Dermatology · Medicine
Keloid and Hypertrophic Scar
Also known as Keloid · Hypertrophic scar · Keloid scar · Cheloid · Cheloid scar · Crab-claw scar
Keloids extend beyond the original wound; hypertrophic scars remain within it. Diagnosis is usually clinical, atypical lesions need histology, and treatment is individualized because comparative evidence is heterogeneous.
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The wound boundary gives the exam answer. A keloid is a benign fibroproliferative scar that grows into adjacent clinically unwounded skin. A hypertrophic scar is raised but confined to the original injury. Both may itch, hurt and impair function, but their natural histories differ: keloids usually persist, whereas hypertrophic scars may soften and flatten with time.[2][4]
The distinction is clinical, not a claim that the two lesions share one proven molecular pathway. Modern reviews describe overlapping scar phenotypes and incompletely defined mechanisms.[3][4]
Both lesions are the remodelling phase of wound healing failing to switch off, but only one overruns its borders. That single fact separates them at the bedside and in every viva.[1][4]

Keloid
Beyond the original wound
- Lobulated, firm or rubbery growth into adjacent skin
- Usually persists and may continue to enlarge
- Pruritus, pain or tenderness may be prominent
- Recurrence is common; outcome depends on site, treatment and follow-up
Hypertrophic scar
Within the original wound
- Raised scar that follows the wound shape
- Often appears during active wound maturation
- May flatten, soften and fade, but regression is variable
- Burn scars may contract and restrict movement
Normal or atrophic scar
Not a raised proliferative scar
- Normal mature scar is flat and confined to the wound
- Atrophic scar is depressed below the surrounding surface
- Neither should be relabelled as a keloid merely because colour differs
Keloids are a disease of skin of colour and of youth, and they love skin under tension. The single biggest risk factor is Fitzpatrick IV to VI; reported in roughly 4.5 to 16 per cent of African, Asian and Hispanic populations versus under 1 per cent of Caucasians. Peak onset is 10 to 30 years, when dermal fibroblasts are most active.[2][4]
Use association language, not biological race. Keloids are reported more often in some populations with darker skin phototypes and in several ancestry groups, but estimates vary with case definition, ascertainment, access to care and the populations sampled. Phototype, ancestry, social exposure and treatment access are not interchangeable, and none predicts an individual outcome with certainty.[4][11]
Familial clustering is real, but keloid susceptibility is genetically heterogeneous rather than a single universal Mendelian trait. A personal or family history therefore changes counselling, not the diagnosis by itself.[11]
Common clinical risk contexts include prior keloid formation, wounds under mechanical tension, delayed healing or inflammation, burns, surgery, acne, piercing, vaccination and other trauma. Chest, shoulder, upper back, jaw and ear are familiar sites. Keloids on palms, soles or genital skin are uncommon, not impossible.[2][4][19]
Pathophysiology
Pathological scarring is a failure of coordinated repair, not one proven switch in remodelling. Normal wound repair has overlapping haemostatic, inflammatory, proliferative and remodelling processes. In keloids and hypertrophic scars, persistent inflammation, fibroblast heterogeneity, dysregulated extracellular-matrix turnover and mechanical signalling are implicated.[1][4][19]

Mechanism → consequence → clinical lever
Inflammation persists
Cytokine and immune-cell signalling can remain active beyond orderly repair.
Fibroblast responses vary
Fibroblast subpopulations differ in proliferation, contractility and matrix production.
Matrix turnover is dysregulated
Collagen synthesis and degradation no longer return cleanly to baseline.
Mechanical tension sustains signalling
Stretch and wound geometry can reinforce fibroproliferative activity.
The phenotype diverges
Keloid growth crosses the clinical wound boundary; hypertrophic growth remains inside it.
TGF-beta/SMAD signalling is important in experimental and clinical scar research, but exact cytokine ratios, collagen-per-cell multipliers and fixed MMP/TIMP panels should not be presented as universal diagnostic facts.[3][4][19]
Clinical Presentation
Keloid: firm, smooth, shiny, nodular or lobulated tissue extending beyond a known injury. Colour varies with activity and baseline pigmentation. Symptoms may include itch, pain, burning and tenderness. Growth can remain active; speed alone does not prove malignancy, but an unusual change in behaviour lowers the threshold for biopsy.[2][4]
Hypertrophic scar: raised erythematous or pigmented tissue that traces the original wound. Burn-related lesions may be broad, pruritic and contractile. Spontaneous improvement is possible but not guaranteed.[4][8]
Clinical priorities are the patient's dominant symptom, lesion activity, site, range of motion, sleep, body image and previous treatment response—not thickness alone.[3][4]
Differential Diagnosis
A typical lesion is diagnosed clinically; an atypical scar-like mass earns tissue. Ask whether there was a wound, whether the lesion respects that boundary and whether its behaviour fits the history.[2][4]
Dermatofibrosarcoma protuberans
Malignant mimic
- Indurated plaque or nodules
- Progressive local growth or fixation
- Storiform CD34-positive spindle-cell tumour on histology
Squamous cell carcinoma in a scar
Malignant mimic
- Ulceration, bleeding or destructive change
- New pain or rapid change in a chronic scar
- Atypical keratinocytes on biopsy
Scar sarcoidosis
Inflammatory mimic
- New violaceous or infiltrated change in an old scar
- May coexist with systemic clues
- Non-caseating granulomas on biopsy
Dermatofibroma / desmoid / infection
Other mimics
- Dermatofibroma is a dermal nodule, often with dimpling
- Desmoid is deeper and fixed
- Deep fungal or atypical infection depends on exposure and immune status
Biopsy when the diagnosis is uncertain, especially with ulceration, fixation, destructive change, an unexplained scar-like mass or behaviour discordant with a known keloid. Choose a specimen deep enough to sample the relevant dermis and exclude a spindle-cell tumour; coordinate with the surgical team when biopsy planning could affect definitive excision.[2][4]
Clinical & Bedside Assessment
Measure what matters before treating. Record trigger, timing, previous scars, itch, pain, tenderness, sleep, function, mood, prior treatments and the patient's priority. Examine the original wound boundary, length, width, elevation, colour, pliability, ulceration, fixation and joint range of motion. Take standardised photographs with consent.[3][4][8]
Scar scores without false precision
- Vancouver Scar Scale (VSS): records vascularity, pigmentation, pliability and height. It was developed for burn scars; versions and reported totals vary, so name the version used rather than claiming one universal maximum.[8]
- POSAS: the original scale has six patient items and six observer items, each scored 1–10. Each six-item subscale therefore totals 6–60; the overall-opinion item is recorded separately. Later versions differ, so document the version.[12]
Investigations
No routine blood test or scan confirms a typical keloid. Histology is for diagnostic uncertainty or an atypical lesion. Ultrasound can quantify thickness when available; MRI is reserved for a genuinely deep or invasive differential, not routine scar follow-up.[2][4]
Histopathology
Keloids classically show broad, glassy, hyalinised eosinophilic collagen (“keloidal collagen”). Hypertrophic scars more often show nodular, relatively aligned collagen with myofibroblastic activity. These patterns overlap, and histology cannot reconstruct the original clinical wound boundary; clinicopathological correlation is essential.[4][19]
No cytological atypia is expected in either benign scar. Atypia, infiltrative storiform spindle cells, destructive epithelial proliferation or granulomatous inflammation redirects the diagnosis.[2][4]
Management — Resuscitation
These scars do not usually require resuscitation. Urgency comes from functional compromise: contracture restricting a joint or orifice, severe secondary infection, or a suspected malignant mimic. Stabilise the immediate problem and obtain the relevant burns, plastic-surgery, dermatology or oncology input.[4][8]
Management — Definitive & Stepwise
There is no universal gold standard. Match treatment to diagnosis, site, activity, symptoms, previous response, pigmentary risk, comorbidity, patient preference and local expertise. Explain that most trials are small and heterogeneous and that recurrence definitions and follow-up vary.[2][3]

Prevention and early scar care
A safe prevention conversation
Discuss individual risk
Prior keloid, family history, wound site, tension and the necessity of the procedure.
Reduce avoidable trauma
Defer optional piercing or surgery when the likely scar burden outweighs benefit.
Optimise closure
Control infection and inflammation, handle tissue gently and reduce wound tension.
Wait for epithelialisation
Silicone gel or sheeting is applied only after the wound is fully closed; protocols vary.
Review early change
New elevation, itch, pain or contracture prompts reassessment rather than an automatic recipe.
Silicone gel may help prevent or treat hypertrophic scarring, but the 2022 meta-analysis found many trials at high risk of bias and did not establish simple equivalence between all gels, sheets and additive products. Present benefit as possible, not guaranteed.[10]
For burn-related hypertrophic scars, a specialist pressure programme may be considered alongside rehabilitation. A 2023 systematic review suggested starting within two months, using at least 20–25 mmHg and continuing at least 12 months, preferably 18–24 months; these are review-derived suggestions, not a universal prescription, and tolerance/adherence require monitoring.[14]

Intralesional corticosteroid
Intralesional triamcinolone is a common first-line treatment for symptomatic keloids. The 2024 KECORT e-Delphi preferred 40 mg/mL, a four-week interval, and a maximum 80 mg per month, while also finding no full consensus on dosing. Use those numbers as expert-consensus practice, not a one-size-fits-all mandate; individualise injected volume and stop when risk outweighs benefit.[13]
Inject into the lesion rather than subcutaneous fat. Counsel about pain, atrophy, telangiectasia and hypo- or hyperpigmentation. Dyspigmentation risk matters across skin phototypes; it is not a reason to dose by race.[2][13]
Refractory lesions and combinations
- Intralesional 5-fluorouracil, bleomycin or verapamil may be considered by experienced clinicians, usually in combination or after inadequate response. Evidence is mixed; exact recipes are protocol-specific.[3][7]
- Cryotherapy can be an adjunct, especially for smaller lesions. Pain, blistering and pigmentary change require counselling, particularly when dyschromia would be consequential.[2][3]
- Laser treatment is an adjunct rather than a proven standard ladder step. A Cochrane review of 15 randomised trials involving 604 participants found low- or very-low-certainty evidence for most comparisons.[15]
- Silicone, pressure and rehabilitation may remain useful for symptoms or function, but their role differs between a focal keloid and an extensive burn hypertrophic scar.[8][10][14]
Surgery and postoperative radiotherapy
Excision creates another wound, so recurrence is high when surgery is used alone. Before operating, agree the indication, closure strategy, adjuvant plan and follow-up. Options include intralesional treatment, silicone or pressure where feasible, and selected postoperative radiotherapy.[2][3][7]
Radiotherapy is most defensible for selected adults with recurrent or refractory keloids after specialist assessment. A 2017 meta-analysis reported 22% overall postoperative recurrence, with subgroup estimates of 15% after brachytherapy, 23% after x-ray therapy and 23% after electron therapy; chest lesions recurred most often. These pooled observational data do not establish one universally superior regimen.[16]
Prompt treatment after excision is common practice, but a timing meta-analysis did not demonstrate a significant recurrence advantage for immediate over delayed postoperative radiotherapy. Dose, fractionation, modality, timing and shielding therefore belong to the radiation-oncology plan rather than a universal dermatology recipe.[17][18]
Discuss pigmentary change, telangiectasia, fibrosis and the small long-term malignancy concern. Modern reviews judge the secondary-malignancy risk low when sensitive organs are protected, but the evidence is not zero-risk. Avoid radiotherapy during pregnancy and generally defer it in children because of the longer risk horizon and radiosensitive tissues.[18]
Specific Subtypes & Scenarios
Earlobe keloid
Confirm that the lesion truly arose from piercing or trauma and map both surfaces of the lobule. Excision may be combined with compression and/or intralesional treatment, but recurrence estimates depend on protocol and follow-up. One 60-patient ear-keloid RCT compared postoperative 5-fluorouracil plus triamcinolone with radiotherapy at six months; it does not establish a universal ear-keloid recipe.[9]
Chest, shoulder and other high-tension sites
Mechanical tension and site-specific recurrence matter. Use shared decision-making and multimodal planning rather than promising that five simultaneous treatments will prevent recurrence.[3][16][19]
Burn-related hypertrophic scar
Prioritise range of motion, splinting/positioning, physiotherapy or occupational therapy, itch control and scar monitoring within a burns rehabilitation service. Consider silicone or monitored pressure therapy; a mature functional contracture may need release and reconstruction.[4][8][14]
Acne-associated keloid
Control active acne to reduce new inflammatory injury, then treat the established scar according to symptoms and site. Do not confuse truncal keloids with acne keloidalis nuchae, a distinct follicular disorder.[2][4]
Complications & Pitfalls
- Recurrence: common and reported inconsistently; document the follow-up interval when quoting a rate.[2][3]
- Functional restriction: contracture across a joint or orifice changes the goal from cosmesis to function.[4]
- Psychological burden: ask about pain, itch, sleep, clothing, intimacy, stigma and mood without assuming what matters most.[4]
- Treatment harm: steroid atrophy/dyspigmentation, cryotherapy pigment change, laser uncertainty and radiotherapy late effects belong in consent.[13][15][18]
- Diagnostic anchoring: a prior keloid history does not make every new mass a keloid.[2][4]
Prognosis & Disposition
Set goals that can be measured: less itch or pain, flatter contour, improved pliability, restored movement, or acceptable appearance. Complete eradication is not a safe promise. Hypertrophic scars may improve without intervention; keloids may remain active or recur after apparently successful therapy.[2][3][4]
Follow-up should match the intervention and recurrence risk. Review during an active injection, pressure, postoperative or radiotherapy course according to that protocol, then continue long enough to detect clinically meaningful recurrence. Many studies have short or inconsistent follow-up, so avoid inventing a universal three-monthly or annual schedule.[3][16]
Special Populations
- Children: confirm the diagnosis and prioritise conservative, function-preserving care. Intralesional treatment requires an age-appropriate pain plan. Radiotherapy is generally deferred; any surgery needs a non-radiation adjuvant discussion.[3][18]
- Pregnancy: defer elective procedures when possible. Avoid radiotherapy and obtain obstetric/pharmacy advice before any intralesional cytotoxic or systemic treatment; do not label an unsourced dose “safe.”[3][18]
- Darker phototypes: discuss observed epidemiologic associations and the possibility of treatment-related dyspigmentation. Individualise therapy by lesion, site, prior response and patient priorities—not ancestry or race.[4][11][13]
- Immunocompromised patients: broaden the differential for a new scar-like lesion to include infection and malignancy; biopsy when the clinical diagnosis is uncertain.[4]
- Burn survivors: use multidisciplinary rehabilitation and monitor growth, function, itch and skin integrity; pressure parameters require specialist fitting and review.[4][14]
Evidence, Guidelines & Regional Differences
International recommendations support silicone and intralesional corticosteroid as established options, while later reviews emphasise individualized combinations. These documents are consensus or evidence syntheses, not interchangeable national rules.[6][7][8]
The 2023 systematic review included 108 prospective studies but found heterogeneous interventions, small samples and inconsistent outcomes. It supports silicone and corticosteroids as first-line options, mixed evidence for intralesional alternatives, combination use of lasers, and postoperative radiotherapy as an option—without establishing one universally low-recurrence gold standard.[3]
The Nippon Medical School protocol is a detailed single-centre Japanese strategy. It is useful as one model of organized multimodal care, but it should not be presented as an international consensus or automatically exported to every health system.[5]
Regional practice differs through access to scar clinics, burns rehabilitation, pressure-garment services, laser platforms and radiation oncology. Name the actual local protocol when giving a dose or schedule; do not attribute a position to AAD, BAD, NICE, IADVL or ICMR without a live guideline source.[3][8]
Exam Pearls
BOUNDARY
B-O-U-N-D-A-R-Y
Keloid crosses the original wound boundary.
Reconstruct the injury before naming the scar.
Especially with ulceration, fixation or destructive change.
Evidence is heterogeneous and recurrence definitions vary.
Symptoms, function, dimensions, photos and score version.
Do not create a new wound without a recurrence strategy.
Specialist adult option; regimen and timing are individualized.
Pain, itch, movement and appearance may carry different priorities.
Worked stems
A raised burn scar remains inside the graft boundary and is tightening the elbow. What matters first?
A presumed keloid becomes ulcerated and fixed. What changes?
The patient asks for the best radiotherapy dose. What is the safe answer?
References
- [1]Wang PH, Huang BS, Horng HC, et al. Wound healing J Chin Med Assoc, 2018.PMID 29169897
- [2]Ekstein SF, Wyles SP, Moran SL, et al. Keloids: a review of therapeutic management Int J Dermatol, 2021.PMID 32905614
- [3]Walsh LA, Wu E, Pontes D, et al. Keloid treatments: an evidence-based systematic review of recent advances Syst Rev, 2023.PMID 36918908
- [4]Jeschke MG, Wood FM, Middelkoop E, et al. Scars Nat Rev Dis Primers, 2023.PMID 37973792
- [5]Ogawa R, Dohi T, Tosa M, et al. The Latest Strategy for Keloid and Hypertrophic Scar Prevention and Treatment: The Nippon Medical School (NMS) Protocol J Nippon Med Sch, 2021.PMID 32741903
- [6]Mustoe TA, Cooter RD, Gold MH, et al. International clinical recommendations on scar management Plast Reconstr Surg, 2002.PMID 12142678
- [7]Gold MH, McGuire M, Mustoe TA, et al. Updated international clinical recommendations on scar management: part 2--algorithms for scar prevention and treatment Dermatol Surg, 2014.PMID 25068544
- [8]Monstrey S, Middelkoop E, Vranckx JJ, et al. Updated scar management practical guidelines: non-invasive and invasive measures J Plast Reconstr Aesthet Surg, 2014.PMID 24888226
- [9]Khalid FA, Farooq UK, Saleem M, et al. The efficacy of excision followed by intralesional 5-fluorouracil and triamcinolone acetonide versus excision followed by radiotherapy in the treatment of ear keloids: A randomized control trial Burns, 2018.PMID 29534885
- [10]De Decker I, Hoeksema H, Verbelen J, et al. The use of fluid silicone gels in the prevention and treatment of hypertrophic scars: a systematic review and meta-analysis Burns, 2022.PMID 35367089
- [11]Shih B, Bayat A Genetics of keloid scarring Arch Dermatol Res, 2010.PMID 20130896
- [12]Draaijers LJ, Tempelman FR, Botman YA, et al. The patient and observer scar assessment scale: a reliable and feasible tool for scar evaluation Plast Reconstr Surg, 2004.PMID 15253184
- [13]Yin Q, Wolkerstorfer A, Lapid O, et al. KECORT Study: An International e-Delphi Study on the Treatment of KEloids Using Intralesional CORTicosteroids in Clinical Practice Am J Clin Dermatol, 2024.PMID 39298112
- [14]De Decker I, Beeckman A, Hoeksema H, et al. Pressure therapy for scars: Myth or reality? A systematic review Burns, 2023.PMID 36941176
- [15]Leszczynski R, da Silva CA, Pinto ACPN, et al. Laser therapy for treating hypertrophic and keloid scars Cochrane Database Syst Rev, 2022.PMID 36161591
- [16]Mankowski P, Kanevsky J, Tomlinson J, et al. Optimizing Radiotherapy for Keloids: A Meta-Analysis Systematic Review Comparing Recurrence Rates Between Different Radiation Modalities Ann Plast Surg, 2017.PMID 28177974
- [17]Hsieh CL, Chi KY, Lin WY, et al. Timing of Adjuvant Radiotherapy After Keloid Excision: A Systematic Review and Meta-Analysis Dermatol Surg, 2021.PMID 34417379
- [18]Liu EK, Cohen RF, Chiu ES Radiation therapy modalities for keloid management: A critical review J Plast Reconstr Aesthet Surg, 2022.PMID 35817711
- [19]Ogawa R Keloid and Hypertrophic Scars Are the Result of Chronic Inflammation in the Reticular Dermis Int J Mol Sci, 2017.PMID 28287424