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Low Level Laser Therapy Mary Dyson PhD, FCSP Emeritus Reader in the Biology of Tissue Repair, Former Professor, Department of Physical Therapy
& Rehabilitation Sciences, University of Kansas Medical Center, Kansas
City, USA. INTRODUCTION Low level laser therapy (LLLT) is widely used to accelerate
tissue repair including wound healing.
It is also used to alleviate skin conditions such as acne (Hirsch and
Shalita, 2003) and scarring (Patel and Clement 2002). These conditions involve tissue injury,
sometimes acquired many years ago. Their
improvement is achieved by tissue repair, which can be initiated and stimulated
by exposure to low intensities of red light and to some other forms of
electromagnetic radiation such as infrared (IR) electromagnetic radiation.
Exposure to red light increases blood flow to the skin thus improving its
metabolism and stimulates the manufacture of collagen, the protein that gives
strength to the skin (Bjerring et al 2002). Other uses of red light and
infrared irradiation include accelerating the resolution of inflammation (Dyson
2004) and the reduction of pain (Moore et al 1988; Chow and Barnsley 2005). The laser technique used
to deliver this light is usually termed low level laser therapy (LLLT),
also referred to as low intensity laser therapy (LILT), low energy
photon therapy (LEPT) and phototherapy. Unlike the high intensity medical lasers used
to cut and coagulate tissues, LLLT involves the use of medical lasers such as
the Beurer SoftLaserTM and Laser Therapeutics SL50 Cluster Laser that
operate at intensities too low to damage living tissues. Unlike most LLLT
devices that are relatively large and designed for clinical use, the Beurer
SoftLaserTM is a small, single-diode, hand held device emitting red
light and designed for home use. The
Laser Therapeutics SL50 Cluster Laser consists of twelve laser diodes combined
in a treatment head but smaller than the devices designed for clinical use.
These devices are now available for home use; the Laser Therapeutics Inc. SL50 Cluster
Laser is an example of a cluster probe suitable for home use. It contains 8
laser diodes that emit red light at 640-660 nm and 4 laser diodes that emit
infrared (IR) electromagnetic radiation at 775-795 nm.   Wound
healing can be stimulated by photons from the visible and infrared parts of the
electromagnetic spectrum when applied to the skin and mucous membranes by low
level lasers and light-emitting diodes (LEDs) at appropriate wavelengths,
powers and durations. When absorbed these photons induce cellular changes which
accelerate tissue repair (Fulop et al 2009) and relieve pain (Chow, Barnsley
2005). Changes induced by photons in immune cells and stem cells assist in the
acceleration of wound healing (Dyson 2008); changes induced in nerve conduction
assist in the short term relief of pain (Baxter 1994) LIGHT Light consists of photons transmitted at wavelengths of the
electromagnetic spectrum that are visible to the human eye. This part of the spectrum
extends from violet to red. Infrared (IR) is just beyond the visible range. The
perceived colour depends on the wavelength. White light is a mixture of all the
visible wavelengths. For photons to reach the skin, all that is required is
that it be either exposed to air or to be covered by a transparent dressing.
Exposure to red light and/or infrared radiation can stimulate the healing of
both chronic injuries of the skin (Mester et al 1985) and acute injuries (Dyson
& Young 1986). Photons are
quanta of electromagnetic radiation that originate in the burning gases of the
sun. They have zero mass, are
electrically neutral, behave both as particles and as waves and are pure
energy. When they are absorbed this
energy is transferred to the chemicals that absorb them, for example
cytochromes (coloured materials present in all cells). Absorption of photons by cytochrome C
oxidase in mitochondria increases the
amount of energy-rich ATP the mitochondria
produce, (Karu 1988) and also temporarily increases cell membrane
permeability to calcium ions, the latter acting as a stimulus for cell activity
(Young et al 1990). Depending on their
type and metabolic status, the cells are induced to proliferate, manufacture
proteins, secrete mediators, contract, conduct, phagocytose pathogens or kill
cancer cells. Following absorption,
photons trigger metabolic activities that stimulate wound healing and relieve
pain. They can be delivered in effective
wavelengths and doses by low level laser therapy (LLLT) devices (Tuner, Hode
2002). LASER This is an acronym for Light
Amplification by the Stimulated Emission of Radiation.
The stimulated emission of radiation occurs when a photon interacts with an
energized atom. When an atom is energized, for example by electricity, one of
its electrons is excited, i.e. raised to a higher energy orbit than its orbit
when in the resting state. If the energy
of the incident photon is equal to the energy difference between the electron’s
excited and resting states, then stimulated emission of a photon occurs and the
excited electron returns to its resting state. This photon has the same
properties as the incident photon, which is also emitted. This process is repeated in the adjacent
energized atoms, producing a laser beam. Unlike light from non-laser sources,
this light is: ·
Monochromatic,
i.e. of a single wavelength ·
Collimated,
i.e. its light rays are non-divergent ·
Coherent,
i.e. in phase, the troughs and peaks of the waves coincide in time and space. With regard to the biomedical effects of LLLT, wavelength
is particularly important. To produce an effect, the light must be absorbed,
and absorption is wavelength-specific. Different substances absorb light of
different wavelengths. Mitochondria, present in all mammalian cells except
erythrocytes, contain cytochromes that absorb red light. Light
emitting diodes emitting effective wavelengths are now often used instead of
the more expensive lasers, making phototherapy more economical. Light
could now be substituted for Laser in the LLLT acronym. Only low powers (5-500 milliwatts) are required for
effectiveness. The duration for which the photons are applied is clinically
important because there is a temporal window of effectiveness. Within this
window longer treatments are more effective than shorter treatments in
accelerating healing, probably because they allow more of the circulating
immune cells and stem cells of the body to be exposed to photons. Energy (power x duration) doses of 4-20
Joules/cm2 are usually effective in stimulating wound healing and
relieving pain (Tuner, Hode 2002). Generally red or infrared electromagnetic radiation is
employed using either single-diode probes to irradiate small areas such as
acupuncture points and trigger points or cluster probes to irradiate larger
areas such as wounds or joints. LLLT
EQUIPMENT This has three essential components: 1.
Lasing medium, which is capable of being energized
sufficiently for light amplification by the stimulated emission of radiation to
occur 2.
Resonating cavity containing the lasing medium 3.
Power source that transmits energy into the lasing medium. The
type of lasing medium used determines the wavelength, and therefore the
colour, of the laser beam. For example, a HeNe laser, in which the lasing
medium is a mixture of helium and neon gases, produces red light with a
wavelength of 632.8 nm. Gallium, aluminium and arsenide, the lasing medium of
GaAlAs semiconductor diodes, also produces monochromatic radiation, the
wavelength of which depends on the ratio of these three materials and is in the
red-infrared range of the electromagnetic spectrum, typically 630-950 nm. The resonating cavity
containing the lasing medium has two parallel surfaces, one being totally
reflecting, the other being partially reflecting. Photons emitted from the
lasing medium are reflected between these surfaces, some of them leaving
through the partially reflecting surface as the laser beam. The cavity of a
HeNe laser is many cms long, whereas that of a GaAlAs semiconductor diode is
tiny, the diode being the lasing medium and its polished ends the reflecting
surfaces. Modern low intensity laser therapy devices are generally of the GaAlAs type. Their treatment heads may contain either one or many diodes. Those with one diode resemble laser pointers and are designed to treat acupuncture and trigger points; they can also be used to treat points in and around skin injuries. Those with many diodes are generally called cluster probes and allow large areas to be treated rapidly. The diodes may be housed in a rigid head or in a flexible material. The latter can be applied around curved surfaces such as the shoulder. Each diode emits either red or IR radiation. Red light is absorbed by all cells, whereas different wavelengths in the infrared range appear to target specific cell types. The power source for a LLLT device may be
either a battery or mains electricity. Many LLLT devices are portable. The main
function of the power source is to energize the lasing medium. HOW
LLLT PRODUCES ITS EFFECTS For LLLT to be
effective, the tissue targeted must absorb photons. Absorption is wavelength
dependent. Red light is absorbed by cytochromes in the mitochondria; all human
cells, other than mature red blood cells (erythrocytes) contain mitochondria.
Provided that appropriate wavelengths and energy densities are used, cell
activity can be stimulated if it is suboptimal. Cells in which this has been
investigated include mammalian keratinocytes, lymphocytes, macrophages, mast
cells, fibroblasts and endothelial cells, all cells of significance in tissue
repair. Much of the research on this has been reviewed by Baxter (1994) and by
Tuner and Hode (2002). Cells affected by
LLLT show a temporary increase in permeability of their cell membranes to
calcium ions (Young et al 1990). This may be an important component of the
mechanism by which LLLT modulates cell activity; other electrotherapeutic
modalities, such as ultrasound, may act in a similar fashion (Dyson 2004). The triggering of cell activity
by reversible changes in membrane permeability when photons are absorbed could
be responsible for the stimulation of tissue repair (Young & Dyson 1993).
Increase in calcium uptake by macrophages exposed to red light and IR in
vitro has been shown to be wavelength and energy density dependent. Of the
wavelengths tested, 660, 820 and 870 nm were effective; 880 nm was ineffective.
These same wavelengths also affected growth factor production by the
macrophages, 660, 820 and 870 nm being stimulatory, whereas 880 nm was not.
Energy densities of 4 and 8 J/cm2 were found to be effective; 2 and
19 J/cm2 were not (Young et al 1990). Red light of 660 nm wavelength is absorbed by
the cytochromes of mitochondria, where it stimulates ATP production and
increases cytoplasmic H+ concentration, which can affect cell
membrane permeability (Karu 1988). IR radiation of 820 and 870 nm may be
absorbed by components of the cell membrane.
Some of these components vary in different cell types, which may be why
the IR wavelengths absorbed by cells differ according to the cell type. For
example, 870 nm affects macrophages (Young et al 1990) but not mast cells (El
Sayed & Dyson 1990). It may be possible to selectively stimulate
macrophages but not mast cells in vivo by exposure to an 870 nm probe. Following a reversible
change in membrane permeability to calcium ions, the cells respond by doing
what they are programmed to do. In the case of macrophages, this is to produce soluble
protein mediators such as growth factors and to phagocytose debris, whereas
fibroblasts manufacture collagen and other extracellular components of the
dermis. The molecular mechanisms by which LLLT
affects cell activity begin with photoreception, when the photons are absorbed.
This is followed by signal transduction, amplification and a photoresponse,
e.g. cell proliferation, protein synthesis and growth factor production, all of
which assist in tissue repair. Membrane structure differs according to the cell
type, which, if IR is absorbed by parts of the membrane, may explain why
different cell types absorb different wavelengths of IR. Theoretically, it
should be possible, by the judicious selection of IR wavelengths, to affect
some cell types while leaving others unaffected. In contrast red light, since
it is absorbed by the mitochondrial cytochromes present in all mammalian cells
other than erythrocytes, and also by the haemoglobin contained in erythrocytes,
affects all mammalian cells. WOUND HEALING Wound healing consists of a closely regulated cascade of events
that follow injury and in skin normally result in the regeneration of the
epidermis and the replacement of the damaged dermis with scar tissue. The events can be grouped into the sequential
and overlapping phases of inflammation,
proliferation, and remodeling. If the dermis is damaged, haemostasis is the
initial major component of inflammation, following which debris and damaged
tissue are removed from the wound site by neutrophils and macrophages. Antigens
are also detected and presented to T-lymphocytes by macrophages such as
Langerhans cells. All these cells are components of the immune system. During
proliferation, angiogenesis and the formation of matrix rich in type III
collagen results in the production of granulation tissue over which the
epidermis migrates and regenerates. Myofibroblasts which develop in the
granulation tissue produce wound contraction, reducing the size of the wound.
During remodeling, the granulation tissue is gradually transformed into less
vascular, less cellular and more collagenous scar tissue which replaces the
injured dermis. Much of the type III
collagen is replaced by stronger type I collagen arranged in wider fibre bundles,
increasing the tensile strength of the scar tissue although this remains weaker
than uninjured dermis (Ovington, Schultz 2004). Regulation
of wound healing For wound healing to be successful, the multitude of events
comprising it must be spatially and temporally regulated. This regulation is dependent
on intercellular communication. Soluble
protein mediators (SPMs), produced initially by immune cells and consisting of
chemokines, cytokines and growth factors, together with hormones,
neurotransmitters and their receptors are involved in this communication;
protease and protease inhibitors modify the wound bed and affect the ease with
which cells can migrate within it. (Ovington and Schultz 2004). SPMs
are produced mainly by immune cells, eg neutrophils, macrophages and
lymphocytes, but also by peripheral nerve fibres, fibroblasts, endothelial
cells and other non-immune cells.
Following SPM synthesis and secretion, the SPMs diffuse to target cells
involved in the healing process or are transported to them in blood and lymph
vessels. They bind to specific receptor
sites on the target cell surface.
Binding triggers cell activation, the activity depending on the target
cell type. For example, myofibroblasts will contract, fibroblasts will
(depending on their stage of differentiation) either proliferate or secrete
matrix materials, endothelial cells will produce new blood capillaries. SPM actions during wound healing include
the following: 1. Initiation of
inflammation, by Il-1, TNF, etc. 2.
Cell recruitment to wound bed, by PAF, Il-1, Il-3, Il-6,
TNF, etc. 3.
Debris removal, by Il-1, Il-2, Il-4, Il-5, Il-6, TNF, etc. 4.
Promotion of proliferative phase of healing, by FGF, PDGF,
TGF-b, Il-1, Il-6, TNF etc Key: Il = Interleukin; TNF = Tumor necrosis factor,
PAF = Platelet activating factor, FGF = Fibroblast growth factor, PDGF = Platelet derived growth factor, TGF-b = Transforming growth factor-beta. Acute
inflammation is a vital stage in healing, setting the stage for the
proliferative phase by the removal of
debris and pathogens, and by the secretion of regulatory SPMs. In contrast, chronic inflammation inhibits
healing. For chronic wounds to heal, acute inflammation must be induced in them
by, for example, debridement. LLLT ACCELERATES WOUND HEALING Many publications during the last 30
years report the acceleration of delayed healing by LLLT and other forms of
phototherapy when used appropriately. To quote from a recent meta-analysis ‘…our
findings leave no doubt whatsoever that phototherapy promotes tissue repair’
(Fulop et al 2009). In addition to treating the wound bed, it is
recommended that the intact tissue around the wound also be treated (Baxter
1994). This will induce the peripheral nerve fibres and immune cells present in
epidermis and dermis to secrete SPMs.
Acute inflammation is a vital part of wound healing. Its resolution
should be accelerated so that the proliferative phase of repair begins earlier,
thus accelerating the healing process. Cells that have absorbed sufficient
quantities of photons of effective wavelengths will secrete these SPMs earlier
and thus accelerate healing. In
contrast, chronic inflammation inhibits repair; it has to be converted to acute
inflammation for healing to progress.
This may require debridement and should be followed as soon as possible
by phototherapy so that the immune cells are stimulated to secrete SPMs. It is recommended that this be continued,
ideally on a daily basis or at every dressing change, throughout the acute
inflammatory phase of repair. Continuing the treatment into the proliferative
phase may also be of value since phototherapy can stimulate the proliferation
of endothelial cells (Ghali, Dyson 1992) and fibroblasts (Hawkins, Abrahamse
2006), accelerating the development of
the granulation tissue over which epidermal cells migrate. The Beurer SoftLaserTM This hand-held LLLT device is a low power Class
2M laser manufactured by Beurer GmbH. It
contains a single 5 mW GaAlAs diode producing red light of 635-670 nm
wavelength. It is powered by 2 AAA batteries. Application of SoftLaserTM to Skin The probe is placed in contact with clean
skin or over a transparent dressing at right angles to the skin’s surface and
moved slowly over the region to be treated for a few minutes, typically 3-6
minutes for a region of about 1 cm diameter.
A convenient way to use it is twice daily, shortly after cleansing the
skin in the morning and evening, and before the application of a moisturizing
cream and/or cosmetics. Laser Therapeutics Inc. SL50 The Laser Therapeutics Inc.
SL50 is an example of a cluster probe suitable for home use. It has 8 laser
diodes that emit red light at 640-660 nm and 4 laser diodes that emit infrared
electromagnetic radiation at 775-795 nm.
Application of Laser Therapeutics Inc. SL50 to Skin The cluster probe is
placed in contact with clean skin, or, if the skin has an open wound, over a
transparent wound dressing. The cluster
probe does not operate if contact is broken and there is no need to move the
cluster during the treatment period, typically 5 minutes per point. LLLT EFFECTS ON DAMAGED SKIN Effects of the Laser
Therapeutics SL50 Cluster Laser and Beurer SoftLaserTM on Skin The Laser Therapeutics
SL50 Cluster Laser and Beurer SoftLaserTM have been reported by its
users to: ·
Reduce
wrinkles ·
Make
scars less visible ·
Tighten
large pores ·
Elevate
pock marks ·
Improve
skin tone ·
Give
a temporary radiance to the skin ·
Soften
chapped lips ·
Accelerate
wound healing Treatment of damaged
skin with red light accelerates the resolution of acute inflammation, leading
to faster repair (Dyson 2004). The stimulated
secretion of collagen by fibroblasts at the site of a wrinkle or of a pock mark
will increase the thickness of the dermis locally, helping to fill in the
tissue deficit. The gradual removal of excessive scar tissue may be due to the
activation of fibroblasts, fibrocytes and other cells in and around the scar. As with any other
technique, tissue repair can only be stimulated by LLLT if it is absent or
delayed. In these circumstances, epithelialisation and granulation tissue
production can be stimulated by LLLT as can wound contraction (Dyson &
Young 1986) which reduces the area in which scar tissue is produced resulting
in less obvious scarring. THE
IMMUNE SYSTEM The immune system plays a vital role in the response of the
body to pathogens, cancer and injury.
The main cellular components of the immune system are lymphocytes and
macrophages, including the Langerhans cells of the epidermis. These are located either in peripheral
tissues such as the epidermis and dermis of the skin, the epithelium and lamina
propria of mucous membranes and superficial lymph nodes or in deeper organs
such as the deep lymph nodes. The key molecular components of the immune system
are antibodies and SPMs such as cytokines and growth factors. All the components of the immune system are linked by blood
vessels and lymphatic vessels, via which immune cells and the molecules they
secrete are carried around the body.
SPMs released from peripheral immune cells such as Langerhans cells in
response to the direct action of absorbed
photons can be transported to and affect cells that have not been exposed to
photons. Injuries other than those
directly exposed to photons can therefore be affected by them indirectly. Peripheral immune cells are located mainly located in the
skin associated lymphoid tissue (SALT) and mucous membrane
associated lymphoid tissue (MALT). Their
superficial location renders them accessible to photons during phototherapy.
Other immune cells, the natural killer (NK) cells, patrol the body in the blood
and lymph, lysing cancer cells and virus-infected cells. The initial response of the immune system is
non-specific and immediate. It is
enhanced by cytotoxins secreted by the NK cells. During it neutrophils,
macrophages, NK cells, T lymphocytes and antimicrobial proteins inhibit the
spread of the invading substances. SPMs released locally recruit immune cells
to the infected region and promote tissue repair. SPMs consist of 3 groups: 1.
CHEMOKINES, for example fractalkine, are chemotactic
molecules that attract and activate inflammatory cells 2.
CYTOKINES, for example interleukins, are molecules that
regulate division and differentiation of immune (inflammatory) cells 3.
GROWTH FACTORS, for example platelet derived growth factor
(PDGF), are molecules that stimulate division of both immune and non-immune
(non-inflammatory) cells. Immune or inflammatory cells include Langerhans cells,
neutrophils, natural killer cells, monocytes, macrophages, T & B
lymphocytes, plasma cells and mast cells. All play significant roles during the
inflammatory and proliferative phases of wound healing (Martin, Leibovich 2005). Non-immune or non-inflammatory cells that are
of importance during wound healing include epidermal cells, endothelial cells,
fibroblasts and myofibroblasts. Photons can be absorbed not only by the superficially-located immune cells of the SALT and MALT and but also by immune cells and stem cells in transit through the superficially-located blood and lymph capillaries of the skin and mucous membranes. Phototherapy can have a direct effect on the secretion of SPMs by these cells. By doing so it can accelerate the resolution of inflammation and thereby accelerate repair if this is delayed. The deeper cells of the immune system and also non-immune cells of injured tissues can be affected indirectly by SPMs released from peripherally-located cells that have absorbed photons. Phototherapy thus has both local and systemic effects. Cells of injured tissues are more sensitive to phototherapy that cells of intact tissues, so lower power and energy levels can affect them while leaving less susceptible cells unaffected. The secretion of different SPMs may assist chronic wounds to heal by allowing them to progress from inflammation to the proliferative phase of wound healing when granulation tissue is formed and re-epithelialization occurs. Because of the indirect, systemic, effects of photons, the treatment of one wound of a patient may lead to improvements not only in this wound but in the patient’s other wounds. Link
between cutaneous nerves and SALT Cutaneous contact hypersensitivity (CH) reactions are
closely correlated with Langerhans cells (LC), macrophages that arise from stem
cells in the bone marrow and migrate into the epidermis (Streilen et al 1999). Also known as
epidermal dendritic cells they help to activate the immune system by presenting
antigens to lymphocytes. LCs may be linked synaptically to cutaneous nerve
termini containing calcitonin gene-related peptide (CGRP), suggesting that
there is a link between innervation and immune responses in the skin. It has
been proposed that ‘cutaneous nerves dictate whether antigen applied to the
skin will lead to sensitivity or tolerance’(Streilen et al 1999), linking the
nervous system to the immune system. There is evidence that phototherapy can
affect mast cell degranulation (El Sayed and Dyson 1990) resulting in
activation of pain fibres. Nerve conduction (Vinck et al 2005) is
also affected by phototherapy, supporting the hypothesis that it may affect the
immune system via the nervous system. CLINICAL RELEVANCE OF
EFFECTS OF LLLT ON IMMUNE SYSTEM TO WOUND HEALING Phototherapy has been used for many decades to treat the
chronic wounds of patients (Mester et al 1985). It is suggested that treatment of the intact
skin around chronic wounds may, provided that the correct parameters are used,
activate immune cells of the SALT. This will increase the efficiency with which
pathogens and debris are removed and stimulate the release of cytokines of
value in the inflammatory and proliferative phases of repair. Furthermore latent SPMs such as transforming
growth factor–beta 1 (TGF-ß1), of crucial importance in wound healing, can be
activated by phototherapy. In addition
to exposing SALT to phototherapy, irradiation of peripheral lymph nodes could
also be of value in that more immune cells will be exposed to the beneficial
effects of phototherapy. Immune cells from these nodes will enter the
lymphatics and be transported to the wounds where they and the cytokines they
secrete can assist in the healing process (Dyson 2008). It is
possible that variation in the treatment parameters used may determine which
SPMs are secreted. Different mediators
are necessary for different activities during wound healing, including the
initiation of inflammation, the recruitment of inflammatory and
non-inflammatory cells to the wound bed, debris removal by neutrophils and
macrophages, and the induction of granulation tissue formation. Chronic wounds
may be trapped in the inflammatory phase of healing; compared with healing
wounds, they have more inflammatory cytokines, higher protease activity, lower
mitogenic activity and contain fewer mitotically competent cells (Dyson 2008).
Selection of appropriate treatment parameters may move them on to the proliferative
phase of healing. What these parameters
are remains to be determined. Antibody array screening allows the rapid
monitoring of the induction of different SPMs (Chang et al 2009). Selection of
the best parameters could optimize the treatment of chronic wounds with
phototherapy, helping improve the quality of life of millions of people world
wide. Cellular effects
relevant to skin repair The cellular effects of LLLT relevant to skin
repair include the stimulation of ·
adenosine
triphosphate (ATP) production ·
growth
factor release by macrophages ·
keratinocyte
proliferation ·
collagen
synthesis ·
angiogenesis. All of the above are
required for skin to renew itself and repair the damage done to it by, for
example, environmental factors such as excessive exposure to the elements,
damage that accumulates with age. Temporary vasodilatation
following the exposure to red light improves the transport of essential
nutrients and oxygen to the skin and the removal of toxic waste materials from
it. It also gives sallow skin a radiant
glow. PAIN RELIEF BY LLLT Although many of the reports of pain relief
following exposure to LLLT are anecdotal, there have been a number of reports
based on trials aimed at assessing LLLT as an antinociceptive or analgesic
modality, one of the earliest being that of Walker 1983 who implicated
alteration in serotonin metabolism as one mechanism of LLLT-mediated analgesia.
Rheumatoid pain Walker et al (1987)
reported a highly significant reduction (p<0.001) in the levels of pain and analgesic
medication intake reported by rheumatic patients either treated with low
intensity red laser or sham-irradiated, pain relief being greater in
those given laser treatment. Palmgren et al (1989) found that treatment of the
small joints of the hand in rheumatic patients with low intensity infrared
laser was followed by reduced pain and swelling, reduced early morning
stiffness and increased grip strength and range of movement. In contrast
Basford et al (1987) found that red laser irradiation of the osteoarthritic
thumbs of patients was not followed by significant reduction in pain; however,
the power and energy levels used (0.9 mW and 0.081J) are well below those
recommended for clinical application (Baxter 1994) and may have been sub
threshold. Chronic neurogenic pain Moore et al (1988a) have
investigated the effect of red laser in the treatment of patients with chronic
neurogenic pain including that of post-herpetic neuralgia. It was found that there was a significant
reduction in reported pain following treatment in comparison to that in
sham-irradiated patients. Similar effects have been reported by Hong et al
(1990) using the same equipment. Mechanisms It has been suggested by
Obata et al (1990) that laser-mediated relief of rheumatic pain may be linked
to autonomic changes that produce vasodilatation and slight increases in local
temperature. It is also possible that laser treatment affects the synthesis,
release and metabolism of a range of neurochemicals involved in nerve
transmission and pain relief (Walker 1983).
Relief following the stimulation of acupuncture points with LILT has
been ascribed to the production of endogenous opiate-like peptides and
serotonin (Zhong et al 1989). CONCLUSIONS Cells of the immune system initiate acute
inflammation, an essential part of the healing process. The peripheral components of the immune
system such as the Langerhans cells of the epidermis are readily accessible to
photons and can be affected by them directly, triggering the release of a
variety of SPMs which orchestrate the sequential events of the inflammatory,
proliferative and remodeling phases of wound healing. These SPMs can either diffuse or be
transported by blood and lymph vessels to the other parts of the immune system
and to distant injured tissue where they can initiate reparative changes, thus
amplifying the direct effects of the superficially absorbed photons. Cells can
therefore be affected indirectly by photons without the need to absorb them.
Photon-induced changes in peripherally located nerve fibers and in the
endocrine system can also modulate wound healing and relieve pain either
directly or indirectly. There is some evidence that exposure of immune cells to different parameters of phototherapy can
alter the types of SPMs produced.
Further research on the effects of different parameters on SPM
production by immune cells is indicated. It may therefore be possible to select
the most effective parameters to use to accelerate healing where it is either
delayed or chronic. Scarring associated with
acne and skin deterioration due to ageing and sun damage can be alleviated by
LLLT. These skin conditions involve tissue injury, the repair of which is
improved by exposure to LLLT in the form of red and IR radiation. LLLT can
reduce the duration of inflammation, improving tissue repair where this is
delayed or defective. It can also reduce both acute and chronic pain. By
assisting in the resolution of inflammation, the proliferative phase of tissue
repair begins earlier and the reparative process is completed earlier. Cell
activity is jump-started by changes in membrane permeability. This occurs when
the cells absorb red and/or infrared radiation. The cells are also energized
when red light is absorbed by their mitochondria, stimulating the synthesis of
ATP and thus providing readily available energy for cell activity. The
improvement in the skin produced by LLLT has been described as skin
rejuvenation (Lee 2002). The portable Beurer SoftLaserTM and the Laser Therapeutics Inc. SL50 take LLLT from the clinic into the
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blind crossover trial of low level laser therapy in the treatment of post
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relief effects of serotonin in laser acupuncture analgesia. Am J Acupuncture
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learning approach. Edited by Morison MJ, Ovington LG, Wilkie K, 83-100.
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dye laser. Dermatol Surg 28:942-945 Streilen JW, Alard P, Niizeki H 1999 A new concept of
skin-associated lymphoid tissue (SALT): UVB light impaired cutaneous immunity
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for pain of rheumatoid arthritis. Clin J Pain 3:54-59 Young SR, Dyson M, Bolton P 1990 Effect of light on calcium
uptake by macrophages. Laser Therapy 2:53-57 Young SR, Dyson M 1993 The effect of ultrasound and light
therapy on tissue repair. In: Macleod DAD, Maughan C, Williams CR, Sharo JCM,
Nutton R (eds) Intermittent high intensity exercise. Chapman and Hall, Zhong X et al 1989 Correlation between endogenous
opiate-like peptides and low-power laser therapy in rheumatoid arthritis by
thermography. Laser Ther 2:28 CURRICULUM VITAE NAME: Dr. Mary Dyson (nee DEPLEDGE) BSc
PhD MIBiol CBiol FCSP(Hon) FAIUM(Hon) FZS LHD(Hon) PRIVATE ADDRESS Chestnuts 33
King’s Road Berkhamsted
Hertfordshire HP4 3BH TELEPHONE: +44
(0)1442 874427 CELL PHONE +44
(0)07866 456 532 FAX +44
(0)1442 384859 E-MAIL md41139@aol.com DATE OF BIRTH MARITAL STATUS Widowed DEGREES 1961 BSc Class I Special Honours in Zoology Specialist
Subject: Embryology 1965
PhD Topic: Wound Healing ADDITIONAL ACADEMIC
AWARDS 1958 State
Scholarship Pfeiffer
Scholarship ( West
Riding of 1961
Busk-Howell
Research Scholarship ( Department of Scientific &
Industrial Research Postgraduate Scholarship 1988 History of Medical Ultrasound
Pioneer Award (presented by the American Institute of Ultrasound in Medicine
and the World Federation for Ultrasound in Medicine and Biology, in recognition
of contributions to the development of medical ultrasound) 1989 Elected Honorary Fellow of the
American Institute of Ultrasound in Medicine for “outstanding contributions to
the field of medical ultrasound” 1990 Elected Honorary Fellow of the
Chartered Society of Physiotherapy for
research into the biological effects of electrotherapy 1992 Elected President of the
International Laser Therapy Association 1996
Awarded
the degree of Doctor of Humane Letters (honoris causa) by the Pennsylvania
College of Podiatric Medicine 1998
Elected
Honorary Member of the World Association of Laser Therapy 1998 Conferred
with the title of Emeritus Reader in Biology of Tissue Repair by King’s College
London, PRESENT APPOINTMENTS Since 1991: Biomedical
Consultant and Director, Dyderm Ltd. Since 1996: Research
Director, Quality Medical Instruments Ltd. Since 1998: Emeritus
Reader in Biology of Tissue Repair, University of Since 1998: Director
of Research & Development, Longport Inc. Since 1998: Member
of Board of Directors of World Walk Foundation. Since 2000: Executive Vice-President, Longport Inc. PAST EMPLOYMENT 1964-70
Research
Associate Department of Anatomy Guy’s 1970-75
Lecturer
Department of Anatomy Guy’s 1975-87
Senior
Lecturer Department of Anatomy Guy’s 1987-98 Reader
in Biology of Tissue Repair Head,
Tissue Repair Research Unit Department
of Anatomy Guy’s 1998-2000
Director
of Research and Development Longport Inc PROFESSIONAL
APPOINTMENTS Teaching 1974
Recognised
as a Teacher of the 1974-98
Member
of the Board of Studies in Human Anatomy and Morphology, 1976-98
Examiner
in Cytology and Histology, Guy’s 1976-98
Examiner
in Anatomy, Guy’s 1981-98
Member
of the Preclinical Subjects Sub-Committee of the Board of Studies in Dentistry,
1985-98
Member
of the Panel of Visiting Examiners in Anatomy, 1987-88
Member
of Working Party considering introduction of projects into the clinical curriculum
(UMDS Education Committee) 1987 Appointed as a Teacher of the 1988
Elected
by the Board of Studies in Human Anatomy and Morphology as Chairman of the
Course-Unit Approval Sub-Committee and Chairman of the Panel of Course Unit
Examiners, 1989-95 Admissions Tutor (Medical), United
Medical and Dental Schools of Guy’s and St Thomas’ Hospitals (UMDS) 1992-95
Organiser
of Access Course for prospective medical and dental students at UMDS in
conjunction with EDITORIAL Since 1977 Member
of Advisory Editorial Board of
“Ultrasound in Medicine and Biology” 1979-87
Associate
Editor of “Gray’s Anatomy” 36th edition Since 1985 Member
of the Advisory Editorial Board on
“Physiotherapy Practice” 1989
Appointed
as an Editor of “ Gray’s Anatomy” 37th edition 1991 Appointed
to the Editorial Board of “Gray’s Anatomy” 38th edition 1990
Appointed
Section Co-Editor of “Gray’s Anatomy” 38th edition. ADVISORY 1973-74
Adviser
to the Bureau of Radiological Health of the Food and Drugs Administration on
the performance requirements of ultrasonic therapy equipment 1980
Member
of the Scientific Committee of the 10th LH Gray Conference, University of Since 1983 Member
of the International Anatomical Nomenclature Committee 1984-93
Member
of the European Committee for Ultrasonic Radiation Safety 1986
Appointed
as a Reviewer by the American Medical Association 1986-87
Adviser
to the Electrotherapy Working Party of the Chartered Society of Physiotherapy 1988-90
Honorary
Treasurer of the International Laser Therapy Association 1989
Member
of Chief Scientist’s Assessment Group, Department of Health, for the Nursing
Practice Research Unit, Since 1989 Academic Board of UMDS Representative to
Lewisham and North Southwark Ethical Committee (now the Guy’s Hospital Local
Research Ethics Committee) 1990-95
Member
of the Special Advisory Committee in Health Studies, University of 1990-92
President
Elect of the International Laser Therapy Association 1992-94
President
of the International Laser Therapy Association Since 1991 Member of the Electrotherapy Advisory
Group of the Chartered Society of Physiotherapy 1992-96 Vice-Chairman,
Division of Biological Services, UMDS CURRENT MEMBERSHIP OF
EDITORIAL BOARDS Laser Therapy, Physical Therapy Reviews, Physiotherapy
Research International, Physiotherapy Practice, Ultrasound in Medicine and
Biology. REVIEWING
2.Grant Applications submitted to the
Medical Research Council (MRC), Science and Engineering Research Council (SERC)
and Wellcome Trust. MEMBERSHIP OF
SOCIETIES Anatomical Society of Great Britain and
Ireland, British Connective Tissue Society, British Medical Ultrasound Society,
British Orthopaedic Research Society, British Society for Cell Biology, British
Society for Developmental Biology, Institute of Biology, World Association of
Laser Therapy, North American Association of Laser Therapy, Zoological Society
of London. EXAMINING 2nd BDS and BMS (UMDS); Anatomy
Course Units (UMDS); 2nd BDS (University of Birmingham); BSc
(Universities of Brighton, London and Salford); MSc (University of London); PhD
(Universities of Aberdeen, Brighton London UK, London Ontario, Manchester,
Queens University Belfast, Ulster). DEPARTMENTAL
RESPONSIBILITIES WHILE EMPLOYED AS READER 1.Teaching (a)
gross
anatomy to preclinical medical and dental students (b)
histology
to preclinical medical and dental students (c)
supervision
of BSc, MPhil, PhD and MBPhD students 2. Research (a)
analysis
of effects of MHz and kHz ultrasound on tissue repair (b)
bioeffects
of low level laser therapy (c)
control
of angiogenesis during wound healing (d)
development
of the Longport Digital Scanner, a noninvasive high resolution instrument
currently utilising 20MHz ultrasound associated with fractal analysis, as a device for assessing structural changes
associated with the development and repair of damage in skin and subcutaneous soft tissue. (e)
diabetes
associated changes in skin of relevance to wound healing (f)
role
of the immune system in wound healing This work was carried out in the Tissue Repair
Research Unit supported by grants obtained from the MRC, SERC, Department of
Health, Department of Trade and Industry, National Fund for Research into
Crippling Diseases, RESEARCH 1.
Dyson, M.
(1965) An experimental study of wound healing in Arion. PhD Thesis, 2.
Joseph, J.
and Dyson, M. (1965) Sex differences in the rate of tissue regeneration in the
rabbit's ear. Nature, 209, 599-600. 3.
Joseph, J.
and Dyson, M. (1966) Tissue replacement in the rabbit's ear. Br.J. Surg.,
53, 372-380. 4.
Joseph, J.
and Dyson, M. (1966) The effect of anabolic androgens on tissue replacement in
the rabbit's ear. Nature, 211, 193-194. 5.
Pond, J.B.
and Dyson, M. (1967) A device for the study of the effect of ultrasound on
tissue growth in rabbits' ears. J. Sci. Instrum., 44, 165-166. 6.
Dyson, M.
and Joseph, J. (1968) The effect of androgens on tissue regeneration. J.
Anat.103, 491-505. 7.
Dyson, M.,
Joseph. J, Pond, J. and Warwick, R. (1968) The stimulation of tissue
regeneration by means of ultrasound. Clin. Sci., 35,273-285. 8.
Joseph, J.
and Dyson, M. (1970) The effect of abdominal wounding on the rate of
regeneration in the rabbit's ear. Experientia, 26, 66-67. 9.
Dyson, M.
and Pond, J. (1970) The effect of pulsed ultrasound on tissue regeneration.
Physiotherapy, 56, 136-142. 10.
Dyson, M.,
Pond, J., Joseph, J., and 11.
Joseph, J.
and Dyson, M. (1970) The effect of mechanical obstruction on tissue
regeneration in the rabbit's ear. Br. J. Surg., 58, 277-285. 12.
Pond, J.,
Woodward, B. and Dyson, M. (1971) A microscope viewing ultrasonic irradiation
chamber. Phys. Med. Biol., 16, 521-524. 13.
Joseph, J.
and Dyson, M. (1971) The effects of oxymethalone on tissue replacement in the
rabbit's ear. Experientia, 27, 1309-1310. 14.
Dyson, M.,
Pond, J. and Woodward, B. (1971) Flow of red blood cells stopped by ultrasound.
Nature, 232, 572-573. 15.
Dyson, M.
and Joseph, J. (1971) The effects of female sex hormones on tissue
regeneration. J. Endocrinol., 51, 685-697. 16.
Taylor, K.
and Dyson, M. (1972) Possible hazards in diagnostic ultrasound. Br. J. Hosp.
Med., 8, 571-577. 17.
Dyson, M.,
Pond, J. and Woodward, B. (1972) The induction of red cell stasis in embryos by
ultrasound. In: "Interaction of ultrasound and biological tissues:
workshop proceedings", edit. J.M. Reid and M.R. Sikov, DHEW
Publication(FDA) 73-8008,139-141. 18.
Dyson, M.
and Pond, J. (1973) The effects of ultrasound on circulation. Physiotherapy,
59, 284-287. 19.
Dyson, M.
and Pond, J. (1973) Biological effects of therapeutic ultrasound. Rheum.
Rehab., 12, 209-212. 20.
Dyson, M.,
Pond, J., Woodward, B. and Broadbent, J. (1974). The production of blood cell
stasis and endothelial damage in the blood vessels of chick embryos treated
with ultrasound in a stationary wave field. Ultrasound Med. Biol., 1, 133-148. *This paper was selected
for publication as a Benchmark paper in "Acoustics in Ultrasonic
Biophysics", edit. F. Dunn and W.D. O'Brien Jr., Hutchinson and Ross,Inc.,
21.
Taylor, K.,
and Dyson, M. (1974) Toxicity studies on the interaction of ultrasound on
embryonic and adult tissues. In: "Proceedings of the 22.
23.
Dyson, M.,
Franks, C. and Suckling, J. (1976) Stimulation of healing of varicose ulcers by
ultrasound. Ultrasonics, 14, 232-236. 24.
Dyson, M.
and Suckling, J. (1978) Stimulation of tissue repair by ultrasound: a survey of
the mechanisms involved. Physiotherapy, 64, 105-108. 25.
ter Haar,
G., Dyson, M. and Talbert, D. (1978) Ultrasonically induced contraction of
mouse uterine smooth muscle in vivo. Ultrasonics, 16, 275-276. 26.
Webster,
D., Harvey, W., Dyson, M. and Pond, J. (1978) The role of ultrasound-induced
cavitation in the in vitro stimulation of protein synthesis in human
fibroblasts by ultrasound. Ultrasound Med. Biol. 4, 343-351. 27.
Webster,
D., Harvey, W. and Dyson, M. (1979) Ultrasonically-induced stimulation of
collagen synthesis in vivo. In: "Proceedings of the Fourth European
Symposium on Ultrasound in Biology and Medicine", edit. P.Greguss, Vol.1,
pp.135-140. 28.
Dyson, M.,
Webster, D.F., Pell, R. and Crowder, M. (1979) Improvement in the mechanical
properties of scar tissue following treatment with therapeutic levels of
ultrasound in vivo. In: Proceedings of the Fourth European Symposium on
Ultrasound in Biology and Medicine, edit. P. Greguss, Vol.1,pp.129-134. 29.
ter Haar,
G., Dyson, M. and Smith, S. (1979) Ultrastructural changes in mouse uterine
blood vessels brought about by ultrasonic irradiation at therapeutic
intensities in standing wave fields. Ultrasound Med. Biol., 5, 167-179. 30.
Webster,
D.F., 31.
Gibson, T.,
Laurent, R., Highton, J., 32.
Dyson, M.
(1980) The effect of ultrasound on the rate of wound healing and the quality of
scar tissue. In: "Proceedings of the International Symposium on
Therapeutic Ultrasound. 33.
Dyson, M.
(1982) Non-thermal cellular effects of ultrasound. Br. J. Cancer,35,suppl.V,
165-171. 34.
Dyson, M.
(1982) Stimulation of tissue repair by therapeutic ultrasound. Infections
Surg., 1, 37-44. 35.
Dyson, M.
and Brookes, M. (1983) Stimulation of bone repair by ultrasound. In:
"Ultrasound '82", edit. R.A. Lerski and P. Morley, Pergamon
Press,Ltd., 36.
Grahame,
R., Armstrong, R., Simons, N., 37.
Dyson, M.
and Smalley, D. (1983) Effects of ultrasound on wound contraction. In:
"Ultrasound Interactions in Biology and Medicine", edit. R. Millner
and U. Corbet, Plenum Publishing Corporation, 38.
Dyson, M.
(1984) Biological and therapeutical effects of ultrasound. In:
"Proceedings of the Centennial Congress of the Italian Surgical Society.
Postgraduate Course on Emerging Technologies in Surgery", edit. L.
Angelini, F. Fegiz and P.N.T. Wells, Masson Italia Editori, 39.
Dyson, M.
(1984) The effect of ultrasound on tissue repair. Scripta Medica (Praha), 57,
212-213. 40.
Dyson, M.
(1985) Therapeutic applications of ultrasound. Clinics Diagnost. Ultrasound,
16, 121-134. 41.
Gibson, T.,
Fagg, N., Highton, J., 42.
Dyson, M.
and Luke, D.A. (1986) Induction of mast cell degranulation in skin by
ultrasound. IEEE Trans. Ultrasonics, Ferroelectics and Frequency Control,
URRC-33 (2), 194-201. 43.
Dyson, M.
and Young, S. (1986) The effects of laser therapy on wound contraction and
cellularity. Lasers. Med. Sci., 1, 125-130. 44.
Dyson, M
(1986) A review of recent experimental evidence on the effects of diagnostic
ultrasound on tissue. Inst. Phys. Sci. Med., Conference Report Series, 47,
1-11. 45.
Crum, 46.
Dyson, M.
(1986) The effect of laser therapy on wound contraction. Med. Laser Reports, 4,
2-8. 47.
Hodgson,
S., Child, A. and Dyson, M. (1987) Endocardial fibro-elastosis: possible
X-linked inheritance. J. Med. Genet., 24, 210-214. 48.
Coleman,
A.J., Saunders, J.E., Crum, L.A and Dyson, M. (1987) Acoustic cavitation
generated by an extra-corporeal shockwave lithotriper. Ultrasound Med. Biol.,
13(2), 69-76. 49.
Dyson, M.
(1987) Review of recent experimental evidence on the effects of diagnostic
ultrasound on tissue. In: "Obstetric and Neonatal Blood Flow", edit.
C.D. Sheldon, D.H. Evans and J.R. Savage. Conference Proceedings 2, Biological
Engineering Society, pp.1-7. 50.
Dyson, M.
(1987) Mechanisms of therapeutic ultrasound. Physiotherapy, 73, 116-120. 51.
Daniels,
S., Blondel, D., Crum, 52.
Crum, 53.
Crum, 54.
Lovell,
C.R., Smolenski, K.A., Duance,V.C., Light, N.D., Young, S. and
Dyson, M. (1987) A study of Type I and III collagen content and fibre
distribution in normal human skin during ageing. Br. J. Dermatol., 117,
419-428. 55.
ter Haar,
G., Dyson, M. and Oakley, E.M. (1987) The use of therapeutic ultrasound by
physiotherapists in 56.
Dyson, M.
(1987) Why membrane changes matter. Euroson '87, edit. S.Bondesram, A. Alanen
and P.Jouppila. Finnish Society for Ultrasound in Medicine and Biology, p.397. 57.
ter Haar,
G., Dyson, M. and Oakley, E.M. (1988) Ultrasound in Physiotherapy in 58.
Mortimer,
A.J. and Dyson, M. (1988) The effect of therapeutic ultrasound on calcium
uptake in fibroblasts. Ultrasound Med. Biol., 14, 499-506. 59.
Dyson, M.,
Young, S., Pendle, C.L., Webster, D.F. and Lang, S.M. (1988) Comparison of the
effects of moist and dry conditions on tissue repair. J. Invest.
Dermatol., 91, 434-439. 60.
Dyson, M.
(1989) The use of ultrasound in sports physiotherapy. In:
"International Perspectives on Physical Therapy". Series
editors: 61.
Dinno,
M.A., Dyson, M., Young, S.R., Mortimer, A.J., Hart, J. and Crum, 62.
Young, S.,
Bolton, P., Dyson, M., 63.
Young, S.R.
and Dyson, M. (1989) The effect of therapeutic ultrasound on angiogenesis.
Ultrasound Med. Biol. 16, 261-269. 64.
Young, S.R.
and Dyson, M. (1990) Effect of therapeutic ultrasound on the healing of
full-thickness excised lesions. Ultrasonics, 28,175-180. 65.
Dyson, M.,
(1990) Role of ultrasound in wound healing. In: Contemporary Perspectives in
Rehabilitation. Editor-in-Chief: S. Wolf. "Wound Healing: Alternatives in
Management", 1st edition. Volume editors: L.C. Kloth, J. Feedar and J.
McCullough, F.A.Davis Company, 66.
Young, S.R.
and Dyson, M. (1990) Macrophage responsiveness to therapeutic ultrasound.
Ultrasound Med. Biol., 16, 809-816. 67.
El-Sayed,
S. and Dyson, M. (1990) A comparison of the effect of multiwave-length light
produced by a cluster of semiconductor diodes and each individual diode on mast
cell number and degranulation in intact and injured skin. Lasers Surg. Med.,
10, 559-568. 68.
Young,
S.R., Dyson, M. and 69.
70.
Dyson, M.
(1990) Electrotherapy: the need for critical evaluation and continuing
education. Physiotherapy Theory and Practice, 6, 105. 71.
Young, S.R.
and Dyson, M. (1991) Het effect van ultrageluid en licht op het genezen van
weefsels. Ned. T. Fysiotherapie, 101, 20-23. 72.
Al Hassan,
J., Dyson, M., Young, S.R., Thompson, M. and Criddle, R.S. (1991) Acceleration
of wound healing responses induced by preparations from the epidermal
secretions of the Arabian Gulf Catfish (Arius lineatus, Valenciennes).
J. Wilderness Med.,2, 153-163. 73.
Young,
S.R., Dyson, M., Hickman, R., Lang, S.M., and Osborne, C. (1991) Comparison of
the effects of semi-occlusive polyurethane dressings and hydrocolloid dressings
on dermal repair - 1: Cellular changes. J. Invest. Dermatol., 97,
586-592. 74.
Young,
S.R., Dyson, M. and 75.
76.
77.
Dyson, M.
(1992) Cellular and subcellular aspects of low level laser therapy. In:
"Progress in Laser Therapy: Selected papers from the 1990 ITLA
Congress", edit. T. Ohshiro and R.G. Calderhead. John Wiley, 78.
Ghali, L
and Dyson, M. (1992) The direct effect of light therapy on endothelial cell
proliferation in vitro. In: "Angiogenesis: Key Principles - Science
- Technology - Medicine", edit. R. Steiner, P.B. Weisz and R. Langer.
Birkhauser Verlag, 79.
80.
Cheetham,
M., Young, S.R. and Dyson, M. (1992) Histological effects of 820 nm laser
irradiation on the healthy growth plate of the rat. Laser Therapy, 4,
59-64. 81.
Whiston,
R.J., Young, S.R., Lynch, J.A., Harding, K.G. and Dyson, M. Application of high
frequency ultrasound to the objective assessment of healing wounds. Proc. 2nd
Conference on Advances in Wound Management. Macmillan Press, 82.
Young,
S.R., Lynch, J.A., Liepins, P.J. (1992) Ultrasound imaging: a non-invasive
method of wound assessment. Proc. 2nd Conference on Advances in
Wound Management. Macmillan Press, 83.
Dyson, M.,
Young, S.R., Hart, J., Lynch, J.A. and Lang, S.M. (1993) Comparison of the
effect of moist and dry conditions on the process of angiogenesis during dermal
repair. J. Invest. Dermatol., 99, 729-733. 84.
Dyson, M.
(1993) Ultrasound, lasers and soft tissue repair. J. Assoc. Chart. Physiother.
Obst. Gyn., 72, 2.3 85.
El Sayed,
S.O. and Dyson, M. (1993) Responses of dermal mast cells to injury. J. Anat.,
182, 369-376. 86.
El Sayed,
S.O. and Dyson, M. (1993) Histochemical heterogeneity of mast cells in rat
skin. Biotech. Histochem., 68, 326-332. 87.
Steinlechner,
C.W.B. and Dyson, M. (1993) The effects of low-level laser therapt on
macrophage-modified keratinocyte proliferation. Laser Therapy, 5, 65-73. 88.
Young, S.R.
and Dyson, M. (1993) The effect of light on tissue repair. Acupuncture in
Medicine, 11, 17-20. 89.
Dyson, M.
(1993) The effect of ultrasound on the biology of soft tissue repair. In:
"The soft tissues - trauma and sports injuries", edit. G.R. McLatchie
and C.M.E. Lennox. Butterworth-Heinemann Ltd., 90.
Young, S.R.
and Dyson, M. (1993) The effect of ultrasound and light therapy on tissue
repair. In "Intermittent high intensity exercise", edit. D.A.D.
Macleod, R.J. Maughan, C. Williams, C.R. Madeley, J.C.M. Sharp and R.W. Nutton.
Chapman and Hall, 91.
Karim, A.,
Young, S.R., Lynch, J.A. and Dyson, M. (1994) A novel method of assessing skin
ultrasound scans. Wounds, 6, 9-15. 92.
Cervi, P.,
Murdock, A., Rees, D., Garner, S., Grant, D., Wright, S. and Dyson, M. (1994)
Splenic Ultrasound - a new wave for immune thrombocytopenic purpura. J. Clin.
Path., 47, 414-417. 93.
Dyson, M.
(1994) Electrotherapy: an overview. 94.
Rajaratnam,
S., 95.
96.
Dyson, M.
(1995) Ultrasound for wound management. In: "Clinical Wound
Management,", edit. P.P. Gogia, Slack, Inc. 97.
Kitchen,S.
and Dyson, M. (1996) Low energy treatments: nonthermal or microthermal? In:
"Clayton's Electrotherapy" 10th Edition, edit. S. Kitchen
and S. Bazin, W.B. Saunders Company Ltd., 98.
Dyson, M.
(1996) Die Rolle von interaktiven Wundverbanden in de Wundheilung. In:
"Wundheilung und Wundauflagen", edit. K.M. Sedlarik and H. Lippert,
Wissenschaftliche Verlagsgesellschaft mbH. 99.
El Sayed,
S. and Dyson, M. (1996) Effect of laser pulse repetition rate and pulse
duration on mast cell number and degranulation. Lasers Surg. Med. 19, 433-437. 100.
Young,
S.R., Erian, A., and Dyson, M. (1996). High frequency diagnostic ultrasound: a
noninvasive, quantitative aid for testing the efficacy of moisturizers. Internat.
J. Aesthetic Restor. Surg., 4(2), 1.5. 101.
Davies,
J.R., Dyson, M., Mustafa, Y., 102.
Nicolopoulos,
N., Cavadias, C., Karameris, A., Dyson, M, Tsourouktsoglou, Kondoyannis, P.
(1996) The use of laser surgery in subtotal meniscectomy and the effect of
low-level laser therapy on the healing potential of rabbit meniscus: an
experimental study. Lasers Med. Sci., 11, 109-115. 103.
Calvin, M.,
Modari, B., Young, S.R., Koffman, G. and Dyson, M. (1997) Pilot study using
high-frequency diagnostic ultrasound to assess surgical wounds in renal
transplant patients. Skin Res. Technol., 3, 60-65. 104.
Dyson, M.
(1997) Advances in wound healing physiology: the comparative perspective.
Veterinary Dermatol., 8, 227-233. 105.
Sussman, C.
and Dyson, M. (1998) Therapeutic and Diagnostic Ultrasound. In: "Wound
Care: A Collaborative Manual for Physical Therapists and Nurses", edit. C.
Sussman and B.M. Bates-Jensen, Aspen Publishers, Inc., 106.
Webb, C.,
Dyson, M. and Lewis, W.H.P. (1998) Stimulatory effect of 660 nm low level laser
energy on hypertrophic scar-derived fibroblasts: possible mechanisms for
increase in cell counts. Lasers Surg. Med. 22, 294-301. 107.
Calvin, M.,
Rymer, J., Young, S.R. and Dyson, M. (1998) Physiological effects of oestrogens
relevant to wound healing. In: "Management of the Menopause: Annual Review
1998", Edit. J. Studd, Parthenon Publishers, pp.27-38. 108.
Agaiby, A.,
Ghali, L and Dyson, M. (1998) Laser modulation of T-lymphocyte proliferation in
vitro. Laser Therapy, 10, 153-158. 109.
Calvin, M.,
Dyson, M., Rymer, J. and Young, S.R. (1998) The effect of ovarian hormone
deficiency on wound contraction in a rat model. Br. J. Obstet. Gyn. 105,
223-227. 110.
Agaiby, A.
and Dyson, M. (1999) Immuno-inflammatory cell dynamics during cutaneous wound
healing. J. Anatomy 195, 531-542. 111.
Mirpuri,
N.G., Dyson, M., Rymer, J., 112.
Chen, L.,
Dyson, M, Rymer, J., Bolton P,A, and Young, S.R. (2001) The use of
high-frequency diagnostic ultrasound to investigate the effect of hormone
replacement therapy on skin thickness. Skin Res. Technol., 7, 95-97. 113.
Dyson, M.
and Lyder, C. (2001) Wound management: physical modalities. In: "The
Prevention and Treatment of Pressure Ulcers", Edit.MJ Morison, Mosby,
Edinburgh, pp.177-193. 114.
Dyson, M.
(2002). The role of high frequency ultrasound in monitoring soft tissue injury
and repair: a new means of investigating laser bioeffects. Proceedings of the 8th
Annual Conference of the Section of Bioengineering of the Royal Academy of
Medicine in Ireland and the 16th Meeting of the Northern Ireland
Biomedical Engineering Society, 8. 115.
Kitchen,
S., Dyson, M. (2002) Low-energy treatments: nonthermal or microthermal? In:
"Electrotherapy: Evidence-based practice", Edit. S.Kitchen, Churchill
Livingstone, Edinburgh, pp.107-112. 116.
Webb, C.,
Dyson, M. (2003) The effect of 880 nm low level laser energy on human
fibroblast cell numbers: a possible role in hypertrophic wound healing. J.
Photochem. Photobiol. B: Biology, 70:39-44. 117.
Dyson, M.,
Moodley, S., Verjee, L, Verling, W., Weinman, J., Wilson, P. (2003) Wound
healing assessment using 20 MHz ultrasound and photography. Skin Res. Technol.
9:116-121. 118. Dyson, M. (2004)
Adjuvant therapies: ultrasound, laser therapy, electrical stimulation,
hyperbaric oxygen and negative pressure therapy. In: "Chronic Wound Care:
a problem-based learning approach". Edit. MJ Morison, LG Ovington, K
Wilkie, Mosby, Edinburgh, pp.129-159. 119. Ebrecht, M., Hextall,
J., Kirtley, L-G., 120.
Loudon J,
Cagle P., Dyson M. (2005) High frequency ultrasound: an overview of potential
uses in physical therapy. Phys. Ther. Rev. 10(4):209-215. 121.
Dyson, M.
(2006) Heat and Cold, Therapeutic. In "Encyclopedia of Medical Devices and
Instrumentation." , 2nd edition, Volume 3. Edit. JG Webster,
John Wiley & Sons, Inc., 122. Quintavalle PR, Lyder
CH, Mertz PJ, Phillips-Jones C, Dyson M. (2006) Use of high-resolution,
high-frequency diagnostic ultrasound to investigate the pathogenesis of
pressure ulcer development. Adv Skin Wound Care. 19(9):498-505. 123.
Dyson, M. (2007)
Adjuvant therapies: ultrasound, laser therapy, electrical stimulation,
hyperbaric oxygen and vacuum-assisted closure therapy. In: "Leg
Ulcers: A problem-based learning approach". Edit. MJ Morison, C Moffatt, P
Franks, Mosby Elsevier Limited, Edinburgh, pp.429-451. 124. Cagle PE, Dyson M,
Gajewski B, Lukert B. 'Can dermal thickness measured by ultrasound
biomicroscopy assist in determining osteoporosis risk?' Skin Research &
Technology 2007, 13:95-100. 125. Dyson M. 'How phototherapy
affects the immune system'. In: 'Mechanisms for Low-Light Therapy III, edited
by Hamblin MR, Waynant RW, Anders J. Proc. of SPIE 2008, 6846:684605-1 -
684605-10. BOOKS Miller, M. and Dyson, M. (1996) “Principles of
Wound Care”, Macmillan Magazines, Ltd. Contributions have been made to the following: 1. “Gray’s
Anatomy” (1996), 35th Edition, edit. R. Warwick and P.L. Williams,
Churchill Livingstone, Edinburgh. 2.
“Fundamental
and Applied Aspects of Non-ionizing Radiation” (1975), edit. S.M. Michelson
and M.W. Miller, Plenum Publishing
Corporation, 3.
“Ultrasonography
in Obstetrics and Gynaecology” (1977), 1st Edition, edit. R.C.
Sanders and A.E. James, Appleton-Century-Crofts, 4.
“Gray’s Anatomy” (1980), 36th
Edition, edit. P.L. Williams and R. Warwick, Churchill Livingstone, Edinburgh. 5.
“Ultrasonography
in Obstetrics and Gynaecology” (1980), 2nd Edition, edit. R.C.
Sanders and A.E. James, Appleton-Century-Crofts, 6.
“The
Surgical Wound” (1981), edit. P. Dineen, Lea and Febiger, 7.
“A
Companion to Dental Studies” (1982) edit. A.H.R. Rowe and R.B. Johns, Blackwell
Scientific Publications, BOOKS CO-EDITED 1.
“Gray’s
Anatomy” (1989) 37th Edition, edit. P.L. Williams, R. Warwick, M.
Dyson and L.H. Bannister, Churchill Livingstone, Edinburgh. 2.
“Gray’s
Anatomy” (1995) 38th Edition, edit. P.L. Williams, L.H. Bannister,
M. Berry, P. Collins, M. Dyson, J.E. Dussek and M.W.J. Ferguson. Churchill Livingstone, Edinburgh. INVITED LECTURES AND COMMUNICATIONS Over 250 invited lectures and over 60
communications have been presented in Europe, the |
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