Bone Fracture and Joint Disease

Key questions

1. Q1Complete vs incomplete?

   Complete = the break goes all the way through the bone. Incomplete = only part of the way (e.g., greenstick in children).
2. Q2Simple (closed) vs compound (open)?

   Simple/closed = skin intact. Compound/open = bone breaks through the skin → high infection risk (mixed-organism osteomyelitis).
3. Q3Comminuted?

   The bone is splintered into multiple fragments.
4. Q4Displaced?

   The fractured ends are no longer aligned. Displaced and comminuted fractures are the ones most likely to heal with deformity.
5. Q5Pathologic fracture?

   A break through bone already weakened by disease — metastasis, tumor, osteoporosis, Paget, osteogenesis imperfecta — often with little trauma.
6. Q6Stress fracture?

   A fracture (often compression, e.g., in the spine, or in the metatarsals/tibia of runners) from repetitive loading rather than one big injury.
7. Q7What must be assessed first after any fracture?

   Vascular supply, neurologic function and soft tissue injury around the break.

Key questions

1. Q8What are the three phases of fracture repair?

   Inflammatory (hematoma), reparative (soft callus → bony callus of woven bone) and remodeling (woven → lamellar bone shaped by weight-bearing).
2. Q9What happens in days 0–1?

   A hematoma forms: fibrin mesh, platelets and inflammatory cells seal the gap; platelets and inflammatory cells release cytokines and growth factors — PDGF, TGF-β and FGF in the inflammatory phase.
3. Q10What happens in weeks 0–3?

   BMPs and VEGF drive the reparative phase: growth factors activate progenitor cells → granulation tissue and a soft (procallus) of fibrocartilage and hyaline cartilage (~week 1–2); osteoblasts then lay woven bone and endochondral ossification converts cartilage → bony callus (~2–3 weeks).
4. Q11What happens after ~3 weeks?

   Weight-bearing drives osteoclasts and osteoblasts to remodel woven bone into lamellar bone over weeks to months; the excess callus is trimmed.
5. Q12What is needed for normal healing?

   Adequate vascular supply and immobilization, plus activation of progenitor cells by cytokines.
6. Q13What causes delayed healing or nonunion?

   Poor immobilization (motion → nonunion/pseudarthrosis), displacement or comminution (deformity), infection, diabetes, immunosuppression, poor blood supply, malnutrition.
7. Q14What is osteonecrosis (bone infarction)?

   Death of bone and marrow from vascular insufficiency; histology shows empty lacunae (dead osteocytes) and necrotic marrow. Covered in detail under LO 4.

Key questions

1. Q15What is osteomyelitis?

   Inflammation — almost always infection — of bone and marrow. Pyogenic (bacterial; acute or chronic) or tuberculous.
2. Q16How do bacteria reach bone?

   Hematogenous spread (most common in children), direct extension from a nearby focus (e.g., diabetic foot ulcer, skin infection), or direct inoculation (open fracture, surgery, puncture).
3. Q17What is the usual organism?

   Staphylococcus aureus in 80–90% of culture-positive cases. Mixed infections are common after open fractures.
4. Q18Where in the bone does it start?

   It depends on the blood supply, which changes with age: in children the metaphysis (slow, looping capillaries) is classic; in neonates infection can cross into the epiphysis and joint; in adults, epiphyses/subchondral bone and the vertebrae. Usually a single long bone.
5. Q19What does acute osteomyelitis look like?

   Neutrophils in marrow with necrotic bone; pus lifts the periosteum and spreads through Haversian canals. Clinically systemic illness, fever and localized pain (subtle in neonates). Diagnose with blood and bone cultures.
6. Q20What are sequestrum and involucrum?

   Sequestrum = dead, necrotic bone cut off from its blood supply. Involucrum = the shell of reactive new bone laid down around it. A draining sinus through the skin is common.
7. Q21What is a Brodie abscess?

   A walled-off chronic abscess (often metaphyseal) from incompletely resolved acute infection: central lucency with a dense sclerotic rim on X-ray.
8. Q22Why does osteomyelitis become chronic, and what can follow?

   5–25% of acute cases persist — due to delayed diagnosis, short antibiotic courses, extensive necrosis, weak host defenses or inadequate debridement. Complications: pathologic fracture, secondary amyloidosis, endocarditis/sepsis, and squamous cell carcinoma in a draining sinus tract.
9. Q23What is tuberculous osteomyelitis?

   Hematogenous spread from a visceral (usually lung) focus; destructive and treatment-resistant; caseating granulomas. Nearly half involve the spine (Pott disease): vertebrae and discs destroyed → compression fractures, gibbus deformity, neurologic deficits, psoas abscess.

Key questions

1. Q24How is bone supplied?

   Nutrient arteries enter the diaphysis to supply the marrow and inner cortex; metaphyseal and epiphyseal vessels supply the ends; periosteal vessels supply the outer cortex. Subchondral bone of convex joint surfaces (femoral head) has an end-arterial, easily interrupted supply.
2. Q25What is osteonecrosis (avascular necrosis)?

   Ischemic death of bone and marrow. Medullary infarcts involve cancellous bone and marrow; subchondral infarcts are wedge-shaped and lie under articular cartilage.
3. Q26Where does it happen most?

   The femoral head (classic). Also humeral head, femoral condyles, scaphoid, talus.
4. Q27What causes it?

   Glucocorticoids (a very common cause), alcohol, trauma/fracture (femoral neck), sickle cell disease and other hemoglobinopathies (sludging), radiation, hypercoagulable states, caisson disease (barotrauma), pregnancy, infection, Gaucher disease, chronic pancreatitis, connective tissue disorders (e.g., lupus — often via steroids), tumors, epiphyseal disorders, idiopathic (Legg-Calvé-Perthes in children).
5. Q28Why is the overlying cartilage preserved?

   Articular cartilage is fed by diffusion from synovial fluid, not by the bone's blood supply — so it survives while the bone underneath dies and collapses.
6. Q29What does it look like?

   Gross: pale, yellow, wedge-shaped subchondral area; the cartilage separates from dead bone as trabeculae collapse (crescent sign). Histology: empty lacunae (dead osteocytes) and necrotic marrow; creeping substitution at the edges.
7. Q30What are the consequences?

   May be asymptomatic, or cause pain with movement and later at rest; collapse of the joint surface → secondary osteoarthritis; often ends in joint replacement.

Key questions

1. Q31What is osteoarthritis?

   The most common joint disease: progressive erosion of articular cartilage with disordered repair — mainly degenerative ("wear and tear") with minimal, secondary inflammation. Primary (aging) or secondary (prior injury, deformity, osteonecrosis, obesity, diabetes, hemochromatosis).
2. Q32What are the phases of OA?

   Chondrocyte injury (biochemical/genetic factors) → early OA: chondrocytes proliferate and release mediators; MMPs degrade type II collagen and proteoglycans faster than repair → fibrillation (cracks) → late OA: chondrocyte loss, cartilage destruction, subchondral bone changes.
3. Q33What are the pathologic findings in OA?

   Fibrillation and cracking of cartilage, full-thickness loss with eburnation (polished exposed bone), subchondral sclerosis, subchondral cysts (synovial fluid forced into bone through damaged cartilage), osteophytes at the margins, and joint mice (loose bodies of cartilage and bone in the joint space).
4. Q34How does OA present?

   Older, obese or previously injured patient; weight-bearing joints (knees, hips), lumbar/cervical spine, DIP and PIP joints and the thumb base; pain worse with use and better with rest; brief morning stiffness (<30 min); crepitus. Heberden (DIP) and Bouchard (PIP) nodes. No systemic features, no serum antibodies. Ultimately a surgical disease.
5. Q35What is rheumatoid arthritis?

   A chronic systemic autoimmune disease: symmetric inflammatory polyarthritis — small joints first (MCP, PIP, wrists) but also elbows, shoulders, knees and ankles — women > men, with extra-articular disease (lung, heart, vessels, eyes, nodules).
6. Q36What drives RA?

   Genetics (HLA-DR4) + environment (smoking) → citrullination of self proteins → CD4 T cells and autoantibodies (ACPA/anti-CCP in up to 70%; RF — IgM or IgA against the Fc of IgG — in ~80%). TNF is a key mediator; inflammation → synovial hyperplasia → pannus that erodes cartilage and bone (osteoclast activation).
7. Q37What does RA synovium look like?

   Synovial hyperplasia with villi, dense lymphocytes and plasma cells (deep, often follicles), neutrophils superficially and in fluid, angiogenesis, fibrin deposition (rice bodies = organized fibrin in the joint), osteoclastic erosion, and pannus.
8. Q38What is a rheumatoid nodule?

   A subcutaneous soft-tissue nodule at pressure points (elbow, forearm, lumbosacral): central fibrinoid necrosis surrounded by palisading macrophages, then lymphocytes and plasma cells.
9. Q39How does RA present and progress?

   Slow onset of malaise and symmetric joint pain with warm, swollen joints and morning stiffness >1 hour that improves with activity. Late: ulnar deviation of fingers, radial deviation of the wrist, swan-neck and boutonnière deformities, joint effusions. X-ray: periarticular osteopenia and marginal erosions.
10. Q40What is juvenile idiopathic arthritis?

    Onset before 16; more large-joint involvement and systemic disease than adult RA; often RF-negative; complications include pericarditis, myocarditis, glomerular disease, pulmonary fibrosis (and uveitis).
11. Q41What tips the balance toward cartilage loss in early OA?

    Inflammatory mediators switch on MMPs (break down collagen and proteoglycans) and BMPs (make chondrocytes proliferate); breakdown outpaces repair, so the cartilage slowly erodes.

Key questions

1. Q42What is gout?

   Hyperuricemia → monosodium urate crystals precipitate in and around joints → recurrent attacks of acute arthritis, tophi and urate kidney disease. Hyperuricemia is necessary but not sufficient.
2. Q43Why do people become hyperuricemic?

   Uric acid is the end product of purine breakdown. Most cases are primary/idiopathic underexcretion (men > women); others overproduce (enzyme defects such as HGPRT deficiency, high cell turnover — tumor lysis, myeloproliferative disease) or underexcrete (renal disease, thiazide and loop diuretics, low-dose aspirin, alcohol). Risk factors: male sex, age, genetics, obesity, alcohol, some medications.
3. Q44How does a gout attack happen?

   Urate crystals precipitate (cooler, peripheral joints) → two arms: macrophages phagocytose crystals (NLRP3 inflammasome → IL-1 and other mediators) and complement activation recruits neutrophils, which also phagocytose crystals. Neutrophils lyse and release LTB4, prostaglandins and free radicals → more neutrophils (positive feedback) → joint injury.
4. Q45What are the four stages?

   Asymptomatic hyperuricemia → acute gouty arthritis → intercritical gout (symptom-free intervals) → chronic tophaceous gout.
5. Q46How does acute gout present?

   Sudden, excruciating, red, hot, swollen joint — classically the 1st MTP (podagra) — often at night after alcohol, a large meal or a diuretic.
6. Q47What does gout show under the microscope?

   Joint fluid: needle-shaped, negatively birefringent urate crystals (yellow when parallel to the compensator) inside neutrophils. Tophus: aggregates of pale crystals (dissolved out in formalin) surrounded by granulomatous inflammation — macrophages and foreign-body giant cells.
7. Q48What is pseudogout?

   Calcium pyrophosphate dihydrate (CPPD) crystal deposition disease — crystal-induced arthritis of older adults; pathogenesis unclear, perhaps triggered by cartilage degradation. Mono- or oligoarticular: knees (most), wrists, elbows, shoulders. May cause chondrocalcinosis (joint calcification) and significant joint damage.
8. Q49What does pseudogout show?

   Basophilic (purple) crystal deposits in articular cartilage; aspirate shows rhomboid (various shapes and sizes), weakly positively birefringent crystals (blue when parallel).