Photodynamic Therapy (PDT) devices serve as precise activation catalysts in the treatment of keloids, functioning far beyond simple light exposure. Their primary role is to emit specific wavelengths of light that trigger photosensitive substances previously absorbed by the lesion, creating a chemical reaction that selectively destroys abnormal tissue.
Core Insight: Photodynamic Therapy represents a shift from suppressing symptoms to targeting the biological engine of the scar. By combining light energy with photosensitive agents to generate reactive oxygen species, PDT devices actively dismantle the abnormal vascular networks and proliferating cells that drive stubborn keloid growth.
The Mechanism of Action
Precise Activation of Agents
PDT devices are designed to deliver a specific wavelength of light matched to a photosensitive drug (photosensitizer).
The device itself does not heal the tissue directly; rather, it acts as the trigger. Once the photosensitizer is delivered to the scar tissue, the device’s light activates it, initiating a localized therapeutic process.
Generation of Reactive Oxygen Species
Upon activation by the device, the photosensitizer generates reactive oxygen species (ROS).
These reactive molecules are the actual "workers" in the therapy. They induce localized oxidative stress, which is lethal to the targeted cells but spares the surrounding healthy tissue.
Biological Impact on Keloid Tissue
Destruction of Proliferating Cells
The primary target of the ROS generated by PDT is the population of actively proliferating cells.
In keloids, these are usually fibroblasts behaving aggressively. By targeting these cells, the therapy effectively halts the expansion of the scar tissue.
Targeting Abnormal Vascular Systems
Keloids are sustained by a network of abnormal blood vessels that feed the scar tissue.
The reactive oxygen species generated by the PDT process precisely target and destroy these abnormal vascular systems. Cutting off this blood supply is critical for reducing the redness and bulk of the lesion.
The Role of Blue Light Wavelengths
Inhibiting Fibroblast Proliferation
Many professional-grade devices utilize blue LED light, typically around 470 nm.
Research indicates that this specific wavelength utilizes Photobiomodulation (PBM) to directly inhibit the rate at which fibroblasts replicate. This reduces the total number of collagen-producing cells within the keloid.
Reducing Recurrence Risks
The application of blue light has been shown to reduce the expression of TGF-beta, a protein signaling molecule heavily involved in scar formation.
By lowering TGF-beta levels, the therapy provides a physical intervention that not only improves the quality of the scar but significantly minimizes the risk of the keloid returning after treatment.
Understanding the Trade-offs
Requirement for Photosensitizers
Unlike simple laser therapy, PDT is a two-part process requiring the administration of a drug before light application.
This adds a layer of complexity to the treatment protocol. Success relies heavily on the proper delivery and uptake of the photosensitive substance into the lesion before the device is used.
Selectivity vs. Penetration
While the generation of ROS is highly selective for abnormal cells, light penetration can be limited by tissue depth.
Thick, stubborn keloids may require specific wavelengths or multiple sessions to ensure the light reaches the deeper layers of the scar tissue where the photosensitizer is located.
Making the Right Choice for Your Goal
- If your primary focus is non-invasive reduction: Look for PDT protocols that emphasize the vascular destruction capability of the device, as cutting off blood supply is the most effective way to flatten raised scars without surgery.
- If your primary focus is preventing recurrence: Prioritize devices or protocols that incorporate blue light (470 nm) photobiomodulation to actively lower TGF-beta expression and inhibit fibroblast proliferation.
Summary: PDT devices offer a sophisticated, non-invasive method for controlling pathological scars by chemically targeting the root biological causes of keloid growth rather than just the surface symptoms.
Summary Table:
| Mechanism Component | Therapeutic Action | Clinical Benefit |
|---|---|---|
| Photosensitizer Activation | Triggers Reactive Oxygen Species (ROS) | Selective destruction of abnormal scar tissue |
| Vascular Targeting | Dismantles abnormal blood vessel networks | Reduces keloid redness, bulk, and nutrition supply |
| Blue Light (470 nm) | Inhibits TGF-beta and fibroblast replication | Prevents recurrence and halts scar expansion |
| Oxidative Stress | Induces localized lethal stress to lesions | Spares surrounding healthy tissue from damage |
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References
- Ya. P. Nahirniy. COMPARISON OF CONSERVATIVE METHODS OF PREVENTION OF PATHOLOGICAL SCARING OF THE HEAD AND NECK. DOI: 10.31718/mep.2022.26.5-6.10
This article is also based on technical information from Belislaser Knowledge Base .
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