LLLT, lllt, laser therapy - biostimulation
The Low Level Laser Therapy -
LLLT Internet Guide

LLLT - laser therapy -
Guest Editorial

This page includes
LaserWorld Guest Editorial,Nr 9 - 2000.
Low level laser therapy (LLLT) - Does it damage DNA?
By Jena e-mail: kog@imb-jena.de website: www.imb-jena.de/greulich

LaserWorld Guest Editorial,Nr 10 - 2000.
Laser and Plaquex treatment on cryoglobolic vasculitis on diabetic foot
(Case report summary)
By Anita Baxas

LaserWorld Guest Editorial,Nr 11 - 2000.
The Roles of Laser Therapy in tissue Repair and Sports Injuries
By Chukuka S. Enwemeka
LaserWorld Guest Editorial, Nr 12 - 2000.
Regulation of Medical Devices in Australia
By Peter A. Jenkins
See other editorials


 

LaserWorld Guest Editorial, Nr 9 - 2000.

 

Low level laser therapy (LLLT) - Does it damage DNA?

K.O.Greulich, Inst.Mol.Biotech Postfach 100813 D 07708
Jena e-mail: kog@imb-jena.de website: www.imb-jena.de/greulich

Low level laser therapy (LLLT) has been found beneficial in a wide variety of therapeutic applications (see for example 1). However, some concern has arisen on possible DNA damage. May it be possible that it benefits the patient only at a first glance but damages DNA and therefore increases the risk of therapy induced disease up to an increased cancer risk ?

What are the facts ? LLLT is usually performed with red (630 nm) or near infrared (830nm ) laser light. Typical accumulated doses per area are of the order of a few Joules per square centimeter. What an effect may such irradiation may have on DNA ? Unfortunately, most studies on the effects of radiation on DNA are performed with ionizing radiation (alpha, beta , gamma rays) or with UV light. There, DNA damage may be dramatic, although such studies have revealed a surprisingly strong DNA repair capacity of otherwise healthy human cells. Even when the overall integrity of a cell's genome is seriously degraded, the damaged DNA can be repaired without directly detectable consequences (although long term mutational damage cannot be completely excluded).

One efficient and comparably simple technique, requiring basically only a fluorescence microscope and a gel electrophoresis device, to study DNA damage and repair is "Single Cell Gel Electrophoresis" (SCGE). Cells are embedded in an electrophoresis gel, their cell nuclei are perforated chemically and subsequently an electric field is applied (2-5). Since under suitable physicochemical conditions DNA is negatively charged, it migrates towards the electrically positive side of the gel. In a given time, small DNA fragments migrate a long distance (10-20 micrometers), large molecules migrate a correspondingly shorter distance. Very large DNA molecules cannot leave the cell nucleus. When the DNA of a cell is undamaged, it remains in the nucleus, which appears in a microscope, after staining with a fluorescence dye, as a sphere, or two dimensionally as a circle. When part of the DNA is damaged, the latter migrates out of the nucleus.After staining, such a cell has the appearance of a comet with bright head and a tail whose length (or a more quantitative parameter called tail moment) is a measure for the degree of damage. Therefore, SCGE is also called the COMET assay.

Using this COMET assay, light induced DNA damage has been studied in the wavelength range from 308 nm (UV) to approx. 450 nm (blue) (6) . While at 308 nm (UV) 0.0001 Joules per square centimeter were sufficient to induce detectable DNA damage, 1 Joule per square centimeter was required at 450 nm. The damage declined exponentially with wavelength. When one extrapolates this to the wavelengths which are used for LLLT, one can estimate that at least a thousandfold dose for 630 nm and a millionfold dose for 830 nm would be required to induce DNA damage detectable by the COMET assay.Probably the effects are even smaller, since in ref.6 a pulsed laser source was used, which often generates more damage than a corresponding continuous laser.

There is still the possibility that the COMET assay is just not sensitive enough to detect minor, but harmful DNA damages. However, one can compare the amount of radiation with that of sunlight. Bright sunlight has a power per area (=intensity) of 0.1345 Watts per square centimeter, which. after irradiation for only ten seconds, results in a dose per area of 1.345 Joule per square centimeter, comparable to what is used in LLLT, integrated over the whole spectral range. When one filters out a wavelength band of +/- 10 nm, Sun radiation for a few minutes is required to accumulate a few Joules per square centimeter. Such an irradiation is not generally supposed to cause disease. Since we are on the red side of the optical spectrum which, as mentioned above, is less DNA damaging than the average sunlight, we are on the safe side when we assume that the doses per area as they are used in LLLT correspond to the DNA damaging effects of a few minutes sunbath. If any DNA breaks are induced by such irradiation, they will be repaired immediately, otherwise even a short sunbath would cause mutations and finally cancer.

May that mean that LLLT does produce no effect at all, that everything is placebo effect ? Again, COMET assay experiments give a hint: when one first irradiates cells of the bacterium Escherichia coli (7) or human lymphocytes (8) with red (He-Ne) laser light (0.054 - 0.27 Joules per square centimeter) and then tries to damage DNA by UV irradiation, DNA fragmentation is much lower than without pre- irradiation with red light. An interpretation of this effect is that the pre-irradiation activates enzymes of the DNA repair machinery which immediately repairs possible UV damages. Since the effect is similar for cells as different as bacterial and mammalian cells one may conclude that it is evolutionarily conserved. In addition, these experiments indicate that low level laser illumination indeed can cause beneficial effects.

In conclusion, COMET assay experiments reveal possible therapeutic effects of LLLT but do not indicate a risk of DNA damage.

References:

  1. Z.Simunovic editor Lasers in Medicine and Dentistry : LLLT 2000 Eur.Med.Laser Association. Access via www.lasermedico.ch
  2. O.Östling, K.J. Johanson Microelectrophoretic study of radiation induced DNA damages in individual mammalian cells 1984 Bioch.Bioph.Res.Comm.123,291-2982
  3. N.Singh, M.Mc Coy, R.Tice, E.Schneider A simple technique for quantification of low levels of DNA damage in individual cells 1988 Exp.Cell Res. 175,184-191
  4. P.L.Olive,D.Wlodek,J.P.Banath DNA double strand breaks measured in individual cells subjected to gel electrophoresis 1991 Cancer Res.51, 4671-4676
  5. A.Rapp, C.Bock, A.Rapp, H.Dittmar, K.O.Greulich 2000 J.Photochem. Photobiol. in press UV-A breakage sensitivity of human chromosomes measured by COMET-FISH depends on gene density and is not dependent on chromosome size,
  6. A.de With, K.O.Greulich Wavelength dependence of laser induced DNA damages in lymphocytes observed by single cell gel electrophoresis 1995 J.Photochem.Photobiol.B,30,71-76
  7. R.Kohli, P.K.Gupta, A.Dube He-Ne laser pre-irradiation induces protection against UV C radiation in wild type E coli strain K12B1157 2000 Rad.Res.153, 181-185
  8. A.Dube, C.Bock, E.Bauer, R.Kohli, P.K.Gupta, K.O.Greulich He-Ne laser protects B-lymphoblasts from UV induced DNA damage 2000 Rad.Env. Bioph.submitted

 

LaserWorld Guest Editorial, Nr 10 - 2000.

  Laser and Plaquex treatment on cryoglobolic vasculitis on diabetic foot
(Case report summary)

By Anita Baxas, Binningen, Switzerland

A 53-year old male patient presented himself with non-insulin-dependent diabetes mellitus since 5 years as well as an active hepatitis C infection of unknown cause and duration. He developed inflamed and swollen blisters on his first and second toes of his right foot over night. The head of the dermatological outpatient clinic at the University hospital of Basel, Switzerland diagnosed a vasculitis due to cryoglobulins caused by the hepatitis C infection. Within a few days the tips of the toes turned purple and the danger of an amputation increased due to the reduced capillary blood flow caused by diabetes (left photo). We treated the patient locally with Low Level Laser therapy to promote wound healing and intravenously with Plaquex infusions to improve capillary blood circulation. After 3 weeks of treatment with a total of 10 Plaquex infusions and daily application of laser therapy (in-office and with home care laser) we could promote granulation to the point that the wounds healed completely without sequel (right photo, after 3 weeks).

Material and Method:

- Doctor's Office:
Laser Model Med-2000 (LASOTRONIC Baar Switzerland), Output 120 mW (3 Diodes plus red pilot light) approx. 30° divergence. Wavelength: 830 nm (infrared). Mode c.w. (continuous wave), distance from wound: 0.5 - 1 cm. Dose: 4 joules/ cm2. Frequency: daily treatments (5 x per week) for 3 weeks (15 treatments). Duration per toe: approx. 30 minutes total.
- Home treatment:
Laser Model Med-130 (LASOTRONIC Baar, Switzerland). Output: 45 mW 830nm (1 Diode, approx. 30° divergence). Mode c.w. (continuous wave), distance from wound: 0.5 - 1 cm. Dose: 4 joules / cm2, 3 - 4 treatments daily for 3 weeks.

INFO:
Anita Baxas, praktische Aerztin,
CH-4102 Binningen

Joachim W. Picht, praktischer Arzt, D-79098 Freiburg Baxamed AG Hauptstrasse 4 CH-4102 Binningen

 


 


LaserWorld Guest Editorial, Nr 11 - 2000.

 

The Roles of Laser Therapy in tissue Repair and Sports Injuries

Chukuka S. Enwemeka, P.T., Ph.D.,
FACSM Professor & Chairman Department of Physical Therapy,
University of Kansas Medical Center,
3901 Rainbow Boulevard, Kansas City,
KS 66160-7601 USA

Connective tissue injuries, such as tendon rupture and ligamentous strains, occur frequently in sports and athletic activities. Unlike most soft tissues that require 7-10 days to heal, primary healing of tendons takes at least six weeks during which they are protected in immobilization casts. Such long periods of immobilization impair motor rehabilitation and predispose a multitude of complications including, muscle atrophy, trophic neural changes, osteoarthritis, skin necrosis, infection, tendo-cutaneous adhesion, re-rupture, and thrombophlebitis.

If healing can be quickened, then, the duration of cast immobilization can be reduced to minimize the deleterious effects of immobilization. In separate studies, we tested the hypothesis that early weight-bearing, ultrasound, He-Ne laser, and Ga-As laser, when used singly or in combination, accelerate the healing process of experimentally tenotomized and repaired rabbit Achilles tendons as evidenced by biochemical, biomechanical, and morphological indices of healing. Our results warrant the conclusions that:
(1) appropriate doses of each modality, i.e., early weight-bearing, ultrasound, He-Ne and Ga-As laser therapy augment collagen synthesis, modulate maturation of newly synthesized collagen, and overall, enhance the biomechanical characteristics of the repaired tendons.
(2) Compared to the physical agents, i.e., ultrasound, and laser therapy, early weight-bearing offers the most potent stimulus for accelerating the healing process of repaired tendons.
(3) Combinations of either of the two lasers with early weight-bearing and either ultrasound or electrical stimulation further promote collagen synthesis when compared to early weight-bearing alone.

However, the biomechanical effects measured in tendons receiving the multi-modality therapy were similar, i.e., not better than the earlier single modality trials. Although healing of repaired human tendons may differ from healing of the rabbit Achilles tendon, these findings suggest that sportsmen and sportswomen with connective tissue injuries, such as Achilles tendon rupture, may benefit from appropriate doses of early weight-bearing, ultrasound, He-Ne laser, and Ga-As laser therapy when used singly or in combination with one another. Furthermore, our preliminary studies indicate that certain wounds and ulcers, as for example, those associated with sports and athletic activities, benefit from appropriate doses of laser therapy as well. Our recent meta-analyses of the laser therapy literature corroborate these findings.

 

LaserWorld Guest Editorial, Nr 12 - 2000.

 

Regulation of Medical Devices in Australia

Peter A. Jenkins MBA, AIMM spectra@spectra-medics.com

In 2001 the Australian Federal Government will introduce new legislation which will substantially change the way medical devices are regulated by the Therapeutic Goods Administration (TGA).

Although the changes will primarily affect manufacturers and sponsors of medical devices, their impact is likely to be felt across the healthcare system in general. Therefore, it's important that medical practitioners are made aware of the changes and the possible ramifications, and gain an understanding of how the new regulations may affect their purchase and subsequent use of medical devices.

Following the signing of a Mutual Recognition Agreement (MRA) with the European Union in 1998, and as a principal member of the Global Harmonisation Task Force (GHTF), Australia has actively pursued international regulatory harmonisation of medical devices. The European Community (EC) approach to medical device regulation, which encompasses Medical Devices Directive 93/42/EEC, is widely recognised as a defacto world standard , and for this reason Australia has chosen to adopt this model.

By aligning Australia's requirements for the quality, safety and performance of medical devices with those of the EC's benchmark regulatory environment, a number of shortcomings in the present Australian system will be redressed.

The new system will introduce rigorous pre-market evaluation procedures for a much broader range of medical devices than is covered by the current system, and will embody a mandatory reporting system for adverse events, and other post-market surveillance procedures.

Manufacturers and sponsors of devices already listed in the Australian Register of Therapeutic Goods (ARTG) at the time the new system is introduced will have a period of five years in which to ensure their devices meet the new requirements.

After the new system is introduced, any new or existing medical device - that is not listed in the ARTG prior to the implementation date of the new regulations - must be included on the ARTG in accordance with the new regulations before it can be legally placed on the market in Australia.

According to the TGA: "Consumers will benefit from the confidence of having comprehensive quality and performance requirements applied to all medical devices used in Australia." Australia's alignment with the EC will also provide timely local access to new and safer medical technologies as they enter the world market.

Over the longer term the new system is expected to assist Australian manufacturers of medical devices to attain and maintain international best practice, ensuring our ongoing competitiveness in an increasingly globalised marketplace and protecting Australia's reputation as a world-class producer of medical technologies.


Disclaimer: This paper is based solely upon the author's understanding of the existing and proposed medical devices regulations. The actual interpretation of these regulations for legal purposes may differ. Therefore, it is recommended that individuals requiring more detailed advice consult the Therapeutic Goods Administration and/or a their professional legal adviser.


The term 'sponsor' refers to the importer or local representative of a medical device, whether this be a retailer, distributor, or an individual practitioner who imports a medical device directly for use on their patients. Therapeutic Goods Administration paper (Feb 2000) 'Background And Information On The Proposed New Harmonised Regulatory Requirements For Medical Devices' p1 Therapeutic Goods Administration Information Sheet: 'Medical Devices - A New Approach to Regulation: General Information' p2 Contact the TGA's Conformity Assessment Branch (02) 6232 8613, or visit the TGA web site at www.health.gov.au/tga for more information.

   

 

 
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