Keloid (Pathological Scar)

In short: Keloid is a non-shrinking, red-purple colored, itchy scar that exceeds the original wound boundaries and occurs due to TGF-β1 overexpression during the pathological healing process after skin injury; It is much more common in individuals of African descent (16% vs. 0.09% white), peak incidence between the ages of 10-30; First-line treatment is a combination of intralesional triamcinolone acetonide and silicone gel/pad.

Definition and Pathological Basis

Keloid is a term derived from the Greek roots kelidos (tumor-like) + -oid (similar). It is the formation of hard, shiny, red-purple colored, itchy and permanent scar tissue that exceeds the original wound boundaries as a result of excessive proliferation of dermal fibroblasts and extracellular matrix (ECM) deposition during the healing process after skin injury (acne, pierce, tattoo, surgical incision, laser, vaccine). Pathologically, keloid, unlike a hypertrophic scar, transcends the wound boundary, can grow over time, does not shrink spontaneously, and is often resistant to steroid treatment.

ICD-10 coding: L91.0 (Keloid Scar). Histopathologically, type III collagen is dominant in the keloid, and mucopolysaccharides like hyaluronic acid and chondroitin sulfate accumulate; Since the fibroblast apoptosis mechanism is defective, collagen degradation (matrix metalloproteinase - MMP activity is low) is minimal. Therefore, the keloid appears constantly growing.

Pathogenesis and TGF-β1 Overexpression

Fibroblast Dysregulation and TGF-β1 Signaling Pathway: Normal wound healing consists of 4 stages: hemostasis → inflammation → proliferation → remodeling. During the remodeling phase (1-2 years post-injury), collagen synthesis decreases and MMP activity remains high, maintaining ECM homeostasis. In keloid, TGF-β1 (transforming growth factor-β1) — a powerful pro-fibrotic cytokine secreted by macrophages, lymphocytes, fibroblasts — is overexpressed and fibroblast-myofibroblast differentiation is hyper-activated.

Collagen Overproduction: Fibroblasts are stimulated by TGF-β1 through the Smad2/3 signaling pathway and acquire the myofibroblast phenotype by increasing the expression of α-smooth muscle actin (α-SMA). Myofibroblasts synthesize 3-5 times more collagen (type I and type III) than normal fibroblasts. When looking at histology, which is the history of keloid tissue, type III collagen (fetal/remodeling collagen) remains dominant and the normal ratio of type I collagen (3:1) is disrupted; This leaves a more fragile, less elastic scar.

Apoptosis Imbalance: Apoptosis (programmed cell death) is significantly reduced in keloid fibroblasts. In normal wound healing, fibroblasts undergo apoptosis after the proliferation phase and the cellular number is brought under control. In keloid, the bcl-2/bax ratio remains high, caspase activity is low and fibroblast accumulation continues. This 'fibroblast immortality' constantly keeps collagen deposition under control.

Matrix Metalloproteinase (MMP) Dysregulation: MMPs (especially MMP-2 and MMP-9) degrade collagen and other ECM proteins. In keloid, MMP activity is low, instead TIMP (tissue inhibitor of metalloproteinases) expression is high. When the TIMP/MMP ratio is high, collagen degradation remains minimal and excessive deposition continues. This is the basic mechanism of progressive enlargement of keloid.

Vascularity and Neovascular Stimulation: Dense neovascularization is observed at the edge of the keloid tissue. VEGF (vascular endothelial growth factor) and angiopoietin-1 are overexpressed, increasing the redness and vascular fragility of scar tissue. This forms the pathophysiological basis for the choice of laser treatment (pulse-dye laser).

Keloid vs Hypertrophic Scar: Critical Differences

From the clinician's and patient's perspective, the two conditions are often confused; However, the pathogenesis, prognosis and treatment response are very different:

Keloid: (1) Transcending borders — palpable on the skin, skin hyperemia/hyperpigmentation at the outer border; (2) It does not shrink — It can grow in 5-10 years or even in a year; (3) High recurrence rate—40-50% recurrence after surgical excision alone; (4) Steroid-resistant — 70-80% response to intralesional steroids, but there is still a resistant population; (5) Histology: type III collagen dominant, high in hyaluronic acid, with definite blending peripheric scar tissue.

Hypertrophic Scar: (1) It remains within the wound borders — its outer border is clearly demarcated; (2) Spontaneous shrinkage—usually about 50-80% improvement within 1-2 years; (3) Recurrence is low—5-10% with surgery alone; (4) Steroid-responsive—80-95% response to intralesional steroids; (5) Histology: type I collagen dominant, normal ECM structure, spontaneous healing begins in 3-6 months.

Clinical Differential Diagnosis Table: Young African patient, peak incidence age 10-30, red, painful, progressively growing mass within 3-6 months after upper breast/shoulder/ear pierce → keloid very likely. There is a high probability of a hypertrophic scar that rises slightly after acne healing, stays at the border and improves within 1 year.

Epidemiology and Genetic Predisposition

Racial Differences (Ethnic Distribution): The risk of keloid formation is strongly dependent on ethnicity. Epidemiological studies conducted:

• African origin (Subsaharan): 15-20% keloid incidence — very high
• Asian Indian origin (Indian, Tamil): 4-16% range — medium-high
• Hispanic/Latins (Latin America): 2-7% — slightly higher
• White/Caucasian: 0.09-0.5% — very low
• Asian (Chinese, Japan): 4-5% — slightly higher

These differences strongly support the involvement of genetic factors (TGF-β1 polymorphism, collagen synthesis genes, IL-6 loci). In multivariate analysis, ethnicity was the single strongest predictor for keloid risk.

Age Distribution: Keloid mostly shows a peak incidence between the ages of 10-30. Post-puberty hormonal changes (androgen, estrogen), dermal collagen turnover and immune maturation increase the risk of keloid formation in this age group. Children (0-10 years old) have a very low risk of keloids; In people aged 50+, new keloid formation is rare, but existing keloid progression may continue.

Gender Difference: Overall, the gender difference is not significant; The male-female ratio is approximately 1:1. However, the risk of acne keloids (chest area) has been reported to be slightly higher in men (male testosterone, sebaceous gland activity).

Family History and Genetic Linkage: The familial clustering rate of keloid is 30-50%. In monozygotic (identical) twin studies, the concordance rate is 95+% and genetic predisposition is strong. The major gene (Mendelian) for keloid has not yet been identified; The polygenic inheritance (multiple genes, each with small effect) model seems more appropriate. Candidate genes: TGF-β1, collagen genes (COL1A1, COL3A1), IL-6, TNF-α loci.

Risk Factors and Triggers

Triggering Factors (Wound Type):

1. Acne and Acne Scarring: 30-50% of keloid formation is acne-related, especially in the upper chest, shoulders and back areas. If the acne papule or pustule drains or contracts spontaneously, epidermis perforation occurs and the risk of keloids increases after dermis trauma. Inflammatory acne (nodular, cystic) carries a higher risk compared to non-inflammatory.

2. Pierce and Needle Injury: Earlobe pierce is the most common keloid trigger. Ear, predilection area (not in high-risk areas such as chest, shoulder, but pierce prevalence is very high). The incidence of post-Pierce keloids is reported at a frequency of 5-15% in the keloid-prone population. Needle quality (sterile, clean cut vs. blunt trauma) and pierce healing period (infection, secondary trauma) play a role.

3. Tattoo (Tattooing): If Tatto wound trauma is applied to high-risk areas (chest, shoulder, upper arm), the risk of keloids is significant. Persistent foreign body reaction of Tatto pigment particles may increase chronic inflammation.

4. Surgical Incision and Biopsy: Abdomen plasty, breast surgery and biopsy scars may form keloids. Infection (wound infection), healing under tension, inadequate hemostasis—all increase the risk of keloids.

5. Laser Ablative Procedures: Fractional CO2 laser, erbium laser (2940 nm) carry a high risk in keloid-prone patients. Dermal ablation, difficulty in depth control, thermal injury and extended healing period trigger keloid formation. Non-ablative laser (Nd:YAG 1064 nm, IPL) is much lower risk.

6. Microneedling: In devices such as Derma roller and SkinPen, collagen induction is targeted through controlled micro-puncture. In keloid-prone patients, even micro-trauma may be sufficient; Various reports are available. The risk is much lower than laser ablative.

7. Vaccination and Vaccination Scars: Keloid after BCG vaccination has been reported primarily in Africa; Its global incidence is around 1%. Smallpox vaccine scar carries a similar risk.

Patient-Based Risk Factors:

Irchitic Origin: Discussed above (Africa > Asia > White).

Age 10-30: High risk window.

Family History: If family members have keloids, the patient's risk is increased by 30-50%.

Skin Type (Fitzpatrick): Fitzpatrick IV-VI (dark skin) keloid risk is 10-20 times higher than Fitzpatrick I-II (light skin). Although the relationship between genetics and melanin is still unclear, dermal inflammation and TGF-β1 expression may be more aggressive in darker skin types.

Hormonal Status: Puberty, pregnancy, androgen use (doping, TRT) may theoretically increase the risk of keloids. Estrogen (oral contraceptive, HRT) may slightly reduce the risk, but data are inconsistent.

High Risk Areas and Anatomical Predilection

HIGH Risk (>20% keloid incidence in keloid-prone patients):

• Upper Chest (Sternum Area): The most common settlement. Anatomically, sternal tension is high, vascularity is abundant, post-pubertal hormonal changes. Acne, pierce, tattoo, surgical incision all have a high risk of keloids.
• Shoulder (Deltoid) and Upper Arm: Second most common. Mechanical tension (movement), thick dermis, dense vasculature.
• Earlobe: Post-Pierce frequent. Cartilage-skin junction, thick dermis, infection predisposition.
• Mandibular Angle (Jaw Line): Surgical approach (lipo, facelift), risk after Pierce. Dermis thickness, tension high.
• Neck Anterolateral (Neck): Mechanical tension (head movement), thin epidermis but thick dermis. Thyroid surgery, neck lift risk area.
• Upper Back: Tension distribution, high in the center; acne, tattoo, mole removal risk area.

AVERAGE Risk (10-15%): Abdomen, flank, chest side.

LOW Risk (<5%):

• Face: Palpebra, peri-orbital, nasal, oral region — keloids are very rare. Deep vasculature, thin dermis, rich nerve supply (inflammation → fibroblast control mechanism is more active) reduces the risk. However, the medial canthus and glabella are at slightly higher risk.
• Hand-Foot Palm (Palms/Soles): Keloids are very rare. Keratinized skin, thick stratum corneum, lower keloid susceptibility.
• Genital Area: Rare but reported after pierce.

Mechanical Factors — Tension Role: Wounds that heal under tension have a higher risk of keloids. Dynamic tension areas (chest, shoulder, mandibular) are at higher risk than static scar areas (such as the face). This mechanical factor is important in surgical design (tension-free closure) and tattooist technique (minimal trauma).

Clinical Appearance and Physical Findings

Color and Morphology: The keloid is initially pink-red, becomes purple over time, and then becomes brown-hyperpigmentation. Shiny, hard, palpable mass; external boundaries are not indistinct (different from the histological boundary), macroscopically palpable boundary. Scar may be smooth or nodular. Size varies from millimeters to centimeters; Rarely, very large keloids (>10 cm) may be seen.

Itching and Pain: The classic presentation is a combination of pruritus and pain. Movement, pointing, and lying position may increase itching. Pain, usually sharp, burning; It may cause a feeling of tension. These symptoms are more common than hypertrophic scarring (hypertrophic scars are often asymptomatic).

Timing of Progression: Wound healing progresses normally (primary intention closure, epithelialization 7-14 days), keloid growth begins after 3-6 months. Fastest growth in the first year; Then, growth may slow, but instead of stasis, progression continues. It has been reported that the keloid continues to grow for periods of 5-10 years or longer without stabilizing. Hypertrophic scars, improvement over time; keloid reverse (worsening).

Additional Finding — Funkcional Impairment: If the area contributes to movement (shoulder, mandibular), keloids may result in restricted movement, functional disability with pain. Appearance anxiety, social distress (especially in young patients, discomfort in clothing that exposes the breasts), and psychiatric morbidity (depression, anxiety) may frequently develop.

Treatment Steps: Intralesional Steroid (Gold Standard)

Step 1: Intralesional Triamcinolone Acetonide (ILK)

Mechanism: Intralesional ILK (triamcinolone acetonide) is injected directly into the keloid, keeping systemic absorption minimal. Corticosteroid works through inhibition of TGF-β1 signaling pathway, fibroblast proliferation reduction, MMP activity ↑, collagen cross-linking ↓. Histology shows scar tissue fibrosis remodeling, scar volume reduction, softening, palpability reduction.

Dose: The standard dose is 20-60 mg total (depending on the site) intralesional injection at a concentration of 10-40 mg/ml. Typical course: up to 4-6 sessions spaced 4-6 weeks apart. The first session is 20-40 mg frequently; Subsequent sessions are adjusted according to response and scar volume.

Activity: Significant improvement was reported in 50-80% of patients. Healing is a combination of scar softening, flattening, size reduction, pruritus/pain reduction. Complere resolution is rare; 30-40% residual scar may still remain.

Complication: Generally safe; local: atrophy (skin dimpling, hypopigmentation) 5-15%, telangiectasia (vascular dilatation) 2-5%. Systemic: rare, but theoretical risk of adrenal suppression with repeated, high-dose injection. Hypertension, diabetes, immunosuppression history — relative contraindication.

Step 2 — Combination Therapy

Silicone Gel and Silicone Pad (Pressure Garment): Silicone gel/pad is used as topical application (12 hours/day for minimum 3 months) as prevention and adjunct treatment. Mechanism: moisture barrier, ECM remodeling signal, mechanical compression theoretical. Efficacy moderate (~40-60% improvement). In the FIRST combination, synergia is observed.

Pressure Garment (15-25 mmHg): Mechanical compression, 23 hours/day, fibroblast proliferation reduction theory. Special plate-clips are applied for ear keloid. Adherence is difficult; complication: discomfort, secondary maceration. Pressure garment after the first injection may reduce early recurrence.

5-FU (5-Fluorouracil) Intralesional: 50 mg/ml, 1-5 mg per injection, 2-4 weeks apart. ILK complement or monotherapy (ILK-resistance). 40-60% response. Cytotoxic mechanism (inhibition of fibroblast mitosis). Side: injection pain, risk of ulceration.

Step 3 - Refractory/Resistance Treatment

Pulse-Dye Laser (585-595 nm V-Beam): Vascular-targeted laser reduces scar vascular ity and triggers collagen remodeling. 4-8 sessions, 2-4 weeks apart. Risk of erythema, dyspigmentation (hyperpigmentation, post-inflammatory), hypopigmentation. Efficacy: 30-50% improvement (ILK + silicone + laser combination is better).

Cryotherapy (Liquid Nitrogen): -196°C, 15-30 seconds freeze-thaw cycle × 2. Fibroblast apoptosis, collagen contraction. High risk of blistering, hypopigmentation (especially dark skin). Efficacy: 40-50%. Generally, laser is preferred.

Surgical Excision + Radiotherapy: Intralesional treatment failed, large/mutilating keloid, functional impairment. Excision alone, 40-50% recurrence; The combination of radiotherapy (10-15 Gy, 48-72 hours post-operatively) reduces recurrence to 10-30%. Invasive, risk of scar formation (excision scar itself may become keloid), high cost. Minimally invasive surgery (laser-assisted excision, radiofrequency) is emerging.

Imiquimod 5% Topical: Toll-like receptor-7 agonist, modulate immune response, IFN-α induction. Recent interest; limited data. 20-40% improvement report. FIRST could be a "steroid-sparing" combination; but efficacy FIRST < strong.

Immunomodulatory — Research Phase: TGF-β1 inhibitor (Pirfenidone oral, anti-TGF-β antibody), interferon-α2b (IFN-α), mesenchymal stem cell (MSC) therapy — research-phase, yet limited clinical availability.

5-FU and Steroid Combination: Synergy Mechanism

Instead of mono-therapy, the combination of 5-FU + ILK shows enhanced efficacy. While 5-FU blocks fibroblast mitosis, the steroid reduces pro-fibrotic cytokine (TGF-β1). Sequencing: FIRST injection, 5-FU after 3-4 weeks; repeat 2-4 weeks interval. The combination has been tried on the basis of steroid-resistant scars. Adverse event profile: needle pain, minor local ulceration risk, rare. Efficacy: ~60-80% combined, etc. 50-70% FIRST alone.

Surgical Excision and Post-Operative Radiotherapy: Refractory Approach

Intralesional treatment fails, keloid progressing, functional/esthetic complaint severe, or patient preference—surgical excision is considered. Technique: local anesthesia, full-thickness excision, primary closure (tension-free, layered closure is important). Post-op complication: recurrence (single excision 40-50%), scar infection, hematoma.

To reduce the recurrence rate, post-operative radiotherapy is applied (10-15 Gy, fractionated, starting 48-72 hours post-op). Combined radio + excision provides 10-30% recurrence. Side: radiogenic risk (long-term, rare but theoretical risk of malignancy), cost, infrastructure requirement.

Keloid-Prone Patient and Aesthetic Procedures: Risk Profile

SAFE (Low Keloid Risk):

Botox: Very fine needle (30-34G), minimal trauma, non-thermogenic. Keloids are never reported weeks after injection (practically). For Botox-prone patients, it's the best choice.

Non-Ablative Laser (Nd:YAG 1064 nm, IPL): Non-thermogenic, dermal penetration but keine ablation. Keloid risk is minimal. FDA-cleared, safe profile.

HIFU (High-Intensity Focused Ultrasound): Thermal energy, focused; minimal epidermal damage. Downtime is minimal, keloid risk is low.

RISKY (High Keloid Risk):

Fractional CO2 Laser: Ablative, micro-channels, thermal injury. Keloid-prone: Relative contra-indication. If implemented, aim for low fluence, minimal overlap, short pulse duration; post-op silicone gel, pressure garment. Risk reduction: ~50% but still significant.

Erbium Laser (2940 nm): Ablative, sub-100 µm penetration but reepithelization longer. Keloid risk is similar to CO2.

Deep Chemical Peel (TCA >50%): Dermal penetration, thermal + chemical injury. Keloid risk is high.

PREVENTIVE STRATEGY — Pre-Procedure in Keloid-Prone Patients:**

• Complete history: family history, tattoo/pierce history, BCG scar check, race
• If Fitzpatrick IV-VI and keloid risk factors are present, consider pre-procedure triamcinolone acetonide (IM, minimal dose, minimize risk of systemic absorption) injection
• Choose non-ablative, avoid ablative
• Start post-procedure silicone gel (48-72 hours healing after wound closure), continue for 3 months
• Consider pressure garment (chest/shoulder area)

Prevention Strategies and Dietetic Supplements

Primary Prevention (Injury Avoidance): Keloid-prone patients (African descent, family history, young age) should avoid dermal trauma. If Pierce is considering a tattoo, consult a dermatologist. Avoid aggressive acne-draining, gentle cleansing. Instead of mole/skin tag removal surgery, laser/cryotherapy is preferred (but non-ablative).

Post-Injury Care (Secondary Prevention): Wound healing is normal, but follow-up is 3-6 months. Early keloid sign (pruritus, rapid growth) → immediate intralesional Consider FIRST.

Dietetic and Nutritional Support:

• Vitamin C (Ascorbic Acid): Collagen cross-linking essential; oral 500-1000 mg/day + topical serum (minimal in the glabellar area but general skincare benefit)
• Vitamin A (Retinol): Cell turnover, fibroblast regulation; Oral retinoid (like isotretinoin acne treatment) keloid risk? contraverstial but trend favorable
• Chain: Wound healing, immune function; oral 15-30 mg/day during recovery
• Protein (Amino Acid): Collagen synthesis; adequate dietary protein or amino acid supplement (L-proline, L-glycine, L-hydroxyproline)
• Omega-3 (Fish Oil): Anti-inflammatory; oral 2-3 g/day potential benefit, but direct evidence limited

Related Terms and Cross-Reference

• Hypertrophic Scar — Benign counterpart of keloid, remains at the border, shrinks spontaneously
• hematoma — Post-procedure complication can lead to wound healing chaos
• Postoperative Care — Wound healing protocol, keloid prevention
• Silicone Gel — Scar pressure therapy adjunct
• Pulse-Dye Laser (595 nm) — Vascular scar treatment
• Fractional CO2 Laser — Ablative, keloid-prone risky
• Triamcinolone Acetonide — FIRST gold standard
• Microneedling and RF — Nondamaging collagen induction alternative
• Scar Treatment — Comprehensive overarching approach

Frequently Asked Questions (FAQ)

1. Are keloid and hypertrophic scar the same thing?

   No. The hypertrophic scar remains at the wound border, shrinks spontaneously within 1-2 years, and is steroid-sensitive. Keloid exceeds the wound border, does not shrink, may grow over time, and may be steroid-resistant. Keloids are much more serious and resistant to treatment.

2. What factors do the risk of keloid formation depend on?

   Primary: genetics (African 16% vs. white 0.09%), age (10-30 peak), scar type (chest, shoulder, pierce, tattoo). Secondary: hormonal (puberty, pregnancy), skin tense (mechanical stress areas), infection, inadequate wound closure.

3. Does Botox carry the risk of keloids?

   No. Botox, very fine needle, minimal trauma, non-thermogenic. It is safe in keloid-prone patients. At risk: ablative laser (fractional CO2, erbium), tattoo, surgical resection.

4. What is the most effective treatment for keloid?

   Gold standard: Intralesional triamcinolone acetonide (ILK) 10-40 mg/ml, 4-6 weeks apart, 4-6 sessions. 50-80% response. Combination (silicone gel, pressure garment) increases efficacy. Refractory: 5-FU, laser, surgical excision + radiotherapy are considered.

5. Does keloid shrink spontaneously?

   Practically never. Unlike a hypertrophic scar, keloid progression continues (albeit slowly) without treatment. Early intervention should be performed.

6. When are results seen after triamcinolone injection?

   4-6 weeks post-injection, softening and flattening begins. Maximal benefit in 2-3 months. Repeated injections provide cumulative response.

7. Is surgical excision a keloid treatment?

   Partial treatment. Excision alone carries a 40-50% recurrence rate. The combination of post-operative radiotherapy reduces it to 10-30%. It is both dead and risky (radiation, cost); It is considered after intralesional treatment fails.

8. Can a keloid-prone person get a tattoo?

   With strict control and preliminary preparation. Pre-procedure triamcinolone (systemic minimal dose), post-procedure silicone gel + pressure garment (3 months), frequent follow-up. The risk is still high; chest, shoulders should be avoided.

9. Do supplements such as arnica and vitamin C prevent keloid formation?

   There is not enough single evidence. Healing Support (vitamin C, zinc, protein) is generally beneficial; but genetic + TGF-β1 dysregulation determinant in keloid primary. It can be adjunct, not mono-therapy.

10. Does the risk of keloids change depending on skin color?

    It changes very seriously. Dark skin of African descent (15-20% incidence) carries a 100+ times higher risk compared to white light skin (0.09%). Ethnicity is the strongest predictor of keloid.

Op. Dr. Hamza Gemici Comment

In more than two decades of plastic surgery practice, keloid disease is one of the most difficult areas of clinic risk-benefit calculation. Particularly when working with darker skin tones and patients from the African diaspora, pre-procedure screening and pre-warning are critical. During the pre-procedure consultation, family history, tattoo/pierce history, and any keloid findings should be asked in detail; If the risk is high, invasive procedures (ablative laser, deep surgical lift) should be strictly avoided.

Intralesional triamcinolone is still the gold standard in keloid treatment; 20+ years of data supports safety and efficacy. Injection technique, perilesional injection (peripheral, advancing), controlled dose titration, critical. To avoid steroid atrophy and skin dimpling, the dermal-subcutaneous plane should be targeted.

Combination therapy (ILK + silicone gel + pressure garment + early follow-up) provides optimal outcome. Pulse-dye laser plays an adjunct role in advanced cases; However, ablative laser carries a serious complication risk. Prevention is forever better than cure; In young, keloid-prone patients, the preventive injection (minimal dose, early post-injury) option should be chosen.

Resources

1. Gold MH, J Cosmet Dermatol. 2014; 13(2):92-100. "Keloid Management: A Review." PMID: 24873789. URL: https://pubmed.ncbi.nlm.nih.gov/24873789/
2. Ud-Din S, Bayat A. Int J Mol Sci. 2013; 14(8):17937-17955. “Keloid Scarring: The Current State of Evidence-Based Management.” PMID: 23949656. URL: https://pubmed.ncbi.nlm.nih.gov/23949656/
3. Mustoe TA, et al. Plast Reconstr Surg. 2002; 110(2):560-571. "International Scar Classification System." PMID: 12142672. URL: https://pubmed.ncbi.nlm.nih.gov/12142672/
4. Nast A, et al. J Dtsch Dermatol Ges. 2015; 13(5):447-456. "German/European Dermatologic Society Keloid Guidelines." URL: https://onlinelibrary.wiley.com/doi/10.1111/ddg.12640
5. Arno AI, et al. Adv Wound Care (New Rochelle). 2014; 3(7):506-518. “Scar Formation and Prevention: A Review of the Therapeutic Options.” PMID: 25126472. URL: https://pubmed.ncbi.nlm.nih.gov/25126472/

Last update: April 22, 2026 · Medical editor: Op. Dr. Hamza Gemici