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Dermatology
Plastic Surgery
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Basal Cell Carcinoma (BCC)

High EvidenceUpdated: 2025-12-24

On This Page

Red Flags

  • H-Zone Location (Eyes, Nose, Lips, Ears)
  • Morphoeic/Infiltrative Subtype
  • Perineural Invasion
  • Recurrent BCC
  • Large Size (>2cm)
Overview

Basal Cell Carcinoma (BCC)

1. Topic Overview (Clinical Overview)

Summary

Basal Cell Carcinoma (BCC) is the most common skin cancer and the most common malignancy in humans overall. It arises from basal keratinocytes in the epidermis and is almost always caused by cumulative UV sun exposure. BCC is locally invasive but, crucially, almost NEVER metastasises (<0.1%). This makes it highly curable if detected and treated appropriately. However, if neglected, BCC can cause significant local destruction ("rodent ulcer"), particularly on the face. Management depends on subtype, location, and patient factors, ranging from simple excision to Mohs micrographic surgery for high-risk lesions.

Key Facts

  • Commonest Cancer: ~75% of all skin cancers. ~150,000/year in UK.
  • Metastasis Rate: <0.1%. Cure is the norm.
  • Cause: Cumulative UV exposure (UVB primarily).
  • Classic Appearance: Pearly/translucent nodule with rolled edge, telangiectasia. +/- Central ulceration (Rodent Ulcer).
  • Subtypes: Nodular (most common), Superficial, Morphoeic/Infiltrative (aggressive).
  • Treatment: Surgical excision (4mm margin standard). Mohs surgery for high-risk sites. Topical/ablative for superficial.
  • Key Guideline: NICE CSG8 / BAD Guidelines on Skin Cancer.

Clinical Pearls

"The H-Zone": The central face (around Eyes, Nose, Lips, Ears, Temples) is high-risk. BCCs here require careful management (often Mohs) due to complex anatomy and risk of incomplete excision.

"If it bleeds, crusts, and never heals": This is the classic patient description of a BCC. Any skin lesion that repeatedly crusts and bleeds without fully healing should raise suspicion.

Morphoeic = Malignant Scar: The morphoeic subtype looks like a scar (flat, white, waxy). It has indistinct borders and is often much larger subclinically than it appears. Always think of it if a "scar" appears without a history of trauma.

Hedgehog Pathway: BCC is driven by aberrant activation of the Hedgehog signalling pathway (PTCH1, SMO genes). This is the target for oral drugs like Vismodegib in advanced BCC.

Why This Matters Clinically

While BCC is rarely life-threatening, it is incredibly common. Every clinician will encounter it. Recognising the subtypes and understanding which lesions need specialist referral (vs. GP excision) is essential. Inappropriate management of morphoeic or H-zone BCCs can lead to incomplete excision and recurrence, requiring more complex surgery later.


2. Epidemiology

Incidence & Prevalence

  • UK Incidence: ~150,000 new cases per year.
  • Australia: Highest incidence globally (>1000 per 100,000).
  • Lifetime Risk (UK): ~1 in 5-6 for fair-skinned individuals.
  • Trend: Incidence is rising (ageing population, sun exposure habits).

Demographics

FactorAssociation
AgeRisk increases with age. Peak 60-80 years. Can occur younger in sun-seekers.
SexHistorically Male > Female (occupational exposure). Now equalising.
Skin TypeFitzpatrick I-II (Fair skin, burns easily) highest risk. Rare in dark skin.
LocationSun-Exposed Sites: Face (80%), especially nose. Trunk (Superficial BCC).

Risk Factors

Risk FactorNotes
Cumulative UV Exposure (UVB)Primary cause. Lifelong sun exposure.
Sunburn HistoryEspecially childhood burns.
Fair Skin (Fitzpatrick I-II)Poor melanin protection.
ImmunosuppressionOrgan transplant recipients: 10-16x increased risk.
Previous BCC30-50% chance of another BCC within 5 years.
Genetic SyndromesGorlin Syndrome (Naevoid BCC Syndrome) – PTCH1 mutation. Multiple BCCs.
Ionising RadiationHistory of radiotherapy.
Arsenic ExposureHistorical risk (drinking water).

3. Pathophysiology

UV Damage & Hedgehog Pathway

The molecular driver of BCC.

  1. UVB Radiation: Causes direct DNA damage (pyrimidine dimers).
  2. Failed Repair: Accumulated mutations in tumour suppressor genes.
  3. PTCH1 Mutation: PTCH1 normally inhibits SMO (Smoothened) in the Hedgehog (Hh) pathway.
    • Inactivating mutation in PTCH1 -> SMO is constitutively active.
    • Activated Hh pathway -> Uncontrolled basal cell proliferation.
  4. p53 Mutation: Common. Contributes to tumour progression.

Key Genes

GeneRole
PTCH1Tumour suppressor. Gatekeeper of Hedgehog pathway. Mutated in ~90% of sporadic BCCs.
SMO (Smoothened)Oncogene when activated. Target for Vismodegib.
p53Tumour suppressor. Mutated in >0% of BCCs.
GLI1/GLI2Transcription factors activated downstream. Drive proliferation.

Gorlin Syndrome (Naevoid BCC Syndrome)

Autosomal Dominant. PTCH1 germline mutation.

  • Features:
    • Multiple BCCs (often >100 by adulthood).
    • Odontogenic Keratocysts (jaw cysts).
    • Palmar/Plantar Pits.
    • Skeletal abnormalities (Rib bifurcation, macrocephaly).
    • Calcification of Falx Cerebri.
    • Medulloblastoma risk.
  • Management: Careful sun avoidance. Regular skin surveillance. Vismodegib may be needed.

4. Clinical Presentation

Classic BCC Appearance

"The Pearly Pink Pimple that never heals."

FeatureDescription
Translucent/Pearly SurfaceHallmark. Shiny, waxy appearance.
Rolled EdgeRaised, rounded border.
TelangiectasiaFine, branching blood vessels visible on surface.
Central Ulceration"Rodent Ulcer". Crusted, bleeding.
Slow GrowthMonths to years.

BCC Subtypes

SubtypePrevalenceAppearanceBehaviour
Nodular~60%Classic pearly nodule. Telangiectasia. Central ulceration.Most common. Well-defined.
Superficial~25%Flat, red, scaly plaque. Often on trunk. Thin, pink, erosion.Least aggressive. Often multiple.
Morphoeic / Infiltrative~10%Pale, waxy, scar-like. Indistinct borders. Firm.Most Aggressive. Subclinical spread. Difficult to excise.
Pigmented<5%Nodular or superficial with brown/black pigment.Can mimic Melanoma.
BasosquamousRareMixed BCC and SCC features.Higher recurrence/metastasis risk.

High-Risk Features

FeatureWhy High-Risk
Location in H-ZoneCentral face – complex anatomy, cosmetic importance, higher recurrence.
Size >cmIndicates longer duration, higher recurrence risk.
Morphoeic/Infiltrative SubtypeIndistinct borders, subclinical spread.
Recurrent BCCPrevious incomplete excision. More aggressive behaviour.
Perineural InvasionOn histology. Risk of spread along nerves.
ImmunosuppressionMore aggressive BCCs in transplant patients.

5. Clinical Examination

Dermoscopy Findings

FeatureDescription
Arborising (Tree-like) VesselsBranching telangiectasia. Highly specific for BCC.
Leaf-Like StructuresBrown/grey pigment. In pigmented BCC.
Blue-Grey Ovoid NestsPigment clusters.
Spoke-Wheel AreasPigment spokes radiating from centre.
UlcerationSurface disruption.
Shiny White Structures / BlotchesSeen with polarised dermoscopy.
Absence of Pigment NetworkDifferentiates from benign naevi and Melanoma (which have a network).

Differential Diagnosis

ConditionDistinguishing Feature
Intradermal NaevusFlesh-coloured papule. Softer. No telangiectasia/ulceration.
Sebaceous HyperplasiaYellow papules. Central dell. No rolled edge.
Molluscum ContagiosumMultiple, umbilicated. Paediatric.
KeratoacanthomaRapid growth. Central keratin plug. May regress.
SCCMore keratinised, crusty. Faster growing. Tender.
Melanoma (Nodular)For pigmented BCC. Dermoscopy differentiates.
Fibrous Papule (Nose)Small, firm, dome-shaped. No telangiectasia.

6. Investigations

BCC is a clinical and histological diagnosis.

Diagnosis

InvestigationPurpose
Clinical ExaminationStandard. Dermoscopy aids accuracy.
DermoscopyIncreases diagnostic accuracy. Identifies subtype features.
BiopsyConfirms diagnosis. Identifies subtype. Punch or Shave.
Excision BiopsyDiagnostic AND therapeutic for small, well-defined lesions.

Imaging (Rarely Needed)

IndicationInvestigation
Suspected Perineural InvasionMRI
Suspected Bone InvasionCT
Gorlin Syndrome WorkupCT Brain (Falx calcification), OPG (Jaw cysts).

7. Management

Management Algorithm (NICE / BAD)

┌─────────────────────────────────────────────────────────────────────┐
│                        BCC DIAGNOSED                                │
├─────────────────────────────────────────────────────────────────────┤
│                                                                     │
│  STEP 1: Assess Risk                                                │
│  ├── Low Risk: Small (&lt;2cm), Non-H-Zone, Nodular/Superficial.       │
│  └── High Risk: H-Zone, Morphoeic, Recurrent, &gt;2cm, Immunosuppr.    │
│                                                                     │
│  STEP 2: Select Treatment                                           │
│                                                                     │
│  LOW RISK (Nodular):                                                │
│  └── Standard Surgical Excision (4mm margin).                       │
│                                                                     │
│  LOW RISK (Superficial):                                            │
│  ├── Curettage & Cautery (C&C).                                     │
│  ├── Topical Imiquimod (5 days/week x 6 weeks).                     │
│  ├── Topical 5-FU (Fluorouracil).                                   │
│  ├── Photodynamic Therapy (PDT).                                    │
│  └── Cryotherapy.                                                   │
│                                                                     │
│  HIGH RISK:                                                         │
│  ├── Refer to Specialist (Dermatology / Plastics).                  │
│  ├── Mohs Micrographic Surgery (H-Zone, Morphoeic, Recurrent).      │
│  └── Excision with Wider Margins (if Mohs not available).           │
│                                                                     │
│  LOCALLY ADVANCED / INOPERABLE:                                     │
│  ├── Radiotherapy.                                                  │
│  └── Hedgehog Inhibitors (Vismodegib / Sonidegib).                  │
│                                                                     │
└─────────────────────────────────────────────────────────────────────┘
8. Surgical Atlas: Reconstruction

After excising the BCC, we are left with a defect. The "Reconstructive Ladder" applies.

  1. Secondary Intention (Heal by itself). Good for concave surfaces (inner canthus, conchal bowl). Poor for convex surfaces (nose tip).
  2. Direct Closure. Ellipse. Orientation along Relaxed Skin Tension Lines (RSTLs).
  3. Skin Graft. Full Thickness (FTSG) preferred for face (better colour match). Donor: Pre/Post-auricular, Supraclavicular.
  4. Local Flaps. The workhorse of facial reconstruction.

Common Facial Flaps

  • Transposition Flaps: The Bilobed Flap (Zitelli).
    • Indication: Distal nose defect <1.5cm.
    • Concept: Borrow skin from the lax upper nose to fill the tight lower nose.
  • Advancement Flaps: The cheek advancement.
    • Indication: Large cheek defects.
  • Rotation Flaps: The Rieger Flap (Dorsal Nasal Flap).
    • Indication: Large dorsal nasal defects.
  • Interpolation Flaps: The Paramedian Forehead Flap.
    • Indication: Large defects of the nasal tip/ala (>1.5cm).
    • Concept: Forehead skin is the best match for nose skin. Requires 2 stages (pedicle division at 3 weeks).

The H-Zone Danger

  • Reconstruction vs Surveillance:
    • Using a flap hides the deep margin.
    • If your excision wasn't complete, you have buried the tumour under a flap.
    • Rule: Never put a flap over a high-risk tumour unless margins are confirmed clear (Frozen section or Mohs).
    • If no frozen section available, use a Skin Graft or Secondary Intention first.

Mohs Micrographic Surgery (The Process)

  1. Debulking: Visible tumour removed.
  2. Layer 1: A thin disc of tissue (1-2mm) is removed including the whole margin.
  3. Mapping: Tissue is cut into quadrants, colour-coded, and mapped to a diagram.
  4. Freezing: Tissue froze and sectioned horizontally (en face).
  5. Microscopy: Surgeon examines 100% of the peripheral and deep margin.
  6. Targeted Re-excision: If tumour found at "3 o'clock", surgeon goes back ONLY to 3 o'clock.
  7. Reconstruction: Once clear, the hole is repaired.

Surgical Excision

FeatureStandard Excision
Margin4mm peripheral margin. Clear deep margin to fat/fascia.
Cure Rate~95% for primary, well-defined BCC.
IndicationMost nodular BCCs outside H-Zone.

Mohs Micrographic Surgery

The gold standard for high-risk BCC.

FeatureDetails
PrincipleExcise in thin layers. Map and examine 100% of the margin intraoperatively. Continue until margins clear.
AdvantageTissue-sparing. Highest cure rate (99%).
IndicationH-Zone (Nose, Eyes, Ears, Lips). Morphoeic. Recurrent. Large BCCs. Where tissue preservation is critical.
AvailabilitySpecialist centres. Not universally available.

Topical Treatments (Superficial BCC only)

TreatmentRegimenNotes
Imiquimod 5% (Aldara)5 times per week x 6 weeks.Immune modulator. Inflammatory response – warn patient.
5-Fluorouracil (5-FU / Efudix)Twice daily x 4-6 weeks.Anti-metabolite. Erosion, crusting expected.
Photodynamic Therapy (PDT)In-clinic. Photosensitiser + Light.Good cosmesis. Lower cure rate than excision.

Curettage & Cautery (C&C)

  • Indication: Small, low-risk, superficial or nodular BCCs.
  • Technique: Scrape tumour with curette, cauterise base. Repeat 2-3 times.
  • Cure Rate: ~90% for appropriate lesions.
  • Cosmesis: Leaves flat, hypopigmented scar.

Hedgehog Pathway Inhibitors

DrugTargetIndication
VismodegibSMO InhibitorLocally advanced BCC (inoperable). Metastatic BCC (rare). Gorlin Syndrome.
SonidegibSMO InhibitorSecond-line.
Side EffectsMuscle cramps, alopecia, taste disturbance, weight loss. Often limit tolerability.

9. Advanced Pathology & Genetics

The Hedgehog Pathway (Deep Dive)

The discovery of the Hedgehog (Hh) pathway revolutionised our understanding of BCC.

  • Normal State:
    • PTCH1 (Patched) is the receptor. It inhibits SMO (Smoothened).
    • With SMO inhibited, the pathway is OFF. No cell division.
  • Ligand Binding:
    • Sonic Hedgehog (SHH) ligand binds to PTCH1.
    • Binding stops PTCH1 from inhibiting SMO.
    • SMO becomes active -> Activates GLI transcription factors -> Cell Division.
  • In BCC:
    • Mutation: PTCH1 is broken (loss of function).
    • It cannot inhibit SMO.
    • SMO is permanently ON.
    • Cell divides uncontrollably.
  • Treatment: Vismodegib binds to SMO and turns it off. It is a "SMO Inhibitor".

Adnexal Tumours (The Mimics)

BCC arises from the "folliculo-sebaceous-apocrine germ". Many benign tumours also arrive here and look like BCCs.

  1. Trichoepithelioma: Benign hair follicle tumour. Flesh coloured papules on nasolabial folds. Multiple in "Brooke-Spiegler Syndrome". Can look exactly like BCC histologically (but no retraction artefact).
  2. Sebaceous Hyperplasia: Yellowish papules with central dell. "Mature" sebocytes. Benign.
  3. Microcystic Adnexal Carcinoma (MAC): Very dangerous. Looks like a benign lump but invades nerves aggressively. Needs Mohs.

10. Rehabilitation: Scar Management

Facial surgery leaves scars. A poor scar can be devastating.

The Process of Maturation

  • 0-6 Weeks: Red, lumpy, immature. Sutures out at day 5-7 to prevent "railroading".
  • 6 Weeks - 6 Months: Scar remodels. Collagen aligns.
  • 12-18 Months: Final maturation (Pale, flat).

Interventions

  1. Silicone Gel/Sheets: Gold standard. Hydrates the scar, reduces fibroblast activity.
  2. Massage: Breaking down adhesions. Desensitisation.
  3. Sun Protection: Fresh scars hyper-pigment permanently if sunburnt. Factor 50 is mandatory for 1 year.
  4. Steroid Injection (Triamcinolone): For hypertrophic/keloid scars.

11. Evidence and Guidelines (Expanded)

The SINS Trial (Surgery vs Imiquimod for Nodular & Superficial)

  • Findings: Surgery is superior to Imiquimod.
  • Recurrence: 2% (Surgery) vs 17% (Imiquimod) at 5 years.
  • Cosmesis: Better in Imiquimod group.
  • Conclusion: Trade-off. If you want a cure -> Surgery. If you want no scar and accept risk -> Cream.

The M-BCC Study (Morphoeic BCC)

  • Confirmed that morphoeic BCCs extend subclinically far beyond visible margins.
  • Standard 4mm excision often inadequate.
  • Mohs recommended.

12. Patient/Layperson Explanation

(As per original - restored)

What is a BCC?

A Basal Cell Carcinoma (BCC) is a type of skin cancer. It's the most common type and is almost always caused by sun damage over many years. The good news is that BCCs almost never spread to other parts of the body. They grow slowly and are very treatable.

What does it look like?

Often a shiny, pearly lump or a sore that won't heal. It may crust, bleed, and then seem to get a bit better, but never fully heals.

How is it treated?

Usually, it is removed with a small operation under local anaesthetic. For BCCs in difficult areas (like around the eyes or nose), a specialist surgery called Mohs can be used to make sure all the cancer is removed while saving as much healthy skin as possible.

Will it come back?

If completely removed, it is unlikely to come back at the same spot. However, having one BCC means you are at higher risk of getting another somewhere else on your skin in the future.

How can I prevent more?

  • Sun protection: Sunscreen (SPF 30+), hats, protective clothing.
  • Regular skin checks: Check your skin and see your GP if you notice any new or changing spots.

13. References

(As per original)

  1. NICE Improving Outcomes Guidance (CSG8)
  2. British Association of Dermatologists Guidelines
  3. Sekulic A, et al. Efficacy and safety of vismodegib. N Engl J Med. 2012.
  4. Rowe DE, et al. Mohs surgery is the treatment of choice. J Dermatol Surg Oncol. 1989.


Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Clinical decisions should account for individual patient circumstances. If you have a skin lesion you are concerned about, please see a healthcare professional.

Last updated: 2025-12-24

At a Glance

EvidenceHigh
Last Updated2025-12-24

Red Flags

  • H-Zone Location (Eyes, Nose, Lips, Ears)
  • Morphoeic/Infiltrative Subtype
  • Perineural Invasion
  • Recurrent BCC
  • Large Size (&gt;2cm)

Clinical Pearls

  • **"The H-Zone"**: The central face (around Eyes, Nose, Lips, Ears, Temples) is high-risk. BCCs here require careful management (often Mohs) due to complex anatomy and risk of incomplete excision.
  • **"If it bleeds, crusts, and never heals"**: This is the classic patient description of a BCC. Any skin lesion that repeatedly crusts and bleeds without fully healing should raise suspicion.
  • **Hedgehog Pathway**: BCC is driven by aberrant activation of the Hedgehog signalling pathway (PTCH1, SMO genes). This is the target for oral drugs like Vismodegib in advanced BCC.
  • Female (occupational exposure). Now equalising. |
  • SMO is constitutively active.

Guidelines

  • NICE Guidelines
  • BTS Guidelines
  • RCUK Guidelines