Sec 21 Epidermal and Appendegeal Tumors Flashcards
A common feature of all premalignant keratinocyte tumors
Potential to become invasive squamous cell carcinoma
Cutaneous neoplasms consisting of proliferations of cytologically abnormal epidermal keratinocytes that develop in response to prolonged exposure to ultraviolet
Actinic Keratosis or Solar Keratosis
Are the initial lesion in a disease continuum that may progress to SCC
Actinic Keratosis
Risk factors for development of Actinic keratoses
Individual susceptibility (older age, male gender, fair skin that easily burns and freckles, blond or red hair, light-colored eyes)
Cumulative ultraviolet radiation exposure Immunosuppression
Prior history of actinic keratoses or other skin cancers
Genetic syndromes (Xeroderma pigmentosum, Bloom syndrome, Rothmund-Thomson syndrome)
The most important contributing factor in the development of AKs and SCC
Habitual exposure to UV radiation
Play a pivotal role in the initiation of AKs and their development into SCC
Tumor suppressor gene p53
Typical patient is an older, fair-skinned, light-eyed individual who has a history of significant sun exposure, who burns and freckles rather than tans, and who has significant solar elastosis on examination
Actinic keratosis
Presents most commonly as a 2-6 mm erythematous, flat, rough, gritty or scaly papule; usually more easily felt than seen; most often found against a background of photodamaged skin or dermatoheliosis, with solar elastosis, dyspigmentation, yellow discoloration, ephelides and lentigos, telangiectases, and sagging skin notably prominent
Erythematous AK
Presents as a thicker, scaly, rough papule or plaque that is skin-colored, gray–white, or erythematous; can be found on any habitually sun-exposed site on the body but has a propensity for the dorsal hands, arms, and scalp
Hypertrophic AK
AKA cornu cutaneum; refers to a reaction pattern and not a particular lesion; a type of HAK that presents with a conical hypertrophic protuberance emanating from a skin-colored to erythematous papular base; height is at least one-half of the largest diameter
Cutaneous horn
Pathology underlying Cutaneous horn
Actinic keratosis Squamous cell carcinoma Seborrheic keratosis Filiform verruca vulgaris Trichilemmoma Keratoacanthoma
Represents confluent AKs on the lips, most often the lower lip; presents with red, scaly, chapped lips, and at times erosions or fissures may be present; complain of persistent dryness and cracking of the lips
Actinic cheilitis
May be a marker of progression of AK to SCC
Pain
Inflammation
Treatment: Actinic Keratosis
Lesion-targeted therapies
Liquid nitrogen cryotherapy
Curettage with or without electrosurgery
Shave excision
Treatment: Actinic Keratosis
Topical field therapies
5-fluorouracil cream and solution
Imiquimod cream
3% diclofenac gel
Treatment: Actinic Keratosis
Procedural field therapies
Cryopeeling Dermabrasion Medium-depth chemical peel Deep chemical peel Laser resurfacing Photodynamic therapy
Most common destructive procedure and is typically administered with a spray device or a cotton-tipped applicator with ideal freeze time of 10-15 secs
Liquid nitrogen cryosurgery
Cryosurgery: benefits
Ease of administration in trained hands
Lack of need for anesthetic
Lack of reliance on patient compliance
Cryosurgery: disadvantages
Pain and discomfort Presence of unsightly blisters and crusted wounds for a week or longer Hypopigmentation Scarring Possible alopecia in treated areas
Constitute approximately 80% of all treatments for AKs in the United States
Liquid nitrogen cryosurgery
Curettage with or without electrosurgery
Most appropriate for patients with relatively few AKs; beneficial for treatment of lesions after biopsy and for the treatment of HAKs
Curettage with or without electrosurgery
Involves injection of a local anesthetic followed by tangential excision of the lesion with a surgical blade; most often indicated when a clinically apparent AK is suspicious for SCC or BCC and histopathologic examination is needed
Shave excision
Signs and symptoms that should arouse suspicion of SCC
Marked erythema Pain Ulceration Bleeding Induration Failure to respond to prior destructive therapies
Best used in patients with moderate to severely photodamaged skin and numerous AKs that would be too burdensome and painful to treat with the lesion-targeted therapies
Field therapies
Extensive liquid nitrogen cryosurgery to the areas of discrete AKs as well as to the surrounding actinically damaged skin
Cryopeeling
An older technique that is quite effective in the treatment and prophylaxis of AKs but is now rarely used; causes physical destruction of the AKs with abrasion using either dry-wall sanding sheets or diamond fraises, which are powered or handheld
Dermabrasion
Medium-depth chemical peels used for AK
Jessner’s solution
35% trichloroacetic acid (TCA)
Deep chemical peels used for AK
Phenol
High concentrations of TCA
More effective in treating thick AKs or those with appendageal epithelial atypia but are rarely used because of the potential cardiac and renal toxicity, the greater risk of scarring and infection, and the dramatic hypopigmentation that may occur postoperatively
Deep chemical peels
Two laser systems that have primarily been used for the treatment and prophylaxis of AKs; ablate the epidermis at varying depths allowing reepithelialization with adnexal keratinocytes that are less actinically damaged; effective in short-term clearing of multiple facial and scalp AK and in the long-term prevention of recurrences, and possibly the development of NMSC
Carbon dioxide (CO2) laser Erbium:yttrium-aluminum-garnet (er:YAG)
Another procedural therapy available for the treatment of multiple and diffuse AKs where topically applied ALA or MAL accumulates preferentially in the more rapidly dividing atypical cells and is converted sequentially to protoporphyrin IX, a heme precursor and photosensitizer and when exposed to a light source of the appropriate wavelength, the accumulated protoporphyrin IX generates a phototoxic reaction that destroys the treated cells
Photodynamic therapy
Single most effective means of decreasing the risk of AKs
Avoidance of UV radiation
Precancerous lesions found in association with chronic arsenicism which have the potential to develop into invasive SCC
Arsenical Keratosis
An ubiquitous element that has no color, taste, or odor which has the potential to cause characteristic acute and chronic syndromes in persons exposed to it
Arsenic
How often should regularly scheduled total-body skin examinations and general physical examinations in management of patients with chronic arsenicism and ArKs
Every 6 months
Precancerous lesions that result from long-term exposure to infrared radiation; can progress to squamous cell carcinoma (SCC)
Thermal keratosis
Precursor lesion of Thermal keratosis
Erythema ab igne
Occur in persons who are occupationally exposed to polycyclic aromatic hydrocarbons; can progress to squamous cell carcinoma (SCC); usually on the nostril rims, upper lip, or genitalia
Hydrocarbon keratosis
Pitch keratoses
Tar keratoses
Tar warts
Hyperkeratotic papules or plaques within areas of chronic radiation dermatitis and occasionally on clinically normal skin that may arise years (56 years) after such exposure and may progress to squamous cell carcinoma common on palms, soles, and mucosal surfaces
Chronic radiation keratosis
Precancerous lesions that arise in long-standing scars from various causes
Chronic scar keratoses
Cicatrix keratoses
Malignant changes within a burn scar but can also refer to such changes in chronic ulcers or sinus tracts with sites of predilection being the extremities and overlying joints
Marjolin’s ulcer
Precancerous epithelial lesions with a viral association
Bowenoid papulosis (BP) Epidermodysplasia verruciformis (EV) Vulvar intraepithelial neoplasia (VIN) Anal and perianal intraepithelial neoplasia (AIN and PaIN) Penile intraepithelial neoplasia (PIN)
Characterized clinically by the presence of pink, reddish brown, or violaceous verrucous papules and plaques primarily on the genitalia of predisposed, usually younger, individuals, and histopathologically by the presence of SCC in situ-like changes caused by infection with HPV, particularly subtypes 16 and 18
Bowenoid papulosis (BP)
Histopathology: hyperplastic with atypia, disordered maturation, scattered mitotic figures, and dyskeratotic keratinocytes
Bowenoid papulosis (BP)
Rare inherited skin condition that arises when genetically susceptible individuals are infected with certain HPV subtypes, most notably HPV 5 and 8; present in childhood with numerous thin, pink, flat papules and plaques that resemble verruca plana; can also be widespread scaly, erythematous, or hypopigmented macules and flat papules that appear similar to tinea versicolor
Epidermodysplasia verruciformis (EV)
May occur at any age in adults can be found on any body site, including both sun-exposed and nonsun-exposed regions of the body, although it appears to have a predilection for sun-exposed surfaces such as the head and neck and for the lower legs of women, typically presents as a discrete, slowly enlarging, pink to erythematous thin plaque with well-demarcated, irregular borders and overlying scale or crust resembling a psoriatic plaque
Bowen disease
Can present as an oozing, erythematous, dermatitic plaque or as a pigmented patch or plaque
Intertriginous BD
May appear as an erythematous, scaly, thin plaque around the cuticular margin, a crusted erosion, nail discoloration, erythronychia, onycholysis, a verrucous plaque, or destruction of the nail plate
BD involving the periungual region
Can present as verrucous or polypoid papules and plaques, erythroplakia, or a velvety erythematous plaque
BD of the mucosal surfaces
Histopathology: full-thickness atypia, including in the intraepidermal portions of the adnexal structures with involvement from the stratum corneum to the basal cell layer, but BM is intact; parakeratosis, hyperkeratosis, acanthoses are present, with complete disorganization of the epidermal architecture; throughout the epidermis are numerous atypical, pleomorphic, hyperchromatic keratinocytes which may be vacuolated and have a prominent pale-staining cytoplasm, reminiscent of the cells in Paget disease; show loss of maturation and polarity; upper dermis is typically infiltrated by lymphocytes, plasma cells, and histiocytes
Bowen disease
BD that displays parakeratosis and marked acanthosis with broad, sometimes fused, epidermal rete ridges
Psoriasiform BD
BD that demonstrates a thinned epidermis, but in addition there is full-thickness atypia and lack of maturation, as well as adnexal involvement
Atrophic BD
BD that shows marked acantholysis in the epidermis
Acantholytic BD
BD that has changes of incidental epidermolytic hyperkeratosis (EHK) present
Epidermolytic BD
BD with phenomenon of intraepidermal epithelioma of Borst-Jadassohn which is nesting of the atypical cells within the epidermis
Pagetoid BD
Treatment: Bowen disease
Surgical and destructive therapies
Excision
Mohs micrographic surgery
Curettage with or without electrosurgery
Liquid nitrogen cryosurgery
Treatment: Bowen disease
Topical therapies
5-Fluorouracil (5% cream bid for 6–16 weeks)
5% imiquimod (daily for 16 weeks)
Treatment: Bowen disease
Nonsurgical ablative therapies
Laser ablation
Radiotherapy
Photodynamic therapy
HPV: Bowenoid papulosis (BP)
HPV-16,18
HPV: Epidermodysplasia verruciformis (EV)
HPV-5,8
HPV: Vulvar intraepithelial neoplasia (VIN)
Anal intraepithelial neoplasia (AIN)
Perianal intraepithelial neoplasia (PaIN)
Penile intraepithelial neoplasia (PIN)
Digital or periungual Bowen disease
HPV-16
Predominantly white lesion of the oral mucosa that cannot be rubbed off or characterized by any other definable lesion or known disease; most common precancerous lesion of the oral mucosa, with the potential to become oral SCC
Leukoplakia
Presents mostly as white, flat, uniform lesion that may have shallow cracks and a smooth, wrinkled, or corrugated surface that is consistent throughout
Homogeneous oral leukoplakia
Presents mostly as white or white and red lesion (erythroleukoplakia) that may be irregular and flat, nodular (speckled), ulcerative, or verrucous; has a higher risk of malignant transformation
Nonhomogeneous oral leukoplakia
Precancerous lesion of stratified squamous epithelium characterized by cellular atypia and loss of normal maturation and stratification short of carcinoma in situ
Epithelial dysplasia
A lesion in which the full thickness, or almost the full thickness, of squamous epithelium shows the cellular features of carcinoma without stromal invasion
Carcinoma in situ of the oral cavity
Most important risk factor for the conversion of oral leukoplakia into oral squamous cell carcinoma
Presence of epithelial dysplasia
Other risk factors for the conversion of oral leukoplakia into oral squamous cell carcinoma
Female gender Long duration of oral leukoplakia (OL) OL in nonsmokers Location on the floor of the mouth or tongue Size >200 mm3 Nonhomogeneous type of OL
A red macule or patch on a mucosal surface
that cannot be categorized as any other known disease entity caused by inflammatory, vascular, or traumatic factors; can involve any mucosal surface but most commonly occurs on the oral mucosa in more than half of all cases; considered to be the most dangerous and carries the greatest risk of progressing to or harboring invasive carcinoma
Erythroplakia or Erythroplasia
Most common areas or oral erythroplakia in the oral cavity
Soft palate
Floor of the mouth
Buccal mucosa
Presents as a solitary, subtle, asymptomatic, erythematous macule or patch; most often <1.5 cm in its widest diameter; sharply demarcated from the surrounding pink mucosa, and surface is most often smooth and homogeneous in color; occasionally lesions of demonstrate a pebbled or stippled surface change and on palpation may have a soft and velvety feel
Erythroplakia or Erythroplasia
Predisposing factors for SCC
Precursor lesions (actinic keratosis, Bowen disease)
Ultraviolet radiation exposure
Ionizing radiation exposure
Exposure to environmental carcinogens Immunosuppression
Scars
Burns or long-term heat exposure
Chronic scarring or inflammatory dermatoses
Human papillomavirus infection
Genodermatoses (albinism, xeroderma pigmentosum, porokeratosis, epidermolysis bullosa)
Considered the predominant risk factor for SCC
UV radiation
Associated 30-fold increase in non-melanoma skin cancers, most of which are SCCs
Long term PUVA therapy
Virus recently identified in approximately 15% of cutaneous SCCs from immunocompetent patients
MCPyV polyoma virus
Disorder of DNA repair, is also characterized by early development of SCCs
Xeroderma pigmentosum
Apoptosis of keratinocytes that have sustained UV radiation-induced DNA damage, requires the p53 tumor suppressor and represents a key protective mechanism against skin cancer by removing premalignant cells that have acquired mutations
Sunburn cells
Associated with nodal metastasis in oral SCC
Bcl-2-associated athanogene 1 (BAG-1)
May present as firm, flesh-colored or erythematous, keratotic papule or plaque but may also be pigmented; may also present as an an ulcer, a smooth nodule, or a thick cutaneous horn; may also be verrucous or present as an abscess, particularly if in a periungual location; margins may be indistinct; with enlargement, there is usually increased firmness and elevation
Squamous cell carcinoma
Usually occurs in patients with a long history of cigarette smoking, tobacco chewing, or alcohol use with male predominance; most commonly evolves from lesions of erythroplakia and is usually asymptomatic; may also present as a peritonsillar abscess
Squamous cell carcinoma of oral cavity
Most common sites of oral SCC
Palate
Tongue
High risk sites of oral SCC
Floor of the mouth
Ventrolateral tongue
Soft palate
Begins as a roughened papule of actinic cheilitis or scaly leukoplakia, with slow progression to a tumor nodule; usually associated with persistent lip chapping with localized scale or crust, red and white blotchy atrophic vermilion zone of the lip, indistinct or “wandering” vermilion border, and small fissuring; or ulceration within an area of indurated actinic cheilitis
SCC of the lower lip
Most commonly occurs on the anterior labia majora, beginning as a small warty nodule or an erosive erythematosus plaque; may be asymptomatic but more often are associated with pruritus or bleeding
SCC of the vulva
Begins as a small pruritic verrucous lesion that becomes friable with increasing size in the genitalia
SCC of the scrotum
Usually occurs in uncircumcised males and, may account for 10% of cancers in places where genital hygiene is poor
SCC of the penis
Distinct precursor of penile SCC characterized by a velvety red plaque
Erythroplasia of Queyrat
Common precursor of SCC of the vulva
Lichen sclerosus
Typically begin decades after injury, with skin breakdown and persistent erosion; most commonly this occurs on the lower extremities at sites of chronic pyogenic or venous stasis ulcers; may be associated with increased pain, drainage, or bleeding
Scar squamous cell carcinoma
Typically presents as a large, smooth, dome-shaped, verrucous nodule with a central keratotic crater in an elderly patient on a sun-exposed site, particularly an extremity with rapid growth, up to several cm in weeks, and then gradual involution over a period of months in most cases
Keratoacanthoma
Associated neoplasms in Keratoacanthoma
Sebaceous neoplasms Gastrointestinal malignancies (Muir-Torre syndrome)
Form of SCC that encompasses several clinical entities, all characterized by slow-growing exophytic tumors with a cauliflower-like appearance that develop at sites of chronic irritation; may be clinically mistaken for giant warts
Verrucous carcinoma
Type of Verrucous carcinoma that consists of oral tumors on the buccal mucosa of elderly male tobacco chewers representing 2%–12% of all oral cancers; these tumors are most commonly found on the buccal mucosa, tongue, gingiva, and floor of the mouth
Type I - oral florid papillomatosis
Type of Verrucous carcinoma that occurs on the glans penis of young uncircumcised males, on the scrotum, on the perianal region in both sexes, and, less commonly, on the female genitalia
Type II - anogenital type
Type of Verrucous carcinoma that is a malodorous tumor often found on the plantar area in elderly men; usually involves the skin underlying the first metatarsal head and tends to form draining sinuses that are like rabbit burrows in appearance
Type III - epithelioma cuniculatum
Type of Verrucous carcinoma that occurs at other sites, including the scalp, trunk, and extremities; detection of sequences from HPV types 6, 11, 16, and 18 in epithelioma cuniculatum and type 11 sequences in oral verrucous carcinoma raises the possibility that these tumors evolve from verruca vulgaris
Type IV
May be signaled by a palpable lymph node near the site of treatment of a previous SCC; May present as large keratotic papules or nodules resembling the primary lesion; Or may be clusters of firm pink or red papules that may be keratotic centrally
Metastatic SCC
Histopathology: extension of atypical keratinocytes beyond the basement membrane and into the dermis; tumor may appear as single cells, small groups or nests of cells, or a single mass; squamous differentiation is seen as foci of keratinization in concentric rings of squamous cells called horn pearls
Squamous cell carcinoma
Histologic grading of SCC is based on
Degree of cellular differentiation
Broders’ Grading System for Squamous Cell Carcinoma
1 - <25; uniform cells, resembling mature keratinocytes, with intracellular bridges and keratin production
2 - <50
3 - <75
4 - >75; atypical cells, loss of intracellular bridges, and minimal or absent keratin production
Histopathology: SCC variant with tubular microscopic pattern and keratinocyte acantholysis
Adenoid (or pseudoglandular) SCC
Histopathology: SCC variant with keratinocytes that appear clear as a result of hydropic cytoplasmic swelling and accumulation of lipid vacuoles
Clear cell SCC
Histopathology: SCC variant with spindle-shaped atypical cells
Spindle cell SCC
Histopathology: SCC variant with characterized by concentric rings composed of keratin and large vacuoles corresponding to markedly dilated endoplasmic reticulum
Signet-ring cell SCC
Histopathology: the superficial component resembles verruca vulgaris with prominent acanthosis and papillomatosis, whereas the deeper component extends downward, displacing collagen bundles
Verrucous carcinoma
Histopathology: reveals a symmetric keratin-filled crater, with the epidermis on each side extending over to form a distinct lip
Keratoacanthoma
Diagnosis of Squamous cell carcinoma
Skin biopsy
High risk Squamous cell carcinoma
Diameter >2 cm Depth >4 mm and Clark level IV or V Tumor involvement of bone, muscle, nerve Location on ear, lip Tumor arising in scar Broders grade 3 or 4 Patient immunosuppression Absence of inflammatory infiltrate
Treatment: Squamous cell carcinoma
Nonexcisional ablative techniques (in situ disease only, or in special circumstances) Mohs micrographic surgery Conventional surgical excision Topical therapy (in situ disease only) Radiation therapy
Treatment of choice for small primary SCCs
Conventional surgical excision
Margins for excision of small primary SCCs
4 mm - for low-risk lesions or SCCs with a depth of less than 2 mm
Mohs micrographic surgery - for lesions with a depth of more than 6mm or a diameter >1 cm
Indications for Mohs Micrographic Surgery
Infiltrative squamous cell carcinoma (SCC)
Poorly dedined clinical margins
Location on lip, ear, nail bed, nasal tip, eyelid, genitalia
History of radiation at site
Involvement of nerve, bone, muscle
Immunosuppressed patient
Recurrence of large SCC
Verrucous carcinoma
SCC arising from chronic scarring conditions
Can be used to treat superficially invasive to moderate-risk lesions and serves as an important adjuvant to excisional surgery in treating residual microscopic disease and providing prophylaxis against metastatic disease; may also be used as adjuvant therapy in cases in which perineural SCC was identified in surgical pathologic specimens but treatment failures occurred
Radiation therapy
Treatment: Squamous cell carcinoma (topical)
5-Fluorouracil once or twice daily for 2-4 weeks
Imiquimod 3-5 times per week for 2-4 months
May be due to enhanced interferon-γ production and effector function of T cells infiltrating the tumor
Imiquimod
Recurrence rate: Mohs micrographic surgery (Primary SCC)
3.1%
Recurrence rate: electrodesiccation and curettage (Primary SCC)
3.7%
Recurrence rate: excisional surgery (Primary SCC)
8.1%
Recurrence rate: radiation (Primary SCC)
10%
Recurrence rate: Mohs micrographic surgery (Lip SCC)
2.3%
Recurrence rate: Mohs micrographic surgery (Ear SCC)
5.3%
Most common cancer in humans and accounts for approximately 75% of all nonmelanoma skin cancers; more common in elderly; develops on sun-exposed skin of lighter skinned individuals
Basal cell carcinoma
Risk factors: Basal cell carcinoma
Ultraviolet light (UVL) exposure
Light hair and eye color
Northern European ancestry
Inability to tan
The pivotal abnormality in all BCCs, and there is evidence that little more than this upregulation is required for BCC carcinogenesis.
Hedgehog (HH) pathway
Heritable conditions pre- disposing to the development of BCC
Nevoid basal call carcinoma syndrome or basal cell nevus syndrome (BCNS)
Bazex syndrome
Rombo syndrome
May develop hundreds of BCCs and may exhibit a broad nasal root, borderline intelligence, jaw cysts, palmar pits, and multiple skeletal abnormalities;occurs due to mutations in the tumor suppressor PTCH gene
Basal cell nevus syndrome
Transmitted in an X-linked dominant fashion; have multiple BCCs, follicular atrophoderma, dilated follicular ostia with ice pick scars, hypotrichosis, and hypohidrosis
Bazex syndrome
Transmitted in an autosomal dominant fashion; have vermiculate atrophoderma, milia, hypertrichosis, trichoepitheliomas, BCCs, and peripheral vasodilation; no hypohidrosis
Rombo syndrome
Presents with a friable, nonhealing lesion that bled briefly then healed completely, only to recur; usually develops on sun-exposed areas of the head and neck but can occur anywhere on the body with features include translucency, ulceration, telangiectasias, and the presence of a rolled border
Basal cell carcinoma
Most common clinical subtype of BCC which most commonly on the sun-exposed areas of the head and neck and appears as a translucent papule or nodule depending on duration; usually with telangiectasias and a rolled border; larger lesions with central necrosis are referred to by the historical term rodent ulcer
Nodular basal cell carcinoma
Subtype of BCC that exhibits increased melanization; appears as a hyperpigmented, translucent papule, which may also be eroded
Pigmented basal cell carcinoma
Subtype of BCC that occurs most commonly on the trunk and appears as an erythematous patch often well demarcated that resembles eczema that does not respond to treatment
Superficial basal cell carcinoma
An aggressive growth variant of BCC with a distinct clinical and histologic appearance; lesions may have an ivory-white appearance and may resemble a scar or a small lesion of morphea
Morpheaform (Sclerosing) basal cell carcinoma
Presents as a pink papule, usually on the lower back which may be difficult to distinguish from an acrochordon or skin tag; express androgen receptors
Fibroepithelioma of Pinkus
Seen most often with recurrent tumors located in the preauricular and malar areas; occurs most often in histologically aggressive or recurrent lesions; has been correlated with recurrent lesions, increased duration and size of lesions, and orbital invasion; may manifest as pain, paresthesias, weakness, or paralysis
Perineural invasion
Metastasis of BCC occurs only rarely, with rates varying from
0.0028 - 0.55%.
Site of predilection: BCC
Nodular and morpheaform - head and neck
Superficial - trunk
Histopathology: account for half of all BCCs and are characterized by nodules of large basophilic cells and stromal retraction; characterized by discrete nests of basaloid cells in either the papillary or reticular dermis accompanied
Nodular basal cell carcinoma
Histopathology: melanocytes are interspersed between tumor cells and contain numerous melanin granules in their cytoplasm and dendrites; tumor cells contain little melanin but numerous melanophages populate the stroma surrounding the tumor
Pigmented basal cell carcinoma
Histopathology: microscopically by buds of malignant cells extending into the dermis from the basal layer of the epidermis; peripheral layer shows palisading cells; there may be epidermal atrophy, and dermal invasion is usually minimal; there may be a chronic inflammatory infiltrate in the upper dermis
Superficial basal cell carcinoma
Histopathology: consists of strands of tumor cells embedded within a dense fibrous stroma; tumor cells are closely packed columns and, in some cases, only 1-2 cells thick enmeshed in a densely collagenized fibrous stroma; strands of tumor extend deeply into the dermis
Morpheaform (Sclerosing or Infiltrative) basal cell carcinoma
Histopathology: long strands of interwoven basiloma cells are embedded in fibrous stroma with abundant collagen.
Fibroepithelioma of Pinkus
Histopathology: shows infiltrating jagged tongues of tumor cells admixed with other areas that show squamous intercellular bridge formation and cytoplasmic keratinization
Basosquamous carcinoma
Gold standard for treating basal cell carcinoma
Excision with clear margins
Offers superior histologic analysis of tumor margins while permitting maximal conservation of tissue compared with standard excisional surgery
Mohs micrographic surgery
Treatment of choice for morpheaform, poorly delineated, incompletely removed, and otherwise high-risk primary BCCs; preferred treatment for recurrent BCC and for any BCC that occurs at a site where tissue conservation is desired; used in treating BCCs at high-risk anatomic sites, including the nasofacial junction and retroauricular sulcus
Mohs micrographic surgery
Margins needed in excision for BCC
<2cm - 4 mm <1 cm - 0.5-cm 1-2 cm - 0.8-cm margin >2 cm - 1.2- cm 5 mm - primary morpheaform BCC
One of the most frequently used treatment modalities for BCC that is operator-dependent
Curettage and Desiccation
Destructive modality that has been used in the treatment of BCC; 2 freeze-thaw cycles with a tissue temperature of −50°C (−58°F) are required to destroy BCC with a margin of clinically normal tissue destroyed
Cryosurgery
Potential serious adverse outcome with cryosurgery for BCC
Obscuring of tumor recurrence by fibrous scar tissue
