Most Common Anatomical Locations of Keloids

Primary Sites of Keloid Formation

Keloids demonstrate distinct anatomical predilection sites that are consistently reported across multiple populations and ethnic groups. The chest region represents the most frequently affected area, accounting for 25.7% of documented keloid locations in large cohort studies (Swenson et al., 2023). This is followed by the ear (24.4%) and back (10.9%) (Swenson et al., 2023).

Additional commonly affected sites include:

• Shoulders and deltoid region (12.1-17%) (Swenson et al., 2023; Chike-Obi et al., 2009)

• Upper limbs (13-20%) (Swenson et al., 2023; Shaheen et al., 2016)

• Neck (9.8%) (Anaba et al., 2019)

• Abdomen (8.3%) (Swenson et al., 2023)

• Cheeks (11.18%) (Anaba et al., 2019)

Anatomical Distribution by Ethnicity

The distribution of keloid locations varies significantly among different ethnic populations (Swenson et al., 2023). Among Asian patients, the most common sites are chest (35.0%), ear (14.6%), and shoulder/deltoid (12.1%) (Swenson et al., 2023). For Black patients, ear keloids predominate (33.1%), followed by chest (20.8%) and abdomen (8.3%) (Swenson et al., 2023). White patients most frequently develop keloids on the chest (27.5%), ear (19.6%), and back (14.1%) (Swenson et al., 2023).

High-Risk Anatomical Sites

Keloids preferentially develop in areas characterized by high skin tension and mechanical stress (Chike-Obi et al., 2009). The presternal region, shoulders, upper back, posterior neck, and earlobes represent the classic high-risk zones (Chike-Obi et al., 2009). These locations experience constant stretching during normal movement, contributing to the mechanical factors underlying keloid pathogenesis (Limandjaja et al., 2021).

Conversely, certain anatomical sites demonstrate lower susceptibility to keloid formation, including eyelids, cornea, palms, mucous membranes, genitalia, and soles (Shaheen, 2017).

Causes and Risk Factors

Genetic Predisposition

Keloids demonstrate a strong genetic component with clear familial clustering patterns (Halim et al., 2012; Marneros et al., 2001). Approximately one-third of patients with keloids have a first-degree blood relative who also develops keloids (Kelly & Ramakrishnan, 1974). Studies of identical twins further support genetic susceptibility, with multiple case reports documenting twin pairs developing keloids simultaneously (Kelly & Ramakrishnan, 1974; Marneros et al., 2001).

The inheritance pattern appears to follow an autosomal dominant mode with incomplete penetrance and variable expression (Marneros et al., 2001). However, approximately 6.8% of gene carriers remain unaffected (obligate unaffected carriers), indicating incomplete penetrance (Marneros et al., 2001).

Ethnic and Demographic Factors

Keloid prevalence varies dramatically among ethnic populations. Individuals of African, Asian, and Hispanic descent demonstrate significantly higher susceptibility compared to Caucasian populations (Kelly & Ramakrishnan, 1974; Mayo Clinic, 2023). The frequency of keloid occurrence is 15 times higher in highly pigmented individuals (Kelly & Ramakrishnan, 1974). Among ethnic Chinese in Asia, keloids represent the most common skin condition (Kelly & Ramakrishnan, 1974).

Age distribution shows peak incidence between 10-30 years, with particular susceptibility during adolescence and young adulthood (Chike-Obi et al., 2009; Mayo Clinic, 2023; Walsh et al., 2023). This age predilection may relate to hormonal influences and increased healing activity during these developmental periods.

Triggering Factors

Keloids can develop following virtually any form of skin trauma or inflammation (McGinty & Siddiqui, 2024; Mayo Clinic, 2023). The most common precipitating factors include:

• Trauma (50% of cases) (Shaheen et al., 2016)

• Acne (15%) (Shaheen et al., 2016)

• Surgical procedures (10-32%) (Shaheen et al., 2016; Khan et al., 2005)

• Burns (5-30%) (Shaheen et al., 2016; Khan et al., 2005)

• Ear piercing (common cause of auricular keloids) (Bashir et al., 2011)

• Vaccinations, insect bites, scratches (Mayo Clinic, 2023)

Approximately 10-13.4% of keloids develop spontaneously without identifiable trauma, though this may reflect unrecognized minor injuries (Shaheen et al., 2016; Shaheen et al., 2016).

Pathophysiological Mechanisms

The underlying pathophysiology involves dysregulated wound healing with excessive collagen deposition (Nangole & Agak, 2019; Walsh et al., 2023). Keloid fibroblasts demonstrate genetically programmed hyperactivity, producing abnormally large volumes of collagen fibers (Nangole & Agak, 2019). These cells exhibit:

• Increased proliferation rates with decreased apoptosis (Nangole & Agak, 2019)

• Enhanced response to growth factors (particularly TGF-β1) (Nangole & Agak, 2019)

• Paracrine effects stimulating surrounding fibroblast activation (Nangole & Agak, 2019)

The inflammatory component plays a crucial role, with keloid tissues containing high concentrations of macrophages, lymphocytes, and mast cells (Nangole & Agak, 2019). Patients with keloids often demonstrate elevated serum levels of pro-inflammatory cytokines including interleukin-6 and TGF-β1 (Nangole & Agak, 2019).

Treatment Modalities

First-Line Therapies

Intralesional corticosteroid injection represents the gold standard first-line treatment for keloids (Coppola et al., 2018; Jiang et al., 2020; Walsh et al., 2023). Triamcinolone acetonide (TAC) is the most commonly used agent, typically administered at concentrations of 10-40 mg/mL (Coppola et al., 2018; Anaba et al., 2019). Treatment protocols generally involve:

• Monthly injections for 4-6 sessions (Jiang et al., 2020)

• Response rates of 50-100% regression (Coppola et al., 2018)

• Recurrence rates of 33% at 1 year and 50% at 5 years (Coppola et al., 2018)

Silicone gel sheeting with compression therapy represents another first-line approach, particularly effective for prevention and early intervention (Lee et al., 2021; Walsh et al., 2023).

Combination Therapies

Combined treatment modalities consistently demonstrate superior outcomes compared to monotherapy (Coppola et al., 2018; Khan et al., 2005). Effective combinations include:

TAC + 5-Fluorouracil

This combination shows comparable or superior efficacy to TAC alone while reducing injection-site adverse effects (Coppola et al., 2018; Jiang et al., 2020). The addition of 5-FU appears to diminish TAC-related complications such as skin atrophy and telangiectasia (Coppola et al., 2018).

TAC + Verapamil

Studies demonstrate significant overall improvements with long-term stable results when combining these agents (Coppola et al., 2018). Verapamil (2.5 mg/mL) works by reducing collagen production through calcium channel antagonism (Jiang et al., 2020).

Surgical Excision + Adjuvant Therapy

Surgical excision alone carries recurrence rates of 45-100% (Limandjaja et al., 2021). However, when combined with immediate adjuvant treatments, outcomes improve dramatically (Khan et al., 2005):

• Excision + TAC injections: Lower recurrence rates with longer intervals to recurrence (10 months vs. 6 months for injection alone) (Khan et al., 2005)

• Excision + Radiotherapy: Recurrence rates of 27-32.7% in optimized protocols (Boesoirie et al., 2025; Siddiqui et al., 2025)

Advanced Treatment Options

Radiotherapy

Post-surgical radiotherapy represents an effective adjuvant therapy, functioning by inhibiting fibroblast proliferation and excessive collagen synthesis (Boesoirie et al., 2025). Optimal protocols involve:

• 15-20 Gy delivered over 5-6 sessions (Lee et al., 2021)

• Immediate post-operative timing (within 24-48 hours) (Boesoirie et al., 2025)

• Recurrence rates of 6.7-32.7% depending on protocol (Siddiqui et al., 2025)

Laser Therapy

Multiple laser modalities show promise when combined with intralesional treatments (Coppola et al., 2018). CO₂, pulsed-dye, and Nd:YAG lasers combined with TAC injections demonstrate better results than laser monotherapy (Coppola et al., 2018).

Cryotherapy

Liquid nitrogen cryotherapy combined with intralesional steroids shows efficacy in reducing keloid dimensions (Hassan & Khan, 2025). Recent studies report 75% of patients achieving ≥50% reduction in keloid size with combination protocols (Hassan & Khan, 2025).

Prognosis and Clinical Outcomes

Recurrence Patterns

Keloid recurrence represents the primary challenge in management, with rates varying significantly by treatment modality and patient factors (Siddiqui et al., 2025; Chhaya et al., 2023). Key prognostic factors include:

Treatment-Specific Recurrence Rates

• Surgical excision alone: 45-100% (Limandjaja et al., 2021)

• Intralesional steroids: 33-50% at 1-5 years (Coppola et al., 2018)

• Excision + radiotherapy: 27-65% depending on protocol (Boesoirie et al., 2025; Siddiqui et al., 2025)

• Combination therapies: Generally lower than monotherapy (Khan et al., 2005)

Timing of Recurrence

Most keloid recurrences occur within the first 24 months following treatment (Siddiqui et al., 2025; Chhaya et al., 2023). In pediatric populations, median time to recurrence is approximately 23 months (Chhaya et al., 2023). Early recurrence (within 6 months) occurs in 55% of recurrent cases (Siddiqui et al., 2025).

Predictive Factors for Recurrence

Several factors influence treatment outcomes and recurrence risk:

Patient Demographics

• Age: Patients under 10 years show higher recurrence rates (50%) (Chhaya et al., 2023)

• Ethnicity: African American patients demonstrate slightly elevated recurrence rates (32%) (Chhaya et al., 2023)

• Family history: Positive family history correlates with treatment resistance (Siddiqui et al., 2025)

Keloid Characteristics

• Size: Larger keloids (>3 cm) show higher recurrence rates (Swenson et al., 2023)

• Location: Neck keloids demonstrate increased recurrence with surgical excision (Khan et al., 2005)

• Etiology: Burn and acne-related keloids more likely to develop in multiple sites (Shaheen et al., 2016)

Treatment Adherence

Studies demonstrate that adherence to evidence-based treatment algorithms significantly reduces recurrence rates (27% vs. 55% for non-adherent protocols) (Khan et al., 2005).

Quality of Life Impact

Keloids significantly impact physical and psychological well-being (Hassan & Khan, 2025). Common symptoms include:

• Pain and pruritus: Reported in 46% and 86% of patients respectively (Chike-Obi et al., 2009)

• Functional impairment: Particularly over joints with mobility restriction (Kelly & Ramakrishnan, 1974)

• Cosmetic disfigurement: Leading to psychological distress and social withdrawal (Boesoirie et al., 2025)

Treatment success should be measured not only by dimensional reduction but also by symptom improvement and patient satisfaction (Khan et al., 2005; Al-Chalabi et al., 2023).

Assessment Tools

Several validated scales facilitate standardized keloid assessment:

Vancouver Scar Scale (VSS)

The VSS evaluates vascularity, pigmentation, pliability, and height with scores ranging 0-15 (Al-Chalabi et al., 2023). Severity classification includes:

• Mild: 0-5 points

• Moderate: 6-10 points

• Severe: 11-15 points (Al-Chalabi et al., 2023)

Detroit Keloid Scale (DKS)

The DKS offers superior inter-rater reliability compared to VSS and incorporates both patient-reported and observer assessments specifically designed for keloid evaluation (Al-Chalabi et al., 2023).

Prevention Strategies

Primary Prevention

• Avoidance of unnecessary trauma in susceptible individuals

• Proper wound care with gentle tissue handling

• Early intervention with silicone sheeting for high-risk wounds (Lee et al., 2021)

Secondary Prevention

• Immediate post-surgical adjuvant therapy for excised keloids

• Long-term monitoring for early recurrence detection

• Patient education regarding keloid susceptibility and prevention strategies

Conclusions

Keloids represent a complex, genetically-influenced disorder with significant clinical and psychosocial impact. The chest, ears, and shoulders constitute the most common anatomical sites, with clear ethnic and demographic risk patterns. While multiple treatment modalities exist, combination therapies consistently demonstrate superior outcomes compared to monotherapy approaches. Intralesional corticosteroids remain the first-line treatment, with surgical excision plus adjuvant therapy reserved for recalcitrant cases. Recurrence rates remain substantial across all treatment modalities, emphasizing the importance of realistic patient expectations and long-term management strategies. Future research should focus on standardized outcome measures, larger randomized controlled trials, and development of targeted therapies based on improved understanding of keloid pathophysiology.

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