Log in
Diseases of the skin

Keloid

A keloid is a benign dermal fibroproliferative growth that extends beyond the original wound margins due to abnormal wound healing. It occurs most often in individuals with darker skin pigmentation (African, Hispanic, and Asian populations) and typically arises after skin trauma, surgery, piercings, or acne. The single most testable fact: unlike hypertrophic scars, keloids grow beyond the boundaries of the original injury and rarely regress spontaneously.

ICD-10L91.0
Typical patientDark-skinned young adult with prior skin injury
Key findingFirm, raised scar extending beyond original wound margins
First-line treatmentIntralesional corticosteroid injection (triamcinolone)
5 min readFor medical studentsUpdated 2026-10-14

Definition and epidemiology

A keloid is an abnormal, benign dermal scar that results from excessive fibroblast proliferation and collagen deposition during wound healing, extending beyond the borders of the original skin injury. This distinguishes it from a hypertrophic scar, which remains confined to the wound site and often regresses over time.

  • Keloids are far more common in people with darker skin tones, with incidence estimated to be up to 15 times higher in Black and Hispanic populations compared with White populations.
  • Peak incidence occurs between ages 10 and 30 years; keloids are rare in young children and the elderly.
  • There is a strong familial predisposition, suggesting a genetic component, though no single causative gene has been identified.
  • Common sites include the earlobes, shoulders, upper chest, and back — areas of higher skin tension.
High-yield for exams
  • Keloids extend beyond the original wound margins; hypertrophic scars stay within them.
  • Highest risk in darker-skinned individuals, ages 10-30, with family history.
  • Earlobe piercing is a classic exam trigger for keloid formation.
  • Pathophysiology involves excessive TGF-beta signaling and fibroblast resistance to apoptosis.
  • Histology shows thick, hyalinized, haphazard collagen bundles.
  • First-line treatment is intralesional corticosteroid injection.
  • Surgical excision alone has high recurrence; combine with adjuvant therapy (steroids or radiation).
  • Keloids are benign and do not become malignant.

Etiology and risk factors

Keloids form after any process that disrupts the dermis, triggering a dysregulated wound-healing response.

Common triggers

  • Surgical incisions
  • Ear piercings (a classic board-exam trigger)
  • Burns and lacerations
  • Acne vulgaris and folliculitis
  • Vaccination sites and insect bites
  • Tattoos

Risk factors

  • Darker skin pigmentation (highest risk group)
  • Family history of keloids
  • Younger age (10-30 years)
  • Wound location over high-tension areas (sternum, shoulders, earlobes)
  • Delayed wound healing or wound infection
  • Hormonal influences (keloids may enlarge during pregnancy and puberty)

Pathophysiology

Keloid formation reflects a prolonged, dysregulated fibroproliferative response to dermal injury.

  • Normal wound healing involves inflammation, proliferation, and remodeling, with eventual balance between collagen synthesis and degradation.
  • In keloids, fibroblasts show increased proliferation and resistance to apoptosis, leading to excessive production of collagen (particularly type I and type III) and extracellular matrix.
  • There is upregulation of transforming growth factor-beta (TGF-beta) signaling, which drives continued fibroblast activity and reduced collagen breakdown.
  • Collagen bundles in keloids are thick, haphazardly arranged, and hyalinized, unlike the organized parallel bundles seen in normal scars or hypertrophic scars.
  • The inflammatory phase is prolonged, and the lesion continues to grow beyond the original wound margins because the abnormal fibroblast activity extends into surrounding normal tissue.

Clinical features

Keloids present as scar tissue that outgrows the boundary of the inciting injury.

  • Firm, rubbery, raised nodules or plaques with a smooth, shiny surface.
  • Color ranges from pink or red (early) to brown or hyperpigmented (later), often darker than surrounding skin.
  • Lesions extend beyond the original wound edges, sometimes with claw-like projections.
  • Commonly pruritic and may be tender or painful, especially during active growth.
  • No spontaneous regression in most cases; lesions tend to persist or slowly enlarge over months to years.
  • Most frequent sites: earlobes, chest, shoulders, upper back, and jawline.

Diagnosis

Keloid diagnosis is primarily clinical, based on history and physical examination.

  • History of preceding skin trauma, surgery, piercing, or acne at the site.
  • Physical exam shows a firm, hyperpigmented or erythematous growth extending beyond the original wound margins — this feature differentiates it from a hypertrophic scar.
  • Biopsy is not routinely needed but may be performed if the diagnosis is uncertain or malignancy is suspected (e.g., atypical growth, ulceration, rapid change).
  • Histology (if performed) shows thick, hyalinized, haphazardly arranged collagen bundles with increased fibroblasts and reduced blood vessels compared with normal dermis.
  • No laboratory or imaging studies are routinely required.

Differential diagnosis

ConditionDistinguishing feature
Hypertrophic scarConfined to original wound borders, often regresses over time
DermatofibromaSmall, firm nodule with a positive "dimple sign" on lateral compression
Dermatofibrosarcoma protuberansProgressive, infiltrative growth; biopsy needed to exclude malignancy
Keloidal morphea/scleroderma plaquesAssociated with systemic sclerosis features, different histology
Foreign body granulomaHistory of retained material (e.g., suture, piercing debris)
Lobomycosis (chronic cases)Rare fungal infection mimicking keloid in endemic regions

Management

Treatment aims to reduce size, symptoms, and recurrence, but no single therapy guarantees cure, and recurrence rates remain significant across all modalities.

First-line

  • Intralesional corticosteroid injections (triamcinolone) — reduce fibroblast proliferation and collagen synthesis; often combined with other modalities.
  • Silicone gel sheeting and pressure therapy — supportive, especially for prevention and smaller lesions.

Other options

  • Intralesional 5-fluorouracil or bleomycin, often combined with corticosteroids, for resistant lesions.
  • Cryotherapy, particularly for smaller keloids.
  • Laser therapy (pulsed dye laser) to reduce erythema and improve texture.
  • Surgical excision — effective but carries high recurrence risk (up to 50 percent or more) if used alone; typically combined with adjuvant therapy such as intralesional steroids or radiation.
  • Postoperative radiation therapy — reserved for high-risk or recurrent keloids, used adjunctively after excision.
  • Pressure therapy and silicone sheeting are also used post-excision to reduce recurrence.

Prevention

  • Avoid elective procedures (e.g., ear piercing, cosmetic surgery) in high-risk individuals when possible.
  • Early use of silicone sheeting or pressure dressings on new wounds in predisposed patients.
  • Guideline consensus (international scar management guidelines) favors combination therapy over any single modality for established keloids, as monotherapy has higher recurrence rates.

Complications and prognosis

  • Chronic pruritus and pain can impair quality of life.
  • Cosmetic disfigurement, particularly on the face, ears, and chest.
  • Contractures and functional limitation if located over joints.
  • High recurrence rate after treatment, especially with excision alone.
  • Keloids are benign and do not undergo malignant transformation, though rare case reports of associated squamous cell carcinoma exist in long-standing lesions.
  • Lesions may stabilize or slowly regress over many years but often persist indefinitely without treatment.
Mnemonic

"KELOID": Keeps growing beyond wound, Ethnicity (dark skin) predisposes, Localized to high-tension areas (ears, chest, shoulders), Overactive fibroblasts/TGF-beta, Intralesional steroids are first-line, Doesn't regress spontaneously.

Practice questions

1. A 22-year-old Black woman presents 6 months after an ear piercing with a firm, raised, dark pink nodule that has grown progressively larger than the original piercing site and extends onto the adjacent earlobe skin. It is mildly itchy but not painful. Which of the following best describes the underlying pathologic process?

Answer: B. The clinical description (growth beyond the original wound site, firm texture, in a patient of African descent after piercing) is classic for a keloid. The underlying process is excessive fibroblast activity and collagen deposition driven by dysregulated TGF-beta signaling, with lesion growth extending into previously uninjured skin. This differentiates it from a hypertrophic scar, which would remain within the wound margins.

2. A 30-year-old man has a keloid on his chest that recurred twice after prior surgical excisions. He wants a treatment approach that minimizes further recurrence. Which management strategy is most appropriate?

Answer: D. Excision alone has a high recurrence rate, especially in a patient with prior recurrences. Current guideline consensus favors combining surgical excision with adjuvant therapy such as intralesional corticosteroids or postoperative radiation to reduce recurrence risk. Systemic antibiotics and systemic corticosteroids have no established role in keloid management.

3. A dermatopathologist examines a biopsy from a chest wall lesion in a patient with a history of a prior burn. The sample shows thick, hyalinized collagen bundles arranged haphazardly, with increased fibroblast density and reduced vascularity compared to normal dermis. Which diagnosis is most consistent with these findings?

Answer: B. The histologic description of thick, hyalinized, haphazardly arranged collagen bundles with increased fibroblasts is characteristic of a keloid. Dermatofibromas show a different pattern with storiform fibrohistiocytic proliferation, and the other listed options have distinct histologic features unrelated to excessive collagen deposition from abnormal wound healing.

Frequently asked questions

What causes a keloid?

A keloid is caused by an abnormal wound-healing response in which fibroblasts overproduce collagen after skin injury. Common triggers include surgical cuts, ear piercings, burns, acne, and vaccination sites. Genetic predisposition and darker skin pigmentation significantly increase risk, and the exact molecular trigger for the exaggerated TGF-beta driven fibrosis is still not fully understood.

What are the first signs of a keloid?

The first sign is usually a firm, raised, pink or red bump that forms at the site of a healed injury and continues to grow beyond the original wound edges. It is often itchy or tender in the early stages. Over weeks to months, the lesion becomes firmer, smoother, and may darken in color, especially in pigmented skin.

How is a keloid diagnosed?

Keloids are diagnosed clinically based on the appearance of a firm scar extending beyond the boundaries of the original wound. A biopsy is rarely necessary but can be done if the diagnosis is unclear or to rule out a malignant growth. No blood tests or imaging are routinely required for diagnosis.

Is a keloid curable?

Keloids are not reliably curable, and recurrence after treatment is common even with combination therapy. Treatments such as corticosteroid injections, laser therapy, and surgical excision with adjuvant therapy can shrink or flatten keloids and relieve symptoms, but complete and permanent removal cannot be guaranteed. Ongoing maintenance therapy is often needed to control regrowth.

Keloid vs hypertrophic scar — what is the difference?

The key difference is that a keloid grows beyond the borders of the original wound, while a hypertrophic scar stays confined within the wound margins. Hypertrophic scars often improve or flatten over time without treatment, whereas keloids tend to persist or enlarge. Keloids are also more strongly associated with darker skin pigmentation and genetic predisposition.

Key drugs

Triamcinolone5-fluorouracilBleomycinVerapamil (intralesional, adjunct)Imiquimod (topical, adjunct)
Hypertrophic scarDermatofibromaDermatofibrosarcoma protuberansScleroderma (morphea)Acne vulgarisBurn scar contractureForeign body granulomaSquamous cell carcinoma (rare, in chronic lesions)

Sources and further reading

StatPearls (NCBI Bookshelf)MedlinePlusWHO ICD-10: L91.0

Educational content for medical students, prepared by the WhiteCoat Pro editorial team with AI assistance; every page is reviewed by a second AI model for factual errors. It is not medical advice and does not replace the product label, local guidelines or a clinician.