guarding and trigger points as they attempt to stabilize the degenerating joint. In knee OA, hamstrings, ITB/TFL, and gastrocnemius become hypertonic; in hip OA, piriformis, adductors, and TFL develop trigger points.
• The vicious cycle: Pain → reduced movement → arthrogenic inhibition and contracture → loss of synovial fluid pumping → accelerated cartilage decay → more pain. This cycle is the primary rationale for MT intervention — breaking the cycle at the muscular level preserves joint nutrition and function.

Nodal OA (Hands)

• Heberden nodes (DIP joints) and Bouchard nodes (PIP joints) are bony osteophyte enlargements specific to hand OA. They represent the same osteophyte formation process occurring at the finger joints.
• Heberden nodes are more common and appear earlier; Bouchard nodes indicate more advanced hand involvement. Both are diagnostically significant because they confirm OA over RA (RA affects the MCP and PIP joints but spares the DIP).

Signs and Symptoms

Early Stage (Mild)

• Deep, aching pain in the affected joint that worsens with activity and is relieved by rest
• Brief "gelling" stiffness after inactivity (sitting, sleeping) lasting less than 30 minutes — improves with gentle movement as synovial fluid redistributes
• Occasional clicking or catching; intermittent mild swelling after prolonged use
• Function largely preserved; pain is activity-dependent

Moderate Stage

• Pain becomes more persistent; may occur during routine daily activities (stairs, walking, gripping)
• Crepitus (grating or grinding) palpable or audible during joint movement — reflects the irregular cartilage surfaces articulating
• Visible joint enlargement from osteophytes (bony, non-tender) — Heberden and Bouchard nodes in the hands; bony prominence around the knee
• ROM progressively restricted by osteophytes and capsular fibrosis; capsular pattern emerges
• Periarticular muscle atrophy (quadriceps wasting in knee OA; gluteal wasting in hip OA) from arthrogenic inhibition
• Episodes of mild warmth and effusion (reactive synovitis from loose bodies)

Advanced Stage

• Pain at rest and at night, disrupting sleep
• Significant ROM loss with bony end-feel at end-range
• Joint deformity: genu varum (bow-legs) in medial compartment knee OA; genu valgum in lateral compartment; fixed flexion contracture at hip
• Marked muscle atrophy and weakness; functional dependence (difficulty with stairs, rising from a chair, walking distances)
• Joint instability from ligament laxity secondary to chronic effusion and capsular distension

Assessment Profile

Subjective Presentation

• Chief complaint: Deep, aching pain in the joint that is worst after activity or prolonged use; "my knee grinds when I go up stairs"; "my hip is stiff every morning but loosens up after a few minutes"
• Pain quality: Deep, dull, aching — not sharp or burning (sharp pain suggests loose body or meniscal involvement); pain is localized to the joint, not radiating (radiating pain suggests nerve involvement and warrants further investigation)
• Onset: Insidious, gradual onset over months to years; may have a history of prior injury to the joint decades earlier; progressive worsening over time with periodic flare-ups
• Aggravating factors: Weight-bearing activities (walking, stairs, standing), prolonged use, cold and damp weather (increases joint stiffness via synovial fluid viscosity changes), end-range movements
• Easing factors: Rest, warmth (improves synovial fluid viscosity and reduces stiffness), gentle movement after gelling (synovial fluid redistribution), activity modification
• Red flags: Sudden onset of hot, red, swollen joint → suspect septic arthritis or crystalline arthropathy (gout, pseudogout) — refer for urgent medical evaluation; do not treat as OA flare

Observation

• Local inspection: Bony joint enlargement (hard, non-tender — osteophytes); Heberden nodes (DIP) and Bouchard nodes (PIP) in hand OA; genu varum or valgum deformity in knee OA; visible quadriceps or gluteal atrophy; mild effusion may be present
• Posture: Antalgic posture favoring the affected joint; lateral trunk lean toward the affected side in hip OA (to reduce abductor demand); increased lumbar lordosis to compensate for hip flexion contracture; forward-flexed trunk in bilateral hip OA
• Gait: Antalgic gait with shortened stance phase on the affected side; Trendelenburg gait (pelvic drop) if gluteus medius is weakened in hip OA; stiff-legged gait avoiding full knee extension in advanced knee OA

Palpation

• Tone: Compensatory hypertonicity in muscles crossing the affected joint — knee OA: hamstrings, ITB/TFL, gastrocnemius, and popliteus; hip OA: piriformis, adductors, TFL, and rectus femoris; hand OA: forearm flexors and extensors. Simultaneous arthrogenic inhibition of primary stabilizers (quadriceps in knee OA, gluteus medius in hip OA) as described in Pathophysiology. The combination of hypertonic secondary stabilizers and inhibited primary stabilizers is a characteristic finding.
• Tenderness: Joint line tenderness on palpation (medial joint line in medial compartment knee OA; lateral joint line in lateral compartment); periarticular tenderness at muscle-tendon junctions from compensatory overload; trigger points in compensatory muscles (vastus medialis in knee OA, piriformis in hip OA); Heberden and Bouchard nodes are bony and non-tender unless acutely inflamed
• Temperature: Usually normal or slightly cool; mild warmth indicates reactive synovitis from loose cartilage fragments — if the joint is hot and markedly swollen, rule out septic arthritis or crystalline arthropathy before proceeding
• Tissue quality: Bony, hard enlargement at joint margins (osteophytes). Crepitus palpable during passive joint motion. Periarticular muscle wasting with fibrotic, ropy texture in chronically hypertonic compensators. Capsular thickening palpable around the joint. Effusion detectable by patellar tap or ballottement in knee OA.

Motion Assessment

• AROM: Progressively restricted with a pattern that improves with gentle warm-up ("gelling" resolves as synovial fluid redistributes with movement). Capsular pattern: hip — IR most restricted, then flexion, then abduction; knee — flexion more restricted than extension; hand — grip strength reduced. Pain primarily at end-range. Crepitus audible or palpable through the arc of movement
• PROM / end-feel: PROM may slightly exceed AROM (due to arthrogenic inhibition reducing active force generation), but both are restricted. End-feel progresses from capsular (firm, leathery) in early/moderate OA to bony (hard, abrupt) in advanced OA as osteophytes create a mechanical block. The end-feel type is diagnostically significant: hard end-feel = structural bony change; capsular end-feel = soft tissue fibrosis still amenable to treatment
• Resisted testing: Weakness in muscles crossing the affected joint due to arthrogenic inhibition and disuse atrophy — quadriceps weakness is the hallmark in knee OA (specifically VMO); gluteus medius weakness in hip OA (positive Trendelenburg). Resisted testing is typically pain-free or mildly painful (the joint is degenerative, not acutely contractile), which distinguishes OA from tendinopathy

Special Test Cluster

For knee OA with mechanical symptoms (locking, catching, giving way), add McMurray's test to rule out concurrent meniscal pathology. For hip OA with groin pain, add FABER to differentiate SIJ involvement.

Differential Assessment