Dr Mary Dyson “Low Level Laser Therapy”

“Low Level Laser Therapy”
Mary Dyson PhD, FCSP
Emeritus Reader in the Biology of Tissue Repair, Kings College London, UK;
Former Professor, Department of Physical Therapy & Rehabilitation Sciences, University of
Kansas Medical Center, Kansas City, USA.

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 Softlaser Plus, formerly the Beurer SoftLaserTM
and Laser Therapeutics SL50Evolution 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 SoftLaser Plus is a small, single-diode, hand held device emitting red light and designed for home use. The Laser
Therapeutics SL50 Evolution 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 SL50 Evolution Cluster Laser is an example of a cluster probe suitable for home
use. It contains 8 laser diodes that emit red light at 635 nm and 4 laser diodes that emit infrared
(IR) electromagnetic radiation at 830nm.

The Softlaser Plus



The SL50 Evolution Cluster Laser

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 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).


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.


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.


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 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 Tlymphocytes
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
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.


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 Softlaser Plus (formerly Beurer SoftLaserTM)

This hand-held LLLT device is a low power Class 2M laser manufactured by Health and Beauty. It
contains a single 5 mW GaAlAs diode producing red light of 635 nm wavelength. It is
powered by 2 AAA batteries.

Application of Softlaser Plus 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.

The SL50 Evolution

The SL50 Evolution is an example of a cluster probe suitable for home use. It has 8
laser diodes that emit red light at 635 nm and 4 laser diodes that emit infrared electromagnetic
radiation at 830 nm.

Application of the SL50 Evolution 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.


Effects of the SL50 Evolution Cluster Laser and the Softlaser Plus on Skin

The SL50 Evolution Cluster Laser and the Softlaser Plus have been reported by its users
 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 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
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.


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.


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.


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).


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 jumpstarted
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 home
where it can be used regularly for skin care and pain relief.

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NAME: Dr. Mary Dyson (nee DEPLEDGE)
BSc PhD MIBiol CBiol FCSP(Hon) FAIUM(Hon) FZS LHD(Hon)
33 King’s Road
United Kingdom
TELEPHONE: +44 (0)1442 874427
CELL PHONE +44 (0)07866 456 532
FAX +44 (0)1442 384859
E-MAIL md41139@aol.com
WEB www.marydyson.com

DEGREES 1961 BSc Class I Special Honours in Zoology
Specialist Subject: Embryology
Bedford College, University of London
1965 PhD
Topic: Wound Healing
Bedford College, University of London
1958 State Scholarship
Pfeiffer Scholarship (University of London)
West Riding of Yorkshire County Major Scholarship (Honorary)
1961 Busk-Howell Research Scholarship (University of London)
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, University of London, in recognition of services to the University and the subject
of Tissue Repair.
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 London
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.
1964-70 Research Associate
Department of Anatomy
Guy’s Hospital Medical School
University of London
1970-75 Lecturer
Department of Anatomy
Guy’s Hospital Medical School
University of London
1975-87 Senior Lecturer
Department of Anatomy
Guy’s Hospital Medical School
University of London
1987-98 Reader in Biology of Tissue Repair
Head, Tissue Repair Research Unit
Department of Anatomy
Guy’s Hospital Medical School (later United Medical and Dental Schools of
Guy’s and St Thomas’s Hospitals)
University of London
1998-2000 Director of Research and Development
Longport Inc
740 South Chester Road, Suite A
Swarthmore, PA 19081, USA
1974 Recognised as a Teacher of the University of London
1974-98 Member of the Board of Studies in Human Anatomy and Morphology,
University of London
1976-98 Examiner in Cytology and Histology, Guy’s Hospital Medical School
1976-98 Examiner in Anatomy, Guy’s Hospital Medical School
1981-98 Member of the Preclinical Subjects Sub-Committee of the Board of Studies in
Dentistry, University of London
1985-98 Member of the Panel of Visiting Examiners in Anatomy, University of London
1987-88 Member of Working Party considering introduction o