Discover how laser and light-based treatments effectively reduce keloids and improve skin healing.
Keloids are an overgrowth of fibrotic tissue that extends beyond the original wound margins and arises from defective wound healing. Unlike hypertrophic scars, which remain confined to the initial injury site, keloids grow outward and persist. Both lesions result from dysregulated fibroblast proliferation and collagen deposition after skin trauma. Keloids can impair function, appearance, and psychosocial wellbeing; quality-of-life studies report intense pain, pruritus, reddish discoloration, and continuous expansion. These scars are unique to humans and do not develop spontaneously in animals, and the absence of faithful animal models has slowed research into their pathogenesis and therapy.
Management options include surgical excision, intralesional or topical corticosteroids, intralesional 5-fluorouracil, bleomycin or interferon, topical imiquimod, compression, cryotherapy, radiation, silicone sheeting, and laser or light-based modalities. Recurrence remains frequent even with combined approaches. Laser and light technologies offer additional strategies that may improve appearance, relieve symptoms, and possibly lower relapse rates. These devices fall into three broad groups: ablative lasers, non-ablative lasers, and non-coherent light sources.
Non-ablative lasers act on hemoglobin or melanin. The 585–595 nm pulsed-dye laser (PDL), whose primary chromophore is oxyhemoglobin, also targets melanin, so pigmentary changes must be monitored. PDL is thought to diminish keloids by selectively injuring scar vasculature. The 980 nm diode laser affects both hemoglobin and melanin, while the 1064 nm neodymium-doped yttrium-aluminum-garnet and 532 nm neodymium-doped vanadate lasers are believed to damage deeper dermal vessels.
Non-laser light sources—intense pulsed light (IPL), light-emitting diode (LED) phototherapy, and photodynamic therapy (PDT)—are also employed. These methods deliver light energy that may modulate keloid fibroblast activity. IPL emits broadband pulsed light that targets pigment and vessels. LED phototherapy is hypothesized to photomodulate mitochondrial cytochrome c oxidase, thereby altering intracellular signaling. PDT entails topical application of a photosensitizer such as 5-aminolevulinic acid, which is preferentially taken up by metabolically active or highly vascular tissue and converted to protoporphyrin IX. Light activation generates reactive oxygen species that can be cytotoxic and may also modify extracellular-matrix turnover and cytokine expression.
The precise mechanisms by which topical PDT improves abnormal scars are unclear, but they likely involve downstream effects of the generated reactive oxygen species: membrane and mitochondrial injury activates signaling molecules such as TNF-α and interleukins 1 and 6, leading to cell death via apoptosis, necrosis, or autophagy. These events may shift growth-factor and cytokine profiles, thereby modulating collagen synthesis and matrix organization.
Because PDT penetrates only superficially, it may serve as an adjunct immediately after keloid excision to help reduce postoperative recurrence.
PMC overview on scar pathophysiology PubMed search for keloid light therapies
