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Photodisinfection

Photodisinfection is a topical, broad spectrum antimicrobial technology, targeting virus, fungi and bacteria. The process efficiently destroys endo- and exotoxins, directly reduces inflammation, is capable of eliminating both intracellular and extracellular pathogens and is highly effective against cross-linked biofilm matrix, a characteristic feature of CRS pathology. Photodisinfection has demonstrated pathogen reduction, including antibiotic resistant CRS polymicrobial biofilms, by >99.9% immediately after a single treatment.

The induced effect is target-specific to only those organisms that have absorbed the photosensitizer and are exposed to a specific wavelength of light, and has no effect on human tissue. Photodisinfection is equally effective against normal strains and antibiotic resistant pathogens. Furthermore, there is no evidence of bacterial resistance occurring after repeated photodisinfection treatment cycles. The photodynamic mechanism of pathogenic cell destruction is by perforation of the cell membrane or wall by photodisinfection-induced singlet oxygen and oxygen radicals, thereby allowing the dye to be further translocated into the cell. Once there, the photosensitizer, when activated, causes cellular damage, membrane lysis, protein inactivation and induces rapid cell death. The photodisinfection mechanism of microbial cell death is different to the cell death of oral and systemic antimicrobial agents. There is no metabolic or thermal action involved with this non-systemic therapy.

Photodisinfection may also be deployed as an adjunct to Functional Endoscopic Sinus Surgery (FESS) or Functional Endoscopic Dilation of the Sinus (FEDS) procedures, thereby enhancing patient outcomes, providing an alternative to patients for whom few or no alternate therapies exist, and increasing the number of referrals made by the General Practitioner.

Photodisinfection Rapidly Destroys Pathogens

The photodisinfection reaction is well understood and follows this simplified mechanism:

1. A photosensitizing solution is applied to the treatment site where the photosensitizer molecules preferentially bind to the targeted microbes. The photosensitizer molecules are inactive at this stage.
2. A light of a specific wavelength and intensity illuminates the treatment site. The wavelength is carefully chosen to maximize absorption of light energy by the photosensitizer.
3. A photocatalytic reaction occurs. This results in the destruction of the targeted microbes and their virulence factors1, without damaging host cells. This reaction involves the formation of short-lived, highly reactive free-radical oxygen species. These radicals cause a physical disruption of the microbial cell membrane through oxidative reactions, resulting in immediate rupture and destruction of the cell. The process has also been shown to eliminate a multitude of virulence factors, leading to a clinically observable anti-inflammatory effect.
4. When the light is removed the photocatalytic reaction ceases.

Unlike antibiotics, which require hours to days to exert their effect, photodisinfection works instantaneously, destroying microbes upon light activation. The speed at which the reaction occurs, its broad range of targets and other features make it highly unlikely that microorganisms will develop resistance to photodisinfection2,3, thus positioning photodisinfection as an important alternative to antibiotic treatment for non-systemic infections.

Photodisinfection therapy is well suited to the treatment of chronic sinusitis because of the technology’s proven immediate antimicrobial and anti-inflammatory effects.


1. Darveau R et al. Antimicrobial Photodynamic Therapy May Promote Periodontal Healing Through Multiple Mechanisms. Journal of Periodontology. 2009, Vol. 80, No. 11, Pages 1790-1798
2. Pedigo, LA et al. Absence of bacterial resistance following repeat exposure to photodynamic therapy. Proc. SPIE, Vol. 7380, 73803H (2009).
3. Tavares, A et al. Antimicrobial Photodynamic Therapy: Study of Bacterial Recovery Viability and Potential Development of Resistance after Treatment. Mar Drugs. 2010 January; 8(1): 91–105.