This document discusses benign skin lesions. It notes that most skin lesions are benign, but some require diagnosis for patient reassurance. Key characteristics to consider include those outside the lesion, physical characteristics of the lesion, and histologic characteristics. Common benign lesions include seborrheic keratoses, dermatosis papulosa nigra, stucco keratoses, and inverted follicular keratoses. Seborrheic keratoses are usually benign growths that appear in middle age and are often multiple, with waxy and varied coloring. Diagnosis is usually based on visual characteristics but histology may also be examined.
This document discusses benign skin lesions. It notes that most skin lesions are benign, but some require diagnosis for patient reassurance. Key characteristics to consider include those outside the lesion, physical characteristics of the lesion, and histologic characteristics. Common benign lesions include seborrheic keratoses, dermatosis papulosa nigra, stucco keratoses, and inverted follicular keratoses. Seborrheic keratoses are usually benign growths that appear in middle age and are often multiple, with waxy and varied coloring. Diagnosis is usually based on visual characteristics but histology may also be examined.
This document discusses benign skin lesions. It notes that most skin lesions are benign, but some require diagnosis for patient reassurance. Key characteristics to consider include those outside the lesion, physical characteristics of the lesion, and histologic characteristics. Common benign lesions include seborrheic keratoses, dermatosis papulosa nigra, stucco keratoses, and inverted follicular keratoses. Seborrheic keratoses are usually benign growths that appear in middle age and are often multiple, with waxy and varied coloring. Diagnosis is usually based on visual characteristics but histology may also be examined.
This document discusses benign skin lesions. It notes that most skin lesions are benign, but some require diagnosis for patient reassurance. Key characteristics to consider include those outside the lesion, physical characteristics of the lesion, and histologic characteristics. Common benign lesions include seborrheic keratoses, dermatosis papulosa nigra, stucco keratoses, and inverted follicular keratoses. Seborrheic keratoses are usually benign growths that appear in middle age and are often multiple, with waxy and varied coloring. Diagnosis is usually based on visual characteristics but histology may also be examined.
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Most skin lesions are benign; however, some concern has caused the patient to make an inquiry, and a correct diagnosis is important. The following 3 general types of characteristics must been considered when defining a benign lesion: 1. Characteristics outside of the lesion e.g. patient age, ethnicity, presence of associated symptoms, related systemic disorders, and location. 2. Physical characteristics of the lesion 3. Histologic characteristics of the lesion Initially, benign lesions must be differentiated from malignant lesions. This is best done by being familiar with characteristics of common malignant lesions. The clinician should try to categorize any skin lesion as one of the following: a. most likely benign, b. most likely malignant, c. or unclear. the last 2 categories should be biopsied. Benign lesions of the surface epithelium. Cutaneous Cysts. Benign Melanocytic Neoplasms Neoplasms and proliferations of follicular lineage Neoplasms and proliferations with sebaceous differentiation Neoplasms and proliferations with apocrine differentiation Neoplasms and proliferations with eccrine differentiation Fibrous and Fibrohistiocytic Proliferations of the Skin and Tendons Muscle, Adipose and Cartilage Neoplasms Vascular Neoplasms MULTIPLE SOLITARY LINEAR 1. Seborrheic keratosis 1. Inverted follicular 1. Epidermal nevus 2. DPN keratosis 2. ILVEN 3. Stucco keratosis 2. Keratoacanthoma 3. Linear porokeratosis 4. Disseminated superficial 3. Cutaneous horn 4. Nevus comedonicus actinic porokeratosis 4. Clear cell acanthoma 5. Mosaic form of Darier 5. Porokeratosis palmaris 5. Warty dyskeratoma disease et plantaris disseminata 6. Lichenoid keratosis 6. Acrokeratosis verruciformis of Hopf SKs usually begin to appear during and after the fourth decade and continue to arise throughout life. An apparent familial predisposition with a postulated autosomal dominant inheritance. They only occur on hair bearing skin. Can arise on all body surfaces except mucosa, palms and soles. Though harmless, SKs can occasionally become irritated or can be cosmetically bothersome. The exact cause of seborrhoeic keratoses is not known may be; 1. There is a familial predisposition in those with hundreds of lesions. 2. Sun exposure (Although SKs are common in areas covered by clothing) higher prevalence of SKs within sun-exposed areas such as the head and neck in contrast to non-sun exposed areas in the same subjects. 3. Very rarely, eruptive SKs may denote an underlying internal malignancy. The syndrome is known as the sign of Leser-Trélat. 4. Neoplastic origin (somatic mutations). 5. HPV may be implicated. Typically appear as sharply marginated, pigmented lesions. They may be macules, papules, plaques or even pedunculated, depending on their stage of development. Color is variable even within the same lesion (pink, yellow, flesh colored, tan, brown, black). Surface is usually waxy and the texture can vary from smooth, velvety to verrucous. Often multiple & can be extensive. Keratotic plugging with follicular prominence. They have a stuck-on quality. SKs can develop on the face, neck and trunk (especially the upper back), as well as the extremities. Usually measure about 1 cm in diameter but they can become quite large, i.e. > 5 cm in diameter. Lesions may become inflamed due to rupture of the small pseudocysts they contain or from trauma, or rarely from infection with microorganisms such as Staphylococcus aureus. Conditions associated with an abrupt “flare” of lesions followed by regression include pregnancy, coexisting inflammatory dermatoses (in particular erythroderma) and malignancy. Velvety, dark brown Light tan or Verrucous, tan almost skin colored Multiple SKs Multiple SKs If you are in doubt of the diagnosis, try gently picking or scratching the lesion. It may crumble, hyperkeratotic scale, or lift off, revealing that superficial waxy character. This SK has been partially picked off (If picked off or curetted, SKs will leave a pink moist base with minimal bleeding) • Use dermoscopy to look for keratin pseudocysts. • These are small white spots commonly found in seborrheic keratoses. Seborrheic keratosis clinical white spots are directly comparable with the horn pseudocysts which is it histological equivalent. Dermoscopy of SKs showing horny pseudocysts Leser-Trélat sign It is not precancerous. SCC cutaneous melanoma, BCC, keratoacanthoma, and SCC in situ have all been rarely observed in association with SKs. This represents a coincidental neoplasm developing in adjacent skin. The sign of Leser–Trélat is a rare cutaneous marker of internal malignancy (in particular gastric (60%) or colonic adenocarcinoma, breast carcinoma, and lymphoma). It is considered to be a paraneoplastic cutaneous syndrome characterized by an abrupt and striking in the number and/or size of SKs occurring before, during or after an internal malignancy has been detected majority and of the lesions are located on the back, followed by the extremities, face and abdomen and usually associated with pruritus. Neoplasm may secrete TGF-alpha epithelial hyperplasia. I. IRRITATED SEBORRHOEIC KERATOSIS II. DERMATOSIS PAPULOSA NIGRA III. STUCCO KERATOSES IV. INVERTED FOLLICULAR KERATOSES • Inflamed lesion, often red, edematous and crusted. Irritated SKs erythematous, edematous and crusty Multiple, small, symmetric hyperpigmented, sessile to filiform, smooth-surfaced papules measuring from 1 to 5 mm. Arise in darker skin types, usually on the cheeks, temples. Less often, lesions are on the neck, chest and back. It has a strong familial predisposition. Women are twice as likely to be affected as men. It tends to have an earlier age of onset (during adolescence) than that of SKs. HP pattern quite similar to the acanthotic type of SK. DPN Small white-gray papules or plaques scattered on dorsal feet and ankles of older fair-skinned individuals. Lesions are “stuck on”, and when scraped off, with a fingernail and there is usually minimal, if any, bleeding. A collarette of dry scale may remain The papules may number in the hundreds. They are usually small, measuring from 1 to 4 mm, but rarely individual plaques may be as large as a few centim- eters. There is no familial predilection. Men are four times more likely to be affected than women. It displays prominent orthokeratotic hyperkeratosis and papillomatosis, often showing “church spire” pattern. Asymptomatic solitary firm, white to light-tan or pinkish papules usually less than 1 cm in diameter on face or neck of middle-aged and older adults. They are typically stable and persistent lesions, but may regress. Benign endophytic variant of irritated SK. It is derived from the infundibulum of the hair follicle. Histologically, The keratinocyte proliferation seems to surround one or several follicular canals that open to the surface. squamous eddies and inflammation are common. Histopathology of IFK There are at least six histologic types of SK but different histologic features are often present in the same lesion: 1. Acanthotic: the most common. 2. Hyperkeratotic: more prominent hyperkeratosis and papillomatosis. 3. Reticulated: delicate strands of epithelium that extend from the epidermis in an interlacing pattern. 4. Irritated: perivascular, diffuse or lichenoid lymphoid infiltrate. Squamous eddies are common findings. 5. Clonal: well defined nests of loosely packed uniform cells in the epithelium. 6. Melanoacanthoma: shows dendritic melanocytes packed with melanin which is absent in keratinocytes. Usually presents as a smooth surfaced, dome - shaped papule. Slight hyperkeratosis and papillomatosis are often present, while the greatly thickened epidermis typically contains a preponderance of basaloid cells. Sharply demarcated horizontal base called “string”. Papillae may be narrow in some lesions. Invaginated horn pseudocysts are most prevalent in this variant. This type often contains an amount of pigment superior in quantity than others; it is primarily concentrated in keratinocytes and is transferred from neighboring melanocytes and deeply pigmented lesions contain abundant melanin in basaloid cells. Acanthotic type Hyperkeratotic type with church spires of papillomatosis and hyperkeratosis & preponderance of squamous cells relative to basaloid cells Reticulated type with delicate, lace-like strands of interconnecting epithelium composed of a double row or more of hyperpigmented basaloid cells and interspersed horn pseudocysts Reticulated type Irritated type exophytic lesion with papillomatosis, hyperkeratosis, hemorrhagic crust and dermal inflammation Clonal type with Borst–Jadassohn phenomenon* characterized by well-demarcated nests of keratinocytes within the epidermis * ‘clones’ of basaloid, squamatized, or pale keratinocytes in epidermis appear different than their neighbors Assurance. Superficial destructive means mainly for cosmetic reasons; 1. Cryotherapy: The most commonly used method but can result in hypopigmentation in dark individuals. 2. Curettage. 3. Electrodessication (very light) is often safe. 4. Shave excision 5. Scissor snip (pedunculated lesions & DPN). 6. Laser ablation (pulsed CO2, erbium: YAG) Full thickness excision: if melanoma is considered in the differential diagnosis for histology. They are due to an hamartoma of the epidermis present at birth (50%) or develop during childhood (mostly in the first year of life) and persist indefinitely. The abnormality arises from a defect in the ectoderm (outer layer of the embryo that gives rise to epidermis and neural tissue). Most commonly, hyperpigmented papillomatous papules and plaques appear in a linear array along Blaschko’s lines. The incidence of epidermal nevus is estimated to be 1 in 1000 infants. Sporadic rarely inherited. Blaschko’s lines Originate from pluripotent cells in the basal layer of the embryonic epidermis. Mosaicism (skin cells that have the active abnormal gene spread out to form the epidermal naevus, whereas the remaining skin cells form the other areas of apparently normal skin) for activating mutations in the gene that encodes fibroblast growth factor receptor 3 (FGFR3) was demonstrated in “common” epidermal nevi. While these lesions are classically referred to as “epidermal” nevi, the hamartomatous process also involves at least some portion of the dermis, especially the papillary dermis. Epidermal Naevi Epidermal Naevi Epidermal nevi most commonly present as a single linear lesion, but sometimes multiple unilateral or bilateral linear plaques are seen. Asymptomatic well circumscribed, hyperpigmented, papillomatous papules or plaques. The earliest lesions may be macular once developed, it become thickened and more verrucous, especially over joints and in flexural areas. Occur most commonly on trunk, extremities or neck following Blaschko’s lines. TYPES OF EPIDERMAL NAEVI: 1. Localized Linear Epidermal Naevus (Nevus Verrucosus) 2. Naevus Unius Lateris 3. Systematised Epidermal Naevus (Ichthyosis Hystrix) 4. ILVEN 5. Epidermolytic Epidermal Naevus 6. Acantholytic Epidermal Naevus NEVUS UNIUS LATERIS: It is a variant in which there are extensive unilateral plaques, often involving the trunk. SYSTEMATIZED EPIDERMAL NEVUS (ICHTHYOSIS HYSTRIX) It is a variant with extensive bilateral involvement, also usually on the trunk. EPIDERMAL NEVUS SYNDROME is diagnosed when epidermal nevi occur in combination with other developmental anomalies. These abnormalities most commonly involve the neurologic or musculoskel- etal systems. All epidermal nevi are characterized by epidermal hyperplasia, hyperkeratosis, acanthosis, papillomatosis, and variable parakeratosis. Other findings such as epidermolytic hyperkeratosis and focal acantholytic dyskerato- sis may be prominent features. Neoplasms such as BCC, SCC and keratoacanthoma may rarely develop in association with epidermal nevi. Infants and children with epidermal nevi, particularly multiple or extensive lesions, require a thorough evaluation for systemic abnormalities. MEDICAL: 1. Topical therapies such as corticosteroids, retinoic acid, tars, anthralin, 5-fluorouracil and podophyllin have all been used, but they are of limited benefit. 2. Oral therapy with systemic retinoids for long term has been reported to be effective at decreasing the thickness of systematized epidermal nevi, although it does not result in resolution. SURGICAL: 1. Superficial destructive means (e.g. by cryotherapy, shave excision or curettage) recurrence is common as only the epidermis is removed. Laser ablation may also be undertaken, but, to be effective, it must induce scarring and fibrosis of at least the papillary dermis. Therefore, this treatment is often not cosmetically acceptable to patients and test sites are recommended. 2. Full thickness surgical excision is curative but can be complicated by hypertrophic scars or keloid formation. It is relatively rare, linear, psoriasiform plaque that usually presents on one extremity and appears before the age of 5 years in 75% of patients. Four times more common in girls. The definitive cause is unknown. As it bears some resemblance to psoriasis histologically, some believe that the two conditions share a common pathogenesis. Rarely arthritis may be associated with ILVEN. ILVEN Psoriasiform appearance. Significant pruritus. Scaly, erythematous papules coalesce to form a linear plaque, almost always unilateral on a limb of a child. Most lesions spontaneously resolve by adulthood. Psoriasiform histology. Elongated rete ridges. Broad zones of parakeratosis without an underlying granular layer alternate abruptly with depressed regions of orthokeratosis and hypergranulosis. There is often exocytosis of lymphocytes and neutrophils into the spongiotic papillomatous epidermis and occasionally Munro’s microabscesses may be seen. ILVEN is difficult to treat. Treatments that are successful in psoriasis are only partially effective for ILVEN. MEDICAL: 1. Combination therapy with topical tretinoin and 5-fluorouracil creams has been employed with beneficial results, but long-term success can only be achieved with maintenance therapy. 2. Calcipotriol may be partially effective. SURGICAL: 1. Pulsed dye laser has been used successfully in some cases. 2. Surgical excision is effective but results in scarring. Rare benign hamartoma of the pilosebaceous unit resulting in numerous dilated, keratin filled comedones usually arising before the age of 10 years. It is due to genetic mosaicism with FGFR2 mutation. Sometimes follow the lines of Blaschko. Hormonal influences of puberty often worsen the condition. Nevus Comedonicus Usually a single circumscribed area or linear streak composed of clusters of dilated follicular ostia with central keratinous plugs contain firm, darkly pigmented, cornified material. Their size is variable and they can range from a few centimeters in diameter to extensive lesions affecting half of the body. The site most commonly affected is the face, followed by the trunk, neck and upper extremity. These nevi may also arise in areas that are devoid of hair follicles such as the palms, soles and glans penis. When present on the elbows and knees, lesions can be verrucous in appearance. Rarely, at puberty or later, it may develop inflammatory acne-like lesions within it. These can lead to cysts, recurrent bacterial infections, abscesses, and scarring. Grouped undeveloped hair follicles, presenting as dilated invaginations filled with cornified debris devoid of hair shafts. MEDICAL: 1. Keratolytic agents e.g. salicylic acid, tretinoin and ammonium lactate may be helpful, but they are not curative. 2. Isotretinoin is not usually recommended owing to the long term treatment required, but it may be beneficial in preventing cyst formation. 3. Antibiotics may be necessary to treat secondary infections. SURGICAL: 1. Manual comedo extraction, laser, dermabrasion may be done but it is not curative. 2. Excision of localized lesions, although it is often difficult to excise larger lesions. KA is a rapidly growing skin tumor that considered by some to be a variant of SCC and by others to represent benign tumors (i.e. pseudomalignancy) this remains in question, although based on a systematic review keratoacanthoma cannot be considered malignant. Comparing the clinical behaviors of both KA and SCC found that none of KA resulted in distant metastases or death*. * Savage JA, Maize JC Sr. Keratoacanthoma clinical behavior: a systematic review. Am J Dermatopathol. May 2014;36(5):422-9. It tends to occur in males more often than in females, with a male- to-female ratio of 3-4:1. The peak incidence of KA is between ages 50 and 70. This tumour is rare before 40 years of age. More common in fair skinned people. The most common denominator appears to be sun exposure. Some KAs appear to be related to infection with HPV but the majority of KAs are not found to be due to HPV. Genetic predisposition in case of multiple KAs e.g. KAs associated with Muir–Torre syndrome, Multiple spontaneously regressing KAs of Ferguson-Smith. KA A predictable clinical sequence occurs, which consists first of the development of a spontaneous dome- shaped papule that is red to flesh colored. The papule undergoes an rapid growth phase over a few weeks, forming a large sharply circumscribed crater-like nodule with a keratotic core. Over the next few months, the tumor may slowly resolve to leave an atrophic scar. Size usually 1-2 cm in diameter. Most lesions occur on the head and neck or in sun-exposed areas of the extremities, with or without symptoms of pain or tenderness. Most common presentation is the solitary KA. Three growth phases are described:
1. Proliferative phase: a solitary papule appears
suddenly and then rapidly grows to its maximum size over 2 to 4 weeks. 2. Mature phase: the lesion is stable in size and appearance for weeks to months; it may appear crateriform if the core has been partially removed. 3. Resolving phase: the base becomes indurated, the central core is expelled, and the base resorbs, leaving a atrophic scar. This phase may last several months. Keratoacanthoma centrifugum marginatum Progressive peripheral expansion and central involution with residual atrophy Grzybowski syndrome Multiple spontaneously regressing KAs of Ferguson-Smith The patient had approximately 40 firm, 1- to 2-cm, dome-shaped, red-to-flesh colored, hyperkeratotic nodules on the lateral upper arm and extensor forearms. Giant keratoacanthoma with a yellow–red color and a history of rapid growth SEVERAL DISTINCT CLINICAL PRESENTATIONS OF KA CLINICAL VARIETIES FEATURES 1. Generalized eruptive severely itchy multiple non-regressing KAs hundreds KA (of Gryzbowski) of papules resembling milia or early eruptive xanthomas 2. Multiple spontaneously autosomal dominant condition, where multiple KAs appear in regressing KAs of patients aged 20-30 ys typically regress over weeks to months. Ferguson-Smith 3. KA centrifugum is characterized by multiple grouped keratoacanthomas may marginatum reach several cms in diameter resolve more slowly than solitary KA 4. Actinic KAs when KAs develop in sun-exposed skin associated with AK 5. KAs associated with may have sebaceous differentiation [“seboacanthoma”]. Muir–Torre syndrome 6. Giant KA several centimeters in diameter 7. Subugual KA associated with underlying bony destruction 8. Intraoral KA 9. KAs associated with immunosuppression 10. KAs associated with HPV infection Typically has a “volcano-like” architecture with overall hemispheric shape with a keratin-filled crater and overhanging edges. Mitotic figures are present, secondary to the accelerated growth. Basaloid cells are found toward the periphery. Inflammatory cells eosinophils, lymphocytes and neutrophils also may be common. Cytologic atypia is usually minimal. An overall slight mild pleomorphism is detected. In general, the squamous epithelium is well differentiated and has an abundant glassy eosinophilic cytoplasm. KA Histologic features Pseudocarcinomatous infiltration in keratoacanthoma typically presents a smooth, regular, well-demarcated front that does not extend beyond the level of the sweat glands. Perineural and vascular invasion also can be observed. As the lesion regresses, the dome- shaped architecture flattens and fibrosis develops at the base of the lesion. Immunohistochemical staining can help differentiate KA from other epidermal carcinomas. Filaggrin is ubiquitous in KA but uncommon in carcinoma. While the lesion is generally self-limited it should be treated for several reasons; 1. To obtain pathology: KA can be difficult to distinguish from invasive SCC. 2. To be rid of an unsightly, tender or worrisome lesion 3. To minimize the scar, due to potential cosmetic compromise with the healing of the lesion. Treatment requires destruction of the lesion. Options include: 1. Surgical Excision (the treatment of choice) 2. Cryotherapy 3. Curettage and Electrodesiccation 4. Laser 5. Radiotherapy Treatment of Multiple KAs: 1. Acitretin 2. Isotretinoin 3. 5-Fluorouracil 4. Methotrexate 5. Cyclophosphamide Clinical term for a hard conical white to yellow brown projection from the skin, made of compact keratin. So named as it resemble an animal’s horn. It arise from benign, premalignant or malignant skin lesions. Sun-exposed areas are the most common locations. Cutaneous Horn Cutaneous Horn Cutaneous Horn Cutaneous horns are more common in older patients, with the peak incidence in those between 60 and 70. Men are affected more frequently than women and there is a higher risk of the lesion being malignant in men. They are more common in people with fairer skins (skin phototype I and II). SYMPTOMS:
Cutaneous horns are usually asymptomatic, however
as they are protuberant, they can be injured causing pain and inflammation. APPEARANCE: Cutaneous horns generally present as curved hard yellow brown horns. They can be surrounded by normal skin or have a border of thickened skin. The side of the horn may be terrace-like with horizontal ridges. The base of the horn may be flat, protruding, or like a crater. Inflammation may be present, due to recurrent injury. SIZE: Typically, the horn is taller than twice the width at the base. It may vary from a few millimeters to several centimetres in size. LOCATION: Cutaneous horns are usually single, but can be multiple. They can occur anywhere on the body, but are more common on sun-exposed areas especially the head and ears, dorsum of hands and forearms. They may also occur on the chest, neck, shoulder and penis. Dermoscopy of Cutaneous Horn Terrace morphology is an orderly structural dermoscopic feature It shows hyperkeratosis, parakeratosis associated with variable acanthosis. Orderly horizontal parallel layers of keratin are associated more with benign lesions. Rapidly growing malignant lesions exhibit a more erratic growth. The base of the lesion shows features of the underlying lesion e.g. atypical keratinocytes of actinic keratosis. BENIGN PREMALIGNANT AND MALIGNANT 1. Seborrhoeic keratosis 1. Actinic keratosis 2. Viral warts 2. SCC in situ or invasive 3. Epidermal naevus 3. Malignant melanoma (rare) 4. Molluscum contagiosum 5. Psoriasis 6. Hypertrophic lichen planus 7. Keratoacanthoma 8. Tumors derived from follicular epithelium, especially tricholemmoma. 1. Excision biopsy with local destruction; – It is the most common treatment. – This must be done deeply enough to allow the pathologist to see the dermis beneath the horn in order to evaluate the possibility of dermal involvement by invasive carcinoma. – Excision to adipose is best when invasion is suspected. In that case, induration of the dermis is detected, as opposed to the thickness related only to the horn. 2. Cryotherapy after paring of the horn. It is uncommon, usually solitary lesion of unknown etiology appearing on the lower legs but there have been rare cases of multiple lesions occurring. They occur mostly in adults of middle- age or older. It may be suspected by astute clini- cians, but usually a biopsy is required to establish the diagnosis. Lesions are almost always asymptomatic. Slightly elevated to dome-shaped rounded papule, plaque or nodule. Colour varies from pink to brown, but is most commonly blood red and shiny. Lesions are blanchable. Usually develop slowly, most commonly over a period of 2–10 years. Can be from 0.3 to 2 cm in diameter. Wafer-like scale may be stuck round the edges of the lesion. A moist or bleeding surface may result if scale is removed. Dermoscopic view of Clear Cell Acanthoma characteristic looped blood vessels within the dermal papillae create red dots in lines. Psoriasiform histology i.e. acanthosis with elongation of rete ridges with well-demarcated zone containing characteristic accumulation of clear to pale glycogen-containing keratinocytes that stain positively with PAS. The epidermis is eroded and neu- trophils extend from the papillary dermis into the stratum spinosum, aggregating in the overlying thin crust. They may persist for years and years without changing or causing any complications. Simple destruction or excision is adequate for removal. Shave excision or curettage combined with electrofulguration is a common form of treatment. Most lesions do not recur. Uncommon, usually solitary papule or nodule with a central keratotic plug. Usually located on the head or neck. It is more prevalent in men, usually appearing between the fifth and seventh decades of life. Acantholytic dyskeratosis seen at the base and side of a cup-like epidermal invagination. Lesions should be biopsied to exclude the possibility of a malignancy. Excision is curative. It presents as a solitary, rarely multiple, verrucous, often crusted, skin-colored to red– brown papule or nodule with a central pore and a keratotic plug. Lesions grow slowly, and they are located most commonly on the scalp, cheek, temple, forehead, postauricular area and nose. Lesions have been found beneath the nail plate and in the mouth, especially on the hard palate and alveolar ridge. It typically range in size from several millimeters to 2 cm in diameter. Most warty dyskeratomas are asymptomatic, but patients may rarely complain of pruritus or burning. Bleeding and discharge of foulsmelling cornified material may occur. Usually involves at least one dilated folliculosebaceous unit. There is a central cuplike invagination lined with epithelium displaying acantholysis and individual cell necrosis, corps ronds and grains, most closely resembling Darier disease. The central crater is filled with cornified debris. The wall has multiple villi, sometimes composed of only a single layer of basal cells, often project upward from the invaginated hyperplastic base. Warty Dyskeratoma Bolognia 3rd ed. dermnetnz.org http://emedicine.medscape.com http://www.globalskinatlas.com AAD; Benign Skin Lesions (Presentation) Skin Tumors by Seyed Morteza Mahmoodi (Presentation)