Soft Tissue Concepts

Mr R van Bever Donker

What are Soft Tissues?

• 4 groups
– Muscle
– Nerve
– Connective Tissue
– Epithelial tissue

MUSCLES

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 Muscles
• 3 types of muscle:

– Voluntary – skeletal / striated muscle

– Involuntary – smooth / unstriated

– Cardiac muscle

Muscles
• Skeletal muscle
– Consists of both contractile and non-contractile
tissue
– Mm fibers surrounded by CT membrane called
endomysium
– Muscle fiber bundles (fascicles) bound together by
tougher CT envelope called perimysium
– Whole muscle covered by course sheet called
epimysium

Muscles

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 Muscles
• All the CT in a muscle is continuous with the
tendon – each fiber pulls on the tendon
– Tendon – a strong cord from mm to the fibrous
periostium
– Aponeurosis – same CT but merges with CT of
another muscle

Muscles
• Tension in muscles:
– Active tension – contractile components
– Passive tension – parallel connective tissue
structures
– A tendon however is only under tension when the
muscle is in a shortened state i.e. during
contraction
– Mid-ROM is optimal sarcomere length therefor
strongest contraction – mm testing

Muscles
• Tension in muscles:
– Governed by the golgi tendon organ, the muscle
spindle and joint receptors. Together they protect the
muscle by constantly monitoring changes in muscle
length
• The golgi tendon organs are in the tendon and are activated
by an active contraction of the muscle or excessive passive
stretch – they tell the nervous system to inhibit the muscle.
• The muscle spindles are sensitive to stretch eg tendon reflex
• Joint capsule and ligament receptors can influence the
muscle activity eg pain and swelling.

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 Muscles
• Fiber types
– Type 1 – slow twitch; resistant to fatigue, slow
contraction velocity
– Type 2a – intermediate; fast contraction velocity
but resistant to fatigue
– Type 2b – fast twitch; fast contraction velocity,
fatigues easily
• Distribution in a muscle varies depending on
function

Muscles
• Motor unit
– Motor neuron to the fibers that axon innervates
– Also fast and slow twitch motor units
– Some are large (more fibers) others are small
(fewer fibers) depending on function, training etc
– When a motor unit is activated all the fibers in
that unit contract
– Degree of desired contraction in a mm is regulated
through the activation (or not) of motor units in a
motor pool

Muscle Physiology
• Physiology of muscle action – excitation and
contraction
– Impulse from motor neuron triggers
neurotransmitter acetylcholine
– Acetylcholine crosses neuromuscular junction and
binds to receptors on motor endplate of fiber
– Stimulation of acetylcholine receptors initiates an
impulse along sarcolemma through T tubules to
sarcoplasmic reticulum (SR)

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 Muscle Physiology
• Excitation and contraction
– Ca++ is released from SR into sarcoplasm, where it
binds to troponin molecules in the thin myofilaments
– Tropomysin molecules in the thin myofilaments shift,
exposing actin’s active sites
– Energized myosin cross bridges of the thick
myofilaments bind to actin, and use their energy to
pull the thin myofilaments towards the centre of each
sarcomere. This cycle repeats many times per second
as long as there is ATP

Muscle Physiology
• Excitation and contraction
– As the thin filaments slide past the thick
myofilaments, the entire muscle fiber shortens

Muscle Physiology

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 Muscle Physiology
• Relaxation
– After impulse is over, the SR begins actively
pumping Ca++ back into its sacs
– As Ca++ is stripped from troponin molecules in the
thin myofilaments, tropomyosin returns to its
position, blocking actin’s active sites

Muscle Physiology
• Relaxation
– Myosin cross bridges are prevented from binding
to actin and thus can no longer sustain the
contraction
– Thick and thin myofilaments no longer connected,
muscle fiber returns to its longer resting length

Muscle Physiology

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 CONNECTIVE
TISSUE

Connective Tissue
• Four classes of connective tissue:
– Connective tissue proper
– Cartilage
– Bone
– Blood

Connective Tissue
• Connective tissue make-up
– Cells
– Extracellular matrix
• Fibrillar Component
• Interfibrillar Component

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 Connective Tissue
• Cells
– Fibroblasts
• basic cell of most connective tissue
• Produces extracellular matrix
• Specialise into – chondroblasts (cartilage), tenoblasts
(tendon), osteoblasts (bone) – once mature and less
metabolically active they become chondrocytes,
tenocytes and osteocytes

Connective Tissue
• Extracellular Matrix (outside cells)
– Determines the tissues function
– Contains mostly protein and water
– As mentioned before – fibrillar and interfibrillar
components

Connective Tissue
• Fibrillar (fibrous) component
– Contains 2 major classes of protein
• Collagen
– resists tensile forces, tensile strength of steel
– Type I – found almost everywhere, gives tensile strength
– Type II – cartilage and intervertebral discs
– Type III – skin, joint capsules, muscle and tendon
sheaths, and in heeling tissues
• Elastin
– allows tissue to stretch, varied amount depending on
function
– Example: ligamentum nuchae = 75% elastic + 15%
collagen, achilles tendon = 4.4% elastin + 86% collagen

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 Connective Tissue
• Interfibrillar
– Contains water and proteins
– These proteins are fundamental in the healing process
------------------------------------------

– Collagen type, cross-links, protein type and amount

are affected by type and amount of stress applied

– For a detailed description of connective tissue,

specific structural differences, make-up and response
to loading see Joint Structure and function pg 67 – 87
(see reference list)

HEALING

Physiology and Healing

• Management of healing soft tissue structures
– Evidence points to carefully graded mobilisation of
soft tissues to restore tensile strength and
functional biomechanical properties
– SSTM is a standardised, more sensitive and
specific use of manual therapy to treat benign soft
tissue disorders

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 Physiology and Healing
• Soft tissues have a tensile load threshold
• After tissue overload the tolerable amount of
force decreases, therefor treatment has a major
emphasis on promoting tissue’s ability to adapt to
the forces demanded by functional activities
• To achieve this the T must perform a detailed
assessment, specifically and progressively load
affected tissues and restore optimal kinetic
control

Physiology and Healing

• Biomechanical properties
– Stress / strain to failure

Physiology and Healing

• Biomechanical properties
1. Toe region
2. Linear region
3. Fibre failure
4. Ultimate failure point

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 Physiology and Healing
• Biomechanical properties
– The stress strain curve

Physiology and Healing

• Biomechanical properties
– Stress strain curve
• The steeper the line the more stiff the tissue, and the
more resistance is felt on tensioning. It depicts not only
the final failure point, but also the rate of tensioning
• The area under the line determines the amount of
energy stored in the tissue. We aim to increase this
value in order to improve the tissues ability to
withstand stress
• Above 2 points influenced by tissue viscoelastic
properties. Strain=rate of loading.

Physiology and Healing

• Biomechanical properties
– Stress strain curve
• Elastic (return to original) – plastic (permanent
deformation)
• Hysteresis occurs in viscoelastic materials – energy is
lost during stretch and return cycles due to mechanical
damage and internal friction – reduces stiffness
• Creep is continued deformation at a fixed load. Low
load and long duration

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 Physiology and Healing
• Tissue healing can be divided into 3 stages
– Inflammatory
– Fibroblastic
– Remodeling
• There is no clear and definite time frame but
there are guidelines

Physiology and Healing

• Inflammatory Phase
– Last for 4 – 6 days
– Revascularisation in preparation for fibroblastic phase
– Weak Type III fibrin – to try and stabilise the area but
it is very vulnerable
• Management
– PRICE
– Ice may prevent secondary hypoxia, U/S may be useful

Physiology and Healing

• Fibroblastic Phase
– Collagen synthesis: Type I – strong for scar tissue
– Random orientation of fibres that restore structure
but hamper function
– Cross-linkage increase – provides more stability
• Management:
– Careful tensioning (SSTM) of healing tissue orientates
fibres along lines of stress, improves collagen
synthesis, increase cross-linkage formation
– This increases tensile strength and reduces healing
time

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 Physiology and Healing
• Remodelling Phase
– Improved tensile strength due to cross linkage
formation between collagen fibres – maturation of
process started in fibroblastic phase
– Tissue is stiffer and less likely to tolerate
functional stresses
– Synthesis-lysis balance
• Management
– SSTM promotes viscoelastic properties by use of
hysteresis, creep and plastic deformation

MANAGEMENT

SSTM’S

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 SSTM’s
• Different aims during different stages of
healing
• After Inflammatory stage the aim is to
promote collagen synthesis, orientation and
bond stability
• Thereafter- alter mechanical properties
especially its viscoelastic response to loading,
based on principles of hysteresis, creep and
plastic deformation

SSTM’s
• There are many variations on how to execute
the SSTM’s but we will follow Hunter’s
method
• Hunter (1998) suggests the following:
– Physiological SSTM
– Accessory SSTM
– Combined SSTM

SSTM’s
• Physiological SSTM
– Physiological joint movement is used to place a
tensile load to the affected muscle fibres
– NB to assess joints over which the injured tissue
acts
– Different combinations of joint movement address
different soft tissue structures – this is not uniaxial
movement. E.g. semi-T
– From supported to most tension position

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 SSTM’s
• Physiological SSTM
– All areas of the soft tissue need to be subjected to
varying combinations of tension
– Once this is achieved, then sufficient tensile
strength to progress
– Different combinations of movement tension
differently, e.g. hamstrings
– Ensure proximal stability is maintained. E.g AIRs
– Also used for ligaments
– Can add accessory joint glides

SSTM’s
• Accessory SSTM
– Applied at 90 ᵒ to the injured tissue and along the
same plane
– DTF apply compressive force, SSTM applies a
displacing force and thereby a longitudinal tension at
the site
– This allows effective assessment of quality of motion,
range and extensibility of tissues as well as what
might be limiting these
– Also, allows to feel what grade can be used at what
stage

SSTM’s
• Image from Hunter (1998)

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 SSTM’s
• Combined SSTM
– Initially SSTM is applied to tissues in relaxed
position, but later with increasing tension
– This tension is formed by performing isometric,
concentric or eccentric muscle actions while
performing SSTM
– It is a combination of physiological SSTM and
accessory SSTM

SSTM’s
• Technique
– Enough force to promote adaptation but not
failure
– Under guidance of SIN and re-assessment
– An oscillatory force is used for first 6-11 days in
mild-moderate lesions to facilitate dispersal of
exudate and gently tension (GrI+II)
– Later, a sustained, slower oscillation is used into
resistance (GrIII -/+ or GrIV) to promote hysteresis,
creep and plastic deformation

SSTM’s
• Technique
– Assess all directions of force and apply treatment
based on physiological response and reassessment
– Stages of progression
1. Physiological / accessory SSTM (GrI/II)
2. Physiological SSTM with more stressing combinations
3. Sustained accessory SSTM, prolonged (GrIII/IV)
4. Physiological SSTM with proximal stabilisation (AIRs)
5. Accessory SSTM with stretch, isometric then resistance
through range

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 MYOFASCIAL
TRIGGER
POINTS

Myofascial Trigger points

• Abbreviated as “MTrP”
• Definition:
– “a hyperirritable spot in skeletal muscle that is
associated with a hypersensitive palpable nodule in a
taut band”
• Classified into active and latent trigger points
– Active – symptom-producing MTrP with local or
referred symptoms
– Latent – only triggers pain when stimulated
• Both active and latent MTrPs are painfull on
compression

Myofascial Trigger points

• Clinical presentation:
– Motor aspects
• Disturbed motor function, mm weakness d/t inhibition,
mm stiffness, restricted ROM
– Sensory aspects
• Local tenderness, referred pain, central and peripheral
sensitisation
– Autonomic components
• Vasoconstriction, vasodilation, lacrimation,
pyloerection

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 Myofascial Trigger points
• Clinical presentation:
– Detailed clinical history, examination of movement
patterns and referred pain patterns can assist in
determining the affected muscle
– Referred pain is Somatic
– In palpation – flat or pincer palpation
– Difference between tender point and MTrP is
MTrP tender point along a tight band in the
muscle. MUST have both

Myofascial Trigger points

• Clinical presentation
– Taught band vs. spasm
– Spasm – increased neuromuscular tone of the
entire muscle, due to nerve-initiated contraction
– Taught band – localised contracture within the
muscle without activation of the motor endplate

Myofascial Trigger points

• Clinical Presentation:
– Local twitch response (LTR) – spinal reflex unique
to MTrP
– LTR is a sudden contraction of fibres within the
taught band when is is stimulated manually
– If LTR is elicited the prognosis is better

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 Myofascial Trigger points
• Key points in palpation
– Reproduction of patient symptoms
– Tender point in taught band
– Somatic referred pain / parasthesia / burning
sensation
– Local twitch response
– Can be a 10-15 second delay in above symptom
reproduction

Myofascial Trigger points

• Clinical presentation:
– Normally skeletal mm nociceptors require high
intensity stimulation and do not respond to
moderate pressure
– MTrPs, however, cause persistent noxious
stimulation which results in an increase in number
of and size of the nociceptor receptor fields, to
which a single neuron in the dorsal horn responds.
This convergence is how referred pain is felt.

Myofascial Trigger points

• Etiology (Dommerholt et al, 2006):
– Low-level muscle contractions “Cinderella
Hypothesis”
– Intramuscular pressure distribution “Otten’s
model”
– Direct trauma (eg WAD) “energy crisis hypothesis”
– Eccentric and (sub)maximal concentric
contractions “weak muscle injury / overload”

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 Myofascial Trigger points

Travell and Simons’ “energy crisis hypothesis”

Myofascial Trigger points

• Integrated Trigger Point Hypothesis
– Evolved from the “energy crisis hypothesis”
– Has a better evidence base

– MTrPs have EMG discharges called “spontaneous

electrical activity” (SEA)
– SEA is in fact end-plate noise (EPN) and is
commonly found close to the endplates of MTrPs
and much less elsewhere in mm

Myofascial Trigger points

• Integrated Trigger Point Hypothesis
– Discharges most likely due to excessive release of
Acetylcholine (Ach), hence indicative of dysfunctional
motor endplates
– Excessive Ach affects the voltage gated Sodium Channels in
sarcoplasmic reticulum which increases intracellular Ca
levels - sustained mm contractures
– Myosin filaments get STUCK in Z-band of the sarcomere
– The relative shortage of ATP may also maintain the
contracture as ATP is essential in breaking down cross
bridges betw. actin and myosin filaments to allow release

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 Myofascial Trigger points
• Integrated Trigger Point Hypothesis
– Simultaneously, the shortened sarcomere
compromises circulation causing ischaemia
– Hypoxia causes release of sensitizing substances
making nociceptors more sensitive
– Combined mechanical and chemical stimuli may cause
• Peripheral sensitization
• Central sensitization
• Resultant hyperalgesia
• Referred pain

Myofascial Trigger points

• Integrated Trigger Point Hypothesis
– The motor and sensory components of MTrPs are
more understood but autonomic components not
so
– Examples:
• When stressed a subject feels more pain in MTrP than
when autogenic relaxation is performed
• Sympathetic nervous system activity blocked with
Phentolamine the electrical activity in MTrPs is reduced

Myofascial Trigger points

• Perpetuating factors
– Mechanical
– Metabolic
– Nutritional
– psychological

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 Myofascial Trigger points
• Mechanical perpetuating factors
– Postural syndromes, skeletal disorders (scoliosis,
leg length), kinematic issues (overuse syndromes),
ergonomic issues, joint issues

– It is important to note that MTrPs may be

secondary to metabolic, nutritional, psychological
and careful assessment and necessary referral
may be required

References
• Simons D, Travell J, Simons L, (1999). Myofascial Pain
and Dysfunction, the Trigger Point Manual: Vol 1,
Upper Half of Body. Philadelphia: Williams and Wilkins
• Dommerholt J, Bron C, Franssen j, (2006) Myofascial
trigger points: an evidence informed review, Journal of
manual and manipulative therapy, Vol 14, no 4 203-221
• McArdle W, Katch F, Katch V, (1996). Exercise
Physiology, energy, nutrition and human performance.
Baltimore: Williams and Wilkins
• Hunter G, (1998) Specific soft tissue mobilisation in the
management of soft tissue dysfunction, Manual
Therapy, 3, 2-11

References
• Patton T, (1996) Anatomy and Physiology, Third edition.
St. Louis: Mosby-year Book, Inc
• Levangie P, Norkin C, (2011) Joint structure and
function, a comprehensive Analysis Fifth Edition.
Philadelphia: FA Davis company
• Petty N, (2006) Neuromusculoskeletal examination and
assessment, third edition Philadelphia: Elsevier
• Travell J, Simons D, (1993). Myofascial Pain and
Dysfunction, the Trigger Point Manual: Volume 2, the
lower extremities. Philadelphia: Lippincott Williams
and Wilkins

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