NMSK - bones

week 1 -

What do holes/depressions do/contain?

They normally contain and protect soft tissue structures such as tendons and nerves

What do these descriptive terms mean?

a) canal

b)fissure

c)foramen (foramina)

d)fossa (fossae)

e) meatus

f) notch

g)sulcus

h)groove

a) a bony tunnel

b) a narrow slit

c) a hole

d) a wide depression/hollow

e)a narrow passage

f)a large groove

g) a groove/furrow

h) an uncovered passage

What do these prefixes mean?

a)demi

b) epi

c) infra

d)inter

e) intra

f)sub

g) supra

a) half

b) above/upon

c)below

d) between

e) within

f) beneath

g) above

What do these descriptive terms mean?

a) anterior

b) distal

c)dorsal

d)external

e)inferior

f) internal

g)lateral

h)medial

i)posterior

j)proximal

k)superior

l)ventral/volar

a) nearer the front of the body

b) further away, the lower end of the body

c)the back surface of the body

d)outside

e)below

f)inside

g)away from the midline of the body

h)nearer the midline of the body

h)nearer the back of the body

i)closer to; the upper end of a bone

k) above

l) nearer the front of the body

j

Explain the histology of compact bone

• very hard and strong

• found mainly in the diaphysis of long bones, where a strong tubular structure is requires

• forms the cortex of all bones

Consists of: Haversian systems (cylindrical structures)

• A central Haversian canal - nerves, blood and lymphatic vessles

• lamellae - concentric (like in a tree trunk) rings/layers of bone around the canal

• lacunae - spaces b/w lamellae containing osteocytes

• Canaliculi - channels carrying nutrient fluid that connect lacunae and communicate with the central canal.

Between the Haversian systems are Volkmann’s canals - they join them together and contain nerve, blood and lymphatic vessels

Explain the histology of spongy bone

• also called cancellous bone

• found where lightness, strength and increased SA are needed.

• mainly in the end of long bones and middle of other bones

• Similar structure to compact bone but no true Haversian systems

• Rings of lamellae have an irregular lattice structure of thin columns of bone called trabeculae.

• Trabeculae provide the internal support structure of bone and are aligned along the directional forces to provide tensile and compressive strength.

• The spaces in the trabeculae help to reduce the overall weight of the bone

• Contain bone marrow

Label this image

Top - spongy bone

Trabeculae

Compact bone

Medullary cavity

Where do we often find compact and cancellous bone on:

a)long bone

b)flat bone

a) Compact - forms outer circular surface

Cancellous - near the ends of long bones

b)Compact - forms the outer/inner flat surfaces

Cancellous - fills the narrow interior of flat bones

What type of tissue is bone?

A connective tissue in which mature bone cells are enclosed in an intercellular matrix of organic collagenous protein fibres called osteoid and a harder inorganic materialised component.

What are the 4 types of cells found in bone matrix?

1- Osteogenic cells - stem cells found in the inner aspect of the periosteum, the endosteum and in communicating channels between the units of bone. They divide to form osteoblasts

2- Osteoblasts - bone-building cells that secrete the osteoid, collagen and other components that build the organic matrix. They start the process of calcification for the inorganic mineral matrix in the spaces b/w collagen fibres

3- Osteocytes - mature bone cells that maintain the normal cellular activity of bone such as nutrient exchange. They are formed from osteoblasts when they become trapped in their matrix and no longer secrete osteoid.

4- Osteoclasts - bone-consuming cells. Large cells made of many monocytes that release strong enzymes to dissolve the bone matrix. Found mainly in the endosteum on the inside of the bone.

What is the difference between laminar and woven bone?

Laminar bone is mature bone

Woven bone is immature

How do we observe bone in microscopy?

Need to stain using Haemotoxylin Eosin stain - appears pink under normal light conditions - stains a wide variety of cytoplasmic, nuclear and extracellular matrix features.

• Then we apply polarised light to the tissue section which enables different structures to be seen slightly differently e.g. haversian canals you acan see osteocytes, volkmann’s canals and haversian systems.

What for and how do we use Schmorl’s stain

• an alternative technique for examining bone, by sawing it into thin wafers using an abrasive surface - produces thin ‘ground’ sections.

• It’s a dark stain which provides high contrast and enables open spaces to be seen in greater detail.

Explain Endochondral ossification

Begins with hyaline cartilage modle that is later replaced by bone. Occurs during most bone development at epiphyseal plates that enable long bones to grow in length.

what is osteogenesis and what are the two stages

A complex process consisting of cell migration, differentiation, extracellular deposition and mineralisation

The two stages are Intramembranous ossification (direct bone formation) and endochondral ossification (cartilage is a precursor to bone)

What is the primary centre of ossification

• Appears in the middle of the diaphysis, osteoblasts appear and the bone matrix tissue is laid down.

• Osteoclasts destroy/resorb bone and mould it to the required shape via remodelling. Responsible for forming the medullary canals/sinuses w/in bone.

• Spreads from the middle of the diaphysis towards the epiphyseal plates at the end of the bone

• Simultaneously bone is being built around the outside of the diaphysis and later forms the periosteum.

• Bone width increases and is maintained by bone formation and turnover in sub-periosteal and endosteal bone surfaces

What are the secondary centres of ossification

Appear at the end of the bone and form epiphysis

• Epiphysis is separated by a thin layer of cartilage (epiphyseal plate/physeal plate/physis) from the diaphysis

• Typically forms the surface of an adjacent joint.

What is intramembranous ossification

• occurs in a connective tissue membrane and begins during fetal development with the differentiation of mesenchymal cells into osteoblasts.

• secretion of osteoids that undergo calcification to produce bone

• Ossification spreads from the centre of the bone outwards

• Forms most flat bones e.g. skull, mandible and clavicles.

What are growth plates

• a thin layer of cartilage b/w the epiphysis and metaphysis of long bones

  Characterised by:

• a resting/’reserve’ zone

• a proliferation zone

• hypertrophic zone

• zone of degeneration

What is cartilage and what 3 types are there

Composed of cells. fibres and a highly-hydrated ground substance.

• fibres provide tensile strength

• proteoglycans in the ground substance make it resilient by trapping water (healthy cartilage should be ~70% water)

• Avascular

3 types:

• Hyaline Cartilage (type 2)

• elastic cartilage (elastic fibres and type 2)

• fibrocartilage (type 1 and 2)

Describe the structure of hyaline cartilage

Lines the articular surfaces of synovial joints, acting as a self-lubricating shock absorber with low friction properties.

articular cartilage doesn’t have a perichondrium on either surface.

• free (articular) space - exposed to synovial fluid within the joint

• basal surface - in direct contact with underlying bone

Articular cartilage is the remnant of hyaline cartilage that formed the template for the developing bone.

limited to interstitial growth because of the absence of the perichondrium

No nerves/blood vessels.

Explain the structure of elastic cartilage

Similar to hyaline but the matrix also contains a dense network of branching elastic fibres - occurs where flexibility is required e.g. epiglottis, external ear and auditory tubes.

Perichondrium (blue)- a dense layer of irregular connective tissue that surrounds cartilage - 2 layers

Inner Chondrogenic layer (dark blue)- contains mesenchymal cells that differentiate into chondroblasts, initiate matrix production (elastin and type 2 collagen) and become immature chondrocytes.

Outer fibrous layer (blue) - fibroblasts produce type 1 collagen on the outer surface of the perichondrium

matrix - fibroblasts that produce type 1 collagen on the outer surface.

chondrocytes - cells within lacunae inside cartilage that occur singularly or in clusters (isogenous groups)

No blood or nerves

What is masson’s trichrome stain?

Stains connective tissue dark blue, smooth muscle and cytoplasm light pink and nuclei dark red-purple to black.

What does Aldehyde fuchsin stain?

elastic fibres pink-purple

Explain fibrocartilage

A mix of hyaline cartilage and regular connective tissue

combines collagen fibre tensile strength with resistance compression of cartilage. Found where tendons attach to bones, minisci and intervertebral disks

• Collagen fibres (type 1 and 2, stained pink/red)

• fibroblasts - scattered w/in fibrous regions with elongated/flattened nuclei

• chondrocytes - dispersed either singularly or in isogenous groups

• matrix - much less surrounds each chondrocyte than in hyaline cartilage - type 2 collagen and proteoglycan ground substance. Basophilia is due to a high content of sulfated glycoaminoglycans (GAGs)

• No perichondrium

Give a brief description of where synovial fluid should be found and what it should look like

Should be clear, pale straw colour/colourless and have the consistency of uncooked egg white (high viscosity due to hyaluronic acid)

Acellular liquid too (relatively)

Image for identifying regions of a bone

Label this image correctly

label this image correctly

Label this image correctly.

Terms - zone of degeneration, zone of hypertrophy, zone of reserve, zone of proliferation and zone of ossification

Define osteoarthritis

progressive deterioration of articular cartilage associates with changes in bone and soft tissue of the joint including loss of cartilage, subchondral bone sclerosis and marginal osteophyte formation

How do we grossly characterise osteoarthritis

Fibrillation, wear lines, erosion (partial/full thickness), peri-articular osteophytes, eburnation (cartilage has gone from spongy and complaint to rock hard)

why is cartilage hard to heal?

it’s avascular

How does osteoarthritis develop?

Where are some common sites of osteoarthritis in horses

distal articular joints (most common) - carpus, fetlock, distal interphalangeal joint (DIP J), hock, Proximal interphalangeal joint (PIP J)

where may we see OA in dogs?

Distal joints and hips (often develops early on and is very painful).

where are common places for OA for cats

distal joints, hips and all along the spide (in particular in the elderly cat).

May not compromise in its gait but the owner may say the cat is struggling to be incontinent or struggling to get into litter tray - due to the OA (can’t turn to clean rear end because of pain).

What happens in osteoarthritis.

It’s a complex condition that affects the whole joint and is now thought to involve cartilage, subchondral bone and the synovium. It’s likely they all have key roles in disease pathogenesis and an association with systemic inflammation could also be present.

Cartilage’s role:

• the innate immune system is activated.

• Chondrocytes express many toll-like receptors that are activated by damage-associated molecular patterns. They also express receptors that bind advanced glycation end products which accumulate with ageing tissue. This resultsin a phenotypic shift to catabolism (why OA is linked to age?)

• These responses may also be a reflection of established cartilage degredation.

• Chondrocytes could be first activated by inflam signals originating from other joint structures

Subchondral bone involvement:

• Forms an interface b/w calcified cartilage below the tidemark and underlying trabecular bone.

• Pronounced changes are seen in structure and composition in cortical plate and trabecular bone in OA

• Features of endochondral ossification are reinitiated in OA and the tidemark advances with associated vascular penetration. Accompanied by osteophyte and subchondral cyst formation.

• Highly innervated bone, likely contributes to the generation of pain in the disease

Synovium role:

• synovitis is an early sign of OA

• proliferation of synoviocytes and tissue hypertrophy are notable, with increased vascularity

• Synoviocytes synthesise lubricants such as hyaluronic acid and lubricin - contribute to optimum joint function.

• Reduced lubrication seen in OA patients.

• Release inflam mediators and degradative enzymes.

What differences can be seen in this image?

• vascular infiltration seen in OA

• larger synovium

• activated macrophages

• broken cartilage

• thin, splits and cuts seen in the cartilage

• lots of inflammation markers

How does OA cause pain?

Pain signals are sent from the joint to both the ‘higher’ brain function of the cerebral cortex, creating the feeling of pain itself.

Pain signals are also sent to the limbic system which results in behavioural changes - not wanting to jump, feeding changes, sleep changes, dream cycle changes, general attitude changes.

What does osteoarthritis look like histologically?

​

Cartilage becomes softer in compression and weaker in tension in OA​

Proteoglycan loss​

Altered collagen structure​

Increased water content

What are osteophytes and why do they form?

In order to try and restore some strength and support to the bone, it may produce osteophytes (proliferation of a new cartilage and bone at joint edges).

what may osteophytes look like on a radiograph?

• grainy, extra pieces of bone, give the impression that the bone isn’t smooth/has additional growth

what are some causes of osteophytes

• ageing

• mechanincal instability

• secondary to synovitis

• response to forces

• tissue attachments

How can we diagnose OA?

• TAKE A GOOD HISTORY

• listen to what the owner says about the animal’s behaviour and how it’s changed

• radiography and ultrasonography (used to confirm what we know, as the ultimate care plan won’t change that much)

• Joint fluid analysis (synovial fluid SF)

• MRI/CT

• arthroscopy

Give an overview of synovial fluid

• an ultrafiltrate of plasma and hyaluronic acid

Gross appearance:

• Protein - increases with synovitis and increasing inflammation (>2.5g/dl abnormal, >4g/dl sepsis)

• viscosity - finger test - 2.5-5cm stretch

• ctyology - OA horse: 5000-10000 cells/ml, OA dos 500-5000cells/ml, <10%neutrophils

• clot formation - rapidity and size roughly proportionate to severity of synovitis

• mucinous precipitate quality - 0.5ml fluid into 2 ml 2% acetic acid, quality of clot and clarity of solution, not very accurate.

What are the main goals for treating OA

• identify and treat underlying cause (abnormal forces on the joint, i.e. articular fracture, cruciate rupture, or normal forces on an abnormal joint i.e. osteochondrosis, HD)

• block inflammatory cascade and permit repair if possible

• pain relief and long term management

• weight control and physical therapy

Give some examples and name the 2 groups of anti-inflammatories and analgesics

NSAIDs (Non Steroidal Anti-inflammatory drugs)

• COX-2 inhibitors

• side effects

• potentially decrease PG synthesis

• Dosing

Corticosteroids:

• Intra-articular (equine)

• Phospholipase inhibitors

• Effects on cartilage metabolism

What do we need to be careful of with COX related drugs

Cyclo-oxygenase is needed in the brain, gut and kidneys. If we use COX-inhibitors we risk causing severe damage to these areas e.g. renal failure.

What are preventative measures we can take to reduce the risk of OA

• maintain joint mobility and muscle strength

• minimise additional joint destruction

• weight management

what are some examples of adjunctive treatments

• Hyaluronic acid - intra-articular, intra-venous, anti-inflammatory

• Pentosan polysulfate (not a lot of evidence to support its use) - anabolic effect (build), HA synthesis, catabolic enzyme inhibitioin, clinical improvement

• PSGAGs (also criticised, not a lot of evidence to support their use) - intra-articular, intra-muscular, oral, anti-inflammatory, HA synthesis, complications?

• IRAP - interleukin-1 receptor antagonist protein, harvested from the animal’s own blood and put into the joint.

• PRP - platelet rich plasma, autologous (produced by the animal’s own body), anti-inflammatory, harvested, spun, treated and put into the joint.

• Stem cells (actually mesenchymal cells), put into the tendon and supposedly signal what’s wrong with the area and how to fix it.

ALWAYS QUESTION AND SCRUTINISE NEW DRUGS

What is Anti-nerve growth factor and what are some complications/questions around it at the moment

It’s a monoclonal antibody designed for dogs that neutralises the nerve growth factor (NGF), a key player in OA for dogs, so it reduces pain. It’s eliminated by the body with minimal involvement of the liver/kidney.

Bedinvetmab - administered monthly as an injection, saw a reduction in OA pain. Some mild reactions were seen (swelling and heat). well tolerated at the recommended dose, not additional side effects were observed at overdose.

What is an extreme way we can reduce the effect of OA

Surgery:

• Correct the underlying tissue, HD, cruciate rupture, elbow dysplasia, OCD etc.

• salvage procedure - femoral, head and neck ostectomy, joint replacement, arthrodesis

• joint resurfacing (not proven)

Suggest some ideas for the future of OA care

• synthetic matrix and/or mesenchymal stromal cells, subchondral bone

• suppression of matrix degradation (curative?)

• gene therapy - synthesis of natural inhibitors of cartilage damage

• synthesis of cartilage matrix

Why does the body need a skeleton

• structural support

• protection of vital organs from trauma

• locomotion

• mineral reservoir

what are some limitations of bones

• rigid

• hard/brittle

• unable to expand from within - limited growth potential, can only expand at existing surfaces

What makes up bone tissue?

• matrix - inorganic and organic

• cells - osteo- cytes/blasts/clasts

• vascular spaces (areas that vessels go through the bone)

What is the organic component of the bone matrix - outline it.

OSTEOID = ground substance in which numerous collagen fibres are embedded - it’s what becomes bone (in the image it’s labelled). Over time it will harden and form proper bone

synthesised by osteoblasts

secreted onto existing bone surface

embedded in a ground substance of water and:

• glycoproteins - osteonectin, osteocalcin (bind collagen and minerals)

• proteoglycans - byglycan, decorin (bind growth factors)

• bone sialoproteins - osteopontin, thrombospondin (associated with cell adhesion)

What is the inorganic bone matrix

bone minerals:

• 60-70% dry weight

• confer hardness and rigidty

• make bone radio-opaque

• composed largely of crystals: hydroxyapatite, (Ca10(PO4)6(OH)2), carbonate, calcium phosphate.

How do the components of bone change over time?

younger - during birth, not proper bone yet (would seriously harm the mother if it was), also ensures that when the young fall, they don’t break lots of bones.

in humans at around 18-21, bones will be fully mature.

Older - more brittle

How does bone form?

Mineralisation

• commences as soon as osteoid is secreted

• reaches 70-80% final in around 3 weeks (in utero)

• takes years to complete

What are the two ways in which collagen fibres deposited, organise themselves?

1. woven bone - haphazard collage, ‘quick and dirty’ formation. Young growing animal, fracture, repair. Mineralises quickly. Looks woven, not a lot of strength.

2. Lamellar bone - parallel fibre bone. Thin layers of osteoid within which collagen fibres are parallel. Structurally superior. Collagen fibres deposited in different organisational structures.

what does circumferential mean

slicing in half - used to look at bone microscopically.

Outline osteons

• A round structure in formation that has blood vessels in the middle

• Forms tubes that run the length of the bone, pack together and provide strength to the bone.

• Primary and secondary osteons

• secondary osteons are formed off a primary one (e.g. motorway is the big main road, country roads come off it)

• secondary osteons are more likely to move across the bone (width), transversely.

• White arrows are the primary, black arrows are the secondary (hard to tell apart)

How does bone grow?

• bone is living tissue, therefore it can be replaced and redistributed as loading requirements change.

• grown from the inside, out.

outline primary osteons

• formed in appositional bone growth, when bone increases in diameter.

• Formed from existing blood vessels on the periosteum of the bone - the osteoblasts underneath the blood vessels in the periosteum have a decreased rate of osteoid production, whereas other side has an increased rate

• Once ridges form, they fuse and form a tunnel around the blood vessel lined with the endosteum

• Concentric lamellae formation: osteoblasts in endosteum build them onto the valls of the tunnel, filling inward until just enough space for the blood vessel

• circumferential lamellae form as the bone continues to grow outward as the osteoblasts in the periosteum build them

• Run parallel to the acix of the bone, contain one or more vascular canals are are ALWAYS surrounded by woven bone.

Outline secondary osteon structure

• Contain a haversian canal (contains the nerves, blood and lymphatic vessels), canaliculi (contain cytoplasmic processes of osteocytes), cement line (around the whole osteon) and osteocytes (within lacuna(e)).

• formed from an primary osteon

• often formed due to remodelling needs

• both primary and secondary have similar structure

What can we also call a Haversian system

• osteon

and vice versa

Outline bone cells

1. Osteoblasts

   • derived from mesenchymal stem cells

   • synthesise and secrete osteoid

   • active in mineralisation process

2. Osteocytes

• scattered within the matrix

• interconnected by dendritic processes

• derived from osteoblasts but stopped synthesis of matrix and dividing

• reside within ‘lacunae’ which are interconnected by ‘canaliculi

• long-lived

• maintain the matrix

3. Osteoclasts

• responsible for bone resorption

• large, multinuclei cells

• release protons, leads to an acid environment, leads to demineralisation

• secrete proteases that destroy the organic matrix

• derived from bone marrow

How is bone modelled/remodelled

Cellular mechanisms

• coordinated action of osteoblasts/clasts

• bone is excavated - osteoclasts excavate a cylindrical tunnel from a cutting cone (50 micro metres a day) - parallel to other osteons

• bone is replaced - osteoblasts follow, form concentric lamellae of lamellar bone on walls, surrounding a centrally in-growing blood vessel

• form a secondary osteon

• facilitates: change in shape, material, repair of damaged bone, release of mineral ions

What are and what causes stress fractures

• a syndrome involving localised bone injury associated with fatigue damage subsequent to repetitive loading/mechanical stress

• common in performance animals

• underlying cause of lameness

Over time:

• may lead to a catastrophic break (shatter/break completely) over time.

How can we locate stress fractures?

Micro CT - very high resolution imagine (can’t be used on anything high alive).

Often can’t be seen on X-ray - will see behavioural signs of discomfort.

How does the body try to repair stress fractures?

• Osteoclast will burrow in the area of the fracture, creating more holes so that nutrients can reach the area for it to start healing

• this in turn makes the bone even weaker before it can start healing

outline the pathophysiology of stress fractures using this image

• stress = force per unit area

• strain = percentage of elongation

• stiffness = resistance to deformation

• elastic region = measure of elasticity

• yield point = point at which the structure will no longer return to its original shape

• plastic region = structure deformed and moving towards failure.

• fatigue = progressive decline in mineral properties over time

cyclical loading of quite intense loads may steadily weaken the bone

• we can predict with race horses, how many steps they need to take before obtaining a stress fracture - look at strain vs number of cycles to failure

• the higher intensity of training, the less time it will take to reach that dangerous point.

why is microdamage dangerous

• causes structural damage at various levels

• can cause cell death

• can cause vascular disruption

• leads to remodelling of the bone, which if continuously re broken, will lead to the catastrophic break.

Where are common locations for stress fractures?

How can we diagnose/manage stress fractures

History:

• intense training?

• none - ‘incidental finding’

• none - spontaneous catastrophic fracture

• subtle loss of performance

• acute-onset lameness associated with work

Modify exercise patterns:

• combination of load, repetition and inadequate recovery will lead to a stress fracture

• essential feature of treatment is to break the cycle (change intensity, level and/or type of exercise)

Where do we find cartilage

Joints - flexible interface b/w bones, smooth bearing surface

flexible support - outer ear, sternum, larynx, tracheal rings

How does cartilage grow?

Interstitially

• difficult as cartilage is avascular and aneural

What does matrix include

• NOT just osteoid without the mineral

• different biochemistry, microstructure, metabolism and cell types found

• avascular and aneural

Outline hyaline/articular cartilage

Typical form of cartilage

Found:

• joint surfaces including synovial joints and sternum

• precursors to bone in embryonic skeleton (embryonic ossification)

• present inside bones, serving as a centre of ossification or bone growth

• predominantly type 2 collagen.

Function:

• withstand and distribute load

• act as an elastic shock absorber

• provides a wear resistant surface to articulating joints

• self maintaining

• avascular, aneural and alymphatic

what does Alizarin red stain do?

stains cartilage

• used to see cartilage as a precursor in foetuses.

Outline fibrocartilage

white fibrocartilage

• found in areas requiring tough support/great tensile strength e.g. intervertebral disks, symphyses

• lines surface of bony grooves for tendons - flexor digital sheath, palmar surface of navicular bone

• interface ligament/tendon and bone

• contains more collagen than hyaline cartilage

• contains type 1 and 2

• lacks a perichondrium

outline elastic cartilage

yellow/elastic cartilage

• found in pinna and several tubes (auditory and eustachian canals, larynx, epiglottis and arytenoids)

• keeps tubes permanently open

• similar to hyaline but contains elastic bundles (elastin) scattered throughout the matrix

what are chondrocytes

• the only cells found in cartilage

• produce and maintain the cartilage matrix

• low density

• obtain nutrition and O2 by diffusion

• chondrocytes continue secreting new matrix when embedded in the matrix (interstitial growth, internal expansion)

• chondrocytes are capable of division within the matrix

How many kinds of chondrocytes are there

4 - superficial, middle, deep and calcified

all have distinct biochemical and physiological properties.

morphology varies with depth - see image

What about hyaline articular cartilage structure?

• characteristic zonal microstructure

• collagen framework embedded in a highly hydrated ground substance (carbohydrate and water rich)

• type 2 collagen - 50% dry weight (type 1 collagen in fibrocartilage ± elastic fibres in elastic cartilage

What is the 2-phase composite of articular cartilage

1. 3D latticework of type 2 collagen fibres, orientation of fibres is divided into zones, deeper (interface with bone) layer calcifies

2. Hydrated gel (chondrocytes, no blood vessels, lymphatics or nerves, deeper portion calcifies)

• fills (expands) space b/w collagen fibres

• held together by other ‘structural’ molecules such as collagen XI, collagen IX, fibromodulin, decorin, COMP.

What is aggrecan

a proteoglycan

• core protein

• glycoaminoglycan chains form

• around 10,000 negative groups

• attracts Ca+

• osmotic (pulls water in)

• linked to long hyaluronan to form long chains

How do our joints resist compression?

• articular cartilage - VISCOELASTIC

• allows the ground substance to move in and out of the gaps

• moves out when pressure is applied

• moves back in when pressure is released

What can a high strain rate (as we see for race horses) lead to?

The cartilage snaps

• doesn’t have enough time to move to allow the water molecules out

• the molecules force themselves out due to the pressure

• results in the cartilage breaking

What is a cement line

• junction betwen outermost lamellae of new osteon and some pre-existing older bone

• contains a lot of proteoglycan that stick the old and new bone together

What other kinds of fractures are there?

• hairline

• greenstick

• transverse

• spiral

• comminuted

• compound

outline how stress fractures lead to catastrophic injuries (general cycle)

• fatigue damage leads to microdamage

• cyclical loading leads to an accumulation of microdamage

• leads to a stress fracture

What happens to the forces on the limb at rest

• horses rest standing most of the time

• equal balance of body weight

• forelimbs carry 58.6% and hind limbs carry 41.4%

• bones will be slightly compressed

what happens to the forces on the limb during locomotion

• force distribution varies in accordance with the sequence and timing with limb contacts and overlaps

• how they change their gate depending on activitiy carried out

• different forces acting on the bones (gravitational etc.)

How do bones deform when at rest

• strength of the bone can be weakened and cause deformation when not exercising

• overweight, meaning the load on the joints is too heavy resulting in damage

• generally, less deformation than during locomotion

• elastic deformation at rest

how do we get bone deformation during locomotion

• bones can change shape and remodel during locomotion which can lead to deformation to try and strengthen, need time to recover

• various types on different joints around the body

• more likely to cause plastic deformation than elastic at rest

Identify the regions on this graph

1. Elastic region - measure of elasticity (return to original shape)

2. yield point - point at which the structure will no longer return to its original shape

3. plastic region - structure is deformed and moving towards failure

4. failure point- where the material breaks

What is happening in this graph

Fatigue:

• a progressive decline in material properties (pink and orange line)

• failure point occurs at lower stress with repetition, as the bone weakens

• cyclical loading of quite intense loads may steadily weaken the bone