Keloids and Keloid Scars

🧠 Standard of Care & Symptoms

Keloids are benign, hyperplastic growths of fibrous tissue that form in the skin at the site of a previous injury. Unlike normal scars or hypertrophic scars, keloids grow beyond the margins of the original wound and do not regress over time.

• Presentation: Key symptoms.
  • *Overgrowing Borders:* Scars that spread laterally into surrounding healthy skin, often claw-like or bulbous in shape.
  • *Consistency:* Firm, rubbery, or tough nodules or plaques, often with a shiny, hairless surface.
  • *Color Progression:* Early keloids are erythematous (red) or violaceous, gradually maturing into hyperpigmented or skin-colored growths.
  • *Subjective Distress:* Frequently accompanied by severe, localized itching (pruritus), tenderness, sharp pain, or hyperesthesia.

🧬 Diagnostics & Fibrotic Pathophysiology

Diagnosis is primarily clinical. Skin biopsy is reserved for atypical lesions to rule out malignant mimics like dermatofibrosarcoma protuberans.

• Diagnostic Markers: Key elements.
  • Clinical Assessment: History of trauma followed by progressive, border-crossing scar expansion, typically in high-tension areas (chest, shoulders, upper back, earlobes).
  • Histopathological Confirmation: Biopsy shows thick, glassy, disorganized collagen bundles (referred to as **keloidal collagen**) in the reticular dermis, with an abundance of active myofibroblasts and mucinous ground substance.
  • Hypertrophic Scar Differentiation: Hypertrophic scars remain confined to the original wound margins and tend to regress spontaneously over months, whereas keloids persist and expand.

Pathophysiology of Keloidogenesis

The development of keloids is driven by abnormal wound healing and cytokine signaling:

• TGF-Beta Pathway Overexpression: Dermal fibroblasts in keloids show elevated sensitivity to and production of transforming growth factor-beta (**TGF-beta-1** and **TGF-beta-2**), while showing down-regulated expression of inhibitory TGF-beta-3. This leads to continuous fibroblast proliferation and resistance to apoptosis.
• Collagen Type I & III Hyperdeposition: Activated myofibroblasts produce excessive amounts of **extracellular matrix**, particularly Type I and Type III collagen. The ratio of Type I to Type III collagen is significantly increased compared to normal skin.
• Inflammatory Stimuli: Persistent, low-grade inflammation in the reticular dermis releases pro-fibrotic cytokines, maintaining the myofibroblast activation loop long after the initial epithelial barrier is repaired.

💊 Intralesional Therapy & Surgical Excision

Management is challenging due to recurrence rates exceeding 50% with surgery alone. Successful therapy requires a combination of modalities.

First-Line Intralesional Therapies

• Intralesional Corticosteroids: The primary medical treatment. **Triamcinolone Acetonide** (TAC, 10-40 mg/mL injected directly into the scar every 4-6 weeks) reduces fibroblast proliferation, inhibits collagen synthesis, and suppresses local inflammation.
• 5-Fluorouracil (5-FU) Combinations: Combining TAC with 5-FU (an antimetabolite) inhibits DNA synthesis in active fibroblasts, improving flatting rates and reducing skin atrophy associated with high-dose steroids.

Surgical Excision and Adjuvant Therapy

• Excision with Immediate Adjuvants: Surgical removal alone carries a 50-80% recurrence rate. Excising the keloid must be paired with immediate postoperative **superficial radiation therapy** (SRT, within 24 hours of excision) or serial intralesional injections to prevent recurrence.
• Cryotherapy: Localized freezing with liquid nitrogen (either contact or intralesional cryotherapy) destroys cellular structures and induces vascular thrombosis, flattening the scar.
• Silicone Gel Sheeting: Increases skin hydration and downregulates basic fibroblast growth factor (bFGF), acting as a safe home-care preventative option.

🔬 Active Clinical Trials

Clinical trials are currently evaluating targeted biologics, novel topical formulations, and optimized radiation dosing protocols.

🗺️ Next Steps After Diagnosis

If you are seeking treatment for a keloid scar, establish these clinical care pathways:

1. Consult a Board-Certified Dermatologist: Determine if your scar is a keloid or a hypertrophic scar, as their treatment pathways differ.
2. Begin First-Line Injections: Discuss starting a schedule of intralesional triamcinolone injections to reduce size, pain, and itching.
3. Use Silicone Sheets: Wear medical-grade silicone gel or sheets over the scar for 12-24 hours a day to prevent further growth.
4. Avoid Unnecessary Skin Trauma: Avoid elective surgeries, body piercings, or tattoos, particularly in high-tension areas (shoulders, chest).

❓ Patient FAQ

Q: Why do keloids itch and hurt?
A: The rapid, disorganized growth of collagen fibers and persistent inflammation put pressure on localized sensory nerves in the skin. Additionally, mast cells are often abundant in keloid tissue, releasing histamine which causes itching.

Q: Can keloid scars be completely removed?
A: While treatments like steroid injections and cryotherapy can flatten keloids and relieve pain, completely removing them is difficult because they frequently grow back after surgery. Combining surgical removal with radiotherapy or steroid injections is essential to minimize this risk.