Fracture Flashcards
What comprises the organic (osteoid) part of bone?
- 90% type I collagen
- 10 % non collagenous proteins
- Osteocalcin (Ca binding protein)
- Osteopontin (glycoprotein)
- Proteoglycans
What comprises the inorganic part of bone?
- Hydroxyapatite (Ca(PO)OH)
- Carbonate, citrate, sodium, magnesium
What comprises the axial skeleton? What is the rest of the skeleton referred to as?
- Skull, ribcage, and vertebral column
- Appendicular skeleton
What are the two types of bone and different names for them?
- Cortical, dense, compact
- Trabecular, spongy cancellous
Gross structure of a long bone?
- The epiphysis is the rounded end of a long bone, covered in articular cartilage. Between the epiphysis and diaphysis (the long midsection of the long bone) lies the metaphysis, including the epiphyseal plate (growth plate - sometimes also called the physis).
- The metaphysis and diaphysis have porous bone
Structure of periosteum?
- Outer fibrous lining, anchored to bone by Sharpey fibres
- 2 layers:
Outer –> fibroblasts, type I collagen, nerves, BVs
Inner –> periosteal cells (osteoprogenitor and bone lining cells)
Structure of endosteum?
- Inner cellular lining of compact and spongy bone
- One layer –> endosteal cells (osteoprogenitor and bone lining cells)
What are osteoblast precursors?
- osteoprogenitor cells
- mesenchymal cells
What are osteoclast precursors?
- Myeloid/ hematopoietic progenitor cells (granulocyte/ monocyte progenitors)
Role of osteoblasts
- Lay down and mineralize matrix
- Secrete type I collagen, glycoproteins, proteoglycans, alkaline phosphatase (calcification)
- Bone surface lining cells in quiescent adult bone
Role/ location of osteoclasts
- Resorb bone tissue, release minerals and growth factors
- Occupy Howship’s lacuna
Role/ location of osteocytes
- Calcium regulation, maintain bone tissue, communication
- Live blasts that are embedded in the bone matrix in lacuna
- Have processes on canaliculi to communicate via gap junctions (transducing stress signals)
- If mechanical stress will secrete matrix, can also degrade it for calcium homeostasis
- Secrete sclerostin (inhibits bone formation)
How do osteoblast/clast progenitors develop and regulate each other>
- Osteoclast precursor expresses RANK and will become an inactive osteoclast if it binds RANK-L (from stromal cells or activated T cells)
- Osteoblasts release OPG which binds and inhibits RANK-L (inhibits osteoclast formation)
Describe intramembranous bone formation. Which bones develop this way?
- richly vascularized mesenchymal tissue (no cartilage model)
- flat bones of the skull/face/mandible/clavicle
Describe endochondral bone formation. Which bones develop this way?
- Cartilage model acts as a precursor for bone
- Mesenchymal cells differentiate into chondrocytes which make cartilage –> bony collar forms around cartilage –> hypertrophic chondrocytes secrete alkaline phosphatase –> chondrocytes die and matrix breaks down leading to the marrow cavity –> bvs grow through the thin bone collar –> osteoprogenitor cells contact bone spicules and become osteoblasts (PRIMARY OSSIFICATION CENTER - first site where bone forms in diaphysis) –> bvs grow through epiphyses (SECONDARY OSS CENTERS) –> epiphyseal cartilage forms between the epiphysis and diaphysis (GROWTH PLATE)
- Axial bones that bear weight
What happens when max bone growth is reached?
- Cartilage proliferation in the epiphyseal plate stops, deposition will occur until no more cartilage left –> epiphyseal closure
What are the different names for bone growth (length vs width)? How do they work?
Length –> Interstitial, endochondral ossification at epiphysis
Width –> Appositional, periosteal growth at diaphysis (blasts work outer and clasts work inner)
Differences between immature (woven) and mature (compact) bone?
Immature –> no organized lamellae, more cells per unit area, less mineralization
Mature –> each Osteon has a Haversian canal (BV and nerve supply), concentric lamellae, canaliculi, interstitial lamellae, Volkmann canals (horizontal)
Bone modelling vs remodelling
Modelling - how bone gets its shape, appositional and interstitial growth
Remodelling - adapting to function and injury (Haversian remodelling) i.e tissue renewal, changes in physical activity, fracture repair, malunion, surgical realignment
What is an osteon? How does it develop?
- rings of concentric lamellae with a Haversian canal (blasts and capillary) in the middle
- rings develop inwards during transformation from trabecular to compact bone
Difference of trabecular bone from cortical.
- Also lamellar but doesn’t contain osteons
- Trabeculae are surrounded by marrow
How does bone shape modelling occur?
- metaphysical inwaisting
- influenced by soft tissue (tendons/ joint capsule)
BMU
- Bone metabolizing unit
- contains blasts/ cytes/ clasts
- consists of osteons in cortical, trabeculae in cancellous
- Clasts cut a hole and blasts narrow it (Haversian remodelling)
Phases of Bone remodelling?
- Activation –> clast recruitment (3-7d)
- Resorption –> clast tunneling (2-4w)
- Reversal –> time between resorption and deposition
- Formation –> blasts lay down and mineralize (4-6m)
Wolff’s Law
- bone will adapt to the loads it is placed under (more loading = stronger bone)
What stimulates and inhibits remodelling?
(+) –> growth, thyroid and parathyroid hormones, vit D
(-) –> calcitonin, cortisone, calcium
Stages of Fracture Healing
- Inflammation –> hematoma, necrotic tissues resorbed (few weeks)
- granulation tissue forms, blasts proliferate, progenitor cells - Repair –> soft callus replaced by endochondral ossified hard callus (weeks to months)
- still too soft to weight bear, amount of callus is proportional to motion at the fracture - Remodelling –> bone reshapes (continues for years)
- woven bone replaced by cortical via Haversian remodelling
How does metaphysical (cancellous) bone heal?
Internal callus (similar mechanisms and stages as cortical bone)
Ways to fixate a femur fracture? What ages?
- 0-3m –> Pavlik Harness
- 3-36m –> Spica cast, traction
- 2-10y –> flexible nails
- 11-16y –> plates, trochanteric intramedullary nails (will still get callus) –> increases healing rate by causing inflammation, increases anatomy and function
- Mature –> adult IM nail
- Joints in general do not tolerate immobility
Primary Bone Healing
- rigidly fixed fractures, direct osteonal healing, some gap healing if under 1mm, 20% direct contact btwn fragment ends
How do you classify physeal fractures?
salter-harris classification (refer to images)
How long does a metaphysical fracture take to heal? When can you expect normal bone strength? What factors may lengthen or shorten this?
- 6-8 weeks, normal strength around 1 year
- double it if elderly/ cortical bone/ open fracture (lower union rates)/ smoker/ non-compliant
- halve it for children
Role of bone morphogenic proteins (BMP)
TGF-B
IGF-11
Platelet-derived GF
–> bone healing and formation
–> induces mesenchymal cells to make type II collagen
–> stimulates type I collagen, bone formation, cartilage matrix synthesis
–> attracts inflammatory cells to fracture
How do TH/PTH, cortisone, and GH affect bones?
TH/PTH –> increases callus, affects remodelling
Cortisone –> anti-inflammatory thus decreasing callus
GH –> increases callus volume
What are some causes of non-union?
instability, locking plates, decreased vascularization, infection, nicotine (vasoconstriction), NSAIDs, steroids
What can cause avascular necrosis of the femoral head?
- disruption of the medial branch of the circumflex ring
What are child abuse red flags?
- fracture in pre-ambulatory/ non-verbal child
- no hx of injury/ not plausible
- spiral fracture
- rib fracture, corner fractures
- multiple injuries with different stages of healing
- delay in care seeking
- TEN4FACESP (when bruising is suspicious) –> trunk, ears, neck, under 4 years, frenulum, angle of jaw, cheeks, eyelids, sclera, patterned
Important tests if child abuse suspected
- head CT/MRI
- check retina within 24 hours
- LFT/ amylase/lipase to assess for liver or pancreatic injury
What do you do if you suspect child abuse?
- legal duty to report (welfare worker/ MCFD)
- SCAN (suspected child abuse and neglect clinics) or CPSU (child protection service unit)
- DO NOT interview or probe the child, just report
What constitutes Physical/ Emotional/ Sexual abuse and neglect?
Physical –> child under 2 and over 12, unreasonable force, incapable of learning, bodily injury, head, degrading, use of an object
Emotional –> violence in a relationship, development of anxiety/depression/agression/withdrawal in a child
Sexual –> exposure to sexual material, exploitation involves manipulation in exchange for something
Neglect –> failure to provide basic needs (food, shelter, supervision, healthcare)
Risk factors for abuse?
- premature, disease, disabled, SUD, young or single parents, poverty, domestic violence, criminal behaviour
Different types of fractures?
Open (Compound) –> bone comes through the skin
Transverse –> horizontal line, all the way through
Oblique fractures –> what it sounds like, all the way through
Impacted (Comminuted) –> bone shatters into more than 2 pieces
Spiral –> bone breaks in a spiral fashion
Greenstick –> only one side, not all the way through
Most common cause of clavicle fracture? Where does it normally break?
- fall on shoulder, then direct trauma or FOOSH
What does a bony callus on x-ray indicate?
The fracture is at least 2 weeks old
What type of bone issue cannot be compensated for naturally?
- rotational malalignments
- angular deformities can be corrected to a certain degree
What are causes of pathological bone fracture?
- osteoporosis, hyperparathyroidism, Cushing’s, Paget’s, osteogenesis imperfecta, osteosarcoma, multiple myeloma, metastatic breast and prostate cancer
What are risk factors for osteoporosis?
- female, smoking, menopause, old age, caucasian, dementia, estrogen deficiency, genetics, decreased calcium and vitamin D, low weight, inadequate physical activity
Paget’s
- mechanism
- common in
- diagnosis
- 3 different types
- signs and symptoms
- treatment
- indications for treatment
- resorption and formation are decoupled, faster turnover
- clasts increase in number and size, overactive blasts
- increase in bone size but more brittle due to deformities
- increases with age, more common in white males
- diagnosed on x-ray (pelvis, femur, skull, tibia)
- Lytic (clasts)
- Mixed (blasts lay down disorganized bone)
- Sclerotic (no clast or blast activity)
- increased urinary excretion of hydroxyproline (increased breakdown) and increased serum alkaline phosphatase (rapid rebuilding)
- osteoarthritis, fracture, bone pain and deformity, spinal stenosis or CN palsy, malignancy: osteosarcoma (though rare)
- bisphosphonates (zoldronate) or calcitonin IV
- before ortho surgery, hypercalcemia/calciuria, pain, fractures, radiculopathy, serum alkaline phosphatase or hydroxyproline 2x above normal
Tests for Bone Pain?
What would increased Ca/PO4/ALP suggest?
- CBC, electrolytes, Ca, PO4, ALP, urine
- DRE (could be metastatic prostate cancer)
- would suggest active resorption of bone
Bone Metastases
Treatment?
- bone metastases are more common than primary neoplasms
- 75% are prostate (esp. lumbar vertebrae), breast, lung, kidney
- lytic lesions are the most common
- Tx –> systemic chemo, radiation, bisphosphonates, denosumab, surgery
Different bone lesion types?
Lytic –> tumor releases things that increase RANK-L and thus clasts
Sclerotic –> tumor releases things that increase blasts
Leg discrepancy treatments?
1-2cm –> usually well-tolerated
2-8cm –> epiphysiodesis of longer leg (ablation of physis)
8-10cm –> distraction osteogenesis (stretching bone)
