"Systemic skeletal disorder characterised by low bone mass, micro-architectural deterioration of bone tissue, leading to bone fragility and consequent increase in fracture risk." ^[1]

Why this matters from first principles: Bone is not static. It constantly remodels – osteoclasts resorb old bone, osteoblasts lay down new bone. When resorption exceeds formation (↑ osteoclast activity or ↓ osteoblast activity), net bone mass falls. The trabeculae thin and disconnect, cortices thin, and the bone loses its structural scaffold, making it fracture with forces that would never break healthy bone.

Most common metabolic bone disease. 1 in 3 postmenopausal women, 1 in 5 men ≥50 years will sustain an osteoporotic fracture in their lifetime. 1 osteoporotic fracture occurs every 3 seconds worldwide. ^[2]

• Hip and vertebral fractures are the hallmark complications ^[2].
• > 50% of hip fracture survivors cannot return to their premorbid state; 10% need extra help in daily care ^[1].
• 1-year mortality after hip fracture in the elderly is approximately 20–30% (mostly from medical complications: PE, pneumonia, MI).

Age-stratified 12-month mortality after hip fracture (local data shown on slides) ^[1]:

Death rates within a year after a hip fracture are up to 4.5 times higher than death rates among same-age women who have not broken a hip (LeBlanc et al., Arch Intern Med 2011) ^[1].

• T-score: number of standard deviations below the peak bone mass of a 30-year-old of same sex and ethnicity. Used in postmenopausal women and men ≥50.
• Z-score: compared to age-matched controls. Used in premenopausal women and men < 50. If Z ≤ −2.0 → suspect secondary cause ^[3].
• FRAX score: 10-year probability of major osteoporotic fracture (MOF) or hip fracture. Useful for treatment decisions in osteopenia ^[3].

Osteoporosis diagnosis is shown on the lecture slide with the DEXA thresholds ^[1].

The lecture categorises risk factors into two groups ^[1]:

A. Increased risk of FALLS:

B. Loss of bone strength:

Secondary causes worth screening for: Cushing's/exogenous steroids, hyperthyroidism, hyperparathyroidism, hypogonadism, myeloma, CKD (renal osteodystrophy), IBD, RA, drugs (PPI, cyclosporine) ^[3][4].

82-year-old woman, walks with stick, IHD on aspirin, slip and fall on level ground, left hip pain, unable to walk. ^[1]

Physical exam findings:

• Left hip painful to any movement
• Lower limb shortened
• Externally rotated ^[1]

Why shortened and externally rotated? The hip flexors (iliopsoas) and external rotators pull the distal fragment upward and outward once the femoral neck fractures. The leg cannot resist gravity and muscle pull, so it shortens and rotates externally. This is the classic posture of a displaced neck of femur fracture.

Shenton's line is an imaginary curved line drawn along the inferior border of the superior pubic ramus and the medial border of the femoral neck. If this line is disrupted (broken), a femoral neck fracture is present ^[1].

This is a simple, high-yield radiological sign on AP pelvis X-ray.

The proximal femur is divided into distinct fracture zones ^[1]:

• Intracapsular – femoral neck (within the hip joint capsule)
• Extracapsular – subdivided into:
  • Trochanteric: basal, pertrochanteric, intertrochanteric (transtrochanteric)
  • Subtrochanteric: defined as the region within 5 cm below the lesser trochanter ^[1]

This classification determines blood-supply risk and implant choice.

The blood supply to the femoral head is retrograde – retinacular arteries from the medial and lateral circumflex femoral arteries run along the neck beneath the capsule to reach the head. The ligamentum teres artery is NOT effective in adults. The epiphyseal blood supply is dominant. ^[1]

Key vascular anatomy (from slide diagrams) ^[1]:

• The medial femoral circumflex artery (branch of profunda femoris) is the dominant supply; it forms an extracapsular arterial ring around the base of the femoral neck.
• From this ring, ascending cervical (retinacular) arteries travel within the retinacula of Weitbrecht along the femoral neck to form a subsynovial intracapsular arterial ring near the femoral head.
• The lateral femoral circumflex artery contributes ascending, transverse, and descending branches.
• The foveolar artery (from the obturator artery via the ligamentum teres) supplies only a small area around the fovea and is insufficient in adults.

Why this is critical: An intracapsular fracture can tear these retinacular vessels. Because the blood supply runs retrogradely (from distal to proximal along the neck), any displacement of an intracapsular fracture risks devascularising the femoral head → avascular necrosis (AVN). This is the entire rationale for the surgical decision tree.

Intracapsular fracture – worry of AVN, non-union. Extracapsular fracture – worry of fixation stability and mechanical alignment. ^[1]

Garden classification is the standard classification for femoral neck fractures ^[1]:

Simplified for clinical practice: Garden I & II = undisplaced; Garden III & IV = displaced ^[1].

AVN risk ^[1]:

• Minimally displaced fracture → < 10% AVN risk
• Displaced fracture → ~50% AVN risk

Trabecular pattern: compressive (medial calcar) and tensile (lateral) trabeculae are shown on the slide. The alignment of these trabeculae on X-ray helps determine the Garden grade ^[1].

Considerations: AGE, Displacement, Save the femoral head in young age / undisplaced ^[1].

Other factors ^[1]:

• Time of presentation → AVN risk increases after 6 hours
• Patient's general health
• Risk factors for internal fixation failure: osteoporosis, too comminuted, sepsis

Factors with increased risk for fixation failure: Old age, Osteoporosis, Vertical fracture pattern, Delayed presentation ^[1]

Garden I (valgus impacted fracture) → internal fixation to prevent displacement ^[1]

What the Garden films show: valgus-impacted neck (Garden I) with subtle trabecular angulation vs frankly displaced Garden IV head–neck discontinuity — undisplaced → screws; displaced elderly → arthroplasty. ^[1]

41/F, Garden IV fracture → Reduction and Internal Fixation (not hemiarthroplasty) because she is young ^[1]. At 6 months: union achieved, no collapse/shortening, returned to recreational walking status.

Total Tip Apex Index = 12 mm (measured on immediate post-op X-ray) ^[1]. The tip-apex distance (TAD) measures how close the screw tip sits to the apex of the femoral head on AP + lateral views combined. A TAD < 25 mm is the target to minimise risk of screw cut-out.

Hemiarthroplasty types ^[1]:

• Cemented vs uncemented: Cemented prostheses (e.g. Thompson) provide immediate stability and allow immediate weight-bearing; uncemented (Austin Moore) rely on bone in-growth.
• Mono-bloc vs Modular: Modular allows intra-operative adjustment of head size.

Post-operative precautions (to prevent dislocation) ^[5]:

• Do not squat or cross legs
• Do not flex hip > 90°
• Use abduction pillow
• Use high-low chair

85-year-old woman, fall on level ground, right hip pain → X-ray shows extracapsular fracture ^[1].

Aim: Return to pre-injury status ^[1]

Restoration of neck-shaft angle. Avoid varus alignment of proximal fragment. Stabilize fracture to facilitate early mobilization. ^[1]

Why avoid varus? The normal neck-shaft angle is ~130°. If the proximal fragment tilts into varus (angle decreases), the abductor mechanism moment arm shortens → Trendelenburg gait and increased stress on the implant → fixation failure.

Two types of pertrochanteric fractures ^[1]:

Recognize the unstable patterns and choose an intramedullary device to reduce risk of fixation failure ^[1]

DHS length: 2 holes as good as 4 holes (Bolhofner JOT 1999, McLoughin JOT 2000) ^[1]

Why does the DHS allow "sliding"? The lag screw passes through a barrel on the side plate. As the fracture settles (bone resorbs at the fracture site), the screw slides within the barrel, allowing controlled impaction. This converts shear forces to compressive forces at the fracture site → promotes healing. However, in unstable patterns, excessive sliding leads to varus collapse.

Why is intramedullary fixation biomechanically stronger? The nail sits inside the medullary canal, closer to the mechanical axis. The bending moment (distance from load to implant) is much smaller than with an extramedullary plate, so less stress on the implant.

The lecture shows the AO classification ^[1] – used to categorise fracture complexity and guide implant choice. The key clinical takeaway is the stable vs unstable distinction described above.

AO stability spectrum ^[1]: The AO 31-A classification subdivides trochanteric fractures into a 3 × 3 grid (A1.1–A3.3). A curved dividing line separates stable from unstable patterns:

As comminution and fracture complexity increase (A1 → A3, .1 → .3), the pattern shifts from stable to unstable, guiding the switch from DHS to cephalomedullary nail ^[1].

A: Extra-articular (within width of joint) – Colles or Smith fracture ^[1] B: Partial articular – Barton fracture ^[1] C: Complete articular ^[1]

Problems with acute displacement of distal radius fractures ^[1]:

• Pain
• Unstable fracture
• Nerve impingement (median nerve)
• Loss of reduction
• Skin and tendon impingement

Changes in wrist mechanics may lead to arthrosis, especially with intra-articular steps ^[1]. Even small articular incongruities (step-offs) at the radiocarpal joint accelerate cartilage degeneration.

"Reduction if necessary, Stabilization if necessary, Rehabilitation ALWAYS" ^[1]

Steps for closed management:

1. Hematoma block – inject local anaesthetic into the fracture haematoma ^[1]
2. Closed reduction – longitudinal traction → disimpact fragment ^[1]
3. Casting – 3-point fixation ^[1]

BEWARE: Bad cast (too tight or too loose) → loss of reduction ^[1]

Evaluate patient's functional demand, do a neurological exam (median nerve), fluoroscopy, CT assessment ^[1]

Most do NOT need an operation: non-displaced fractures, well reduced stable fractures, very low demand patients, geriatric ^[1]

Absolute indications for surgery: ^[1]

• High-grade open fracture
• Acute (progressing) median nerve palsy
• Associated carpal dislocation

Operative treatment: Open Reduction Internal Fixation (ORIF) with locking plate – used for displaced intra-articular fractures ^[1].

F70, fall injury and back pain ^[1] – typical presentation of an osteoporotic vertebral compression fracture.

Clinical features:

• Acute mechanical back pain after minimal trauma (or spontaneous)
• Height loss, progressive kyphosis ("dowager's hump")
• Pain worse with sitting/standing, better lying down
• Tenderness on percussion over affected spinous process

Radiological signs ^[1]:

• Intravertebral vacuum cleft – a horizontal radiolucent line within the collapsed vertebral body (seen on lateral X-ray), indicating osteonecrosis/non-union of the vertebral body.

What the vertebral XR panel shows: thoracolumbar wedge compression on lateral film, sometimes with a blue-arrowed intravertebral vacuum cleft — fragility collapse, not always “just a sprain.” ^[1]

• Kyphotic angle (θ) – measured between lines drawn along the superior and inferior endplates of the fractured vertebra on lateral X-ray or sagittal CT. Progressive kyphosis (e.g. > 40°) may warrant intervention.
• Anterior wedging of the vertebral body is the hallmark deformity on lateral imaging.

Principle: Reduction if necessary, Stabilization if necessary, Rehabilitation ALWAYS ^[1]

From GC 031 ^[2]:

• Conservative: Symptoms usually improve in 6-8 weeks. Analgesia, bracing, physiotherapy.
• Vertebral body augmentation: Kyphoplasty / Vertebroplasty – inject cement into collapsed vertebral body.
• Open surgical intervention – indications ^[2]:
  • Significant neurological deficits
  • Progressive and severe kyphotic deformity
  • Intractable pain

Reduced bone turnover → microfractures accumulation → stress fracture → eventual displacement with minimal trauma ^[1]

Bisphosphonates inhibit osteoclasts so effectively that bone remodelling virtually stops. While this prevents bone resorption, it also prevents the normal repair of micro-damage. Over years, these micro-cracks accumulate → eventually a stress fracture develops → completes with trivial force.

Cellular mechanism of bisphosphonate action (slide diagram) ^[1]:

1. Panel A – Untreated postmenopausal bone: Osteoclasts actively resorb bone → resorption > formation → high bone turnover, net bone loss.
2. Panel B – Early bisphosphonate therapy: Bisphosphonate molecules bind to bone mineral at sites of active resorption and accumulate in bone. Resorption still exceeds formation; turnover remains high initially.
3. Panel C – After ~6 months of therapy: Osteoclasts undergo early apoptosis → fewer osteoclasts → resorption ≈ formation → low steady-state bone turnover similar to premenopausal rates. However, this suppressed turnover also reduces the capacity to repair micro-damage, which over years leads to atypical fracture risk.

• Prodromal bilateral thigh pain (the lecture case: F72 with bilateral pain for 5 months before fracture) ^[1]
• Mechanical pain with walking
• Pain on percussion, rotation, and axial loading of the thigh ^[1]
• History of bisphosphonate use > 3 years ^[1]

"Beak" sign on X-ray and "dreaded black line" ^[1]

The beak sign is a cortical thickening ("bumpy") on the lateral cortex of the femoral shaft with a small transverse lucent line – the stress fracture. The dreaded black line is a wider transverse radiolucent line indicating incomplete fracture propagation.

• Both-sided open reduction if bilateral involvement ^[1]
• Stop bisphosphonate, consider switching to teriparatide (anabolic agent) to promote bone formation and healing.

Benefit of bisphosphonates still outweighs risks ^[1] – atypical fractures are rare compared to the huge number of fragility fractures prevented.

Fractures prevented vs bisphosphonate-associated AFFs per 100,000 women (slide data) ^[1]:

The benefit-to-risk ratio narrows with prolonged use (especially > 5 years in Asian women), supporting the practice of bisphosphonate drug holidays after 3–5 years in lower-risk patients ^[1].

Non-pharmacological: ^[1]

• Exercise (weight-bearing)
• Sunlight (endogenous vitamin D synthesis)
• Nutritional (Vitamin D + Calcium) – Ca 1200 mg/day, Vit D 800-1000 IU/day
• Risk factor modification (smoking cessation, alcohol reduction)

Pharmacological: ^[1]

• Glucocorticoid-induced osteoporosis → treat with alendronate (bisphosphonate) ^[8]
• Iatrogenic steroid (e.g. repeated knee injections for OA) → most likely cause of osteoporosis in a middle-aged man ^[9]
• Teriparatide side effect = dizziness (not atypical fracture, not GI reflux, not hypocalcaemia) ^[10]
• Long-term PPI → bone fractures (proven association) ^[11]
• Post-hip fracture DVT → classic SAQ scenario (see 2024 SAQ Q8) ^[12]