After reading this note you will be able to describe the definition, relevant anatomy, causes, risk factors and basic pathophysiology of osteoarthritis, and you will know that drug doses and local protocols must be checked against the Kenya MoH guideline and the hospital formulary.
Definition
Osteoarthritis (OA) is a chronic, progressive, degenerative joint disease characterised by loss of articular cartilage, sub‑chondral bone remodelling, osteophyte formation and synovial inflammation, leading to pain, stiffness and functional limitation.
Anatomy and physiology you need
| Structure | Relevance to OA |
|---|---|
| Articular cartilage | Provides smooth, low‑friction surface; loss initiates OA |
| Sub‑chondral bone | Thickens and remodels as cartilage thins; osteophytes arise here |
| Synovial membrane | Produces fluid; becomes inflamed secondary to cartilage debris |
| Joint capsule & ligaments | Stabilise joint; may become lax with chronic degeneration |
| Peri‑articular muscles | Weakness contributes to abnormal loading and progression |
Key points: cartilage is avascular, relies on diffusion from synovial fluid; chondrocytes maintain matrix balance. Disruption of this balance → net matrix loss.
Causes and risk factors
| Category | Specific factors in Kenya |
|---|---|
| Age | Incidence rises after 45 years |
| Sex | Slight female predominance, especially post‑menopause |
| Obesity | Increases mechanical load on weight‑bearing joints |
| Joint injury | Post‑traumatic OA common after road‑traffic accidents |
| Occupation | Repetitive kneeling, squatting, heavy lifting (farmers, construction) |
| Genetics | Family history of early OA |
| Metabolic | Diabetes mellitus, dyslipidaemia |
| Infectious / Tropical | HIV (synovial inflammation, altered bone metabolism), chronic TB arthritis (joint damage), malaria‑related hemolysis in sickle‑cell disease causing joint pain, sickle‑cell disease itself (avascular necrosis mimics OA), endemic rheumatic fever (post‑streptococcal joint damage) |
| Other systemic | Hyperuricaemia, hypothyroidism |
Pathophysiology
Mechanical stress → chondrocyte injury → release of inflammatory cytokines (IL‑1, TNF‑α) → up‑regulation of matrix‑degrading enzymes (MMPs, ADAMTS) → loss of collagen & proteoglycans → cartilage thinning → exposed sub‑chondral bone → bone remodelling & osteophyte formation → synovial irritation → pain and stiffness.
Clinical features
| Aspect | Key questions / findings | Why it occurs |
|---|---|---|
| Onset & duration | “When did the pain start? Was it sudden or gradual?” | OA is usually insidious; chronic wear‑and‑tear produces progressive symptoms. |
| Pain pattern | • Pain worsens with use (walking, climbing stairs, rising from a chair) <br>• Improves with rest or after a few minutes of activity (“stiffness that eases”) <br>• Night pain? (usually absent) | Mechanical stress irritates degenerated cartilage and sub‑chondral bone → nociceptor activation. Rest reduces load, relieving pain. Night pain suggests inflammatory or malignant processes. |
| Stiffness | “Do you feel stiffness in the morning? How long does it last?” | Joint capsule and peri‑articular structures become stiff after inactivity; in OA stiffness is <30 min, reflecting limited capsular fibrosis rather than synovitis. |
| Functional limitation | • Difficulty walking, climbing stairs, squatting, kneeling <br>• Need for assistive devices? | Cartilage loss and osteophyte formation limit joint range and alter biomechanics, leading to functional loss. |
| Joint swelling | “Is the joint swollen? Is it hard or soft? Does it fluctuate?” | Swelling may be due to joint effusion (synovial inflammation secondary to cartilage debris) or bony enlargement from osteophytes. |
| Crepitus | “Do you hear or feel grinding when you move the joint?” | Rough articular surfaces rub against each other producing audible/ palpable crepitus. |
| Deformity | “Have you noticed any change in joint shape (e.g., bow‑leg, valgus, ulnar deviation)?” | Osteophytes, sub‑chondral sclerosis and ligament laxity cause malalignment. |
| Systemic symptoms | Fever, weight loss, fatigue? | Absence supports primary OA; presence raises suspicion for inflammatory, infectious or neoplastic disease. |
| Risk‑factor history | • Age, gender, occupation (heavy manual work, squatting) <br>• Prior joint injury or surgery <br>• Obesity, metabolic syndrome <br>• HIV, TB, malaria, sickle‑cell disease, other tropical infections <br>• Family history of early OA | Mechanical overload, metabolic inflammation, and disease‑related joint damage accelerate cartilage loss. |
| Medication & comorbidity review | NSAID use, glucocorticoids, anticoagulants, renal disease, hypertension | Influences choice of analgesic, disease‑modifying options and monitoring needs. |
Examination findings
| Finding | What you look for | Pathophysiologic explanation |
|---|---|---|
| Inspection | Joint swelling, bony enlargement, deformity, muscle wasting | Osteophytes and synovial effusion produce visible enlargement; disuse atrophy of surrounding muscles. |
| Palpation | Tenderness over joint line, crepitus, warmth, effusion | Cartilage breakdown releases inflammatory mediators → localized tenderness; osteophytes create palpable irregularities; effusion feels fluid‑filled. |
| Range of motion (ROM) | ↓ active & passive ROM, especially terminal flexion/extension; pain at extremes | Mechanical obstruction by osteophytes and capsular contracture limits motion; pain limits active use. |
| Gait assessment | Antalgic gait, reduced stride, “shuffling” (hip/knee) | Pain avoidance leads to altered biomechanics; joint instability may cause compensatory gait. |
| Special tests | <br>• Joint line tenderness (knee) – indicates cartilage loss <br>• McMurray / Apley – may be positive if meniscal involvement secondary to OA <br>• Valgus/varus stress – assess ligament laxity | Degenerated cartilage and osteophytes alter joint congruity, making menisci more vulnerable; chronic overload stretches ligaments. |
| Neurovascular | Intact sensation, pulses | Excludes compressive neuropathy or vascular compromise that can mimic or complicate OA. |
Differential diagnosis
| Condition | Points toward it | Distinguishing features |
|---|---|---|
| Primary osteoarthritis | Age >45, mechanical pain, minimal morning stiffness, radiographic osteophytes | Absence of systemic inflammation, normal inflammatory markers, characteristic joint‑space narrowing |
| Rheumatoid arthritis | Symmetrical polyarthritis, prolonged morning stiffness >1 h, rheumatoid nodules | Positive rheumatoid factor/anti‑CCP, erosive changes on X‑ray, systemic features |
| Septic arthritis | Acute severe pain, fever, rapid joint swelling, recent infection or trauma | Synovial fluid with high WBC, positive Gram stain/culture, urgent drainage required |
| Gout / pseudogout | Sudden mono‑articular attack, tophi (gout), calcium pyrophosphate crystals (pseudogout) | Joint aspiration shows monosodium urate or CPPD crystals, serum uric acid may be elevated |
| Post‑infectious (TB) arthritis | History of TB exposure, chronic mono‑arthritis, constitutional symptoms | Positive TB PCR/culture from synovial fluid, MRI shows erosive lesions, responds to anti‑TB therapy |
| HIV‑associated arthropathy | Young adult, HIV infection, polyarticular pain, may coexist with OA | Positive HIV test, may have opportunistic infections, CD4 count guides work‑up |
| Hemophilic arthropathy / sickle‑cell joint disease | Recurrent hemarthroses, chronic pain, history of bleeding disorder | Joint aspirate bloody, factor assays abnormal, sickle‑cell disease history |
| Osteonecrosis (AVN) | Hip/knee pain, limited ROM, risk factors (steroids, alcohol, SCD) | MRI shows sub‑chondral crescent sign, pain out of proportion to OA, no osteophytes early |
Investigations
| Test | What it answers | Interpretation |
|---|---|---|
| Plain radiograph (AP & lateral) | Joint space, osteophytes, sub‑chondral sclerosis, cysts | Joint‑space narrowing + osteophytes = OA; erosions suggest inflammatory arthritis |
| MRI (if indicated) | Early cartilage loss, bone marrow edema, occult fractures, AVN | Bone edema supports active disease; absence of erosions favors OA |
| Synovial fluid analysis | Infection, crystal arthropathy | WBC <5 000 µL and no crystals → OA; >50 000 µL or positive Gram stain → septic arthritis |
| ESR / CRP | Inflammatory activity | Normal/ mildly raised in OA; markedly elevated in inflammatory or infectious processes |
| Serum uric acid | Gout suspicion | Elevated levels support gout but not diagnostic alone |
| HIV test (if risk) | HIV‑related joint disease | Positive serology prompts tailored management |
| TB PCR / culture (if TB risk) | Tuberculous arthritis | Positive result confirms TB joint infection |
| Full blood count | Anemia, leukocytosis | Anemia/chronic disease may accompany inflammatory conditions; leukocytosis suggests infection |
| Metabolic panel (glucose, lipids) | Metabolic contributors to OA | Dysglycemia, dyslipidemia increase OA risk; guide lifestyle advice |
Diagnosis and severity
Diagnostic criteria (clinical + radiographic)
- Symptoms – Persistent joint pain ≥3 months, worsened by activity, improved by rest.
- Signs – Crepitus, limited ROM, bony enlargement, minimal morning stiffness (<30 min).
- Imaging – Radiograph showing at least one of: osteophytes, joint‑space narrowing, sub‑chondral sclerosis, cysts.
If all three domains are present, OA is diagnosed. Absence of significant inflammatory signs (e.g., high ESR/CRP, erosions) helps exclude other arthritides.
Severity grading (Kellgren‑Lawrence or similar)
| Grade | Radiographic features | Clinical correlation |
|---|---|---|
| 0 – No OA | Normal joint | Asymptomatic |
| I – Doubtful | Possible osteophyte | Mild intermittent pain |
| II – Mild | Definite osteophytes, possible joint‑space narrowing | Pain with activity, minimal functional limitation |
| III – Moderate | Multiple osteophytes, definite narrowing, sub‑chondral sclerosis | Pain at end‑range, early gait changes |
| IV – Severe | Large osteophytes, marked narrowing, bone deformity, sclerosis | Constant pain, marked disability, possible deformity |
Severity guides management intensity: mild disease often responds to lifestyle modification and simple analgesics; moderate to severe disease may require intra‑articular steroids, viscosupplementation, or referral for surgical evaluation (arthroplasty). Monitoring includes periodic pain scores, functional questionnaires, and repeat imaging if progression is suspected.
Management
| Phase | Goal | Key Interventions | Monitoring / Safety |
|---|---|---|---|
| Immediate stabilisation | Relieve acute pain, maintain function, prevent falls | • Simple analgesics (paracetamol) <br>• Topical NSAID or capsaicin for focal pain <br>• Short‑term oral NSAID if no contraindication (e.g., ulcer, CKD, uncontrolled hypertension) <br>• Rest of the affected joint, use of crutches or cane | • Pain score 0‑10 every 4‑6 h <br>• GI tolerance, renal function, blood pressure |
| Definitive treatment | Slow disease progression, improve joint mechanics, optimise quality of life | Non‑pharmacological <br>• Structured physiotherapy: quadriceps strengthening, range‑of‑motion exercises, low‑impact aerobic activity <br>• Weight reduction (target ≤ 5 % of body weight) <br>• Joint protection: assistive devices, orthoses, ergonomic modifications <br>Pharmacological <br>• Oral NSAID (if tolerated) <br>• Intra‑articular corticosteroid (single injection for flare) <br>• Intra‑articular hyaluronic acid (where available) <br>• Duloxetine (for chronic pain with central sensitisation) <br>Surgical <br>• Arthroscopy for mechanical symptoms (loose bodies) <br>• Unicompartmental or total knee/hip arthroplasty when severe pain limits daily activities despite optimal medical therapy | • Functional scores (WOMAC, KOOS) every 3 months <br>• Weight, BMI, blood pressure, renal & hepatic labs if NSAID used <br>• Joint range of motion and muscle strength at each physio visit |
| Contra‑indications / safety | Avoid harm from therapy | • NSAID: active peptic ulcer, severe heart failure, eGFR < 30 ml/min/1.73 m², uncontrolled hypertension <br>• Intra‑articular steroid: infection, coagulopathy, uncontrolled diabetes (monitor glucose) <br>• Duloxetine: uncontrolled narrow‑angle glaucoma, recent MAOI use, severe hepatic disease <br>• Surgery: severe cardiopulmonary comorbidity, active infection, poor bone quality without optimisation |
Complications and prognosis
- Joint deformity (varus/valgus, bony enlargements) → progressive loss of function.
- Secondary osteoarthritis in adjacent joints due to altered gait.
- Chronic pain syndromes (central sensitisation) → reduced mobility, depression, sleep disturbance.
- Medication‑related adverse effects (GI bleed, renal impairment, cardiovascular events).
- Surgical complications (infection, prosthesis loosening, thromboembolism).
Prognosis is variable: early lifestyle modification and optimal medical therapy can maintain independence for many years; advanced disease often leads to joint replacement, which restores function but carries its own long‑term risks.
High‑yield exam points
- Look‑alike conditions: rheumatoid arthritis (symmetrical, inflammatory signs, serology), septic arthritis (acute, fever, joint effusion), gout (podagra, urate crystals), avascular necrosis (pain out of proportion, MRI changes).
- Common wrong first step: jumping straight to joint replacement without trial of physiotherapy, weight loss, and analgesia.
- Bedside examiner questions:
- “What features on examination help you differentiate osteoarthritis from inflammatory arthritis?”
- “Why is a crepitus heard on movement important?”
- “Explain the rationale for prescribing a topical NSAID versus an oral NSAID in this patient.”
- “What lifestyle advice would you give a 58‑year‑old farmer with knee OA?”
Clinical case
Patient: 62‑year‑old male farmer, BMI 31 kg/m², presents with 18‑month history of progressive right knee pain. Pain worsens after a day’s work, improves with rest and occasional ibuprofen. He reports morning stiffness lasting < 15 min, occasional swelling, and difficulty climbing stairs. No fever, no rash, no recent trauma. Examination shows: bony enlargement of the joint line, crepitus on flexion, reduced terminal flexion, mild effusion, no warmth, and antalgic gait.
Questions
- What is the most appropriate next step in management?
Answer: Initiate a structured physiotherapy programme focusing on quadriceps strengthening and prescribe a weight‑loss plan; add paracetamol for baseline pain control.
- Which finding would make you reconsider the diagnosis of primary osteoarthritis?
Answer: Presence of prolonged morning stiffness (> 30 min) or symmetrical polyarthritis suggesting inflammatory rheumatism.
- If the patient’s pain remains uncontrolled after 3 months of conservative therapy, what is the next pharmacological option?
Answer: Offer a short course of intra‑articular corticosteroid injection, provided there is no active infection or uncontrolled diabetes.
Practice questions
Question 1
A 55‑year‑old woman with BMI 34 kg/m² presents with dull, worsening pain in the left hip for 9 months. Pain is worse after walking and improves with rest. Examination shows limited internal rotation, no warmth, and a palpable osteophyte. What is the most appropriate next step?
A. Start disease‑modifying antirheumatic drug
B. Order plain radiograph of the pelvis
C. Immediate total hip arthroplasty
D. Begin high‑dose oral NSAID
Answer: B. order plain radiograph of the pelvis
Explanation: Imaging confirms osteoarthritis and grades severity before deciding on further therapy.
Question 2
A 68‑year‑old man with known knee osteoarthritis presents with sudden severe knee pain, swelling, and fever of 38.5 °C. Joint aspiration yields purulent fluid with high neutrophils. Which management is indicated?
A. Increase oral NSAID dose
B. Intra‑articular hyaluronic acid injection
C. Immediate arthroscopic washout and IV antibiotics
D. Continue physiotherapy
Answer: C. immediate arthroscopic washout and IV antibiotics
Explanation: The presentation is classic for septic arthritis, a surgical emergency.
Question 3
Which of the following distinguishes osteoarthritis from rheumatoid arthritis on physical exam?
A. Symmetrical joint involvement
B. Presence of rheumatoid nodules
C. Crepitus on joint movement
D. Morning stiffness lasting > 1 hour
Answer: C. crepitus on joint movement
Explanation: Crepitus is typical of degenerative joint disease, whereas rheumatoid arthritis shows synovitis without crepitus.
Question 4
A patient with knee osteoarthritis is started on an oral NSAID but develops new onset hypertension. What is the safest next analgesic option?
A. Increase NSAID dose
B. Switch to topical NSAID
C. Add low‑dose aspirin
D. Begin opioid analgesic
Answer: B. switch to topical NSAID
Explanation: Topical NSAIDs provide local pain relief with minimal systemic cardiovascular effects.
Question 5
In a patient with moderate knee osteoarthritis, which non‑pharmacological intervention has the strongest evidence for reducing pain and improving function?
A. High‑impact aerobic exercise (running)
B. Quadriceps strengthening program
C. Use of a knee brace alone
D. Complete bed rest
Answer: B. quadriceps strengthening program
Explanation: Strengthening the surrounding musculature improves joint stability and reduces load, leading to symptom improvement.
Drafted with AI assistance from standard references and reviewed for structure. Check details against your lecture notes and the Kenya MoH guideline.