Red Light Therapy for Keloids & Scar Tissue

Keloids and hypertrophic scars represent an overreaction of the wound healing process. Whilst normal scars form, mature, and flatten over time, keloids grow beyond the boundaries of the original wound and hypertrophic scars remain raised and thickened. Both involve excessive collagen deposition, and both are notoriously difficult to treat.

The relationship between red light therapy and keloids is complicated by a fundamental tension: PBM generally stimulates collagen production — which is beneficial for wound healing and anti-ageing, but potentially problematic for a condition caused by too much collagen.

Understanding keloids and hypertrophic scars

Keloids

Keloids extend beyond the margins of the original wound. They are more common in people with darker skin (African, Asian, and Hispanic heritage), can appear months or years after injury, and tend not to regress spontaneously. Common trigger sites include the earlobes, chest, shoulders, and upper back.

Keloid formation involves:

Excessive collagen type I and III deposition — Far beyond what is needed for wound repair
Persistent inflammation — Elevated TGF-beta, IL-6, and other pro-fibrotic mediators
Fibroblast dysfunction — Keloid fibroblasts are hyperactive and resistant to normal apoptosis signals
Altered extracellular matrix remodelling — The balance between collagen synthesis (by fibroblasts) and breakdown (by matrix metalloproteinases) is shifted towards net accumulation

Hypertrophic scars

Hypertrophic scars stay within the wound boundaries but remain raised, red, and thickened. They are more common than keloids and are more likely to improve over time (12–24 months). The underlying biology is similar to keloids but less extreme.

Current treatments

Both conditions are difficult to treat. Options include:

Silicone sheets/gel — Moderate evidence, first-line for hypertrophic scars
Intralesional corticosteroid injection (triamcinolone) — First-line for keloids, reduces collagen synthesis
Pressure therapy — Particularly for burn scars
Cryotherapy — Freezing the scar tissue
Surgical excision — High recurrence rate for keloids (50–80%) unless combined with adjuvant therapy
Radiation — Used post-excision for keloid prevention
5-fluorouracil — Intralesional injection, anti-fibrotic
Laser therapy — Pulsed dye laser and fractional CO2 laser (these are ablative/vascular lasers, not PBM)

The evidence for PBM and keloids

The limited research

Direct clinical evidence for PBM (low-level red/NIR light) treating established keloids is very limited. Most studies examining “laser therapy for keloids” use ablative or vascular lasers (pulsed dye, Nd:YAG, CO2 fractional) that work through entirely different mechanisms — they destroy tissue, coagulate blood vessels, or create controlled micro-injuries. These are not PBM.

A small number of in vitro and animal studies have examined PBM effects on keloid fibroblasts and scar tissue:

Barolet and Bhourizi (2018) examined 660nm LED treatment on keloid fibroblasts in culture. They found that PBM at specific doses reduced keloid fibroblast proliferation and collagen production. Interestingly, the effect was dose-dependent — low doses stimulated fibroblast activity (as expected from normal PBM), whilst higher doses had an inhibitory effect.

Dang et al. (2014) investigated 635nm light on scar tissue in an animal model and reported modulation of TGF-beta signalling — a key pathway in fibrosis and keloid formation. The study suggested PBM could shift the TGF-beta isoform ratio in ways that favour scar remodelling rather than excessive collagen deposition.

Collagen remodelling vs collagen synthesis

This is the critical nuance. PBM’s effect on collagen is not simply “more collagen.” Research suggests PBM can:

Stimulate collagen synthesis in deficient tissue (wound healing, ageing skin) — well established
Promote collagen remodelling — Increasing matrix metalloproteinase (MMP) activity alongside collagen synthesis, resulting in better-organised collagen rather than simply more of it
Modulate fibroblast behaviour — In some contexts, PBM normalises overactive fibroblasts rather than simply stimulating them further

Whether PBM can achieve net collagen remodelling (rather than net accumulation) in keloid tissue specifically is not established. The in vitro studies are suggestive but insufficient.

PBM for scar prevention (post-surgical)

A more promising application may be using PBM during wound healing to promote better scar formation from the outset, rather than trying to treat established keloids:

Carvalho et al. (2010) found that PBM applied during wound healing in animal models produced better-organised collagen fibres and less scar tissue compared to unirradiated wounds.

Taradaj et al. (2013) examined PBM after caesarean section and found improved scar appearance scores at follow-up, suggesting that PBM during the healing phase can influence final scar quality.

This approach — using PBM to prevent problematic scarring rather than treat established keloids — has a stronger biological rationale and is consistent with PBM’s known wound healing effects.

The concern: could PBM worsen keloids?

This is a legitimate question. If PBM stimulates collagen production and fibroblast proliferation (which it does in most contexts), could treating a keloid with red light make it grow faster?

Theoretically possible, but not clearly demonstrated. The in vitro evidence (Barolet and Bhourizi, 2018) suggests that keloid fibroblasts may respond differently to PBM than normal fibroblasts, with certain doses actually inhibiting their activity. But in vitro does not equal in vivo, and the dose-response relationship is complex.

Practical advice: If you have active, growing keloids, do not apply PBM directly to them without guidance from a dermatologist. The risk of stimulating further growth is theoretical but cannot be excluded.

A cautious protocol

For scar prevention (during wound healing)

Wavelength: 660nm (red) — most evidence for wound healing
Dose: 4–8 J/cm²
Timing: Begin 48–72 hours after wound closure (allow initial haemostasis)
Frequency: Daily for 2–4 weeks, then every other day for a further 4 weeks
Application: Directly over the healing wound/incision site

For established hypertrophic scars (NOT keloids)

Wavelength: 660nm or 830nm
Dose: 4–10 J/cm²
Frequency: 3–5 times per week
Duration: 8–12 week trial period
Monitor: Photograph the scar weekly under consistent lighting conditions to objectively assess changes. If the scar appears to be enlarging, stop treatment

For established keloids

Not recommended without dermatologist supervision
The evidence is insufficient to justify PBM for active keloids
If your dermatologist uses PBM as part of a combination treatment protocol (e.g., after intralesional steroid injection), that is a clinical decision based on their expertise

The bottom line

The evidence for PBM and keloids/scarring is limited and nuanced. PBM may help with scar prevention during wound healing and could modestly improve hypertrophic scar appearance. For established keloids, the evidence is insufficient, and there is a theoretical concern about stimulating further collagen deposition.

Do not confuse PBM (low-level red/NIR light) with ablative or vascular laser treatments, which work through entirely different mechanisms and have a more established role in scar management. If you have problematic keloids, see a dermatologist for evidence-based treatment rather than relying on consumer light therapy devices.

The most sensible application of PBM in this context is preventive — using it during wound healing to promote better scar formation. This aligns with PBM’s well-established wound healing effects and avoids the uncertain territory of treating established keloid pathology.