Tissue Mechanics and Injury Flashcards
Describe the three zones in articular cartilage.
Zone 1: parallel fibers, smooth, reduced friction, distribute forces
Zone 2: mesh-like to hold water, absorbs compression
Zone 3: perpendicular, securely holds the calcified cartilage
What is active tension? What does it depend on?
Developed by the active contractile elements of the muscle
Depends on more cross-bridges being formed, by:
- Frequency of motor unit firing
- Numberofmotorunitsfiring
- Sizeofmotorunitsfiring
- Diameter of the axon in motor unit (conduction velocity)
Describe the basics of muscle breakdown. How can age, immobility and injury, individually affect muscles. Give three possible pain mechanisms.
Age: reduced cross sectional area (# and size of fibers), decreased ROM and power
Immobility: decreased force production (smaller fibers, impaired activation)
Injury: decreased force production (damaged sarcomeres, pain inhibition)
Possible pain mechanisms
• Reflex inhibition of motor units (to prevent further injury)• Central descending inhibition of injured muscles
• Decreased motivation (cognitive effective)
Is the healing process made of clear steps of is it more of a continuum? Explain.
The healing process is a continuum
Not distinct phases
The healing process overlap one another
No definitive beginning or end points
What is bone composed of? What are its two layers and two types of cells?
- Primarily type I collagen
- Mineral (Ca2+)
Two layers:
• Cancellous (spongy)
- Compact (cortical)
- Osteoblasts versus osteoclasts
What are the different structural properties that a tissue can have? What does a steep stress/strain curve represent? A gradual curve?
• The slope of the line represents the stiffness and compliance of the tissue
- Steep curve: high stiffness, low compliance
- Gradual curve: low stiffness, high compliance
What are the intrinsic, systemic and extrinsic factors that impact healing?
INTRINSIC
Extent of Injury
Edema
Hemorrhage
Poor vascular Supply
Tissue Separation
Muscle Spasm
Atrophy
Scarring
SYSTEMIC
Age
Obesity
Malnutrition
Hormone
Levels
Infection
General Health
EXTRINSIC
Drugs
Dressings
Temperature
Physical
Modalities
Exercise
Give the roles of white blood cells in general/ of leukocytes
- White blood cells – involved in the inflammatory process and categorization depends on the type and age of injury, or if bacteria present
- Mononuclear Leukocytes (agranular): monocyte/macrophage, lymphocyte
- Polymorphonuclear Leukocytes (granular): eosinophil, basophil, neutrophil
What are the signs and symptoms of the fibroblastic repair phase? What are the two main things that are happening during this phase?
- Signs and symptoms include:
- Touch tenderness, pain with stretch to injured site
- Disappears with scar formation
- Deposit new material to reconstruct the injured tissue
- Formulate granulated tissue (highly vascularized)
- Revascularization
- Scar Formation
How are differences in stress-strain determined in ligaments? What happens to ligaments when then have intermittent tensile loads? Are ligaments more, equally or less resistant to tensile stree that tendons? Why?
Differences in stress-strain reflects varied proportion of collagen and type
Similar mechanics to tendons
Increased thickness and strength with intermittent tensile loads
Slightly less resistant to tensile stress than tendons because they must be oriented in multiple directions (but withstand a wider variety of force directions)
Describe the basics of ligaments breakdown.
What happens to its physical properties? What could an external load do to a ligament?
Insertion sites weaken with age, reducing strength and stiffness of tissue
Very sensitive to loading and loading history – without load rapid deterioration of biochemical and mechanical properties (reduced strength and stiffness)
When a ligament is taught for a particular joint position, an external load that results in any deformation of the tissue will exceed the elastic state and the ligament will fail
Ex: ACL tears - stops the tibia to sliding forward on the femur. ACL becomes very tight when you plant your foot on the ground, so if it gets hit at that same time (external load), we will see a tear (ex: soccer)
Describe the behavioural properties (3)
Structural Properties
- Load, force and elongation
- Stress and Strain
Viscoelasticity
Time/Rate-Dependent Properties
- Creep
- Stress Relaxation
- Strain Rate Sensitivity
What are some examples of inert structures? Describes one way that pain can increase in these structures.
- Ligaments, bursae, fascia, nerve roots, capsules, dura mater
- Non-contractile
- Pain is provoked by stretching the tissue
- Pain increases with ACTIVE AND PASSIVE movements (often end-range)
- In the SAME direction
- Resisted movements are not painful
What are some examples of contractile structures? Describes two ways that pain can increase in these structures. Give an example
- Muscle, tendon, tendon-periosteal (TP) junction
- Pain increases with ACTIVE AND RESISTED movements
- In the SAME direction
- Pain increases with PASSIVE movements
- In the OPPOSITE direction
- E.g., painful active and resisted elbow flexion, and passive elbow extension
What are the characteristics of a resting position of an articular joint? Would we see a CPP or a LPP?
- A specific loose packed position
- Minimal congruency between surfaces
- Capsule and ligament have greatest laxity
- Passive separation of joint surfaces, therefore greatest swelling
• Usually the mid-position for the joint
Describe the four stages of bone healing
What is the maturation phase? What is its timeframe? What happens to fibers? What is the apperance of the wound at this point?
Long-term process (3 week to multiple years)
Realignment collagen fibers (no new)
Increases in stress and strain to realign for maximum tension efficiency (more cross-linking bonds)
Fibers to orient themselves along stress line
Normal appearance and function but rarely as strong as the original tissue
Describe the composition of tendons (bone to muscle)
- Similar make up as ligaments
- More type I collagen thought to be an adaptation to larger tensile forces
- Primarily aligned in one direction
Whats is a fibrocartilaginous junction? What is its function?
Gradual change in tendon structure, divided into four zones
Diffuses the load at the tissue-bone interface, perhaps to help prevent injury
What is the difference in cartilage healing between an injury that doesn’t reache the subchondral bone and one that does? Why?
Does not reach the subchondral bone (there is no vascular supply!): becomes necrotic, no healing
If the subchondral bone is reached: access to blood supply
• May resemble healthy tissue, but biochemically and mechanically differ
Fibrillation, fissures and degenerative changes occur
What is the inflammatory response? What is its timeframe? What are its clinical signs? What happens, at the tissue level, during the inflammatory response?
Early, almost immediate response to the injury
0 to 4 days
A protective response intended to eliminate the initial cause of cell injury as well as the necrotic tissues resulting from the original injury
Clinical signs of acute inflammation:
HEAT, REDNESS, SWELLING, PAIN, LOSS OF FUNCTION
Direct injury to the cells that disrupts blood vessels
Immediate coagulation and development of a fibrin clot leading to homeostasis of the injured tissue
Platelets release chemical messengers that change the metabolism of the tissue and initiate the inflammatory response
The later stages of healing can only occur once the inflammatory phase occurs
What are the two main fibrous components of the ECM? One of them has two types, name and describe them.
• Fibrous Component
Collagen – white fibrous, steel-like
strength, rigid
Elastin – yellow fibrous, elastic properties
- Collagen type 1: thick fibers, little elongation• Resists tensile forces well
- Collagen type 2: thinner, less stiff fibers• Resists compression and shear
How is a scar formed?
- Initial fibrin clot breaks down and granulation tissue created
- Fibroblasts, collagen and capillaries (highly vascularized, connective tissue)
- Reddish granular mass filling in the gaps during healing
- Capillary growth accumulates fibroblasts -> ECM synthesis
- Collagen deposited randomly but increases strength of scar (proportionately)
- Fibroblasts diminish with increases in strength (Less collagen that is being laid down)
What are the two characteristics of the cellular response during tissue injury?
Describe the physiology of what happens and the two cell movements that we see in each characteristic.
a) WBCs (white blood cells) leave the vessels moving into the tissues (extravascular space)
• Triggered by chemical mediators supporting dilation and permeability
- Margination: leukocytes adhere to the endothelial cell well of vessel
- Diapedesis: squeezing between cells to leave the vessel
b) Seek and destroy foreign substances
- Chemotaxis: chemical gradient attracts leukocytes to injury site
- Phagocytosis: recognize foreign substance (e.g., bacteria), engulf, degrade
Describe the composition of ligaments (bone to bone)
Cells make up 10-20%
ECM makes up 80-90%
Primarily composed of type I collagen fibrils that are densely packed into fiber bundles arranged in line with the applied tensile force
Depending on the ligament there may be varying directions of tensile force therefore ligaments run in multiple directions (e.g., MCL)
What are some tissue modifiers?
- Age
- Immobility
- Disuse
- Injury
- Medication
• Pain
What is a tissue?
• An aggregate of cells that have similar structure and function
What is the maturation remodeling phase? Use a graph to describe it.
What are the physical characteristics of a mature scar? What is the relative strength of a scar after about 1 week?
- At about 1 week, scar is ~10% of strength of normal skin (or another tissue) strength
- Healing -> reduced angiogenesis (devascularization) -> fewer fibroblasts
• Granulation tissue becomes pale and avascular
- Mature scar will be firm, inelastic, flexible
- Lack physiological function (less strength, not well vascularized)
What are the three main phases of the initial injury healing process?
What is their approximate timeframe and characteristics?
• Initial Injury
1. Inflammatory response – redness, swelling, tenderness, increased temperature,
loss of function, 0-4 days
2. Fibroblastic/Repair phase – diminishing pain tenderness, gradual return to function, 2 days-6 weeks
3. Maturation/Remodeling phase – strong contracted scar develops, increasing strength and full return to function, 3 weeks to 2 years
Describe the basics of tendon breakdown.
What happens to its physical properties? What is the definiton and the difference between acute and chronic tendon breakdown?
- Weaker, stiffer and less likely to deform (common patternt hat we see) (reduced toe region) due to vascular, cellular and collagen-related changes associated with age
- Acute: a known time and method of injury (partial tear to complete rupture)
- Chronic: unknown onset but involves repetitive loading to cause damage
What is passive tension What happens when the muscle is stretched?
Tension developed by passive, non-contractile components of muscle
Parallelelasticcomponents
When the muscle is stretched they resist and contribute to the tension (only in tension stretch not shortening)
- Epimysium
- Perimysium
- Endomysium
Series elastic component
• Tendon (stretch exerts a pull on the tendon)
What are the three types of contractions that a sarcomere can do?
Concentric
Eccentric
Isometric
The outcome and time course of tissue specific healing will vary according to what (3)?
TISSUE SPECIFIC HEALING
• Outcome and time course will vary according to the injury type, severity, extent
- Tendons
- Ligaments
- Muscles
- Closely follow the stages of healing described
- Cartilage and bone vary
What are some of the most common causes of muscle injury (6)?
• Contusions and strains are the most common
- Inadequate muscle flexibility
- Inadequate strength or endurance
- Uncoordinated muscle contraction
- Insufficient warm up
- Poor rehab
What is an end feel? Is it normal or pathological? What is essential when using that technique?
• A sensation that the therapist feels in the joint and tissues at the end of available range of motion during passive movement
- May be normal or pathological (abnormal)
- Must compare the affected and unaffected sides
Give a definition for angiogenesis. What causes it? What has to happend to lead to revascularization (4 steps)?
• Angiogenesis: lack of oxygen stimulates growth of endothelial capillary buds into the wound
The wound can then heal aerobically; increased oxygen delivery
Blood flow to deliver nutrients for tissue regeneration in the area
Vessels tend to be leaky so the tissue appears wet
- Proteolysis of basement membrane
- Migration and chemotaxis at the capillary tip
- Cell proliferation
- Increased permeability through gaps
How are differences in stress-strain determined in tendons?
What does continuous compression do to a tendon?
What does tensile loads over long periods of time do?
- Differences in stress-strain reflects varied proportion of collagen and type
- Cross-sectional area, material and tendon length determine the amount of force that a tendon can resist and the amount of elongation that it can undergo
- Continuous compression modifies composition to resemble cartilage (reducing tensile strength)
- Tensile loads over long periods will increase tissue size, collagen concentration and cross-linking
All joints in the body are composed of what? Give some examples of this type of tissue.
• All joints in the body are composed of connective (inert) tissue
- Bones
- Bursae
- Capsules
- Cartilage
- Discs
- Menisci
- Ligaments
• Tendons
What is fibrocartilage?
Type I > type II collagen
Collagen density to keep the water in the tissue (versus hyaline cartilage that
utilizes collagen and chemical water attraction)
Limited blood supply, nutrient diffusion with compression
E.g., meniscus
• Circumferential fibers (deep zone)• Radial fibers (superficial zone)
Give the role(s) of parenchymal cells, endothelial cells and platelets.
- Parenchymal cell: carries out the function of a tissue or organ
- Endothelial cell: inner blood vessel, form new capillaries “angiogenesis”
- Platelet: an irregular, disc shaped element in the blood to assist with clotting
Describe the basics of cartilage breakdown.
What happens when there’s a lack of cyclical loading? How can it affect other tissues, e.g. bones?
Disruption of synthesis and degradation in the ECM (softening)
Lack of cyclical loading (immobility, bed rest) deprives tissue stresses required for healthy function
• Decreased stress leads to changes in collagen (weaker bonds and unorganized structural changes)
Abnormal force transmission
Less water, increased stiffness, more force translated to other tissues (e.g., bone) and experiences earlier plastic zone
Viscoelasticity: give the definition of elacticity, and viscosity. What does an elastic tissue do, and a viscous one?
- Elasticity: returning to the original length or shape of the material after the load has been removed
- Also known as deformation (proportional to the amount of force)
- Elastic tissue: return to resting length when force is removed
- Viscosity: the material’s resistance to flow
- Force applied to viscous material display time/rate dependent properties
• Viscous tissue: creeps under constant load (plastic does not return shape)
What is hyaline cartilage and where can we find it?
Lines articulating bones and distinguishes synovial joints
Type II collagen throughout the ECM and compresses on the proteoglycan (PG) molecules that hold onto water during load
Articular cartilage has much more PG than other joint structures
Limited blood supply, nutrient diffusion with compression
Describe the loose packed position (LPP) of articular joints.
LOOSE PACKED POSITION (LPP)
- Any position other than CPP
- Not congruent
- Capsule and ligaments are relaxed
- Greatest room for swelling
- Naturally adopted for rest when painful
• Least amount of stress on structures
What happens as a muscle is being pulled apart?
When the muscle is being pulled apart, increase stretch
Passive increases while active decreases, but the overall tension increases as the muscle gets longer
At the black circle: total tension can become stronger than just with active tension
When muscle is shortened: everything is so tightly put together that there is no room to shortnen more, to contract
What are the three types of normal end feels? Give a brief description and an example for each.
Bone to Bone
• Abrupt stop in motion; two bone surfaces coming together (e.g., elbow ext)
Capsular or Soft Tissue Stretch
• Hard-ish stop in motion; spring or slight give (e.g., shoulder lateral rotation)
Soft Tissue Approximation
- Squishy, giving
- Movement stopped by limb hitting again soft tissue of another body part
• e.g., knee flexion
How are contractile tissue fibers grouped? What composes a myofilament? What is a cross-bridge?
- Thousands of fibers grouped into:
- Fascicles
- Myofibrils
- Myofilaments
- Myofilaments: actin, myosin, troponin
- Cross-bridge: Action potential releases Ca2+ to expose binding sites between actin and myosin
What is muscle tension? What is the optimal length, and what happens when a muscles in longer or shorter than its optimal length?
Direct relationship between tension development and muscle length
Optimal length: capable of developing a maximal tension
As a muscle is lengthened or shortened from the optimal length, the amount of tension generated is diminished
Shorter muscle, or too stretched = smaller ability to create a big tension
Passive (green) line in the graph: only contributes to shortening, not lengtening
What are the two cellular components of the ECM? When are they there? Give some examples for each type
• Resident Cells – Always present but depends on tissue
- Fibroblasts (collagen)
- Osteoblasts (bone)
- Chondroblasts (cartilage)
- Circulating Cells – If inflamed or damaged• Lymphocytes
- Macrophages
What are different kinds of strains that we can do to a tissue?
What is the fibroblastic phase (scar forming)?
What is its time frame?
What are the two different possible pathways of scar forming? Which is the most common one? The fibroblastic phase depends on two things… what are they?
Begins within hours to days post-injury
2 days to 6 weeks
Either a REGENERATIVE process to replace necrotic cells with new cells of the same type; OR a REPARATIVE (generally what we see, more common) process to replace necrotic cells with collagen and form scar tissue (type I and III collagen)
Dependent on:
• the extent of the injury (severe vs. mild)
• type of tissue (if its cells can divide or not)
What are the two characteristics of the vascular response during tissue injury? Describe the physiology of what happens and what clinical symptom(s) result from it.
a) Altered blood vessel size to trigger increased blood flow
• Vasoconstriction of vascular walls in the vessels leading away from injured site
- Diminishes oxygen to tissue (anemia)
- Rapid vasodilation to increase blood flow (expand the capillaries, increase fluid) (And that’s how the platelets build up))
• Contributes to heat and redness
b) Structural changes that allow plasma proteins to leave circulation (to heal)
- Vessels become more permeable (increased pressure)
- Fluid leaks out contributing to swelling and fluid accumulation
What is a quantitive way to describe the levels of tendon/ligament breakdown?
What are fibroblasts? What are their functions in injury?
Flat shaped cells in the dermis of skin and structural tissues including ligaments and tendons
Function in injury:
Synthesize collagen for wound closure (forming scar)
ECM remodeling – degradation and production of collagen
What are the two articular joint positions? Identify and describe the most stable one. What happens when it is swollen?
CLOSED PACKED POSITION (CPP) and LOOSE PACKED POSITION (LPP)
- Most stable position
- Greatest protection for the joint
- Usually avoided during assessment
- Greatest congruency of surfaces
- Capsule, ligaments under max tension• If swollen, CPP cannot be reached
What happens after tissue disuse?
TISSUE DISUSE
• Tissues adapt to decreased applied loads
• Active and passive tissues become weaker
• Less stress (load or force) to produce the same amount of strain (deformation)
Which chemicals are released because of cell damage during the inflammatory phase, and what do they do?
What are the two types of response that we can observe?
• Injury to the tissue results in damage to the cells -> release of chemicals
- E.g., bradykinin and histamine
- Releases with injury, triggering free nerve endings, ↑ pain
- Triggers the inflammatory response (2), until:• Stimulus is removed
- Inflammatory mediators are eliminated
Vascular Response
Cellular Response
What is the importance of understanding the healing process?
- The clinician must recognize the signs and symptoms associated with different healing phases to be effective in incorporating the right treatment (e.g., exercise, modality) at the right time and in the right patient
- Understand the: physiological responses of the tissue to injury expected timing of each phase identification of something not right
What are the three things that cartilage does to resist load? What does compression do? What does varied orientations of fibers do?
• To resist load…
Stress developed in the fibrillar portion of ECM
Swelling pressures developed in the interstitial fluid
Frictional drag resulting from fluid flow through the ECM
- Compression reduces volume and increases pressure to push fluid out (rapid initial deformation becoming gradual and stops)
- Varied orientation of fibers through zones creates non-linear behaviour
What is the extracellular matrix composed of (ECM)? What are its roles?
Non-fibrous component (Glycoproteins & Proteoglycans)
- Attracting and binding water
- Supporting substance for fibrous and cellular components
- Contributes to overall strength of connective tissue thereby protecting it
What is a musculotendinous junction?
Muscle cells intertwine with the tendon
Very sensitive to mechanical conditions and becomes flatter with low load
Weakens the junction increasing susceptibility to injury
Loading caution post-immobilization
Describe what happens during the cross bridge cycle.
What are the five types of abnormal end feels? Give a brief description and an example for each.
Empty – movement stopped by pain before resistance is felt (e.g., 10/10 pain)
Spasm – involuntary, vibrant twang (e.g., recent #)
Springy Block – unexpected rebound, non-capsular pattern restriction (e.g., tear)
Abnormal Bone to Bone – early abrupt stop, crepitus or grating (e.g., post- immobilization)
Abnormal Capsular – early hard-ish stop before end range (e.g., frozen shoulder)
Describe the basics of bone breakdown. How can microtraumas, fractures, and osteogenesis (fragile bone) happend?
Cortical bone stays well within the elastic region of the load-deform curve (very little deformation)
Sustained, repetitive loads over time -> microtrauma (happens with a poor balance of activity and rest)
Abrupt, high loads -> fracture
Absent mechanical forces -> osteogenesis (fragile bone)
How does homeostasis affect the inflammatory response during tissue healing?
- Within seconds, to stop blood loss
- Reflexive and transient vasoconstriction (decrease vessel size) -> allows the platelets to build up at the site of the injury, behind the vasoconstriction, and they start binding to the collagen, which generates a snowball effect to recruit more collagen
- Clot formation
- Adhesive platelets – to collagen molecules exposed by injury
- Plug formation – accumulated platelets
Describe the anatomy of a contractile unit (sarcomere).
- The arrangement is regular to give stripped appearance “striated muscle”
- (I) only actin, (A) actin and myosin (H) only myosin
Which type of bone withstands greater force with less deformation than the other?
• Cortical bone withstands greater force with less deformation than cancellous bone
Give some examples of types of bone fractures.
What is a capsular pattern of restriction? In what kind of joints can this occur? What happens and what does this suggest? How is a capsular pattern of restriction determined?
A characteristic pattern of expected proportional limitation of movement, specific to a particular joint
Exists only in those joints controlled by muscle, which have a joint capsule and are lined by a synovial membrane
Suggests that the entire capsule and/or synovial membrane of the joint is involved
Total joint reaction (e.g., post-immobilization)
Determined by passive movements
How can corticosteroids and NSAIDs negaitvely impact tissues.
Corticosteroids
Weakening of passive tissue with prolonged use. Abnormal turnover of collagen fibers
Non-steroidal anti-inflammatory drugs (NSAIDs)
Interference with the healing process. Resultant healed tissue potentially weaker than if no NSAIDs consumed
