# Osteoarthritis Pathology > Osteoarthritis pathology for MBBS Pathology: cartilage degradation mechanisms, osteophytes, Kellgren-Lawrence grading, hand and knee patterns. - Canonical URL: https://prepelephant.com/topics/mbbs/pathology/osteoarthritis-pathology - Exam / course: MBBS · Subject: Pathology - Publisher: PrepElephant (https://prepelephant.com) — Prepared and reviewed by the PrepElephant Academic Review Team - First published: 2026-10-02 - Last updated: 2026-10-02 - How to cite: "Osteoarthritis Pathology", PrepElephant, https://prepelephant.com/topics/mbbs/pathology/osteoarthritis-pathology ## Direct answer Cartilage has no blood vessels and no nerves — which is why osteoarthritis stays painless until subchondral bone and synovium are drawn into the disease. OA is a whole-organ failure of the synovial joint, not passive "wear and tear": mechanical stress and inflammatory cytokines (IL-1-beta, TNF-alpha) drive chondrocytes and their matrix metalloproteinases to degrade type II collagen and aggrecan faster than they are rebuilt, while subchondral bone stiffens and remodels, marginal osteophytes form, and low-grade synovitis advances alongside. Knees dominate Indian practice, where lifelong squatting and cross-legged sitting load the patellofemoral joint; hands follow with the classic nodal pattern. Radiology shows the tetrad of joint-space narrowing, osteophytes, subchondral sclerosis and subchondral cysts, graded 0 to 4 by Kellgren and Lawrence with osteophytes as the anchor. ## What you must remember - **The radiological tetrad and its grade:** joint-space narrowing, marginal osteophytes, subchondral sclerosis, subchondral cysts (geodes); Kellgren-Lawrence grade 4 is end-stage with complete joint-space loss — definite OA needs at least a grade 2 osteophyte. - **Primary versus secondary:** primary is age- and load-related (knees, hips, spine, first carpometacarpal joint, distal interphalangeal nodes); secondary follows trauma, developmental dysplasia, or metabolic diseases — haemochromatosis (second-third metacarpophalangeal), ochronosis, acromegaly, crystal deposition. - **Cartilage events in order:** surface fibrillation and softening, chondrocyte cluster proliferation, aggrecan loss (loss of safranin-O staining), vertical clefts, then eburnation of exposed bone with a polished, ivory-like surface. - **Clinical pattern that scores:** Heberden nodes at the distal and Bouchard nodes at the proximal interphalangeal joints, first CMC squaring, crepitus, bony tenderness, morning stiffness under 30 minutes, worsening with use through the day — the mirror image of rheumatoid stiffness. - **Synovial fluid signature:** non-inflammatory — white cell count under 2,000 per microlitre, high viscosity, good mucin clot — separating it from RA (inflammatory) and septic arthritis (purulent). - **Risk factors for the knee:** obesity is the strongest modifiable factor (each unit of BMI multiplies load), female sex, age, prior meniscectomy or trauma, and deep-flexion occupational and lifestyle postures — squatting and cross-legged sitting being the cited Indian contributors. - **Management skeleton:** education, quadriceps strengthening and weight loss as the core; topical then oral NSAIDs for pain; intra-articular steroid for flares (short-lived); total knee replacement for end-stage disease — Indian joint-replacement volumes having risen steeply as the modality became affordable. ## An OA knee versus a RA knee A 58-year-old woman has a swollen, painful right knee. Two diseases could write this page, and the bedside separates them in minutes. The OA knee is bony-hard, cool or barely warm, with coarse crepitus, varus deformity in established disease, and pain worst after activity; her hands show Heberden nodes, and the stiffness eases within minutes of moving. The RA knee is boggy and warm with a thickened synovial membrane, morning stiffness lasting over an hour, and pain worst at rest and in the small hours; the hands show metacarpophalangeal and proximal interphalangeal soft swelling with ulnar deviation in advanced disease. Aspiration completes the split: OA fluid is viscous with a count under 2,000 cells, RA fluid inflammatory in the thousands to tens of thousands, septic fluid purulent above 50,000 with neutrophil predominance. Add rheumatoid factor, anti-CCP and a radiograph — OA narrows the joint asymmetrically with osteophytes, RA erodes bone with periarticular osteopenia — and the pair is fully resolved. This comparison, reasoned rather than listed, is the answer examiners wait for. ## Where students slip Calling OA degenerative "wear and tear" alone is out of date — chondrocytes actively degrade their matrix under cytokine and mechanotransductive signalling, and anti-catabolic therapies are researched on that basis. Students confuse Heberden (DIP) with Bouchard (PIP) nodes, and forget that primary OA spares the metacarpophalangeal joints, wrists, elbows and ankles — involvement there demands a secondary cause. Erosive hand OA mimics RA but stays nodal and MCP-sparing. Finally, Kellgren-Lawrence grading uses osteophytes as its decisive criterion — the detail that turns a viva answer into a distinction. ## Frequently asked questions ### Which four radiological features characterise osteoarthritis? Joint-space narrowing, marginal osteophytes, subchondral sclerosis and subchondral cysts — the Kellgren-Lawrence tetrad. ### What are Heberden and Bouchard nodes? Bony proliferations at the distal (Heberden) and proximal (Bouchard) interphalangeal joints — the nodal phenotype of hand osteoarthritis. ### What does osteoarthritic synovial fluid show? A non-inflammatory picture — white cells under 2,000 per microlitre, high viscosity and a good mucin clot. ### Why does osteoarthritis spare the metacarpophalangeal joints? Primary OA follows load-bearing and intrinsic joint stress; MCP wrists, elbows and ankles are spared, and their involvement signals secondary OA. ### Which metabolic diseases cause secondary osteoarthritis? Haemochromatosis (especially second and third MCP joints), ochronosis, acromegaly and crystal deposition diseases.