Bone and Joint — FRCS Quiz

18 slides

▸ Slide 14 · Bone and jointBone and Joint · 2 questions expand

Question list

Q1-Q22 questions — tap to reveal all answerslist

What is the theme of this section?
List the bone and joint topics covered in this section.

Answers · Q & A

Q1.What is the theme of this section?

Bone and joint
Title of this section divider slide

Q2.List the bone and joint topics covered in this section.

Not covered in the speaker notes
Topics are covered individually on later slides

▸ Slide 15 · Tell me about boneBone and Joint · 11 questions expand

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Q1-Q1111 questions — tap to reveal all answerslist

What is bone?
What are the functions of bone?
What types of bone are seen macroscopically and where are they found?
What are the microscopic components of bone?
What are the organic and inorganic components of bone ECM?
What mnemonic summarises the lamellar vs woven bone differences?
Differentiate lamellar and woven bone.
Differentiate cortical and cancellous bone.
Describe the structure of the Haversian system.
What is the role of Volkman canals?
What is Wolff's law?

Answers · Q & A

Q1.What is bone?

A solid organ
A specialised connective tissue with several main functions

Q2.What are the functions of bone?

Haematopoiesis
Calcium reservoir
Skeletal framework for locomotion

Q3.What types of bone are seen macroscopically and where are they found?

Lamellar bone (mature) is divided into cortical and cancellous bone
Woven bone (primitive, immature) is found in fracture callus and distraction histiogenesis

Q4.What are the microscopic components of bone?

Comprises cells (10%) and ECM (90%)
Cells: osteoblasts, osteoclasts, osteocytes, bone lining cells, osteoprogenitor cells

Q5.What are the organic and inorganic components of bone ECM?

Organic 40%: type 1 collagen, proteoglycans, matrix proteins (osteocalcin, osteonectin, osteopontin), growth factors and cytokines
Inorganic 60%: HA (hydroxyapatite)

Q6.What mnemonic summarises the lamellar vs woven bone differences?

DLC OBT – Daniel's little cafe offers best tea
Description, Location, Composition, Organisation, Biomechanics, Turnover

Q7.Differentiate lamellar and woven bone.

Lamellar: mature, less cellular, ordered stress-oriented collagen, anisotropic, more stiff/less ductile, low turnover
Lamellar is formed by enchondral or intramembranous ossification
Woven: primitive/immature, more cellular, dense collagen fibres, no lamellae, isotropic, less stiff/more ductile, high turnover

Q8.Differentiate cortical and cancellous bone.

Cortical (compact): diaphysis, osteon/Haversian system along the longitudinal axis, low porosity, higher Young's modulus, low turnover
Cancellous (spongy): metaphysis, 3D lattice of trabeculae, porosity 50-90%, lower Young's modulus, compressive forces, high turnover

Q9.Describe the structure of the Haversian system.

Central neurovascular channel enclosed within concentric lamellae
Each osteon has 5-7 concentric rings; collagen arranged in a herringbone pattern
Separated by a cement line where canniculi and collagen do not cross, an area of relative weakness and fracture propagation
Interstitial lamellae lie between osteons

Q10.What is the role of Volkman canals?

Run perpendicular to the long bone axis
A low pressure system
Make blood flow in the long bone centrifugal (in to out)

Q11.What is Wolff's law?

Bone models and remodels in response to the mechanical stresses it experiences
resulting in a minimal weight structure that is adapted to its applied stresses

▸ Slide 16 · Haematopietic monocyte/ granulocyte cell lineageBone and Joint · 7 questions expand

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Q1-Q77 questions — tap to reveal all answerslist

From which lineage do osteoclasts arise?
What are osteoclasts and how are they activated?
Which enzymes do osteoclasts use to hydrolyse organic matrix?
List the steps of osteoclast bone resorption.
What activates osteoclasts? (PR6)
What inhibits osteoclasts? (CEO)10
Name other multinucleated giant cells.

Answers · Q & A

Q1.From which lineage do osteoclasts arise?

The haematopoietic monocyte/granulocyte cell lineage

Q2.What are osteoclasts and how are they activated?

Multinucleated giant cells responsible for bone resorption
RANKL from osteoblasts binds immature osteoclasts, stimulating differentiation into active mature osteoclasts

Q3.Which enzymes do osteoclasts use to hydrolyse organic matrix?

TRAP (tartrate-resistant isoenzymes of acid phosphatase)
Cysteine proteinases e.g. cathepsins
These are acidic proteolytic lysosomal enzymes

Q4.List the steps of osteoclast bone resorption.

Migrate and attach to bone
Polarisation: orientate the ruffled border to bone
HA dissolution and matrix degradation
Degraded bone resorbed to lacunae
Apoptosis

Q5.What activates osteoclasts? (PR6)

Continuous PTH acting on the osteoblast increases RANKL expression
RANKL (NfkappaB activator ligand) from the osteoblast
IL-6

Q6.What inhibits osteoclasts? (CEO)10

Calcitonin
IL-10
Osteoprotegerin
Estrogen (decreases RANKL)

Q7.Name other multinucleated giant cells.

Normal: osteoclast, megakaryocyte
Inflammation: macrophages, Kupffer cells, Langerhans cells
Neoplasm: Hodgkin, epithelial tumour

▸ Slide 17 · OsteoblastBone and Joint · 9 questions expand

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Q1-Q99 questions — tap to reveal all answerslist

From which cells are osteoblasts derived?
What are the characteristics of osteoblasts?
What are the functions of osteoblasts?
What controls osteoblast differentiation?
What activates osteoblasts? (PED)
What inhibits osteoblasts? (PPS)
What are the osteotropic factors? (PPD11)
Which embryogenesis proteins also regulate osteoblast differentiation?
What is the role of Wnt/beta-catenin signalling in bone?

Answers · Q & A

Q1.From which cells are osteoblasts derived?

Osteoprogenitor cells, a mesenchymal stem cell line
BMP stimulates mesenchymal cells to become osteoprogenitor cells

Q2.What are the characteristics of osteoblasts?

Abundant organelles for synthesis: Golgi apparatus, ER, mitochondria
Increased ALP activity and expression

Q3.What are the functions of osteoblasts?

Bone forming: lay down osteoid (type 1 collagen + GAGs + osteocalcin, osteonectin) and are responsible for its mineralisation
Activate osteoclasts via the RANKL system

Q4.What controls osteoblast differentiation?

Runx2/CBFA1 is the key molecular switch in commitment of osteoprogenitors to the osteoblast lineage, with cofactor Osterix
Osterix plays the important role later, in preosteoblast differentiation into mature osteoblasts

Q5.What activates osteoblasts? (PED)

Pulsatile PTH
Estrogen (inhibits adenyl cyclase, decreasing RANKL synthesis)
1,25 vitamin D (increases osteoblast matrix production and RANKL)

Q6.What inhibits osteoblasts? (PPS)

Glucocorticoid
PTH (continuous)
PGE2 (activates adenyl cyclase)

Q7.What are the osteotropic factors? (PPD11)

Vit D, PGE2, IL 11, PTH
They induce osteoclast formation by upregulating RANKL

Q8.Which embryogenesis proteins also regulate osteoblast differentiation?

HOXA10, DLX and WNT
Typical of embryogenesis but also function in the adult skeleton to support osteoblast differentiation

Q9.What is the role of Wnt/beta-catenin signalling in bone?

Wnt binds frizzled receptors with LRP5/6 co-receptors, stabilising beta-catenin and activating gene transcription
Favours osteoblastic differentiation, osteoblast maturation and survival
Inhibits osteoclast generation by increasing osteoprotegerin (OPG)
Sclerostin (SOST gene, inhibited by RUNX2) antagonises LRP5/6

▸ Slide 18 · Osteoprogenitor cellBone and Joint · 2 questions expand

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Q1-Q22 questions — tap to reveal all answerslist

What can osteoprogenitor cells mature into?
Which theory describes this differentiation?

Answers · Q & A

Q1.What can osteoprogenitor cells mature into?

Osteoblast, chondroblast or fibroblast
Depending on strain and oxygen tension

Q2.Which theory describes this differentiation?

Perren's strain theory
Maturation depends on strain and oxygen tension

▸ Slide 19 · OsteocyteBone and Joint · 4 questions expand

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Q1-Q44 questions — tap to reveal all answerslist

What is an osteocyte?
What are the functions of osteocytes?
What are the characteristics of osteocytes?
What are bone lining cells?

Answers · Q & A

Q1.What is an osteocyte?

Described as an osteoblast trapped in osteoid
Makes up 90% of cells in the mature skeleton

Q2.What are the functions of osteocytes?

Regulate bone response to hormonal and mechanical stimuli
Regulate calcium and phosphorus concentration in bone
Stimulated by calcitonin, inhibited by PTH

Q3.What are the characteristics of osteocytes?

High NC (minimal organelle)
Long cytoplasmic processes
No ALP expression

Q4.What are bone lining cells?

Inactive osteoblasts
Reactive for bone formation, or prepare bone for osteoclastic resorption upon PTH stimulation

▸ Slide 20 · Bone MatrixBone and Joint · 6 questions expand

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Q1-Q66 questions — tap to reveal all answerslist

What are the proportions of organic and inorganic bone matrix?
What does the organic matrix contain and what strength does it provide?
What are the roles of osteocalcin?
What are the roles of osteonectin and osteopontin?
What is the inorganic component of bone matrix?
Which bone matrix markers can be detected in urine and what do they indicate?

Answers · Q & A

Q1.What are the proportions of organic and inorganic bone matrix?

Organic 40%
Inorganic 60%

Q2.What does the organic matrix contain and what strength does it provide?

Collagen type I (90%) for tensile strength; hydroxyproline forms the triple helix with glycine
Proteoglycans for compressive strength
Non-collagen matrix proteins: osteocalcin, osteonectin, osteopontin
Growth factors and cytokines (TGF, IL-1, IL-6)

Q3.What are the roles of osteocalcin?

From the mature osteoblast (marker of osteoblastic differentiation)
Controls osteoclasts: stimulates 1,25 vitamin D, inhibits PTH
Urine detection indicates bone maturation

Q4.What are the roles of osteonectin and osteopontin?

Osteonectin: from osteoblast/platelets, regulates mineralisation, binds calcium
Osteopontin (pont = bond): cell binding

Q5.What is the inorganic component of bone matrix?

Mainly provides compressive strength
Calcium hydroxyapatite Ca10(PO4)6(OH)2
Osteocalcium phosphate

Q6.Which bone matrix markers can be detected in urine and what do they indicate?

Urine hydroxyproline: osteoblast turnover marker
Urine osteocalcin: bone maturation

▸ Slide 21 · CalciumBone and Joint · 5 questions 2 check expand

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Q1-Q55 questions — tap to reveal all answerslist

What is the distribution of calcium in the body?
What are the functions of calcium?
Where and how is calcium taken up?
How is calcium excreted?
What is the distribution and function of phosphate?

Answers · Q & A

Q1.What is the distribution of calcium in the body?

~99% in bone
~1% extracellular, <1% intracellular
Normal level 2.2-2.6 mmol/L

Q2.What are the functions of calcium?

Neuromuscular function
Clotting/metabolic function
Bone mineralisation

Q3.Where and how is calcium taken up?

Duodenum: active transport
Jejunum: passive diffusion

Q4.How is calcium excreted?

Kidney: 98% reabsorbed at proximal tubules (per speaker notes)
Stool

Q5.What is the distribution and function of phosphate?

86% in bone, 14% intracellular, <1% plasma
Bone mineralisation and enzyme/molecular interaction
Uptake from food; kidney 100% resorb (per speaker notes)

Fact check

Kidney reabsorbs 98% of calcium at the proximal tubules — imprecise — 98-99% of filtered calcium is reabsorbed overall; the proximal tubule accounts for only ~60-70%, with the rest reabsorbed in the loop of Henle and distal nephron — source

Kidney 100% resorbs phosphate — misleading — About 80-90% of filtered phosphate is normally reabsorbed (mostly in the proximal tubule); reabsorption approaches 100% only with very low dietary phosphate intake — source

▸ Slide 22Bone and Joint · 4 questions expand

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Q1-Q44 questions — tap to reveal all answerslist

How do PTH and calcitonin differ in their effects on calcium homeostasis?
What is the difference between pulsatile and continuous PTH action on bone?
Describe the activation and actions of vitamin D.
What are the skeletal effects of estrogen and thyroxine (T4)?

Answers · Q & A

Q1.How do PTH and calcitonin differ in their effects on calcium homeostasis?

PTH (parathyroid chief cells): raises serum Ca2+, lowers PO4^3-; released when serum Ca2+ falls
Calcitonin (thyroid parafollicular cells): lowers osteoclast number/activity and renal Ca2+/PO4^3- resorption; released when serum Ca2+ rises
Calcitonin causes only a transient fall in Ca2+

Q2.What is the difference between pulsatile and continuous PTH action on bone?

Pulsatile PTH: increases osteoblast differentiation and decreases osteoblast apoptosis
Continuous PTH: increases osteoclast activity via RANKL and IL-6 from osteoblasts
Osteoclasts do not express PTH receptors

Q3.Describe the activation and actions of vitamin D.

Fat-soluble secosteroid; sources are skin (UVB-generated vitamin D3) and food
Activated to 25-OH-vit D3 in the liver, then to 1,25-OH2-vit D3 in the kidney
Increases intestinal Ca2+ absorption and osteoclastic bone resorption, raising serum Ca2+

Q4.What are the skeletal effects of estrogen and thyroxine (T4)?

Estrogen (ovarian D-ring steroid): decreases bone remodelling and postmenopausal bone loss; benefit when started <5 years postmenopause
Estrogen risks: IHD, thrombo-embolic events and breast cancer
T4 (thyroid): increases skeletal growth and bone remodelling, leading to osteoporosis

▸ Slide 23 · Cutting coneBone and Joint · 5 questions expand

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Q1-Q55 questions — tap to reveal all answerslist

What is the sequence of cellular events in a cutting cone?
What are the labelled components of a cutting cone?
How does the cutting cone tunnel change as it advances?
From which direction do osteoblasts deposit new bone in a cutting cone?
Which cells line the haversian canal after the cutting cone has passed?

Answers · Q & A

Q1.What is the sequence of cellular events in a cutting cone?

Osteoclasts at the front to remove bone
Followed by a layer of osteoblasts depositing successive centripetal layers of lamellae and osteoid
Tunnel size narrows to a haversian canal

Q2.What are the labelled components of a cutting cone?

A osteoclast
B osteoprogenitor cells
C capillary
D mononuclear cell lining reversal zone
E osteoblast apposing bone centripetally
F flattened osteoblast/osteoclast lining haversian canal
G osteoid

Q3.How does the cutting cone tunnel change as it advances?

Tunnel size narrows
Eventually forms the haversian canal

Q4.From which direction do osteoblasts deposit new bone in a cutting cone?

Centripetally (towards the centre of the tunnel)
Deposit successive layers of lamellae and osteoid
Following behind the osteoclast front

Q5.Which cells line the haversian canal after the cutting cone has passed?

Flattened osteoblast/osteoclast lining the haversian canal
Mononuclear cells lining the reversal zone

▸ Slide 24 · Draw a structure of haversian systemBone and Joint · 4 questions expand

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Q1-Q44 questions — tap to reveal all answerslist

What is the haversian system (osteon)?
What is the role of Volkmann canals?
What are osteocytes, lacunae and canaliculi?
What lamellar types are described in cortical bone?

Answers · Q & A

Q1.What is the haversian system (osteon)?

Basic structural unit of cortical bone
Lies parallel to the long axis of bone
Central haversian canal transmits a neurovascular bundle
Concentric lamellae of collagen arranged in a herringbone pattern
Cement lines separate the osteons

Q2.What is the role of Volkmann canals?

Run transversely to the bone long axis
Permit communication between outer periosteal vessels and the haversian canal

Q3.What are osteocytes, lacunae and canaliculi?

Osteocytes are trapped osteoblasts located within lacunae between lamellae
Canaliculi are canals occupied by osteocyte cell processes connecting lacunae
Modulate the response of bone to mechanical stimuli
Allow exchange of nutrients and waste products to maintain osteocyte viability

Q4.What lamellar types are described in cortical bone?

Concentric lamellae
Interstitial lamellae
Separated by cement lines

▸ Slide 25 · Describe the structure of periosteumBone and Joint · 3 questions expand

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Q1-Q33 questions — tap to reveal all answerslist

Describe the structure of periosteum.
What are the functions of periosteum?
Which periosteal layer is osteogenic and why?

Answers · Q & A

Q1.Describe the structure of periosteum.

Outer layer of fibroblasts
Inner layer of osteoblasts (cambial layer)
Outer layer: structural support, less cellular, continuous with joint capsule
Inner cambial layer: vascular, osteogenic, contributes to bone growth and fracture healing

Q2.What are the functions of periosteum?

Medium through which tendon, muscles and ligaments attach
Nutrition
Forms bone when required
Protective membrane for bone tissue

Q3.Which periosteal layer is osteogenic and why?

Inner cambial layer
Vascular and contributes to bone growth and fracture healing

▸ Slide 26 · Tell me about bone healingBone and Joint · 9 questions expand

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Q1-Q99 questions — tap to reveal all answerslist

What is Perren's strain theory?
Describe primary bone healing.
Describe the stages of secondary bone healing.
What adjuncts aid fracture healing?
Differentiate bone modelling from remodelling.
What is the role of fibrinolysis in fracture healing?
Describe enchondral ossification during soft callus formation.
Where does intramembranous ossification occur in secondary bone healing?
What is the bone healing nonunion (BHN) model?

Answers · Q & A

Q1.What is Perren's strain theory?

The degree of interfragmentary strain governs the cellular response and therefore the tissue that forms
<2% = primary bone healing
2-10% = secondary bone healing
>10% = nonunion / fibrous union

Q2.Describe primary bone healing.

It is actually bone remodelling - haversian cutting cones cross the fracture site and directly lay down osteons
It is a process of intramembranous ossification where there is no intermediate step of cartilage formation, therefore no callus formation
Contact healing: direct bone apposition with gap <0.01mm
Gap healing: gap <1mm; vessels grow into the gap and osteoblasts lay lamellar or woven bone
Followed by haviersian remodelling by cutting cones (osteoclast reams, vessel grows in, trailing osteoblasts lay new bone)

Q3.Describe the stages of secondary bone healing.

Hematoma and inflammation (<1wk): haematoma brings in haemtopoetic cells. Inflammatory mediators lead to granulation and angiogenesis; osteoclasts and macrophages remove debris
Soft callus (1 weeks to 1 month): endochondral ossification at intermediate strain/low O2; intramembranous ossification at low strain/high O2
Hard callus (1-4 months): soft calcified chondral callus remodels into hard mineralised osteoid callus
Remodelling: Wolff's law and piezoelectric charges dictate distribution of remodelling

Q4.What adjuncts aid fracture healing?

Low intensity pulsed USG increases nanomotion across the fracture site, increasing healing and callus strength
Bone stimulator (electromagnetic stimulation) increases BMP concentration and osteoblastic differentiation

Q5.Differentiate bone modelling from remodelling.

Modelling: change of shape or growth by independent, simultaneous actions of osteoblast and osteoclast
Remodelling: replacement of the same amount of matrix, sequential osteoblast then osteoclast within the same BMU
Cancellous remodelling: osteoclastic resorption + osteoblastic deposition of lamellar bone
Cortical remodelling: cutting cone

Q6.What is the role of fibrinolysis in fracture healing?

Plays a key transition step from haematoma formation to angiogenesis and fracture healing
Cited from NEJM 2015 O'Keiffe

Q7.Describe enchondral ossification during soft callus formation.

Occurs in areas of intermediate strain and low O2 tension
Stem cells differentiate into chondrocytes, laying down type I collagen and fibrocartilaginous matrix
Followed by vascularisation and osteoblasts laying down bone on the cartilaginous scaffold
Forms the interfragmentary callus and external callus

Q8.Where does intramembranous ossification occur in secondary bone healing?

At sites of low strain and high O2 tension (when fracture strain decreases)
Osteoblasts from the cambrium layer of periosteum directly lay down woven bone
Woven bone is later remodelled to lamellar bone
Forms the medullary callus and periosteal callus

Q9.What is the bone healing nonunion (BHN) model?

Described by Elliot, JBJS 2016
Unifies Perren's strain theory, Wolff's law and Frost's concept of mechanostat
Tissue around a fracture is called a bone healing unit, producing a physiological response to its biological and mechanical environment
The lecturer suggests drawing the graph

▸ Slide 27Bone and Joint · 2 questions expand

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Q1-Q22 questions — tap to reveal all answerslist

What bone and joint topic is shown on this slide?
What are the key learning points from this slide?

Answers · Q & A

Q1.What bone and joint topic is shown on this slide?

Not covered in the speaker notes - the slide image is the only source

Q2.What are the key learning points from this slide?

Not covered in the speaker notes

▸ Slide 28 · Xray showing features of renal osteodystrophyBone and Joint · 6 questions expand

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Q1-Q66 questions — tap to reveal all answerslist

What are the X-ray features of renal osteodystrophy?
How is renal osteodystrophy classified and what causes the bone mineralisation deficiency?
What causes low-turnover renal osteodystrophy?
How does renal osteodystrophy present?
What is the management of renal osteodystrophy?
Describe the pathophysiology of high-turnover renal osteodystrophy.

Answers · Q & A

Q1.What are the X-ray features of renal osteodystrophy?

Subperiosteal resorption
Rugger jersey spine
Brown tumour
Tumoral calcinosis (lecturer advises avoiding this term)
All are features of high bone turnover disease

Q2.How is renal osteodystrophy classified and what causes the bone mineralisation deficiency?

High turnover disease with elevated PTH vs low turnover disease with normal PTH
Bone mineralisation deficiency due to electrolyte and endocrine abnormalities
X-ray features of both osteomalacia (impaired mineralisation) and hyperparathyroidism

Q3.What causes low-turnover renal osteodystrophy?

Aluminium accumulation in renal failure
Excess deposition into bone -> toxic to osteoblasts (differentiation and proliferation)
Also impairs PTH release
PTH is normal

Q4.How does renal osteodystrophy present?

Bony problem: pathological fracture
Soft tissue: tendinitis, tendon rupture, carpal tunnel syndrome
Growth retardation, deformity, SCFE in children

Q5.What is the management of renal osteodystrophy?

Treat the underlying cause, multidisciplinary approach
Aluminium chelator
Calcium supplement
Vitamin D supplement
Bisphosphonates

Q6.Describe the pathophysiology of high-turnover renal osteodystrophy.

Uraemia -> abnormal PO4 excretion -> PO4 retention (glomerular) + kidney unable to convert vitamin D to active form (tubules) -> hypocalcaemia
Failure of 1-alpha hydroxylase -> hypocalcaemia
High PO4 and low Ca -> increased PTH -> hyperplasia of chief cells of the parathyroid gland

▸ Slide 29 · Type of jointBone and Joint · 5 questions expand

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Q1-Q55 questions — tap to reveal all answerslist

How are joints classified?
Classify joints by nature with examples.
Which joints are given as examples of the 6 morphological types of synovial joint?
Classify joints by movement.
How many morphological types of synovial joint are there?

Answers · Q & A

Q1.How are joints classified?

By anatomical composition
By movement allowed

Q2.Classify joints by nature with examples.

Synovial
Cartilaginous: symphysis, synchondrosis, IVD
Fibrous: syndesmosis, suture

Q3.Which joints are given as examples of the 6 morphological types of synovial joint?

C1/2
SCJ
GHJ
Elbow, radiocarpal, 1st CMCJ

Q4.Classify joints by movement.

Diarthrosis
Amphiarthrosis (pubic symphysis)
Synarthrosis (suture)

Q5.How many morphological types of synovial joint are there?

6 types of synovial joint, classified by morphology

▸ Slide 30 · Bone graftBone and Joint · 15 questions expand

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Q1-Q1515 questions — tap to reveal all answerslist

Define bone graft and the properties of an ideal graft.
What are the common uses of bone graft?
How is a cancellous bone graft incorporated?
How is a cortical bone graft incorporated?
Compare autograft with allograft.
What are the methods of allograft preservation?
How are bone grafts classified?
By what mechanisms are bone grafts incorporated into host bone?
What factors affect bone graft uptake?
What are the non-vascularised sources of autograft?
Describe the ASIS autograft harvest and the structure at risk.
Describe the PSIS autograft harvest and the structures at risk.
What are the vascularised sources of autograft?
How is a bone bank set up and allograft processed?
What is the principle of graft fixation - nail vs plate?

Answers · Q & A

Q1.Define bone graft and the properties of an ideal graft.

Implanted materials to promote bone healing
Biological properties: osteoconduction, osteoinduction, osteogenesis, vascularity
Structural support

Q2.What are the common uses of bone graft?

AJR - structural support (bone defect management)
Spine - induce fusion
Trauma - fracture nonunion

Q3.How is a cancellous bone graft incorporated?

Inflammation phase: vascular ingrowth, chemotaxis
Revascularisation phase (0-3 weeks)
Creep substitution (3-12 weeks): angiogenesis, osteoblasts and osteoclasts introduced and work at the same time
Remodelling phase (>12 weeks)
Incorporation can be complete; no osteopenia during incorporation

Q4.How is a cortical bone graft incorporated?

Initial incorporation at the host-graft junction by endochondral bone formation
Sequential action of osteoclast then osteoblast: graft bone removed by cutting cones then new bone laid down
50% loss of strength in 3-6 months, then fully returns over 1-2 years
Incorporation is not complete; initial osteopenia on X-ray during bone absorption
Called reverse creep substitution

Q5.Compare autograft with allograft.

Autograft pros: osteogenesis, no immunogenicity, less chance of infection
Autograft cons: limited supply, donor site morbidity
Allograft requires donor consent, screening, processing and storage
Aim of bone bank processing: decrease immune sensitisation and disease transmission
Other sources include synthetic bone substitute and xenograft

Q6.What are the methods of allograft preservation?

Fresh frozen at -70deg: preserves BMP, better mechanical strength; immunogenic, disease transmission risk; shelf life 2 years at -20deg, 5 years at -70deg
Freeze dry (lyophilise): less immunogenic, less disease transmission, longer shelf life; weak structure, no BMP - purely osteoconductive
Fresh

Q7.How are bone grafts classified?

By source: autograft / allograft / synthetic / xenograft
By structure: cortical or cancellous

Q8.By what mechanisms are bone grafts incorporated into host bone?

Inflammation
Osteoblast differentiation
Osteoinduction and osteoconduction
Remodelling

Q9.What factors affect bone graft uptake?

Biological: local vs systemic
Mechanical
Think of the factors affecting fracture healing

Q10.What are the non-vascularised sources of autograft?

Femoral head
ASIS
PSIS

Q11.Describe the ASIS autograft harvest and the structure at risk.

2cm posterior to ASIS, 3cm wound along the crest
Subperiosteal elevation of iliacus
Lateral cutaneous nerve of thigh is at risk

Q12.Describe the PSIS autograft harvest and the structures at risk.

1cm lateral to PSIS, longitudinal incision
Subperiosteal elevation of gluteal muscle
Superior cluneal nerve L1-3 (6cm lateral to PSIS) at risk
Superior gluteal NV (6cm inferior to PSIS) at risk

Q13.What are the vascularised sources of autograft?

Wrist: 1,2 intercompartmental supraretinacular (ICSR) bone graft for scaphoid; 4,5 ICSR bone graft for lunate AVN
Fibular
Iliac crest (deep iliac circumflex artery)

Q14.How is a bone bank set up and allograft processed?

Donor consent and screening (IVDU, blood for HIV, Hep B/C, syphilis, Rhesus status)
Exclusion criteria: HIV, Hep B/C, malignancy, RA/autoimmune disease, steroid
Processing: physical debridement, ultrasonic processing (remove cells/blood), ethanol (denature protein), antibiotic soak, irradiation, +/- demineralisation
Then storage

Q15.What is the principle of graft fixation - nail vs plate?

Nail > plate
Even stress distribution
Increased time for incorporation, needs a rigid device
Increase contact area
Never remove the implant

▸ Slide 31 · Synthetic:Bone and Joint · 7 questions 2 check expand

Question list

Q1-Q77 questions — tap to reveal all answerslist

What are the synthetic bone graft types?
Describe tricalcium phosphate.
What does DBM contain and not contain?
How do bone morphogenic proteins work?
What are the contraindications to BMP?
What are the complications of BMP?
How is DBM manufactured and what does the acidic extraction leave behind?

Answers · Q & A

Q1.What are the synthetic bone graft types?

Osteoconduction: tricalcium phosphate
Osteoinduction: bone morphogenic protein 2 and 7
Others: demineralised bone matrix, hydroxyapatite, calcium phosphate, calcium sulphate

Q2.Describe tricalcium phosphate.

Ceramic scaffold providing a scaffold for ingrowth of vessels and osteogenic cells
Porosity 50% - balance between mechanical strength and porosity
Macropore 100-500mcg for ingrowth of vessels and cells
Micropore 10mcg increases surface area of remodelling
Available as blocks, wedges and granules; trade name Chronos (Synthes)

Q3.What does DBM contain and not contain?

Contains: collagen, BMP, transforming growth factor-beta, residual calcium
Does NOT contain mesenchymal precursor cells
Made by acidic extraction of bone matrix from allograft, then sterilised (may decrease BMP availability)
Osteoconductive without structural support; minimally osteoinductive
Interproduct and interlot variability common

Q4.How do bone morphogenic proteins work?

Osteoinductive; belong to the TGF-beta superfamily
Stimulate undifferentiated perivascular mesenchymal cells to differentiate into osteoblasts via serine-threonine kinase receptors
Activate intracellular signalling molecules called SMAD
rhBMP-2 and rhBMP-7 are FDA-approved for application in long bones and spine
BMP-2 marketed by Medtronic; BMP-7 by Stryker

Q5.What are the contraindications to BMP?

Pregnancy
Allergy to bovine type I collagen
Infection
Tumor
Skeletal immaturity

Q6.What are the complications of BMP?

Under- or overproduction of bone (heterotopic ossification)
Inflammatory responses / seroma formation
Not for cervical spine - increased cervical swelling
Early bone resorption

Q7.How is DBM manufactured and what does the acidic extraction leave behind?

Acidic extraction of bone matrix from allograft removes the minerals
Leaves collagen, non-collagenous proteins and bone growth factors
BMP quantity is extremely low and variable
Sterilisation may decrease the availability of BMP

Fact check

rhBMP-2 and rhBMP-7 are FDA-approved for application in long bones and spine — outdated / imprecise — rhBMP-2 (INFUSE) is approved for anterior lumbar interbody fusion and acute open tibial shaft fractures; rhBMP-7 (OP-1) was approved via HDE only for recalcitrant long-bone nonunion and is no longer marketed in the US — source

Macropore 100-500mcg and micropore 10mcg increase remodelling surface area — unit error — pore sizes are measured in micrometres (um), not micrograms: macropores ~100-500um and micropores ~10um or less — source

FRCS Quiz — private