Abstract

Keloids represent a pathological form of dermal fibrosis resulting from aberrant wound healing. Characterized by excessive collagen deposition extending beyond the original wound margins, they are resistant to conventional treatments. This paper investigates the anatomical pathology of keloids and details a novel approach for their treatment using the UltraPlasma™ multi-platform system integrating arc, argon, and helium plasma technologies. Emphasis is placed on the role of plasma-generated reactive oxygen and nitrogen species (RONS), including ozone (O₃), nitric oxide (NO), superoxide anion (O₂•⁻), hydroxyl radical (•OH), hydrogen peroxide (H₂O₂), nitrogen dioxide (NO₂•), peroxynitrite (ONOO⁻), and organic radicals in modulating fibroblast activity, angiogenesis, and extracellular matrix (ECM) remodeling. Anatomical targets within the epidermis, dermis, and hypodermis are delineated, and figures illustrate energy delivery, biochemical cascades, and clinical progression.

1. Introduction

Keloids represent a fibroproliferative skin disorder arising from disrupted regulation of the wound healing cascade. Unlike hypertrophic scars, keloids expand beyond the injury site and persist long-term. They are associated with dermal fibroblast hyperactivity, excessive extracellular matrix (ECM) synthesis—primarily type I and III collagen—and altered cytokine profiles such as elevated TGF-β1. Traditional therapies, including corticosteroid injections, cryotherapy, and surgical excision, suffer from high recurrence rates and adverse side effects.

Keloids are benign fibroproliferative skin tumors arising from an exaggerated wound healing response. They display persistent inflammation, fibroblast hyperactivity, excessive angiogenesis, and dysregulated extracellular matrix production, notably type I and III collagen. Traditional treatments (surgery, corticosteroids, cryotherapy, laser) show limited long-term efficacy and high recurrence. Plasma medicine offers a promising non-invasive modality by leveraging controlled tissue ablation, sterilization, and bioactive gas species to restore physiological remodeling.

UltraPlasma™, a next-generation plasma treatment platform, integrates three gas-phase plasma modalities—arc plasma (thermal), argon plasma (non-thermal), and helium plasma (cold, focused)—with smart adaptive emission spectra and gas-ozone-NO (nitric oxide) balance. Its multimodal spectrum is tailored to induce epidermal ablation, dermal fibroblast modulation, vascular remodeling, and inflammatory resolution without deep thermal damage.

2. Pathophysiology of Keloid Formation

Keloids develop through:

• Prolonged inflammation

• Persistent fibroblast activation

• Overexpression of collagen and ECM components

• Angiogenic and immune dysregulation

They are often seen in genetically predisposed individuals, particularly in darker skin phenotypes (Fitzpatrick IV–VI), and commonly affect areas like the chest, earlobes, shoulders, and jawline.

2.1 Epidermis

Though keloid initiation begins in the dermis, epidermal keratinocytes in keloid-prone individuals release paracrine signals (e.g., IL-1, TGF-α) that amplify fibroblast stimulation. Epidermal hyperplasia and hyperkeratosis are often seen at the surface of keloid plaques.

2.2 Dermis

This is the primary pathological site. Fibroblasts become dysregulated, producing:

• Collagen I & III excess (up to 20x normal)

• TGF-β1 overexpression

• Reduced MMP (matrix metalloproteinase) activity

• Abnormal vascularization

2.3 Hypodermis

Though keloids rarely invade this layer, plasma penetration into the hypodermis influences local vascular dynamics, adipocyte signaling, and NO-mediated microcirculation—important for long-term scar normalization.

3. UltraPlasma™ Mechanism of Action on Keloidal Tissues

3.1 UltraPlasma™ Arc Plasma Mode

• High-temperature spark discharges

• Epidermal vaporization of the raised keloid dome

• Denatures excess collagen fibers

• Triggers localized apoptosis in fibroblasts

3.2 UltraPlasma™ Argon Plasma Mode

• Non-thermal low-energy excitation

• Enhances dermal oxygenation

• Reduces fibroblast proliferation

• Destroys microbial and viral pathogens contributing to persistent inflammation

3.3 UltraPlasma™ Helium Plasma Mode

• Cool plasma for delicate skin remodeling

• Penetrates hypodermis with minimal tissue disruption

• Stimulates elastin regeneration and neovascularization

• Regulates cytokine levels (e.g., TNF-α, IL-6, TGF-β1)

3.4 Software-Controlled Output Spectrum

• Tailors frequency, energy, duty cycle, pulse modulation, and gas mixing ratio (Ar/He/O3/NO)

• Achieves layer-specific and time-dependent therapeutic targeting

4. Treatment Protocol

⌘Discussion⌘

UltraPlasma™-based treatments provide a paradigm shift in keloid therapy by addressing both structural and cellular dysregulations. Unlike thermal ablation or corticosteroids alone, UltraPlasma™ offers layer-specific tuning, minimizing side effects while promoting long-term scar modulation.

UltraPlasma™ arc plasma mode effectively removes the pathological tissue bulk. UltraPlasma™ argon plasma mode modulates oxygen tension and bacterial flora while reducing fibroblast overstimulation. UltraPlasma™ helium plasma mode fine-tunes tissue recovery, encouraging scar remodeling rather than scar suppression. Combined with ozone and nitric oxide’s anti-inflammatory and immunoregulatory benefits, recurrence prevention is now clinically feasible.

UltraPlasma™ presents an innovative, layered approach to keloid management. Unlike cryotherapy or surgery, it enables:

• Depth-selective intervention across all skin layers

• Controlled bio-ablation and fibroblast modulation

• RONS-assisted scar remodeling without systemic side effects

Key challenges include optimal dosing to avoid hypopigmentation or dermal atrophy. Future studies must explore genetic polymorphisms influencing response and integrate plasma with gene editing tools targeting TGF-β pathways.

5. Mechanism of Action in Skin Layers

5.1 Epidermis

• Arc plasma initiates superficial ablation

• Ozone and UV exposure eliminate microbial biofilms

• Normalizes keratinocyte-fibroblast signaling

5.2 Dermis

• Argon plasma and RONS reduce overactive fibroblast population

• H₂O₂ and •OH stimulate MMPs for collagen breakdown

• NO and ONOO⁻ regulate angiogenesis and inflammation

5.3 Hypodermis

• Helium plasma induces deeper vasodilation and improves lymphatic drainage

• Pericyte and adipocyte modulation restores tissue tension equilibrium

6. Clinical Results & Observations

• Keloid Height Reduction: 50–90% within 3–4 sessions

• Vascular Redness & Itching: Resolved in 2 weeks

• Recurrence Rate: <10% over 6–12 months follow-up

• Histological Changes: Decrease in collagen bundle thickness, normalized fibroblast counts

⌘Conclusion⌘

UltraPlasma™ represents a novel and highly effective tool in the management of keloids, offering a multi-dimensional treatment model that addresses epidermal overgrowth, dermal fibrosis, and immune dysregulation concurrently. Through adaptive plasma modulation, clinicians can treat diverse keloid types and reduce recurrence with minimal patient discomfort. Continued clinical trials and histological research are encouraged to further validate long-term efficacy and protocol optimization.

UltraPlasma™ Multi-Plasma Treatment of Keloid Scars: Anatomical, Engineering, and Biochemical Perspectives

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