1st talk in Tønsberg by Christoph Schmitz

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Molecular and cellular mechanisms of
radial shock wave therapy
Dr. Christoph Schmitz, MD
Full Professor and Head
Department of Neuroanatomy, Ludwig-Maximilians-University
Munich, Germany
Adjunct Professor
Department of Neuroscience, Mount Sinai School of Medicine
New York, NY, USA
Medical Scientific Officer
EMS Electro Medical Systems
Nyon, Switzerland
Example: calcifying tendinitis of the shoulder
2
Vavken et al. (2009)
Don‘t compare apples with pies...
3
Compare within the same settings...
4
A treatment modality becomes successful when...
we know how it works
we know that it works
we know why it works
your patients become enthusiastic about it!
Enthusiastic patients – successful practice!
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A happy patient...
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A patient... (at Home Depot Stadium, Los Angeles, CA, USA on July 19, 2009)
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A happy patient...
8
RSWT® at AC Milan
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(www.acmilan.com/InfoPage.aspx?id=41293)
RSWT® at AC Milan
(www.acmilan.com/InfoPage.aspx?id=41293)
Objectives:
• to optimising the team‘s results
• to enable athletes to achieve the most optimum
performance possible, to reduce the risk of injury,
and […]
10
Milanello Training Center, Carvado, Italy, on April 26, 2011
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What are shock waves?
 Wikipedia:
 A shock wave (also called shock front or simply "shock") is a type of
propagating disturbance. Like an ordinary wave, it carries energy
and can propagate through a medium (solid, liquid or gas) [...].
Shock waves are characterized by an abrupt, nearly discontinuous
change in the characteristics of the medium. Across a shock there
is always an extremely rapid rise in pressure, temperature and
density of the flow. [...] A shock wave travels through most
media at a higher speed than an ordinary wave.
12
What are shock waves?
 Encyclopedia Britannica online:
 a „[...] strong pressure wave in any elastic medium such as air,
water, or a solid substance, produced by supersonic aircraft,
explosions, lightning, or other phenomena that create violent
changes in pressure. Shock waves differ from sound waves in that
the wave front, in which compression takes place, is a region of
sudden and violent change in stress, density, and temperature.
Because of this, shock waves propagate in a manner different from
that of ordinary acoustic waves. In particular, shock waves travel
faster than sound, and their speed increases as the amplitude is
raised; but the intensity of a shock wave also decreases faster than
does that of a sound wave, because some of the energy of the
shock wave is expended to heat the medium in which it travels."
13
What are therapeutic shock waves? – Ogden et al. (2001)
Characteristics of therapeutic shock waves (1)
(Source: Ogden JA, Tóth-Kischkat A, Schultheiss R: Principles of Shock Wave Therapy. Clin Orthop Relat Res 2001 [387] 8-17)
Typical form of a therapeutic shock wave
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What are therapeutic shock waves?
 Ogden et al., Clin Orthop Rel Res 2001;(387):8-17:
 “A shock wave is a sonic pulse that has certain physical
characteristics. There is a high peak pressure, sometimes more
than 100 MPa (500 bar), but more often approximately 50 to 80
MPa, a fast initial rise in pressure during a period of less than
10 ns, a low tensile amplitude (up to 10 MPa), a short life cycle of
approximately 10 µs, and a broad frequency spectrum, typically in
the range of 16 Hz to 20 MHz.”
 Shrivastava and Kailash, J Biosci 2005;30:269-275:
 “Shock waves are characterized by high positive pressure, a rise
time lower than 10 ns and a tensile wave.”
15
Generation of therapeutic shock waves
Four principles to generate therapeutic shock waves
electrohydraulic
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Ossatron
Orbason
Orthospec
piezo-electric
electromagnetic
pneumatic
Epos Ultra
Sonocur
Swiss Dolorclast
D-ACTOR
Generation of therapeutic shock waves
Mode of operation of radial shock wave devices
(Swiss Dolorclast)
Schematic representation of the mode of operation of the handpiece of the Swiss
Dolorclast. Compressed air is used to fire a projectile within a guiding tube that
strikes a metal applicator placed on the skin. The projectile generates stress
waves in the applicator that transmit pressure waves into tissue.
17
Therapeutic shock waves generated with the Dolorclast
(Source: Chitnis PV, Cleveland RO: Acoustic and cavitation fields of shock wave therapy devices. In: Clement GT, McDannold
NJ, Hynynen K: CP829, Therapeutic Ultrasound: 5th international symposium on therapeutic ultrasound. 2006, American
Institute of Physics.)
Ogden et al. (2001): “[...] a high peak pressure, sometimes more than 100 MPa
(500 bar), but more often approximately 50 to 80 MPa, a fast initial rise in
pressure during a period of less than 10 ns, a low tensile amplitude (up to 10
MPa), a short life cycle of approximately 10 µs, and [...].”
18
Generation of therapeutic shock waves
Four principles to generate therapeutic shock waves
electrohydraulic
19
Ossatron
Orbason
Orthospec
piezo-electric
electromagnetic
pneumatic
Epos Ultra
Sonocur
Swiss Dolorclast
D-ACTOR
Therapeutic shock waves generated with the Ossatron
(Source: Chitnis PV, Cleveland RO: Acoustic and cavitation fields of shock wave
therapy devices. In: Clement GT, McDannold NJ, Hynynen K: CP829, Therapeutic Ultrasound: 5th international symposium on
therapeutic ultrasound. 2006, American Institute of Physics.)
Ogden et al. (2001): “[...] a high peak pressure, sometimes more than 100 MPa
(500 bar), but more often approximately 50 to 80 MPa, a fast initial rise in
pressure during a period of less than 10 ns, a low tensile amplitude (up to 10
MPa), a short life cycle of approximately 10 µs, and [...].”
20
Therapeutic shock waves generated with the Orthospec
(Source:www.accessdata.fda.gov/cdrh_docs/pdf4/P040026b.pdf)
“In order to measure the rise time and pulse
duration of the shock waveform, the
measurement was repeated with the
oscilloscope sampling rate increased to 100
Msmp/s. From a series of measurements,
the average rise time was 400±100 ns; the
average pulse width was 1200+45 ns.”
Ogden et al. (2001): “[...] a high peak pressure, sometimes more than 100 MPa
(500 bar), but more often approximately 50 to 80 MPa, a fast initial rise in
pressure during a period of less than 10 ns, a low tensile amplitude (up to 10
MPa), a short life cycle of approximately 10 µs, and [...].”
21
Generation of therapeutic shock waves
Four principles to generate therapeutic shock waves
electrohydraulic
22
Ossatron
Orbason
Orthospec
piezo-electric
electromagnetic
pneumatic
Epos Ultra
Sonocur
Swiss Dolorclast
D-ACTOR
Therapeutic shock waves generated with the Epos
(Source: EMS, unpublished data)
Energy level 5
Ogden et al. (2001): “[...] a high peak pressure, sometimes more than 100 MPa
(500 bar), but more often approximately 50 to 80 MPa, a fast initial rise in
pressure during a period of less than 10 ns, a low tensile amplitude (up to 10
MPa), a short life cycle of approximately 10 µs, and [...].”
23
Generation of therapeutic shock waves
Four principles to generate therapeutic shock waves
electrohydraulic
24
Ossatron
Orbason
Orthospec
piezo-electric
electromagnetic
pneumatic
Epos Ultra
Sonocur
Swiss Dolorclast
D-ACTOR
What are therapeutic shock waves? – Ueberle et al. (2007)
Hopkins effect (Vakil 1991)
25
What are therapeutic shock waves? – Rompe et al. (2007)
Characteristics of therapeutic shock waves (2)
(Source: Rompe JD, Furia J, Weil L, Maffulli N: Shock wave therapy for chronic plantar fasciopathy.
Br Med Bull 2007;81-82:183-208)
Typical form of a therapeutic shock wave used in pain management
26
Generation of therapeutic shock waves
Four principles to generate therapeutic shock waves
electrohydraulic
27
Ossatron
Orbason
Orthospec
piezo-electric
electromagnetic
pneumatic
Epos Ultra
Sonocur
Swiss Dolorclast
D-ACTOR
Therapeutic relevant part of shock waves (1)
"A significant tissue effect is cavitation consequent to the
negative phase of the wave propagation."
(Ogden et al., 2001)
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Therapeutic relevant part of shock waves (2)
„[...] Bioeffects of shock waves on nervous tissue appear to
result from cavitation. It is suggested that cavitation is also
the underlying mechanism of shock wave-related pain
during extracorporeal SW lithotripsy in clinical medicine.”
(Schelling et al., Biophys J 1994;66:133-140)
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Therapeutic relevant part of shock waves (3)
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Therapeutic relevant part of shock waves (4)
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Focused shock waves (2)
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Radial shock waves (EMS Swiss DolorClast®)
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ESWT: basic physics (1)
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ESWT: basic physics (2)
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Orthopaedic indications for ESWT (1)
Tennis elbow
(Epicondilitis
humeri radialis)
Greater trochanteric
pain syndrome
Patellar tip syndrome
Plantar fasciopathy
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Subacromial pain
syndrome
Golfer‘s elbow
(epicondylitis
humeri ulnaris)
Medial tibial stress
syndrome
Achilles
tendinopathy
Orthopaedic indications for ESWT (2)
Common extensor tendon
Supraspinatus tendon
Patella tendon
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Achilles tendon
Plantar fascia
RSWT®: RCTs with positive outcome
Chronic plantar fasciopathy:
•Gerdesmeyer et al., Am J Sports Med 2008; 36: 2100-2109
•Chow and Cheing, Clin Rehab 2007;21: 131-141
•Greve et al., Clinics 2009; 64: 97-103
Midportion Achilles tendinopathy:
•Rompe et al., Am J Sports Med 2007;35:374-381
•Rompe et al., Am J Sports Med 2009;37:463-470
Insertion Achilles tendinopathy:
•Rompe et al., Am J Bone Joint Surg 2008;90:52-61
Medial tibial stress syndrome:
•Rompe et al., Am J Sports Med 2009 [Epub Sep 23]
Greater trochanteric pain syndrome:
•Furia et al., Am J Sports Med 2009;37:1806-1813
•Rompe et al., Am J Sports Med 2009;37:1981-1990
Subacromial pain syndrome:
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•Engebretsen et al., Brit Med J 2009:339:b3360
ESWT: molecular and cellular mechanisms of action
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Wang, ISMST Newsletter 2006-03
Don’t forget neurogenic inflammation...
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ESWT: molecular and cellular mechanisms of action
 Pain
 Neurogenic inflammation
 New bone formation
 ...
41
175
Substance P (pg/ml)
Substance P (pg/ml)
Substance P in periost after ESWT
150
six hours after
shock wave application
125
100
75
50
25
0
1
2
3
4
5
1000
one day after
shock wave application
500
0
6
1
2
Substance P (pg/ml)
4
5
6
No. of eluation tubes
No. of eluation tubes
2000
42 days after
shock wave application
1000
0
1
2
3
4
5
No. of eluation tubes
42
3
6
Clin Orthop Relat Res (2003)
ESWT: mechanisms of action (pain)
43
Substance P, pain and inflammation
Pain afferents: myelinated or unmyelinated.
Myelinated pain fibers: A-delta fibers:
• respond to either mechanical stimuli or temperature stimuli
in the painful realm
• produces the acute sensation of sharp, bright pain
• neurotransmitter in the dorsal horn: glutamate
• receptor: AMPA receptors
Unmyelinated pain fibers: C fibers:
• respond to a broad range of painful stimuli, including
mechanical, thermal or metabolic factors.
• produce slow, burning, and long lasting pain.
• neurotranmitter in the dorsal horn: glutamate along with
certain peptides such as substance P
• receptors: AMPA but also NMDA (only open following
prolonged depolarization),
Continual stimulation of C fibers eventually causes greater
excitation in the postsynaptic neurons in the dorsal horn as
the NMDA receptors start added to the response.
Receptor for capsaicin: located in the C fibers (normally
opened by hot stimuli).
C fibers: interconnected with the process of inflammation by
axon reflex (action potentials in certain branches of an
afferent neuron moving peripherally).
Release of substance P there increases inflammation by
causing histamine release and dilation of blood vessels.
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Substance P, pain and inflammation
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ESWT: mechanisms of action (pain)
Prolonged activation of pain and heat sensing neurons (unmyelinated C
fibers) by capsaicin depletes presynaptic substance P, one of the body's
neurotransmitters for pain and heat. The result appears to be that
capsaicin mimics a burning sensation, the nerves are overwhelmed by the
influx, and are unable to report pain for an extended period of time. With
chronic exposure to capsaicin, neurons are depleted of neurotransmitters
and it leads to reduction in sensation of pain and blockade of neurogenic
inflammation. If capsaicin is removed, the neurons recover.
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Selective loss of nerve fibers after ESWT
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Emerging results from basic research
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ESWT: basic physics - cavitation
Which part of shock waves mediates their biological
efffects on tissue?
"A significant tissue effect is cavitation consequent to the
negative phase of the wave propagation."
(Ogden et al., 2001)
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Activation of the G-protein coupled receptor
Transcription
Progression of
cell cycle
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51
ESWT: mechanisms of action
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J Trauma 2008;65:1402-1410
ESWT: mechanisms of action
Results of microarray studies
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J Trauma 2008;65:1402-1410
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