2. Basal Cell Carcinomas

3. BASAL CELL CARCINOMA
• Malignant epithelial neoplasm
• Chronic sun exposure
• Slow growing
• Metastasis
• Local tissue destruction

4. EPIDEMIOLOGY
• Australia –Highest incidence
• BCC 788/100,000
• SCC 321/100,000
• Fitzpatrick Types I and II

5. EPIDEMIOLOGY
• Oily skin offers some protection
• History of sunburn
• Cumulative sun exposure
• Incidence increases towards the North

6. DISTRIBUTION
• sun exposed areas and areas of
bioembryological fusion
• Rare on the hand, penis, lower lip

9. DISTRIBUTION
• Upper lip BCC, Lower
lip SCC
• Ext. ear SCC 60%, BCC
40%

10. HISTOGENESIS
• UVA Light 95 %
(315-400nm)
• UVB Light 5 % ----
sunburn, malignant
degeneration
(290-315nm)
• UVA enhances the
carcinogenic effect

11. • UV induced mutation of the p53 tumor
suppressor gene
• 56 % mutation occurs in both p53 alleles
• Aggressiveness of the tumor relates to the
presence of p53 protein
• Mutation in the patched gene PTCH is
responsible for BCC in Gorlin's, XP

12. Carcinogenesis
Initiation - Genetic mutation , DNA changes
Promotion – Changes in cellular environment
Progression – Further genetic alteration.
If erroneous sequences are not repaired propagation
continues during DNA replication.

13. • UV induced immunosuppression – depletion
of Langerhans cells and stimulation of
suppressor T cells – hindering the detection
and destruction of the tumor cells.

14. Non UV
• < 1%
• Arsenic
• Non ionizing radiation
• Immunosuppression
• Tobacco
• Human papilloma virus
• Scars

15. Spread
• BCC’s are stromal
dependant
• Do not survive
transplantation
• Rarely metastasize –
0.1 %

16. Spread
• Aggressive local growth - following the path of
least resistance
• Spreads along:
• periosteum
• Perichondrium
• Fascia
• tarsal plate

17. Spread
• Can spread deeply
between nasal
cartilages
• Embryonic fusion
planes

18. PREDISPOSING CONDITIONS
• Xeroderma Pigmentosum
• Gorlin’s Syndrome - Basal Cell Nevus
Syndrome
• Bazex Syndrome
• Nevus Sebaceous of Jadassohn
• Porokeratosis
• Linear unilateral Basal cell Nevus

19. Xeroderma Pigmentosum
• Autosomal recessive defect
• DNA repair – skin intolerant of
UV light
• Skin normal as infant- becomes
dry,pigmented,cutaneous,
s/c atrophy
• Xerodermic idiocy – progressive
neurological deterioration
• BCC,SCC,Melanomas
• Usually die in second decade

20. Gorlin’s Syndrome
• Basal cell nevus syndrome
• Autosomal dominant with low penetrance
• Mutation in tumor suppressor gene located
on 9q23-q31
Multiple Nevi Reddish Brown, Papular
and
Variously sized
Appear after puberty several to
thousands
76% become invasive BCCs

21. Porokeratosis
Hereditary conditions
Disseminated annular plaques with sharply
raised horny borders
13% BCCs and SCCs
2/5 types of porokeratosis premalignant
Mibelli Porokeratosis
Disseminated superficial actinic porokeratosis

22. ORIGIN
Germinative layers of the skin
• Basal Cells of the Epidermis
• Epithelial cells of the Adenexa

23. CLASSIFICATION
• Emmett and Rourke
• Papulonodular
• Infiltrating
• Multifocal
• Morphoeic / Sclerosing
• Metatypical
• Others – Pigmented , NBCC

24. Papulonodular Bcc
• Commonest - 45%
• PN Solid 38% Smooth, raised,
waxy Translucent, NODULE, thin
epithelial cover,Minute vessels in the
periphery, surface shows fine venules,
Pearly edge, central depression
• PN Cystic 6.9% Pale, pearly pink
Lucid gray with a well defined margin
Acid mucopolysaccharide gel

25. Multifocal Bcc
• 35%
• Multifocal Superficial
Often merely red areas with a patchily adherent
Parakeratotic scales
Pattern with small areas of epithelial discontinuity
Margin ill defined Pearly edge defined on stretch
• Superficial
Early stage of MFS – small red patch with a localized
superficial cluster of BCC cells
• Cicatrizing, Field Fire
Red irregular scaly rim round a whitish healing centre

26. Morphoeic / Sclerosing
• 8.9%
• Flat whitish plaques
• Fine pearly edge
Noticed on stretching the skin at the edge of the
Plaque
• Central regression- skin pit
On stretching the skin the white plaque becomes
Evident may be localized or infiltrating
Synthesize type IV collagenase
Discontinuous basement membrane

27. Infiltrating Bcc
• Primary Infiltrating 8%
No characteristic clinical appearance
Red or gray scaling area
Induration, Ulceration, Whitish plaque
Microscopic examination diagnostic
• Secondary Infiltrating
Parts of the lesion of bcc develops an
Infiltrative character
• Recurrent Infiltrating
Recurrent bcc develops into an
infiltrative
type
D/D Solar Keratoses
Squamous cell ca.

28. Metatypical
• Irregular mammilated pale
pink flesh colored lesion
• Without marginal light reflex
• Without any superficial vv.
• May stay like this for years
• Ulceration

29. Pigmented Type
• Variation in pigment
• Scant flecks to deeper pig.
• Edge - pearly translucence
• Fine superficial venules
• Stromal melanophages
• Central regression
• D/D Melanoma

30. HISTOLOGY
• Cutaneous epithelial tumors
• Nests and sheets of basal
type cells with a large oval
nucleus
• Intercellular bridges not seen
• Peripheral layer is arranged
like a palisade
• Central haphazard arrangement
• Abundant connective tissue
stroma rich in acid
mucopolysaccharides mucinuous
appearance
• Amyloid in 65% bccs

31. Morphological Types
• Solid
• Micronodular
• Cystic
• Multifocal
• Infiltrating
• Sclerosing
• Pigmented
• Metatypical
• Adenoid
• Keratotic
• Infundibulocystic
• Fibroepithelioma

32. Solid, Micronodular
• 70% • Smaller nests
• Islands of Cells • Palisading less
• Peripheral palisading • Infiltration into dermis
• Central haphazard and subcutis
• Retraction spaces • Increased rec.

33. Cystic, Keratotic
• Similar to solid • Similar to solid
• Cystic spaces present • Keratinization towards
towards the centre dt the centre
degeneration of tumor • Very little stroma
cells

34. Infiltrating, Multifocal
• Elongated strands of • Discreet nests of tumor cells
basiloid cells between apparently interconnected
collagen bundles • Multiple small islands of
basiloid cells attached to
• Fibroblasts the extending to the
• Focal infiltration in rec. papillary dermis
Solid in scar

35. Sclerosing, Metatypical
• Thin strands and nests • Plump squamous cells
of cells embedded in a with loss of peripheral
dense fibrous stroma palisading
• Eosinophillic areas - • Represents basiloid and
Morphoeic squamous features

36. Invasive Histological Features
• Microfilaments located on the periphery of the
individual cells with the highest density at the tumor
borders
• Increased type IV collagenase
• Focal gaps in the basement membrane
• Loss of intercellular bridges
• Increased cytokines which stimulate fibroblast
glycosamineglycans synthesis
• Increased peri tumor stroma

37. Differential Diagnosis
• Squamous cell • Non pigmented
carcinoma naevus
• Solar Keratoses • Chondrodermatitis
• Keratoacanthoma Nodularis Helicis
• Melanoma • Seborrhoeic keratoses
• Merkel Cell Tumor • Bowens disease
• Appendegeal tumors
• Pyogenic grannuloma
• Dermatofibroma
• AFX
• Cutaneous sarcoid

38. Differentials
• Noduloulcerative Bcc • Ulcerated Scc
• Slow growing • Fleshy rapidly growing
• Pearly edge • indurated
• Fine venules

39. TREATMENT
• Goals :
Total lesion removal
Preservation of normal tissue
Preservation of function
Optimal cosmesis

40. • Biopsy:
• Excisional
• Punch
• Incisional
• Shave
• Does not affect the natural history

41. • Variables:
Patient Age
Number of lesions
Lesion size
Tumor borders
Primary Vs Recurrent
Anatomic location – sub clinical spread

42. Treatment Modalities
• Curettage and Electrodessication
• 2 mm – 100%, 2-5 mm – 85%

43. • Cryosurgery
• lesions up to 2 cm 97% high morbidity
• lack of microscopic evaluation
• Edema
• hypo pigmentation
• atrophic scars
• Neuropathy
• sub clinical spread
• unpredictable cosmesis

44. • Surgical Excision
• 90% overall success rate
• Nodular lesions <1cm - 2mm margin
• Lesions < 2cm 3-4 mm
• Lesions > 2cm, subclinical spread, aggressive
histology, multifocal - may require margins up
to 10mm

45. • Mohs micrographic surgery:
recurrent bccs, morphoeaform or arising from
scar, anatomic sites with relatively high rates
of treatment failure, critical locations – eyelid
99% primary, 95% recurrent
• Frozen Sections
• Delayed primary repair temporary grafting

46. ADJUNCTS
• Topical Chemotherapy
5 FU with retinoids
Imiquimod – immune response modifier that induces
cytokines including interferons
Radiation Therapy - older patients, adjuvant therapy
where negative margins are difficult to obtain –
nasal, periorbital, periauricular
92%

47. Others
• Alpha-interferon Therapy
• Laser excisions
• Photodynamic Therapy
includes the administration of Dihaematoporphyrine or its
derivative followed by exposure to 630 nm light with a
tunable dye laser .It localizes to the tumor cells and
absorption of light by dihaematoporphyrin ether has a
cytotoxic effect

48. Follow up
• Follow up for 5 yrs
• Recurrence is defined as the reappearance
of a bcc within or contiguous to a scar
resulting from an initial attempt at definitive
treatment

49. Increased Risk
• Long time presence of the lesion
• Location in a high risk area
• Aggressive clinical and histological features

50. • 20% will develop a new lesion within 1 yr of having
been treated
• 36% will develop another lesion by 5 years
• Overall recurrence rate of 2.9 % - 9 %
• 82% recurrence occurs in first 5 years ,18% in 6-10
yrs

51. Incomplete Resection
• 35% recurrence if one margin is involved
• 12% recurrence when tumor within one high
power field of margin