Keloids

Introduction

Keloids are overgrown scar tissues that can climb out of the confines of an injury site, forming firm, shiny bumps that sometimes itch or hurt. People often google “keloid scars” or “how to treat keloids” when they notice these raised lumps after body piercings, acne, surgery or even minor cuts. Clinically, keloids matter because they can impair movment, cause persistent discomfort, and impact self-esteem. In this article, we look through two lenses: modern clinical evidence (studies, guidelines) and practical patient guidance (real-world tips, at-home care). You’ll get the science without the fluff and actionable steps to manage or prevent keloid scars.

Definition

Keloids are benign fibrous growths that develop at the site of skin injury, characterized by an excessive deposition of collagen. Unlike hypertrophic scars, which stay within the original wound boundaries and may regress over time, keloid scars grow beyond these margins and rarely improve without treatment. Medically, they fall under the spectrum of abnormal wound healing disorders—often termed reactive proliferative disorders of the dermis. You might hear terms like “keloid formation” or “keloid fibroplasia” in clinical notes, which basically point to a similar process: uncontrolled scar tissue expansion.

At microscopic level, keloid tissue shows an overgrowth of type I and III collagen fibers arranged in thick bundles, along with an increase in fibroblasts and inflammatory cells. This hyperactive healing response is influenced by various growth factors, especially TGF-β (transforming growth factor beta). Keloids can appear pink, red, or darker than the surrounding skin, and they often take on a smooth, shiny surface. Some patients report itching, tenderness, or even pain—symptoms that can range from mild annoyance to significant discomfort interfering with daily activities.

Keloid scars frequently manifest on the chest, shoulders, earlobes, and jawline, but they can occur anywhere in the body where the skin has been injured—surgical cuts, acne lesions, piercings, tattoos, or even insect bites. They can develop weeks to months after the initial trauma, sometimes even up to a year later—yes it takes that long. While keloids are considered benign and not cancerous, their unpredictable growth pattern and tendency to recur after removal make them clinially important. Patients often seek “keloid removal” or ask “how to get rid of keloids” as soon as they see these persistent bumps.

• Appearance: Firm, raised, smooth, shiny surface, often pink-red or hyperpigmented.
• Symptoms: Itching (pruritus), pain (sometimes sharp or throbbing), and possible restriction of movement.
• Timing: Onset varies—can appear within weeks or delayed up to a year post-injury.
• Distribution: Common on the chest, back, shoulders, earlobes, and jawline—any area of high skin tension.

Recognizing keloids early can be helpful since prompt treatment often leads to better cosmetic outcomes. That said, they’re notoriously stubborn—many treatments yield partial response at best. The term “keloid” itself comes from the Greek word “chele,” meaning crab’s claw, aptly describing how the scar claws its way beyond the original wound edges. If you ever wondered “why do keloids form,” well, science has some answers, but as you’ll see, there’s still a bit of mystery around why some folks get them and others don’t.

Epidemiology

Keloids can affect anyone, but they’re significantly more common in people with darker skin tones—particularly those of African, Asian, or Hispanic descent. Estimates suggest that keloid prevalence ranges from 1% up to 16% in these populations, whereas in lighter-skinned individuals it hovers around 0.1–1.3%. This disparity points to a genetic predisposition, though pinning down specific genes remains an active area of research.

Age at onset typically spans from puberty through early adulthood, peaking between 10 and 30 years of age. Hormonal factors, which may be at play during adolescence, are suspected to influence keloid development, though more evidence is needed to confirm links with estrogen or testosterone levels. Both male and female individuals are affected, with some studies suggesting a slight female predominance, possibly related to higher rates of ear piercing and cosmetic procedures.

Common body sites include the chest, shoulders, upper back, earlobes, and jawline—regions that experience high tension or frequent microtrauma. The lack of standardized reporting and the variety of clinical settings (dermatology clinics, plastic surgery centers, general practice) make it challenging to capture true incidence. Moreover, many people with mild keloids may never seek medical attention, leading to potential underestimation.

Large-scale population studies are scarce, especially in low-resource settings. Hospital-based case series note that keloid scars account for up to 20% of scar-related consultations in specialized clinics, yet these figures likely overrepresent severe cases. Community surveys, when available, often rely on self-reporting and visual inspection, limiting accuracy. Still, the data we have clearly show that keloids represent a global health concern with notable psychosocial impact beyond the mere cosmetic aspect.

Etiology

The etiology of keloids is multifactorial, blending genetic susceptibility, mechanical forces, and various environmental triggers. No single cause explains all cases, so it’s helpful to consider keloid development through four broad categories: genetic, mechanical, biochemical (hormones and cytokines), and local factors like infection or foreign bodies.

Genetic predisposition: Family and twin studies strongly suggest heredity. People with a family history of keloids have significantly higher risk, and certain HLA haplotypes (for example, HLA-DRB1*15) have been implicated. Although genome-wide association studies are limited, some research points to variants in genes governing collagen synthesis and TGF-β signaling.

Mechanical tension and skin stretch: Areas under constant tension—like the chest, shoulders, or near joints—are hot spots for keloid formation. Skin stretching seems to influence fibroblast activity: when the dermis is under chronic mechanical stress, it may trigger more robust healing responses, leading to overproduction of scar tissue.

Biochemical factors: Several growth factors and cytokines orchestrate the wound healing cascade. Transforming growth factor beta (TGF-β), especially isoforms 1 and 2, plays a central role in driving fibroblast proliferation and collagen deposition. Other mediators like connective tissue growth factor (CTGF) and platelet-derived growth factor (PDGF) also contribute. Hormonal influences—estrogen and possibly insulin-like growth factor (IGF)—have been observed, though studies are not always consistent.

Local triggers: Any skin insult—trauma, surgical incision, acne lesion, insect bite, vaccination, tattoo, or body piercing—can initiate keloid formation in susceptible individuals. Chronic irritation, infection, or the presence of foreign materials (like suture threads or implanted devices) may exacerbate the response. Some reports even link keloid growth to minor burns or frictional injuries.

Inflammation and immune response: Keloids may exist as a chronic inflammatory state, with persistent immune cell infiltration. Mast cells, macrophages, and lymphocytes secrete modulators that further activate fibroblasts, perpetuating fibrosis. In rare cases, functional etiologies like autoimmune disorders or viral infections have been postulated, but evidence is preliminary.

Uncommon etiologies include radiation exposure, which can paradoxically both prevent or induce keloid formation, and certain metabolic conditions such as diabetes, where altered wound healing dynamics come into play. Experimental models also suggest that epi-genetics—like DNA methylation and histone modification—could set the stage for keloid fibroblasts to remain in a perpetual “on” state.

In real life, it’s often a perfect storm: a genetic background primed for excess collagen synthesis meets a high-tension area on the skin, and even a small trauma is enough to tip the balance. That’s why you’ll see keloids cropping up after ear piercings more often than on low-stress skin zones—pearls of wisdom for people considering new piercings or cosmetic procedures.

Pathophysiology

The pathophysiology of keloids revolves around a dysregulated wound healing process, where the normal sequence of inflammation, proliferation, and remodeling becomes hijacked, leading to persistent scar formation. In typical wound healing, fibroblasts deposit extracellular matrix (ECM), primarily collagen, to close the breach; then, remodeling enzymes (matrix metalloproteinases, MMPs) and apoptosis gradually reshape and downsize the scar. In keloids, this balance is lost: fibroblasts remain hyperactive, collagen deposition outpaces degradation, and remodeling stalls.

Inflammatory phase gone awry: It starts with an exaggerated inflammatory response. After injury, platelets and immune cells release cytokines—interleukins (IL-6, IL-1β), tumor necrosis factor alpha (TNF-α), and transforming growth factor beta (TGF-β). In keloid-prone skin, the levels and duration of these signals are elevated. Macrophages and mast cells linger longer, prolonging the recruitment of fibroblasts and fueling a feedback loop of inflammation that never quite shuts off.

Fibroblast proliferation and ECM overproduction: The fibroblasts in keloid tissue exhibit a distinct phenotype: they proliferate more rapidly, resist apoptosis, and secrete excess ECM components, especially types I and III collagen, fibronectin, and elastin. TGF-β (particularly TGF-β1 and β2) is a key driver: it stimulates collagen gene transcription and inhibits MMP expression, tipping the balance toward accumulation. Additionally, the TGF-β receptor pathway is upregulated in keloid fibroblasts, amplifying the signal.

Mechanotransduction and tissue tension: Mechanical forces also shape keloid development. Fibroblasts sense tension through integrins and focal adhesion complexes; stretched tissue signals these cells to ramp up ECM production. This is why regions under high stress—like the chest or shoulders—are hotspots for keloid emergence. In vitro studies show that stretching keloid-derived fibroblasts boosts collagen synthesis even more, a vicious circle of tension-begetting-tension.

Angiogenesis and vascular changes: While keloid scars are less vascular than hypertrophic scars, they do show microvascular changes that affect oxygenation and nutrient supply. Hypoxia-inducible factors (HIFs) can activate pro-fibrotic pathways, further supporting fibroblast activity. Yet the vessels in keloid tissue can be dysfunctional, contributing to persistent low-grade hypoxia and chronic fibrotic signaling.

Epigenetic modifications: Emerging evidence points to epigenetic regulation—DNA methylation, histone acetylation, and non-coding RNAs (microRNAs)—as modulators of keloid pathobiology. Certain microRNAs (for example, miR-21 and miR-29) are dysregulated in keloid fibroblasts, affecting collagen production and apoptosis. While this area is still evolving, it offers potential new therapeutic targets.

Cellular cross-talk: Keloid fibroblasts don’t act alone; they interact with keratinocytes, immune cells, and endothelial cells in a complex microenvironment. Keratinocytes in keloids may release specific cytokines that further stimulate fibroblasts, while fibroblasts, in turn, secrete factors that alter keratinocyte behavior, creating a self-perpetuating niche. This cross-talk is part of what makes keloids so stubbornly persistent.

Overall, the pathophysiology of keloids is a tale of runaway repair: inflammation never fully resolves, fibroblasts stay active beyond what’s needed, and tissue mechanics keep feeding the cycle. As a result, the scar tisssue grows like an invasive plant, sprawling beyond the original wound area. Understanding these mechanisms is key to developing treatments that not only reduce symptoms but also correct the underlying biology.

Diagnosis

Diagnosing keloids largely hinges on clinical evaluation. Most patients present with a history of skin injury—piercing, surgery, acne, insect bite—followed by the gradual appearance of a firm, raised scar exceeding the original wound margins. Physicians will gather a detailed history: timing of onset (weeks to months post-injury), progression (slow vs rapid growth), and associated symptoms like itching, pain, or restricted movement.

On physical exam, keloid scars are often shiny, firm, and elastic to the touch. Their color can vary from pinkish-red in early stages to hyperpigmented or hypopigmented later. Size and shape can differ—sometimes nodular, sometimes flat and sheet-like—so clinicians will measure dimensions in centimeters and map the borders relative to the initial injury site. Palpation helps differentiate keloids from softer lesions like lipomas or cysts.

In most cases, no laboratory tests are needed. However, if there’s diagnostic uncertainty—say the lesion is atypical, rapidly changing, or shows unusual features—biopsy can be performed. Histology of keloid tissue reveals broad, disorganized collagen bundles (often described as “keloidal collagen”) and numerous fibroblasts. Immunohistochemical stains may highlight proliferative markers like Ki-67 or elevated TGF-β expression.

Imaging studies (ultrasound or MRI) are rarely required but can be useful for large or deep-seated keloids, especially those limiting joint mobility or encroaching on critical structures. Ultrasound can assess scar thickness and vascularity, while MRI offers superior soft-tissue contrast, helpful for pre-operative planning in complex cases.

It’s also important to consider and rule out other conditions in the differential diagnosis:

• Hypertrophic scars: Similar appearance but stay within wound boundaries and may regress spontaneously.
• Dermatofibroma: A firm, benign skin nodule, usually less than 1 cm and pigmented, does not extend beyond its borders.
• Epidermal inclusion cyst: A round, subdermal nodule with a central punctum, usually softer and mobile.
• Scleroderma/morphea: Autoimmune conditions with hard, indurated skin patches, often accompanied by systemic symptoms.
• Neoplastic lesions: Rarely, skin cancers may mimic keloids in early stages, warranting biopsy if suspicious signs like rapid ulceration or bleeding appear.

In practice, a straightforward history and exam clinch most keloid diagnoses—patients usually know when and where the original injury occurred. Yet, documenting the scar characteristics thoroughly is vital, particularly if you’re considering treatments like steroid injections, laser therapy, or surgical excision, which hinge on accurate staging and sizing of the keloid tissue.

Differential Diagnostics

When faced with a suspicious raised scar, clinicians perform a structured differential diagnosis to separate keloids from hypertrophic scars and other look-alike conditions. The key is to focus on three pillars: clinical history, lesion characteristics, and targeted tests (if needed).

1. History-taking: Note the injury timeline. Keloids typically arise weeks to months after skin trauma and continue to grow beyond six months. Hypertrophic scars peak within 4–6 weeks and often plateau or regress thereafter. Enquire about previous keloid formation, family history, and risk factors like dark skin, body sites under high tension, or immune disorders.

2. Physical exam: Evaluate borders—keloids extend past the original wound edges, forming a broad, bow-shaped or butterfly-like projection. Hypertrophic scars remain confined. Palpation: keloids feel firmer and more irregular. Color can be similar in both, but keloids may become darker over time while hypertrophic scars often lighten.

3. Imaging and biopsy: Reserved for atypical or deep lesions. Use ultrasound to assess thickness; keloids often exceed 5 mm in height. Biopsy shows disorganized, thick collagen bundles and high fibroblast density in keloids versus more parallel collagen patterns in hypertrophic scars.

4. Lab and special tests: Rarely needed unless ruling out underlying systemic diseases. For autoimmune causes (e.g., scleroderma), check ANA or specific autoantibodies. If infection is suspected, cultures or PCR tests can rule out atypical mycobacteria or fungal pathogens.

5. Rule out other conditions:

• Dermatofibrosarcoma protuberans (DFSP): A low-grade sarcoma that can appear as a firm plaque; biopsy is essential to exclude malignancy when the lesion is rapidly growing or bleeding.
• Pyogenic granuloma: A vascular lesion that bleeds easily, unlike keloids which are usually dry.
• Pseudofibroma: Scar-like papule often seen in elderly; history of sun exposure and slower evolution.
• Granuloma annulare: Papular, ring-like lesions, usually without the same firm, raised texture of keloids.

By methodically evaluating onset, growth pattern, tissue characteristics, and complementary tests, clinicians can confidently distinguish keloids from look-alikes. This targeted approach prevents unnecessary aggressive treatments or missing a more serious diagnosis.

Treatment

Managing keloids can feel like trying to tame a stubborn weed—multiple modalities may be necessary, and results vary. Evidence-based treatment generally revolves around reducing fibroblast activity and collagen synthesis, flattening and softening the scar, and preventing recurrence. Here’s a rundown of the main options:

• Intralesional corticosteroid injections: Triamcinolone acetonide is the workhorse: injected directly into the keloid every 4–6 weeks, it reduces fibroblast proliferation and collagen deposition. Typical doses range from 10 to 40 mg/mL. Side effects can include skin atrophy, hypopigmentation or telangiectasias—so dosing wisely is key.
• Silicone gel sheets or topical gels: Available over-the-counter, these work by hydrating the scar and modulating growth factors. Use for at least 12 hours a day over several months. Many patients report softer, flatter scars with consistent use—low risk, easy at-home care.
• Pressure therapy and compression garments: Particularly used for earlobe keloids (post-piercing), chest, or burn scars. Applying constant pressure (24 mmHg or more) for 6–12 months can reduce blood flow and fibroblast activity. Not super comfy, but can be effective when combined with other treatments.
• Cryotherapy: Freezing the keloid with liquid nitrogen induces vascular injury and scar necrosis. Often paired with IL steroid shots. Watch out: risk of blistering and hypopigmentation, especially in darker skin tones.
• Laser therapy: Pulsed-dye lasers (585–595 nm) target blood vessels in scars, diminishing redness and reducing thickness. Fractional CO2 lasers may improve texture. Multiple sessions are usually needed.
• 5-Fluorouracil (5-FU) and bleomycin injections: Anti-fibrotic agents that can be used alone or alongside steroids. 5-FU inhibits fibroblast proliferation, while bleomycin causes DNA strand breaks—both can flair local side effects like pain and ulceration.
• Surgery with adjuvant therapy: Excision alone often leads to recurrence (>50% rate). Combining surgery with immediate post-op radiation therapy (low-dose, 0.5–1 Gy fractions) or steroid injections lowers recurrence to around 10–20%. Imiquimod cream applied post-op may also help reduce keloid return.
• Emerging medical therapies: Interferon, botulinum toxin, and topical imiquimod have shown promise in small studies. ACE inhibitors and Transforming growth factor beta inhibitors are under investigation—stay tuned!

Self-care measures can complement medical treatments. Keeping the area moisturized, protecting from sun exposure (UV can darken scars), and avoiding unnecessary trauma is helpful. Some people try home remedies like onion extract, vitamin E, or aloe vera, but evidence is mixed—no harm in trying, but don’t skip professional advice if the keloid grows.

Choosing the right combination depends on keloid size, location, patient skin type, cost, and tolerance for side effects. A typical plan might start with intralesional steroids plus silicone sheets, adding laser or cryotherapy for stubborn areas, and reserving surgery for large, function-limiting keloids. Remember, no single “cure” fits all—treatments must be personalized, and patience is vital; flattening a keloid can take several months to a year.

Prognosis

Most keloids, while benign, are chronic and have a high recurrence rate, particularly after removal without adjunct therapy. With simple excision alone, up to 70–100% of keloids can come back, sometimes larger than before. Combining treatments—steroid injections, radiation, silicone sheeting—lowers recurrence to roughly 10–30%.

Key factors influencing prognosis include:

• Size and location: Larger keloids on the chest or shoulders tend to be more stubborn than small earlobe keloids.
• Age and genetics: Younger patients and those with a strong family history often see faster regrowth.
• Previous treatment response: A keloid that responded well to steroids in the past may fare better with repeat injections.
• Skin type: Darker skin has both higher risk of keloid formation and potential for pigment changes post-treatment.

Realistically, many patients experience partial improvement—flattening by 30–60%—rather than complete resolution. However, symptom relief (less itching or pain) and cosmetic enhancement are valuable outcomes. Close follow-up is important; early signs of regrowth can be managed promptly to maintain gains. In everyday life, keloids can be controlled, but they rarely disappear entirely without ongoing care.

Safety Considerations, Risks, and Red Flags

While keloids are not life-threatening, certain signs warrant prompt medical evaluation. Watch for:

• Rapid growth: Sudden enlargement or new nodules within a keloid could mimic malignancy and needs biopsy.
• Ulceration or bleeding: Open, weeping areas risk infection and poor healing—seek care if persistent.
• Severe pain or functional impairment: Keloids limiting joint movement (e.g., near the shoulder or knee) can hinder daily activities and may require surgical or physical therapy interventions.
• Signs of infection: Redness, warmth, pus, or fever around a keloid suggests secondary infection and needs antibiotics.

Certain treatments have specific risks. Radiation therapy carries a small risk of secondary malignancy long-term, so it’s usually reserved for recalcitrant keloids in adults. Steroid injections can thin the skin or cause pigment changes. Cryotherapy and laser treatments in darker skin increase hypopigmentation risk. Always discuss potential side effects with your provider.

Delaying care can worsen outcomes. Allowing a keloid to enlarge unchecked makes treatment harder and recurrence more likely. Early intervention—ideally within the first few months of emergence—often leads to better flattening and symptom control. So if you spot a rapidly growing scar, don’t wait months to seek advice.

Modern Scientific Research and Evidence

Research into keloids has accelerated over the last decade, focusing on molecular pathways, novel therapeutics, and predictive markers. Key areas include:

• Genomic studies: Researchers are exploring single nucleotide polymorphisms (SNPs) associated with keloid susceptibility. Early genome-wide association studies (GWAS) hint at loci on chromosomes 2q23 and 7p11, but findings need replication in larger cohorts.
• Epigenetic regulation: Studies of microRNAs (miRNAs) such as miR-21, miR-29, and miR-200 family reveal altered expression in keloid fibroblasts. Modulating these miRNAs in vitro can normalize collagen synthesis, indicating potential RNA-based therapies in the future.
• Targeted biologics: Monoclonal antibodies against TGF-β, CTGF inhibitors, and tyrosine kinase inhibitors are under early-phase trials. For instance, fresolimumab, an anti-TGF-β antibody, showed partial regression in small pilot studies, although side effects remain a concern.
• Stem cell research: Mesenchymal stem cells (MSCs) from adipose tissue display anti-fibrotic effects in animal models, possibly via paracine modulation of fibroblasts. Clinical translation is still in its infancy but holds promise.
• Device-based therapies: Low-level light therapy (LLLT), fractional nanosecond lasers, and radiofrequency ablation are being tested for their ability to remodel scar tissue without thermal damage. Early results indicate moderate improvement in texture and elasticity.

Despite these advances, there are limitations. Many studies are small, lack control arms, or involve cell cultures rather than human subjects. Funding for keloid research is also lower compared with other fibrotic diseases, partly because keloids are benign. Yet, patient advocacy groups and cross-disciplinary collaborations between dermatology, plastic surgery, and immunology are pushing the field forward. Future research aims to personalize keloid care—using genetic and epi-genetic profiling to predict which treatments will work best for each patient.

Myths and Realities

With any stubborn medical issue, misinformation can spread fast. Let’s bust some common keloid myths:

• Myth: Only dark-skinned people get keloids. Reality: While people with darker skin have higher risk, keloids can occur in any race or skin tone. It’s all about genetic predisposition and skin tension, not just melanin.
• Myth: Keloids are contagious. Reality: Keloids are not infectious or spread from person to person. They arise in response to one’s own skin trauma and healing response.
• Myth: Sunscreen cures keloids. Reality: Sunscreen helps prevent darkening of scars (hyperpigmentation) but does not reduce collagen overgrowth. Use SPF to protect healing scars, but don’t expect it to flatten a keloid.
• Myth: Cutting out a keloid guarantees cure. Reality: Excision alone often leads to rapid regrowth—up to 100% recurrence. Surgery must be paired with adjuvant therapy (steroids, radiation, silicone) to improve outcomes.
• Myth: Home remedies like vitamin E oil remove keloids. Reality: Many natural oils and extracts offer moisturizing and anti-inflammatory benefits (e.g., onion extract), but none have strong evidence to completely eliminate established keloids. They can be supportive but not standalone cures.
• Myth: Keloids will always get worse over time. Reality: Some keloids stabilize or even regress slightly after several years. Treatment can also induce involution, and scar behavior varies widely.
• Myth: Anyone can treat keloids at home safely. Reality: While silicone sheets and gentle massage are low-risk, aggressive home treatments (needling, DIY injections) can worsen scarring or cause infection. Always consult a healthcare professional before trying invasive approaches.

Understanding these facts helps set realistic expectations. Keloid care often requires a mix of medical approaches and lifestyle adjustments rather than magical quick fixes.

Conclusion

Keloids represent an overzealous wound healing response, where scar tissue extends beyond the original injury, forming firm, often itchy or painful bumps. Though benign, keloid scars can challenge mobility, self-esteem, and daily comfort. We’ve covered what keloids are, why they happen, how to diagnose them, and the spectrum of treatment—from steroid injections and silicone sheets to surgery with adjuvant therapies—and even emerging gene-based strategies.

While no single “cure all” exists, early detection and a personalized, multi-modal approach offer the best chance for flattening and symptom relief. Recognizing red flags like rapid growth, pain, or ulceration ensures timely intervention and reduces complications. Remember, simple self-care measures—moisturizing, sun protection, and minimizing tension—complement professional treatments and can help keep keloid scars in check.

If you suspect a keloid is forming, don’t brush it off. Seek medical advice rather than guessing online remedies. With the right guidance, you can manage keloid scars effectively and protect your skin from further distress. Stay informed, ask questions, and work with your healthcare team to find the best path forward for your skin health.

Frequently Asked Questions (FAQ)

Q1: What exactly are keloids?
A: Keloids are raised, firm scar tissues that extend beyond the boundaries of the original wound due to excessive collagen deposition.

Q2: What causes keloid scars?
A: Keloids arise from an exaggerated wound healing response influenced by genetics, skin tension, hormones, and local factors like infection or trauma.

Q3: How soon after injury do keloids form?
A: They typically appear within weeks to months post-injury but can take up to a year to become noticeable.

Q4: Can keloids go away on their own?
A: Spontaneous regression is rare; most keloids persist or grow without treatment, though some stabilize over time.

Q5: What’s the difference between keloid and hypertrophic scars?
A: Hypertrophic scars stay within the original wound margins and may regress, whereas keloids extend beyond and rarely shrink.

Q6: Are keloids dangerous?
A: They’re benign but can cause pain, itching, movement restriction, and psychological distress if untreated.

Q7: How are keloids diagnosed?
A: Diagnosis is clinical, based on history of skin injury and exam. Biopsy or imaging is used only when diagnosis is uncertain.

Q8: What are common treatments for keloids?
A: Options include intralesional steroids, silicone gel sheets, pressure therapy, cryotherapy, laser, 5-FU, surgical excision plus adjuvant therapy, among others.

Q9: Can I use home remedies for keloids?
A: Moisturizers, silicone sheets, and gentle massage help, but aggressive home treatments can worsen scars or cause infection; consult a provider first.

Q10: How effective are steroid injections?
A: Steroid shots flatten keloids in about 50–70% of cases, but multiple sessions are usually needed and recurrence can occur.

Q11: Do keloids recur after removal?
A: Yes, especially if treated with excision alone. Combining removal with radiation or steroids reduces recurrence risk significantly.

Q12: Is radiation therapy safe for keloids?
A: Low-dose, targeted radiation can be effective post-excision but carries a small long-term cancer risk, so it’s used judiciously.

Q13: Can people of all skin types get keloids?
A: Absolutely, though darker skin tones have a higher predisposition, keloids can occur in any complexion.

Q14: How can I prevent keloid formation?
A: Avoid unnecessary skin trauma, use silicone sheets after surgery or piercings, protect scars from sun, and apply pressure garments when indicated.

Q15: When should I see a doctor about a keloid?
A: Seek medical advice if the scar grows rapidly, causes pain or itching, limits movement, ulcerates, or shows signs of infection.