Keloid (overview) L91.0

Benign, circumscribed, often painful or itchy (inflammatory) connective tissue proliferations affecting a scar area and the surrounding healthy skin, which rarely occur spontaneously (minimal trauma), otherwise months or even a few years after injury or focal chronic inflammation. The difference to hypertrophic scars is that a keloid by definition exceeds the original scar area, whereas a hypertrophic scar does not. However, fluid transitions are known.

See also under Scar - classification of scars according to Mustoe

Young people, blacks and Asians are particularly predisposed (keloid prevalence: 4.5-16%). The risk of contracting keloid is 15-20 times higher in dark-skinned ethnic groups than in Caucasians.

The exact pathomechanism is unknown.

An increase in collagen synthesis by a factor of 20 has been demonstrated in keloids. Structural proteins such as fibrin, fibronectin, glycosaminoglycans and type III collagen are replaced by extracellular matrix proteins, mainly type I collagen. It is unclear whether keloids are the result of increased collagen synthesis or reduced degradation.

The activity of fibroblasts (keratinocytes) and inflammatory cells is increased in keloids. Fibroblasts overexpress the IGF-I receptor (insulin-like growth factor-I receptor) and produce more potent cytokines such as TGF-beta (transforming growth factor), PDGF (platelet derived growth factor) and CTGF (connective tissue growth factor). Keratinocytes release increased amounts of TGF-beta.

The expression of Runx2 in keloid tissue and human keloid fibroblasts is upregulated compared to normal skin tissue and normal human fibroblasts. After transfection with si-Runx2, the proliferation and migration abilities of keloid fibroblasts can be significantly reduced and the apoptosis rate increases (Lv W et al. 2021).

The plasminogen activator inhibitor I (PAI-I) encoded by the SERPINE1 gene and HIF-I-alpha (hypoxia inducible factor I alpha) are both increased in keloid fibroblasts.

Inhibitors of collagen synthesis such as interferons, interleukin-1 and TNF-α represent starting points for new therapeutic strategies.

The occurrence of itching (or pain) can be explained by the sprouting of regenerating, hypersensitive nerves. Inflammatory mediators and an increased content of NGF intensify this.

Genetics (determining genetic factors): Preference for certain ethnic groups - especially people of color with Fitzpatrick skin types IV-VI, familial clustering, occurrence in connection with various syndromes. Syndromes. These include:

• Rubinstein-Taybi syndrome (mutation in the CREBB gene)
• Dubowitz syndrome (named in 1965 after the pediatric neurologist Victor Dubowitz (* 1931) from Sheffield), OMIM: 223370 (polygenetic syndrome including mutations in the HDAC8 gene which codes for histone deacetylase 8.
• Noonan syndrome (polygenetic syndrome in which mutations in the SOS1, BRAF, KRAS, RAF1 and PTPN11 genes have been detected)
• Goeminne syndrome (Zuffardi and Fraccaro (1982) mapped the locus for this syndrome to Xq28)
• Bethlem myopathy (known mutations in the genes: COL6A1, COL6A2 and COL6A3) (Jfri A et al. 2018)
• Keloid formation in polyfibromatosis (Cinotti E et al. 2013)
• X-linked valvular dysplasia with keloids and arthropathies(FLNA gene mutations/FLNA stands for Filamin-A/AtwalPS et al. 2016)

Predominantly occurring in young adults. Increasingly rare in older age. The average age of first manifestation is 23 years in both sexes (11-30 years/Shaheen A et al. 2016). There is no sex predominance.

Except palms and soles of feet everywhere, especially upper half of the body, pre-sternal, shoulder region, upper arms, earlobes (earrings).

Weeks to months after an injury or spontaneously occurring. Development of a sharply contrasting, plate- or nodular growth of varying thickness, which protrudes above the surrounding area and, due to rapid growth, exceeds the actual scar area and often shows cancer-scissor-like runners at the edges.

Loss of skin relief, hair and sebaceous glands in the affected area. The colour is initially reddish to brown-red, later white-reddish to ivory. More often, telangiectasia occurs on the surface of the skin lesions.

Not infrequently, there is marked pressure or spontaneous pain, but local itching, paresthesia, numbness, contractures (in the case of localization beyond the joint) may also be present. Keloids are very often perceived as a cosmetic impairment by those affected.

Image of a cell-rich fibroma. Unchanged or moderately diluted, more rarely acanthotic epidermis. The regular arrangement of the collagen as in normal scars is abolished. Fresh keloids show numerous fibroblasts, increased myxoidal basic substance, collagenous fibres as well as capillaries and inflammatory infiltrates. Later, cell-poor, dense knots of homogenized fibers. Atrophic hair, sebaceous and sweat glands. Disordered alignment of collagen fibres.

Hypertrophic scar: By definition, it does not extend beyond the original scar area! This makes it easy to distinguish.

Dermatofibroma (histiocytoma): Usually asymptomatic, firm, yellowish-reddish or reddish-brown, with little or no elevation above the surrounding skin level (important differential diagnosis), sometimes centrally depressed, well-defined, and firmly adherent to the epidermis. Size rarely > 1.0 cm.

Dermatofibrosarcoma protuberans: A nodule up to 10 cm in size, very coarse, skin-colored to brownish-livid (it never has the bright red color of a keloid), and bumpy, consisting of a nodular portion and an underlying plate-like portion. Usually painless. The “iceberg phenomenon” is characteristic. Histology is diagnostic.

Leiomyoma: Nodules that are usually smooth on the surface, located in a site atypical for a keloid, barely 0.5 cm in size, and often occurring in clusters. Histology is diagnostic.

Metastasis of a systemic tumor (usually rapid growth; location atypical for a keloid, consistency firm but not hard)  

Cutaneous lymphomas (location atypical for keloids, consistency firm but not hard; histology is diagnostic)  

The treatment of keloids is extremely difficult and time-consuming: Before correction, the keloids should have stabilized—that is, they should no longer be growing. Treatment should also be performed only when strictly indicated (see also Prevention).

• Glucocorticosteroids (Evidence Level III): The first-line treatment is multiple, strictly intralesional injections ofglucocorticoids, e.g.,triamcinolone acetonide and local anesthetics (1 mL Volon A 10 (40) + 1–2 mL of 1%Scandicain). Note: Take your time when injecting, use a thin needle, and apply only minimal force to overcome the internal pressure of the keloid (at this moment, a so-called “"blanching effect" occurs, indicating that a sufficient therapeutic dose has been administered). Administration (depending on size and success), e.g., once a month for 6–12 months. Regression rates between 50–100%; recurrence rates between 9–50%. Sublesional application is simpler, but ineffective.Caution!Risk of adipose tissue atrophy, especially in women!
• Occlusive therapy (Level III evidence); adjunctive therapy: Permanent occlusion and hydration of the stratum corneum using silicone gel film (e.g., Mepiform, Cicacare, Dermatix) or polyurethane patches (Hansaplast Scar Reduction Patch) leads to remarkably good results when used consistently and over the long term (> 3 months).
• Compression therapy (Evidence Level III); Adjunctive therapy: For larger keloids, the approach varies depending on age, size, and location: If topographically feasible, consistent use of a pressure pad over several months. The continuous, sustained pressure and reduced external oxygen supply inhibit fibroblast growth. When initiated early and carried out consistently, this approach is often highly effective. Using elastic bandages, pressure pads, and custom-made compression garments, this approach is easily implemented on joints and the thorax, but is technically more challenging in areas such as the face and neck. This therapy must be continued for at least 1 year.
• Alternative:Cryosurgery: 2-cycle treatment, temperature at the center of the keloid -30 °C. Immediately after thawing, inject 40–80 mg of triamcinolone acetonide into the edematous keloid area. Repeat the procedure if necessary. Possibly in combination with a pressure pad and silicone gel sheet.
• Alternative:Laser therapy: Laser systems for vaporization and ablation. Keloids can be ablated down to skin level using, for example, aCO₂ laser. After removal of the exophytic portions, continue treatment with cryocontact therapy or intralesional glucocorticoid injections. Alternatively, pulsed dye lasers (585–595 nm) are recommended.
• Alternatively:UV therapy: Recent observations also support the use of UVA irradiation following surgical planing/excision at an intensity of 20 J/cm², 4 times per week for 4–6 weeks.
• Alternative: Intralesional5-fluorouracil treatments(once a week; injection concentration: 50 mg/mL. Total dose per injection: 50–150 mg), max. 16 injections (Side effects: Injections are painful; ulceration in rare cases. Note: Experts do not recommend this monotherapy approach! The guidelines recommend monthly intralesional therapy with a combination of 5-fluorouracil and triamcinolone acetonide in a mixing ratio of 9:1 (0.9 mL of 50 mg/mL 5-fluorouracil: 0.1 mL 40 mg/mL triamcinolone acetonide). In various studies, good results were achieved with a mixing ratio of 1:3 (5-fluorouracil/triamcinolone acetonide).  

• Botulinum toxin A (off-label): The intralesional administration of botulinum toxin A (BoNT-A) has been studied as monotherapy and in combination with triamcinolone acetonide for hypertrophic scars and keloids. The evidence to date suggests an improvement in scar quality, particularly in pliability, as well as, in some cases, in pain and pruritus; however, a consistent effect on scar height or thickness and recurrence rate has not been established (Raslan EE et al. 2024; Lai IC et al. 2026). Promising results are also available for the combination with triamcinolone acetonide (Shi J et al. 2024). In a small randomized split-scar pilot study, 4 E of onabotulinumtoxin A and 4 mg of triamcinolone acetonide per 1 cm³ of scar volume were administered intralesionally three times at 4-week intervals; this resulted in a greater reduction in scar thickness and Vancouver Scar Scale score than with BoNT-A alone (Huang SH et al. 2025). A standardized dosing or treatment regimen does not yet exist.

• Alternative (third-line therapy): Surgical partial resection followed immediately by a generous intralesional injection of 40–80 mg of triamcinolone acetonide. Use only for keloids accompanied by restricted movement, in cases of non-response to other therapies, or for very large keloids that are cosmetically highly disfiguring! There is a risk of recurrence that should not be underestimated (50–100% with monotherapeutic surgical intervention!) with, under certain circumstances, more aggressive growth behavior than before and enlargement of the original keloid.
• Alternative (experimental): Avotermin (TGF-beta3), a potent antifibrinolytic cytokine applied to fresh surgical incisions (placebo-controlled studies are available). 
• Alternative (experimental): Treatment of large keloids by tattooing (“pricking with a fine needle”) a bleomycin solution (concentration 1.5 IU/mL and 40 pricks/mm²) represents a good therapeutic alternative.
• Alternative therapy, topical: (Level of evidence III): Onion extracts, heparin, or allantoin are said to inhibit excessive fibroblast proliferation. During treatment-free intervals, massage the keloid several times with a scar treatment (e.g., Contractubex) for several minutes; however, success is generally rather moderate.
• Alternatively, as a last resort and in cases of absolute treatment resistance: combination therapy consisting ofa localcorticosteroid injection immediately following surgery, compression, orsoft X-ray irradiation (ED: 3Gy at weekly intervals, GD: 12 Gy).
• Concluding general remarks:
  • In many cases, due to the complexity of the pathogenesis and the unpredictable response to the chosen treatment, a combination of several therapeutic approaches is recommended, such as compression and/or silicone gel film and/or (if unsuccessful) surgical intervention, possibly combined with internal mass reduction followed immediately by cryosurgery, or compression and/or repeated cryosurgery.
  • The procedure to be used also depends on the specific location, growth pattern, and size of the keloid, as well as the therapist’s experience (e.g., there is no alternative to compression therapy for keloids of the earlobe).
  • In addition to the evidence base, the personal experience of the therapist—who knows how to safely handle the therapeutic agents to be used—is of crucial importance!  

Prevention! Consider the risks of keloid formation before every operation! Avoidance of elective surgery in predisposed patients (own and family history) at a young age, as well as in predisposed areas such as the décolleté, shoulder and back region.

If surgery cannot be avoided, care should be taken to ensure tension-free sutures when closing the wound.

Patch application for 12 weeks can significantly reduce the risk of keloid.

In addition, silicone gels or plasters (see above) can be applied after epithelialization.

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