Benign Skin Lesions

Papules and Plaques

Acrochordon

Acrochordons are extremely common lesions found in middle-aged and older persons. They are frequently found on the cervical region, axilla, upper trunk, and eyelids. Skin tags are of low clinical significance except for the questions and concerns they can generate for the patient. Synonyms for acrochordon are skin tag or fibroepithelial polyp.^{[1, 2]}(An acrochordon is shown in the image below.)

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Papular benign skin lesion: Acrochordon (skin tag).

Acrochordons can be associated with pregnancy, diabetes mellitus, and intestinal polyposis syndromes. They can also occur after trauma. They tend to be located in the intertriginous areas of the axilla, groin, and inframammary regions, as well as in the low cervical area along the collar line. They are soft, fleshy papules and usually, although not necessarily, pedunculated. The lesions are single or multiple and can vary in diameter from 1-6 mm. Acrochordons all consist of a thin squamous epithelium surrounding a fibrovascular core.

Whether this is a specific entity or a common pathway in healing and recovery of several nonspecific inflammatory conditions of the skin is debatable. No treatment is required; however, acrochordons are removed to address bleeding, irritation, cosmesis, and discomfort. Occasionally, a lesion may twist on its stalk and become painful, erythematous, and necrotic. They may be electrodesiccated, shaved, or removed with cryoablation. Larger acrochordons may require surgical excision for the best cosmetic result.

Go to Acrochordon for complete information.

Keratoacanthoma

Keratoacanthoma (KA) is a rapidly growing skin tumor that is considered by many to be a variant of squamous cell carcinoma. The rapid rate of growth of keratoacanthomas may help the clinician to distinguish it from many other cutaneous malignancies. Keratoacanthoma is typically a dome-shaped papule or nodule with a central crater of keratin. It tends to occur in males more often than in females, with a male-to-female ratio of 3-4:1. See the images below.

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Keratoacanthoma

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Keratoacanthoma

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Keratoacanthoma

A predictable clinical sequence occurs, which consists first of the development of a spontaneous nodule that is red to flesh colored. The nodule undergoes an impressive growth phase over a few weeks, forming a large crater-like nodule. Over the next few months, the tumor may slowly resolve.

Numerous subtypes have been described. Generalized eruptive keratoacanthomas (of Gryzbowski) present with multiple nonregressing keratoacanthomas. Multiple regressing keratoacanthomas of Ferguson-Smith is an autosomal dominant condition, where multiple spontaneous regressing keratoacanthomas appear in patients aged 20-30 years. When the nodules developin sun-exposed skin associated with actinic keratoses, they can be referred to as actinic keratoacanthomas. Keratoacanthoma centrifugum marginatum is characterized by multiple grouped keratoacanthomas. Giant and subugual variants have also been described.

Various infections have been implicated, including viral sources. In addition, mineral oil and tar products historically have had some importance. However, the most common denominator appears to be sun exposure.

On histologic examination, keratoacanthomas have an 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. Eosinophils also may be common. An overall slight mild pleomorphism is detected. In general, the epithelium is well differentiated and has an abundant ground-glass cytoplasm. At the margin, evidence of a pushing edge is present. This is characterized by an inflammatory rim with extension into the muscle. Perineural and vascular invasion also can be observed. Immunohistochemical staining can help differentiate keratoacanthomas from other epidermal carcinomas. Filaggrin is a histidine-rich protein that is found in the horny and granule layers of the dermis. It is ubiquitous in keratoacanthoma but uncommon in carcinoma.^{[3, 4]}

While the lesion is generally self-limited, intervention is commonly desired. Intervention is preferred because of the potential cosmetic compromise with the healing of the lesion. Additionally, since it is considered by many to be a variant of squamous cell carcinoma, complete removal is generally preferred by surgical excision, electrodesiccation, and curettage. Because keratoacanthoma can be removed in total with surgical excision, which provides an adequate pathologic specimen, this is generally the treatment of choice.

Whether keratoacanthoma can truly be classified as a malignant variant of squamous cell carcinoma, however, remains in question, although based on a systematic review, Savage and Maize concluded that keratoacanthoma cannot be considered as such. Comparing the clinical behaviors of the two lesions as recorded in 445 cases of keratoacanthoma and 429 cases of squamous cell carcinoma, the investigators found that none of keratoacanthomas resulted in distant metastases or death, while squamous cell carcinoma resulted in 61 cases of metastases and was the direct cause of 24 deaths.^[5]

Go to Keratoacanthoma for complete information on this topic.

Pyogenic granuloma

Pyogenic granuloma is a rapidly proliferating, solitary lesion of mostly disorganized vascular growth known for its bleeding tendencies. Also known as a cutaneous ectasia, it is commonly associated with minor previous trauma to the area. While the size varies, it is usually smaller than 1 cm in greatest dimension and often it has a collarette of scale around the base. Typical locations include the face, fingers, and thorax. Clinically, melanoma must be excluded. These lesions may become eroded, crusted, ulcerated, or even occasionally infected. With light trauma, they can bleed easily.

A pyogenic granuloma is shown in the image below.

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Papular benign skin lesion: Pyogenic granuloma.

Multiple dilated capillaries with prominent swollen endothelial cells are observed. Edema is present in the stroma. A pedunculated gross appearance is common.

Since pyogenic granulomas frequently bleed if untreated, the preferred approach is a shave removal or excision with electrodessication of the base. Application of silver nitrate repeatedly can also be a simple yet effective therapy. Recurrence is common with therapies other than complete excision.

Go to Pyogenic Granuloma for complete information on this topic.

Cutaneous horn

A cutaneous horn, or cornu cutaneum, is a skin lesion made of compacted keratin that forms an exophytic conical projection that becomes curved and resembles a French horn. Patients with cutaneous horns tend to be fair-skinned individuals in their 60s and 70s. This lesion is a clinical finding related to other skin disorders but is not its own unique pathologic entity. Cutaneous horns can arise from other hyperkeratotic lesions, such as actinic keratoses, seborrheic keratoses, benign verrucae, inverted follicular keratoses, and squamous cell carcinomas. Although most cutaneous horns are benign, malignant lesions have been reported to be found at the base of 20% of horns. The most common malignancy is squamous cell carcinoma.

The etiology of the cutaneous horn itself is unclear; the underlying associated skin disorder is the precipitating factor. The horn is composed of compact hyperkeratosis, which may be either orthokeratotic or parakeratotic in nature. Associated acanthosis is a common finding. The base displays features of the pathologic process responsible for the underlying lesion. Because of the potential of malignancy at the base of a cutaneous horn, excisional biopsy is recommended.

Go to Cutaneous Horn for complete information on this topic.

Keloid

Keloids are fibrotic, papular lesions that usually occur as an aberrant healing response to cutaneous injuries, such as acne, trauma, surgery, and piercing.^[1]Common sites for keloid occurrences are the earlobes, chest, lower legs, upper back, and jaw line. Keloids, unlike hypertrophic scars, grow beyond the borders of the original scar. Keloids may be associated with pruritus, pain, and, occasionally, a burning sensation.

A keloid is shown in the image below.

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Papular lesions: Keloids developed from back acne.

Keloids occur in all races; however, they have a higher rate of incidence in persons with darker skin. The rate is equal between men and women, and keloids occur in almost all ages; interestingly, they rarely occur in persons older than 65 years. The complete pathophysiology of keloids is unclear.

Overexuberant proliferation activity of the fibroblast occurs in the keloid scar. Fibroblast generates an excessive amount of extracellular matrix (ECM) proteins, such as collagen and fibronectin. Transforming growth factor beta (TGF-β) plays an important role in regulating fibroblast proliferative function, as well as up-regulating important metalloproteinases that contribute to keloid formation. Collagen type III production is 3 times normal in keloids, and all collagen production is associated with less crosslinking, smaller interfibrillar distance, and a more disorganized fibrillar pattern. Total collagen synthesis is 20 times normal, and the collagen-to-fibroblast ratio is also significantly altered.

A study by Touchi et al indicated that the central portion of keloids is severely ischemic. The investigators found greater expression of hypoxia-induced factor-1α, as well as less vascular density, in the center than on the periphery of these lesions.^[6]

Many different therapies exist, but all treatments have a high rate of keloid recurrence.^[1]Avoidance of keloid development is the best therapy. Most people with a history of keloid development have a high likelihood of developing additional keloids in any other area that undergoes trauma or surgical incision. However, all regions of the skin do not have the same propensity to form keloids. Patients with a history of keloids should take into consideration the development of keloids when deciding to pierce skin or undergo cosmetic or elective surgery.

The mainstay of treatment is intralesional steroids. Corticosteroids have been shown to decrease fibroblast collagen synthesis. Triamcinolone acetonide or diacetate 10 mg/mL, 25 mg/mL, or 40 mg/mL can be injected into the lesion, usually with an additional local anesthetic. Initial injection should be limited to 10 mg/mL, since dermal atrophy and hypopigmentation can occur in certain persons. Multiple injections can be made to the same area over intervals of 6-12 weeks to attain the desired effect. Corticosteroids help to flatten the keloid but do little to decrease its width.

Silicone gel or occlusive sheeting has also been used to help decrease keloid size and prevent further development.^[7]Sheets of these gels, which are commercially available, are applied to the keloid lesion 12-24 hours a day for 6 weeks to 6 months. The mechanism is unclear; however, many theories have been postulated, including increased hydration, increased temperature, and electrical field development providing improvement.

Surgical excision is also an option but, by itself, is associated with a 50-100% recurrence rate and therefore should never be used alone as therapy. Additional modalities of intraoperative or postoperative steroid injections improve the recurrence rate. Preoperative or postoperative low-intensity radiation (900 cGy) has also proved to decrease the keloid formation rate. Other modalities, such as interferon, laser surgery, and intralesional bleomycin, have also been tried with variable results.

A prospective, multicenter study found that intralesional cryotherapy shrank keloid scar volume by an average of 63% at 1-year follow-up. The study, of 27 patients (29 keloid scars), also determined that patient complaints of pain and pruritus were reduced at follow-up. However, 69% of the keloid scars demonstrated persistent hypopigmentation, with the incidence being highest in African American patients, and 24% of the keloids recurred.^[8]

A randomized study by Mourad et al indicated that intralesional cryotherapy is more effective than spray cryotherapy in keloid treatment and requires fewer applications. The study included 50 patients, with a 6-month follow-up.^[9]

A study by Wang et al found that the results of extracorporeal shock wave therapy for keloid scars were comparable to those from intralesional triamcinolone injections. Patients received three treatments of one therapy or the other, with the investigators finding, for example, similar functional outcomes and Patient and Observer Scar Assessment Scale scores between the two groups.^[10]

See also Wound Healing, Widened and Hypertrophic Scar and Keloid and Hypertrophic Scars.

Nevus sebaceus of Jadassohn

Nevus sebaceus of Jadassohn is a congenital, yellowish plaque seen on the head and neck. While this lesion often is included in tumors of the skin adnexum, it is actually an epithelial nevus. On histopathology, nevus sebaceus of Jadassohn, or verrucous epidermal nevi (some consider a variant), has a papillomatosis appearance with acanthosis, sebaceous hyperplasia and often absent hair follicles. The lesion tends to enlarge and become more warty in appearance with time.

A nevus sebaceus of Jadassohn is shown in the image below.

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Macular benign skin lesion: Nevus sebaceous of Jadassohn.

Tumors may arise in nevus sebaceus over time; however, the majority of tumors are benign. The most common two benign tumors which develop are syringocystadenoma papilliferum and trichoblastoma. Rarely, malignant tumors, predominantly basal cell carcinoma, can develop in nevus sebaceus. Nevus sebaceus lesions tend to be yellowish orange, waxy, hairless plaques. An accelerated growth phase may be observed during adolescence secondary to changes in the hormonal milieu.

The natural history of this lesion includes an evolution from a smooth, featureless lesion into a verrucous, thickened plaque with crusting and ulceration. Complete surgical excision is the treatment of choice.

Seborrheic keratosis

Seborrheic keratosis (SK), also known as seborrheic wart, senile keratosis, and basal cell papilloma,^{[11, 12]}is a benign, noninvasive, hyperplastic epidermal lesion with a somewhat misleading title. No known relationship exists between seborrheic keratosis and sebaceous gland function. The term seborrheic relates to their greasy appearance and prevalence in regions of the body with a high concentration of sebaceous glands (ie, face, shoulder, chest, back). These are the most common benign skin tumors of the middle-aged and elderly populations.

A seborrheic keratosis is shown in the images below.

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Macular benign skin lesions: Seborrheic keratoses of back and trunk.

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Macular benign skin lesions: Seborrheic keratoses of the face.

Seborrheic keratoses usually present as small, flesh-colored, waxy papules that have a "stuck-on" appearance. Epidermal hyperplasia can persist, and exophytic growth can cause the lesions to be raised and appear as a cutaneous horn or wart. They can also become pedunculated and have a stalklike growth. Seborrheic keratoses lesions can occur as solitary or multiple lesions. Multiple keratotic papules that occur on the dorsum of the hands, feet, and legs are another variant of seborrheic keratosis and termed stucco keratosis.

In persons with darker skin, multiple small black or dark-brown waxy papules can develop on the forehead, malar, and neck regions. This variant is called dermatosis papulosa nigra and has a familial predisposition. Older seborrheic keratosis lesions can progress to become dark brown or black, causing some concerning confusion with melanoma. Their elevated position, distinct borders, and greasy appearance give clues to the benign nature even when melanotic.

Seborrheic keratoses may be mildly pruritic, but are often asymptomatic. However, if multiple lesions suddenly erupt, this is called the sign of Leser-Trelatand may be a sign of internal malignancy, particularly gastrointestinal neoplasms.

The exact etiology of seborrheic keratosis is unknown. The lesions exist in varying patterns. Generally, the lesion is exophytic with a base level flat with the epidermis. An increased number of basal cells are typically observed. These form cords or sheets of cells with cysts of keratin (horn cysts). When the cysts communicate with the surface, they are visible as keratin plug-filled pits. This assists in the differential diagnosis when discriminating seborrheic keratosis from melanomas and nevi. All seborrheic keratoses have varying degrees of acanthosis, papillomatosis, and hyperkeratosis. Hyperpigmentation of the basal cells may occur with any type and may further confound the diagnosis.

Irritated seborrheic keratosis are characterized by a predominance of basal cells but with whorling sheets of squamous cells. This squamous metaplasia is a consequence of irritation and requires careful discrimination from basosquamous carcinoma. A dermal lymphocytic infiltrate also may be observed, corroborating the inflamed irritated variation.

Inverted follicular keratosis is an endophytic variant associated with a pilosebaceous follicle. Squamous metaplasia also is frequently present. The inverted geometry of the lesion gives it its name.

A study by Kim et al examined diagnostic differences between verruca plana (VP) and VP-like seborrheic keratosis, finding that the latter has a more scattered distribution than VP and more commonly exhibits a brainlike dermoscopic appearance. The investigators, whose report involved a total of 33 patients, recommended that the two conditions can be distinguished via a diagnostic algorithm employing the Koebner phenomenon, dermoscopic findings, biopsy, and lesion distribution.^[13]

Most patients require no specific treatment for seborrheic keratosis. Close patient surveillance and annual clinical evaluations are recommended. For removal, curettage and cryoablation are the most common treatments. Rarely, malignant lesions (eg, Bowen disease) can arise within seborrheic keratoses or malignancies, such as melanoma, can mimic the appearance of a seborrheic keratosis. When malignancy is suspected or diagnosis is indeterminate, an excision biopsy is required. Withhold wide local excision until malignancy is confirmed.

Go to Seborrheic Keratosis for complete information on this topic.

Actinic keratosis

Actinic keratoses (AK), also known as solar or senile keratoses, are scaly cutaneous papules, patches, or plaques on sun-damaged skin. They are most frequently seen in fair-skinned individuals with a history of chronic sun exposure.

These lesions may present on a patient as young as 20 years but are most commonly noticed in individuals older than 50 years. Men are more affected than women. Persons at increased risk for developing actinic keratoses are those who live in warmer, sunnier climates and those who have outdoor professions or hobbies. Immunosuppressed individuals (typically those with a history of organ transplant or lymphoma, or those receiving psoralen and UVA light treatment) are at high risk of developing actinic keratoses and malignant transformation into squamous cell carcinoma with higher rates of metastasis.

A study by Ferrándiz et al reported that in Spain’s dermatologic outpatient population aged 45 years or older, the prevalence of actinic keratosis is 28.6%. The study also found the rate of actinic keratoses in men and women to be 38.4% and 20.8%, respectively, with 45.2% of patients with the lesions being between ages 71 and 80 years.^[14]

Actinic keratoses may demonstrate certain excrescences of keratin, referred to as cutaneous horns. The rough texture of the lesion imparts to the skin a sandpaper-like consistency. The color may be red, yellow, brown, or gray. Actinic keratoses may bear a clinical resemblance to psoriasis, Bowen disease, or Paget disease. The most important attribute is its premalignant potential. The annual incidence of malignant transformation from actinic keratosis to squamous cell carcinoma is likely less than 1% per year per individual lesion.

Ultraviolet solar damage to epidermal keratinocytes is the most likely origin of this lesion. Other nonsolar sources of epidermal damage that are assumed to cause actinic keratoses are artificial UV light, x-ray irradiation, and exposure to aromatic hydrocarbons. The exposed epidermis experiences a sequence of atrophic, dysplastic, and hyperplastic alterations.

The first line of treatment is prevention. Persons with actinic keratoses must avoid further sun damage by habitual use of high-factor sunscreen with each sun exposure. For direct treatment of an actinic keratosis, various treatments are available. Isolated or single lesions can be treated with cryoablation with liquid nitrogen, curettage, or electrodesiccation with local anesthesia. Multiple lesions can be treated with topical 5-fluorouracil (5-FU). Occasionally, a relatively depigmented spot may remain after topical treatment.

Other treatment options include resurfacing with either laser (carbon dioxide or Erbium:YAG) or dermabrasion. An important benefit of topical therapy is its ability to eliminate subclinical actinic keratoses adjacent to the clinically obvious ones. Excision is generally not necessary. Go to Actinic Keratosis for complete information on this topic.

Bowen disease and Bowenoid papulosis

Bowen disease is considered a synonym for squamous cell carcinoma in situ . In contrast, bowenoid papulosis is a term used when histologic changes of squamous cell carcinoma are found within genital warts. The term bowenoid papulosis, and not Bowen disease or squamous cell in situ, for these cases is generally preferred since the papules typically follow a benign course. In bowenoid papulosis, itching is a common symptom. With vulvar involvement, the labia majora tend to be involved more than the labia minora. The lesions are scaly, crusted, erythematous plaques and may be secondary to an infection with HPV-16 or 18.

In Bowen disease, a scaly red plaque is seen on sun-damaged skin, with the potential to turn into invasive squamous cell carcinoma. Squamous cell carcinoma from Bowen disease tends to be more aggressive than that which has degenerated from actinic keratoses, and metastases occur in as many as one third of patients. Its expression is associated with other skin and internal malignancies. Bowen disease (SCC in situ) on the penis is referred to as erythroplasia of Queyrat.

The hallmarks of Bowen disease are atypical epithelial changes. These include cytoplasmic vacuolization, nuclear hyperchromasia, multinucleated keratinocytes, cell dyskeratosis, increased mitoses, and acanthosis. In addition, the pattern and strata of maturation are altered. The most significant finding is that despite the obvious atypia, the dermal-epidermal interface is preserved.^[3]

Curettage and electrodesiccation traditionally have been used in small lesions; however, recurrence rates have been high. Surgical excision generally has been recognized as the standard treatment. Other techniques include cryoablation and irradiation.

A literature review by Matsumoto et al found immunosuppression to be the only factor posing a statistically significant risk for the recurrence of Bowen disease, although the investigators reported that subclinical tumor extension and occult invasive squamous cell carcinoma, which evidence indicates are common in Bowen disease, could also theoretically be recurrence risk factors. The study also mentioned that limited evidence exists that tumor size, depth of follicular extension, and location are associated with increased recurrence risk.^[15]

Go to Bowen Disease for complete information on this topic.

Sebaceous adenoma

Sebaceous adenoma (SA), also known as sebaceous epithelioma (sebaceoma)^[16]and sebocrine adenoma, is a nodular and lobulated lesion that belongs to a family of benign complex skin adnexal tumors with varying degrees of sebaceous differentiation. Sebaceous adenomas occur in areas in which sebaceous glands predominate; they occur primarily in the head and neck regions but can be present in any hair-bearing region of the body. They are usually small (2-10 mm in diameter), tan,reddish-brown, or yellowish in color and occasionally contain central speckles. Infrequently, they can occur on the trunk or legs and have a polypoid appearance. Basal cell carcinoma is challenging to differentiate from sebaceous adenoma, and diagnostic biopsy is often required.

New eruptions of multiple sebaceous adenoma can sometimes be associated with a visceral carcinoma. Adenocarcinomas of the colon, stomach, duodenum, hematologic system, genitourinary tract, endometrium, and larynx that are associated with multiple sebaceous adenomas are termed Muir-Torre syndrome. The carcinomas associated with Muir-Torre syndrome have a more favorable prognosis than nonsyndromic carcinomas.

The etiology of sebaceous adenomas is unclear, but Muir-Torre syndrome is related to a genetic truncating germline mutation. An autosomal dominant inherited germline mutation in one of the DNA mismatch repair genes, most commonly hMSH2, is associated with the syndrome. It is inherited, with a high degree of penetrance and variable expression, with a male-to-female ratio of 3:2.

Sebaceous adenoma is multilobulated with frequent connection to the surface epidermis. At low-power view, it is sharply demarcated from the surrounding tissue with a proliferation of variously sized sebaceous lobules consisting of central, larger, mature sebaceous cells (sebocytes); peripheral, smaller, undifferentiated, germinative basaloid cells; and transitional cells.

The sebocytes contain pale-staining, foamy-to-bubbly cytoplasm, and central, crenated, hyperchromatic nuclei. The smaller, germinative cells contain round-to-oval, vesicular nuclei and basophilic cytoplasm. The transitional cells show more eosinophilic cytoplasm. The ratio of basaloid and transitional cells to sebocytes varies but is traditionally defined as sebaceous adenoma if 50% or more of the cells are sebocytes. The cellular lobules of sebaceous adenoma sometimes comprise ductal structures with holocrine secretion, which may result in occasional cystic degeneration or formation of intralesional cysts. Nuclear hyperchromatism, prominent nucleoli, and mitotic activity are rarely observed in sebaceous adenoma lesions.

Sebaceous adenoma has no malignant potential. Excisional biopsy is recommended for diagnostic distinction if suspicion of basal cell carcinoma exists.

Go to Sebaceous Adenoma for complete information on this topic.

References

Pigmented Lesions

Types of macular skin-colored lesions are described in the image below.

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Macular skin-colored lesions.

Nevus sebaceus of Jadassohn

While this lesion often is included in tumors of the skin adnexum, it is actually an epithelial nevus. Nevus sebaceus of Jadassohn, or verrucous epidermal nevi (some consider a variant), is a hamartomatous lesion expressing elements of sebaceous and apocrine glands, defective hair follicles, acanthosis, and papillomatosis. It is a congenital lesion, usually present on the scalp and face. The lesion tends to enlarge with time.

A nevus sebaceus of Jadassohn is shown in the image below.

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Macular benign skin lesion: Nevus sebaceous of Jadassohn.

The malignant potential of this lesion has been estimated to be 10-50%. Degeneration into basal cell carcinoma is most common; however, other malignancies include adnexal tumors and squamous cell carcinoma. The color tends to be yellowish orange. The lesion is slightly raised, with a waxy appearance. When located on the scalp, it is devoid of hair. An accelerated growth phase may be observed during adolescence secondary to changes in the hormonal milieu.

The natural history of this lesion includes an evolution from a smooth featureless lesion into a verrucous, thickened plaque with crusting and ulceration. This is believed to be a congenital lesion. Microscopically, many sebaceous glands in a vascular stroma with abortive hair follicles are observed. Some of the sebaceous glands communicate with the surface directly. Complete surgical excision is the treatment of choice.

Seborrheic keratosis

Seborrheic keratosis (SK), also known as seborrheic wart, senile wart, and basal cell papilloma,^{[11, 12]}is a benign, noninvasive, hyperplastic epidermal lesion with a somewhat misleading title. No known relationship exists between seborrheic keratosis and sebaceous gland function. The term seborrheic relates to their greasy appearance and prevalence in regions of the body with a high concentration of sebaceous glands (ie, face, shoulder, chest, back). These are the most common benign skin tumors of the middle-aged and elderly populations.

Seborrheic keratosis is shown in the images below.

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Macular benign skin lesions: Seborrheic keratoses of back and trunk.

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Macular benign skin lesions: Seborrheic keratoses of the face.

Seborrheic keratosis has various clinical manifestations. In persons with light skin, most lesions present as small, flesh-colored, waxy papules that have a "stuck-on" appearance. Epidermal hyperplasia can persist, and exophytic growth can cause the lesions to be raised and appear as a cutaneous horn or wart. They can also become pedunculated and have a stalklike growth. Seborrheic keratosis lesions can occur as solitary or multiple lesions. Multiple keratotic papules that occur on the dorsum of the hands, feet, and legs are another variant of seborrheic keratosis and termed stucco keratosis.

These lesions are usually asymptomatic. However, if multiple lesions suddenly occur with or without pruritus, this may be a sign of internal malignancy. Although a rare occurrence, a sudden eruption of seborrheic keratosis lesions that is correlated with internal malignancy is called the Leser-Trelat sign. The validity of the association has recently come into question, but an abrupt development of seborrheic keratoses in a younger person should be investigated for a possible gastrointestinal neoplasm.

The exact etiology of seborrheic keratosis is unknown. The lesions exist in varying patterns. Generally, the lesion is exophytic with a base level flat with the epidermis. An increased number of basal cells are typically observed. These form cords or sheets of cells with cysts of keratin (horn cysts). When the cysts communicate with the surface, they are visible as keratin plug-filled pits. This assists in the differential diagnosis when discriminating seborrheic keratosis from melanomas and nevi. All seborrheic keratoses have varying degrees of acanthosis, papillomatosis, and hyperkeratosis. Subtypes exist. Hyperpigmentation of the basal cells may occur with any type and may further confound the diagnosis.

Irritated seborrheic keratosis is one subtype, characterized by a predominance of basal cells but with whorling sheets of squamous cells. This squamous metaplasia is a consequence of irritation and requires careful discrimination from basosquamous carcinoma. A dermal lymphocytic infiltrate also may be observed, corroborating the inflamed irritated variation.

Inverted follicular keratosis is an endophytic variant associated with a pilosebaceous follicle. Squamous metaplasia also is frequently present. The inverted geometry of the lesion gives it its name.

Most patients require no specific treatment for seborrheic keratosis. Close patient surveillance and annual clinical evaluations are recommended. For removal, curettage and cryoablation are the most common treatments. Alternatively, seborrheic keratoses can be surgically excised to address cosmesis, pruritus, inflammation, and pain. Rarely, malignant lesions (eg, Bowen disease) can arise within seborrheic keratoses. When malignancy is suspected or diagnosis is indeterminate, an excision biopsy is required. Withhold wide local excision until malignancy is confirmed.

Go to Seborrheic Keratosis for complete information on this topic.

Actinic keratosis

Actinic keratoses (AK), also known as solar or senile keratoses, are scaly cutaneous lesions that arise from a cumulative effect of sun exposure. These lesions appear as rough, scaly, erythematous papules or plaques that occur on exposed skin surfaces (eg, face, hands, ears, neck scalp, legs, and sometimes thorax). They are typically seen in fair-skinned individuals with a history of chronic sun exposure.

These lesions may demonstrate certain excrescences of keratin, referred to as cutaneous horns. The rough texture of the lesion imparts to the skin a sandpaper-like consistency. The color may be red, yellow, brown, or gray. Actinic keratosis may bear a clinical resemblance to psoriasis, Bowen disease, or Paget disease. The most important attribute is its premalignant potential. The annual incidence of malignant transformation from actinic keratosis to squamous cell carcinoma varies from 0.25-29.0% per year per individual lesion.

The actinic changes are limited to the interfollicular epidermis; the follicles and the intraepidermal portion of appendageal ducts are spared. The lower layers of the epidermis are the most affected. The stratum corneum undergoes parakeratosis and gives rise to cutaneous horns. The granular layer generally is obliterated except near follicle units. Tonguelike projections of the atypical epidermis may project into the dermis but do not violate the basement membrane. In addition, not infrequently, the basal cells experience some reactive proliferation along with the recruitment of melanocyte activity. These features give actinic keratoses a heavily pigmented appearance and the appearance of a basal cell malignancy. Actinic (solar) changes of the underlying dermis also may occur, and their presence helps in making the diagnosis.^[3]

Other treatment options include resurfacing with either laser (carbon dioxide or Erbium:YAG) or dermabrasion. Topical steroids may be used in tandem with 5-FU to attenuate the inflammatory response. An important benefit of topical therapy is its ability to eliminate subclinical actinic keratoses adjacent to the clinically obvious ones. Excision and primary closure is an uncommon option for actinic keratosis. However, it can be used when lesion diagnosis or progression is in question and, therefore, a full-thickness skin excision biopsy is likely to yield the best diagnostic results.

Go to Actinic Keratosis for complete information on this topic.

Bowen disease

Originally described by Bowen in 1912, these lesions predominantly involve skin that is not exposed to the sun (ie, protected). Classically, Bowen disease, also known as carcinoma in situ and squamous intraepidermoid neoplasia, involves the genitalia. Itching is a common symptom. With vulvar involvement, the labia majora tend to be involved more than the labia minora. The lesions are scaly, crusted, erythematous plaques. This lesion is considered to be a carcinoma in situ without spread beyond the dermal-epidermal junction. Over time, as many as 10% of these lesions experience invasion. Efforts have been made to correlate arsenic and Bowen disease. The results have been inconclusive at best.

Squamous cell carcinoma from Bowen disease tends to be more aggressive than that which has degenerated from actinic keratoses, and metastases occur in as many as one third of patients. Its expression is associated with other skin and internal malignancies.

When a lesion of similar clinical and histologic appearance is found in a sun-exposed location, it is referred to as an actinic keratosis of the bowenoid type. Similarly, when found on the mucous membranes, particularly the glans of the penis, this lesion is referred to as erythroplasia of Queyrat.

Go to Bowen Disease for complete information on this topic.

Sebaceous adenoma

Sebaceous adenoma (SA), also known as sebaceous epithelioma (sebaceoma)^[16]and sebocrine adenoma, is a nodular and lobulated lesion that belongs to a family of benign complex skin adnexal tumors with varying degrees of sebaceous differentiation. Sebaceous adenomas occur in areas in which sebaceous glands predominate; they occur primarily in the head and neck regions but can be present in any hair-bearing region of the body. They are usually small (2-10 mm in diameter), smooth surface lesions that occur usually as macules but also can have papular formations. They commonly are tan to reddish-brown to yellowish in color and occasionally contain central speckles. Infrequently, they can occur on the trunk or legs and have a polypoid appearance. Basal cell carcinoma is challenging to differentiate from sebaceous adenoma, and diagnostic biopsy is often required.

Sebaceous adenoma has no malignant potential. Excisional biopsy is recommended for diagnostic distinction if suspicion of basal cell carcinoma exists.

Go to Sebaceous Adenoma for complete information on this topic.

References

Subepidermal Lesions

Types of subepidermal lesions are described in the image below.

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Subepidermal lesions.

Keratinous cyst

Benign subdermal cysts that pathologically collect normally skin surface secreted materials have long had a number of labels and resultant confusion in the terminology. Descriptors such as keratinous cysts, sebaceous cyst,^[17]wen, atheroma, steatoma, epidermoid/epidermal inclusion cyst [EIC], pilar cyst, and trichilemmal cyst have been previously used interchangeably but not always correctly. Essentially, the two most common types of subdermal cysts are keratinous cysts and sebaceous cysts. Keratinous cysts trap keratin within a pseudo-epithelium sack whereas sebaceous cysts trap sebum produced from apocrine glands. Keratinous cysts are more common and have also been described as epidermoid or epidermal inclusion cysts. Cornified epithelium, a very well demarcated granular layer, and multiple lamellae of keratin without calcification characterize these epidermoid cysts. (See the image of keratinous cyst, below.)

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Subepidermal lesion: Keratinous cyst (epidermal inclusion cyst).

These lesions can be found in almost any location. Variations found on the extremities, particularly the fingers and toes, may be a traumatic form of inclusion. In contrast, the pilar cyst occurs almost exclusively on the scalp. Its hallmark is a trichilemmal keratinization pattern. This pattern is different from the lamellated form because the well-defined granular layer is lacking.

Additionally, focal calcification is common. Amino acid analysis of both types of cysts demonstrates that the epidermoid cyst is most likely to originate from the infundibular portion of hair follicles. Another conclusion is that the trichilemmal cyst tends to have an origin from the epithelium of the hair follicle that is at or distal to the level of sebaceous ducts. In this location, no typical granular layer is present.

The treatment of choice is excision. However, when the cyst is acutely inflamed, incision and drainage is frequently the best approach. Following the resolution of the infection, the lesion is excised. The lesion nearly always is accompanied by a central communicating punctum, which is frequently obvious in the skin surface. They must be excised with an ellipse of skin in continuity. Other techniques of removal include punch biopsy aspiration followed by curettage and avulsion of the cyst wall.

Dermoid cyst

Dermoid cysts are mobile, firm, subepidermal lesions that are often present at birth and occur most commonly on the face and scalp. The lesions are flesh colored and do not transluminate, which differentiates them from the similarly presenting encephalocele. They frequently occur along the superior lateral periorbita but can present anywhere along the lines of embryonic closure as well as along the cervical midline and mastoid area. Rarely, they can occur along the spine, penis, testes, and floor of mouth. In 50% of dermoids, a dermoid sinus (or ‘pit’) is present. They are a cutaneous defect or blind passage that is usually located centrally on the dermoid. A dermoid-appearing lesion with a central pit with protruding hairs is pathognomonic of a dermoid cyst.

A dermoid cyst is a hamartomatous tumor that is usually evident at birth and is caused by a disorder of embryonic epithelium growth at embryonic fusion sites during craniofacial development. Dermoid cysts are a result of the sequestration of skin along the lines of embryonic closure.

The cyst wall is composed of squamous epithelium with associated adnexal structures such as hair follicles and sebaceous glands. These cysts can contain structures from one or more of the 3 primary embryonic germ layers: skin, hair, and teeth.

Differentiation from encephaloceles is critical when assessing for craniofacial dermoid cyst. When a dermoid cyst is present along the facial midline, a CT scan or MRI is essential to distinguish the nature of the lesion and to determine the presence and possible intracranial extension.

Complete resection of a dermoid cyst is curative. If a dermoid cyst is incompletely excised, epithelial remnants might lead to recurrence. Lesions located near the hyoid bone may be impossible to differentiate from a thyroglossal duct cyst intraoperatively. These lesions should be treated with the Sistrunk procedure to avoid the possibility of recurrence, unless frozen section confirms that the resected mass is not a thyroglossal duct cyst.

Go to Dermoid Cyst for complete information on this topic.

Neurofibroma

Neurofibromas are flesh-colored, exophytic papules that can occur anywhere in the body. They can vary in their prominence in the skin. Size also can vary greatly, from small lesions 2-3 mm in diameter to larger growths several centimeters in diameter.

Neurofibromas can present as solitary lesions or as multiple lesions. Multiple neurofibromas can be associated with neurofibromatosis (usually neurofibromatosis type 1 [NF-1], also called von Recklinghausen disease of the skin). Patients with NF-1 also present with classic brown-colored macules called café-au-lait macules. Lesions are soft and can be invaginated when compressed with a fingertip (known as the buttonhole sign). Cutaneous neurofibromas usually remain asymptomatic, but neurofibromas that develop in major peripheral or central nerves can cause motor or sensory dysfunction.

Neurofibromas are composed of Schwann cells, fibroblasts, perineurial cells, masts cells, and axons embedded in extracellular matrix. The lesions present as discrete but unencapsulated tumors. A neurofibroma is composed of interlacing fascicles of Schwann cells that have irregular, wavy, elongated nuclei. The nerve’s perineurium is disrupted, which suggests a breakdown of appropriate signaling between Schwann cells, fibroblasts, and perineurial cells. The part played by each cell type in neurofibroma formation is unclear. On gross inspection, the neurofibroma tumor usually has small fibers coursing through its substance.

Cutaneous neurofibromas can be excised if they cause deformation of surrounding tissues or have become symptomatic. In addition, any lesions suspicious for malignant transformation, evidenced by rapid growth or pain, should also be surgically excised.

Individuals with NF-1 harbor a 7–13% lifetime risk of developing a malignant peripheral nerve sheath tumor, which usually arises in preexisting plexiform or focal subcutaneous neurofibromas. Using the normal clinical signs to evaluate for a potential malignant or transforming premalignant lesion is challenging. In patients with NF-1, new lesions develop and grow continually, so close surveillance is recommended. Neurofibroma can occur in major peripheral nerves, which can cause disruption of nerve function.^[18]Neurofibromas commonly occur within the substance of the nerve, which creates a severe challenge to remove the tumor without causing further nerve dysfunction. Internal neurolysis and nerve grafting are performed as indicated for neurofibromas resection.

Schwannoma

Schwannoma, or neurilemmoma, usually presents as a solitary, painless, flesh-colored lesion of variable size. The lesions are located subepidermally but exhibit protuberance in skin, depending on size and subcutaneous position. Occasionally, a schwannoma may elicit a Tinel sign (tapping of the nerve elicits a tingling, “pins and needle” sensation) if a peripheral nerve is significantly compressed. The pathogenesis of schwannomas is unclear.

Histologically, schwannomas are rounded and encapsulated. They are mostly characterized by the presence of plump S-shaped spindle cells and myxoid stroma. The spindle cells show marked tendency to palisading and irregular configuration, with stellate cells also present in the myxoid stroma. The lesions are also populated with chronic inflammatory cells and hyalinized blood vessels.

If the lesions cause significant compression on peripheral nerves, pain and motor dysfunction can result. These are indications for resection. Unlike neurofibromas, schwannomas are easily dissected from their associated nerves, given their encapsulated nature.

Lipoma

Lipomas are the most common subcutaneous soft tissue tumors, with an annual incidence of nearly 1 in 1000 persons. Lipomas are benign aggregates of slowly growing adipocytes. These tumors usually occur on the trunk and extremities but can occur anywhere on the body. Solitary lesions are the most common, but multiple lesions can occur, with higher frequency in young males.

A lipoma is shown in the image below.

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Subepidermal benign lesion: Lipoma of posterior neck.

Lipomas present as soft, rubbery masses that can sometimes be well-circumscribed and other times have indistinct palpable borders. They are usually not painful or tender, unless they grow to compress an underlying nerve. They are noncompressible and do not transluminate, making them easily distinguishable from a fluid-filled cyst. Most lipomas appear to be small, smooth protuberances of the skin (1-2 cm), but they can present larger than 20 cm in diameter and up to several kilograms.

The etiology of lipsomas is unclear. The tendency to develop a lipoma is not necessarily hereditary, although hereditary conditions, such as familial multiple lipomatosis, may lead to lipoma development. Controversy exists over the so-called posttraumatic lipoma (reported cases in which minor injuries are alleged to have triggered the growth of a lipoma). However, whether the trauma caused the lipoma or simply led to the detection of a preexisting lipoma is unclear.

Lipomas are benign mesenchymal tumors derived from adipocytes. Microscopically, they are composed of fatty tissue with interlacing muscle fibers. Fine-needle aspiration biopsies of a lipoblastoma contain multivacuolated lipoblasts, myxoid areas, and a plexiform capillary network.Several variants have been described. Adenolipomas, a variation of lipomas that may occur in the breast, often have a marked fibrotic component. They are best regarded as hamartomas. Angiolipomas contain many small vessels.

Small, asymptomatic lipomas require no treatment. However, definitive treatment is surgical excision. Indications to excise lipomas vary but are largely performed for cosmetic reasons; to evaluate their histology, particularly when liposarcomas must be ruled out; when they cause symptoms; or when they grow and become larger than 5 cm (because larger lipomas hold a small but increased risk of liposarcoma development). In certain cases, liposuction has been used to remove large lipomas in anatomically sensitive locations.

Inverted follicular keratosis

Inverted follicular keratosis is believed to be an inflammatory variant of seborrheic keratosis. This is an acquired lesion, similar to seborrheic keratosis. It commonly is found on the face and sun-exposed areas of elderly patients. Typically, this lesion is located on the upper eyelid. Anatomically, it represents an upside-down or endophytic process within the epithelium of a pilosebaceous follicle. The lesions tend to be single and present as a papule or nodule.

The hallmarks of this lesion are plentiful squamous eddies. A papillomatous and acanthotic appearance is found reliably. The margins are discrete and lack the inflammatory component found in keratoacanthoma. Since this lesion is benign, simple excision is adequate.

Trichoepithelioma

Trichoepithelioma is an uncommon benign lesion. It is generally pink to flesh-colored. It is frequently multiple and is not ulcerative. These lesions tend to be recapitulations of hair follicles. Initially, they appear during adolescence. Typical areas for this lesion are the central face and scalp and, less commonly, the trunk and neck. A certain familial incidence exists. While these lesions tend to be multiple, solitary lesions can occur. In general, lesions are less than 8-10 mm.

This tumor is characterized by collections of basal cells that are similar to the hair bulb. It is also remarkable for the presence of numerous horn cysts. Both of these tend to be accompanied by an inflammatory stroma that is fibrous. Occasional calcifications and melanin granules also can be found. The abortive hair shafts and follicles are another characteristic of trichoepithelioma. Occasionally, a differential diagnosis from a basal cell carcinoma can be difficult to determine. The most significant distinguishing features are a papillary frondlike orientation of basaloid cells and epithelial tracts consisting of more than one layer of basaloid cells.

Because of the multiplicity of the lesions, the treatment can be difficult; occasionally, palliation is the only achievable goal. Techniques involving cryoablation, dermabrasion, and trichloroacetic acid help control individual lesions and groups of lesions. Unfortunately, any treatment short of complete surgical excision results in the persistence or continued growth and enlargement of these lesions.

Trichilemmoma

Trichilemmoma is a benign tumor with a pattern of globular glycogen-rich clear cells. Occasionally, keratinization in the center is identified grossly. Trichilemmommas can be related to Cowden disease, a multiple hamartoma syndrome with papillomas of the oral mucosa, acrokeratoses, and, most significantly, malignant tumors of the breast, thyroid, and GI tract. Additionally, a rare carcinoma variant of trichilemmoma is known as trichilemmal carcinoma.

Pilomatrixoma

Pilomatrixoma, which is also known as pilomatricoma and the calcified epithelioma of Malherbe, is a variation of the epidermal cyst and should be included in the differential diagnosis. It is a relatively uncommon tumor and tends to occur on the neck, head, and upper extremities of children and young adults. Typically, it presents as a solitary, hard subcutaneous nodule, with attachment to the skin and occasional episodes of inflammation and pain.

The lesion is a nodular subepidermal tumor with elements of hair matrix. Intensely basophilic-staining cells are found peripherally, and eosin-favoring cells are near the center. Also present are shadow or ghost cells, which are cells with eosinophilic cytoplasm with what appear to be vacuolated areas where the nuclei formerly were present. Calcificiation is common.

Simple surgical excision is the cornerstone of treatment. The lesion has a friable capsule. While extremely rare, a malignant counterpart has been named the malignant pilomatrixoma or pilomatrix carcinoma.

References

Benign Dermatoses

Psoriasis

Psoriasis is one of the most common dermatoses (see the image below).^[19]Its prevalence varies from 0.5-3% of the US population. It appears as a chronic, bilaterally symmetric, erythematous plaquelike lesion with a silvery scale. The lesions classically are located over the extensor surfaces, including the elbows, knees, back, buttocks and scalp. Confluent generalized lesions also may occur. A multifactorial inheritance pattern is suggested. These factors include familial clusters, trauma, streptococcal infection, and endocrine changes. However, most cases occur without a precipitating event.

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Psoriasis.

Psoriasis is characterized by exceedingly rapid turnover of skin. This occurs on the order of 7-10 times faster than the normal 28-day cycle of skin renewal. The histomorphologic characteristics include parakeratosis and acanthosis. Characteristics but not pathognomonic findings are spongiform pustules of Kogoj and Munro microabscesses. A spongiform pustule is a local subcorneal neutrophil collection while Munro microabscesses are intracorneal neutrophil collection.

Psoriasis occasionally is associated with other systemic illnesses, particularly psoriatic arthritis. Psoriatic arthritis occurs in approximately a third of patients with psoriasis.

Changes of the nails include onycholysis, pitting, thickening, oil spots and crumbling. At some point, as many as one third of patients may develop a Köbner phenomenon, which is a condition in which new insult or skin trauma is greeted with a development of psoriatic lesions. Greater risk of postsurgical infections also is found, due to a higher-than-normal bacterial colonization of the skin and psoriatic lesions.

Therapy consists of topical steroids, vitamin D3 analogs, tars, and phototherapy. More severe forms of psoriasis can be treated with systemic medications such as immunosuppressants and biologics.^{[19, 20, 21, 22, 23]}Prior to elective procedures, psoriasis should be clinically optimized.

A study by Norlin et al of 2646 patients with psoriasis found that 18% of these patients had moderate to severe psoriasis that persisted even with ongoing systemic therapy. Compared with patients with lower-severity psoriasis, those with persisting moderate to severe psoriasis tended to be younger, have a higher body mass index, suffer from psoriatic arthritis, and more often engage in smoking.^[24]

Discoid lupus erythematosus

Discoid lupus erythematosus and systemic lupus erythematosus are clinically distinct entities. Discoid lupus is a chronic, relatively common dermatitis that is more common in women than in men. It presents as erythematous plaques that vary from an atrophic to a hyperkeratotic appearance in the region of the face, scalp, neck, extremities, and trunk.^[25]It is usually exacerbated by sunlight.^[26]

Histologically, these lesions are characterized by a hyperkeratosis with some atrophy of the epidermis and degeneration of the basal layer. However, none of the histologic findings are pathognomonic. A band of lymphocytic infiltrates can be found along the dermal-epidermal junction. Melanin pigmentation may be discontinuous in extending to the papillary dermis. The follicles and other adnexa tend to be surrounded with an intense lymphocytic infiltrate. Periodic acid-Schiff (PAS) stains demonstrate thickening of the epidermal basement membrane; however, this is nonspecific.

Immunofluorescence of immunoglobulin G, immunoglobulin M, immunoglobulin A, and complement demonstrates a positive lupus band test. This occurs predominantly in the basement membrane and is found in the clinically uninvolved non–sun-exposed skin. Treatment for discoid lupus includes steroids and antimalarial drugs such as hydroxychloroquine.^{[26, 27]}

Despite efforts to control the disease topically, scarring and healing of visible portions of the face may require the attention of a plastic surgeon. Classic reconstruction efforts have been successful using either a full-thickness skin graft or adjacent local flaps after medical control is achieved. As with all chronic scarring processes, the possibility of malignant degeneration into a squamous carcinoma has been reported. Daily protection from sun exposure is essential.^[26]

Morphea

In cutaneous morphea, the lesions often are defined on the trunk or an extremity in a dermatome. The lesions appear to be violations that are lilac-colored and isolated. Occasionally, pruritus is associated with the disease. Morphea may be widespread and chronic, and it may involve the digits of the hand . Histologically, the significant change appears to be in the amount of collagen found. This collagen deposition is indistinguishable from normal collagen levels. The type and proportion of collagen (type 1 or type 3) are similar to those found in the healthy dermis.

When linear morphea affects the face and paramedian forehead causing hemifacial atrophy it is known as morphea en coup de sabre. It manifests as atrophy of the skin, subcutaneous tissues, muscle, and bone. Occasionally, the process resolves spontaneously, but it can be unpredictable in its clinical course. This condition is observed while it remains destructive and progressive. In its burnout quiescent phase, the treatment of choice is self-tissue augmentation.

Neurofibromatosis

Also known as Von Recklinghausen disease, this is a relatively common disorder with a frequency of approximately 1 in 3000.^[28]Nearly 50% of patients with neurofibromatosis have a definable autosomal dominant transmission pattern.^[28]The remaining cases appear to be due to mutations. While the penetrance is 100%, the expressivity is variable.

Clinical patterns include multiple neural tumors anywhere on the body. Findings including six or more café au lait macules (>0.5cm in prepubertal children, >1.5 cm in postpubertal children), axillary or inguinal freckling, optic gliomas, lisch nodules (pigmented iris hamartomas), and sphenoid wind dyplasia. Patients also have an increased risk of tumors including optic glioma, malignant peripheral nerve sheath tumor, neurosarcoma, juvenile myelomonocytic leukemia, rhabdomyosarcomas.

Surgical treatments include excisions of symptomatic lesions or the accompanying soft tissue facial deformity. Frequently, because of critical and eloquent locations, removal of the masses is subtotal. While malignant degeneration is recognized in multiple neurofibromas, practically, it is unfeasible to excise all lesions in most patients. When masses are found at the cerebellopontine angle, this creates the clinical condition recognized as an acoustic neuroma.

Clinical course is difficult to predict. However, to the plastic surgeon, the most significant manifestations of the disease are the multiple and varied facial deformities. The therapeutic plan essentially involves excising the lesions that are bothersome or visible. Occasionally, only palliative partial resection can be accomplished. Bony involvement of the facial skeleton also creates a difficult problem. Total satisfactory excision of all symptomatic lesions is seldom accomplished.

Xeroderma pigmentosum

Xeroderma pigmentosum is an autosomal recessive disorder in which the individual is left essentially unprotected from ionizing radiation. The mechanism is well understood and involves the absence of certain DNA repair mechanisms for pyrimidine dimers that have been formed following actinic radiation change. Within the patient, ultraviolet exposure develops the full spectrum of actinic injury. Basal and squamous cell carcinomas and malignant melanomas may be found. Additionally, pigmentary changes and hyperkeratoses are ubiquitous within the skin surface.

Mainstays of therapy include protection from solar radiation, topical chemotherapeutic agents such as 5-FU, excision or dermabrasion of involved skin, and vigilant surveillance of all premalignant and malignant lesions. These strategies have been successful in expanding the lifespan beyond early adulthood for patients with xeroderma pigmentosum.

Dystrophic epidermolysis bullosa

This is a rare hereditary disease of epithelial, surfaces including skin and mucosa^[29]caused by a defect in collagen 7. Its most obvious clinical characteristic is a bullous formation in the skin following essentially minimal trauma.^{[29, 30]}This heals with scarring and aggressive contracture. The incidence is approximately 1 in 300,000 live births.

Of greatest clinical significance is the involvement of children's hands. A continued unrelenting cycle of injury followed by scarring and contracture with creeping epithelialization occurs until the interdigital and web spaces are completely encased in an epidermal cocoon. A progressive atrophic scar results in the stepwise and eventual total loss of use of the digits of the hand.

While recognizing that variable clinical expression of this disorder exists, all individuals with dystrophic epidermolysis bullosa have some degree of functional loss. While the mucosal services of the hypopharynx and esophagus also are involved, they appear to be less significantly involved clinically than the exposed surfaces of the hands and fingers.

While no medical or surgical cure exists for this affliction, some modicum of benefit has been discovered with the vigorous use of topical steroid therapy. Surgical treatments are frustrating, and one of the larger series of these treatments has been developed at the Ormond Street Hospital for Children in London. In this facility, a highly specialized multidisciplinary approach is used in the perioperative setting to protect all of the epithelial tissues.

One significant clinical contribution from these large series has been the knowledge that within the epithelial cocoon, the digits remain surprisingly mobile, with a greater than expected active and passive range of motion. Skin grafts are used to close the intervening epithelial defects, and they actually heal quite normally. Generally, the donor site heals in an essentially typical fashion.

Another significant clinical observation has been the chronically colonized condition of the blister fluid with beta-hemolytic streptococci. Despite early excellent successes with surgical management, the final common pathway appears to be a recrudescence of the recurrent minor trauma and epithelial encasement. For this reason, treatment is considered only temporary.

Cutis laxa

Cutis laxa is a rare disorder that is principally in the skin but also can involve other organ systems. The pathologic defect consists of degeneration of the elastic fibers of the dermis.^[31]Autosomal dominant, autosomal recessive, and x-linked recessive and acquired forms have been recognized.

Non-cutaneous manifestations include chronic obstructive pulmonary disease (COPD), bladder and GI diverticulosis, great vessel aneurysms, and cardiac abnormalities. These many manifestations, particularly the cardiopulmonary involvement, severely limit the patient's operative candidacy.

Clinically, patients with cutis laxa are recognized by the extreme elasticity of their skin, which permits loose hanging skin. Microscopically, a decrease in the number of fibers, as well as their size, is noted. While the skin is loose, it is not any more fragile. It heals essentially normally and has relatively little elasticity. In some operative candidates, satisfaction can be found with operative correction of the excessive redundant skin. In particular, rhytidectomy has been performed with some satisfaction. Repeated excisions of redundant skin can be beneficial in some patients.

Cutis hyperelastica (Ehlers-Danlos syndrome)

This entity is common to contortionists in that the hyperelasticity and flexibility of the skin and joints permit the achievement of grotesquely exaggerated positions.^[32]There are numerous types of Ehlers-Danlos syndrome with inheritance patterns including autosomal dominant, autosomal recessive and X-linked recessive. Depending on the type, defects in these patients include defects in collagen 5, collagen 3, lysyl hydroxylase (thereby preventing cross-linkage), or the procollagen-N -peptidase enzyme deficiency (impairing the aggregation of collagen fibers) among others.

All patients have variable fragility of the skin and blood vessels. Their response to injury is poor, with easy bruising and blister and hematoma formation following minimal shear injury. Similarly, they heal very poorly. Simple lacerations result in large separated wounds that tend to retract. The overall tensile strength in the skin is poor and fails to adequately hold suture material.

An important distinction remains between Ehlers-Danlos syndrome (cutis hyperelastica) and cutis laxa. Elective procedures should be discouraged in patients with Ehlers-Danlos syndrome because of the poor healing of the skin. The elasticity has some variance in that younger individuals appear to have normal elasticity, but with aging, the skin becomes more relaxed and redundant.

Necrobiosis lipoidica diabeticorum

Necrobiosis lipoidica diabeticorum is a plaquelike, depressed, atrophic yellow lesion typically found in patients with diabetes (see the image below).

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Necrobiosis lipoidica diabeticorum.

It has a strong association with diabetes and actually may be a clinical prodrome of the onset of the disease systemically.^[33]It rarely is found in locations other than the lower extremities and seldom is found in the absence of diabetes. The lesion tends to progress from a red plaque-like area to one with atrophy that occasionally may ulcerate. Controlling the diabetes does not tend to modulate the clinical outcome of this lesion. Successful management occasionally has required resection and skin grafting of the involved areas.

Acne vulgaris

The word acne is a derivative of the Greek word acme, referring to the prime of life. This corresponds with the usual age of onset of acne, which tends to be in early puberty. More than 80% of adults have had some experience with acne.^[34]Clinically significant lesions consist of an open comedone, which corresponds to the term blackhead.^[34]Closed comedones correspond to whiteheads. Additional inflammatory lesions include pustules, papules, and cysts .^[34]The most aggressive forms of acne have chronic scarring coexisting with active inflammatory foci.

The fundamental unit of involvement is the pilosebaceous system. The location of acne manifestation is defined by the distribution of the pilosebaceous glands. Adolescence causes endocrine maturation of the adnexal elements, resulting in an accumulation of cellular products within the ductile systems. In addition to the cellular products are coexistent microorganisms, most commonly Propionibacterium acnes and Staphylococcus epidermidis.

In discussing the pathogenesis, the most common pathophysiologic condition is believed to be that of increased end-organ sensitivity to androgen stimulation. The organism Pacnes also has been demonstrated to produce a lipase that hydrolyses lipases to free fatty acids. These free fatty acids have been shown to produce inflammation in comedones when applied to rabbit ears or when injected intradermally in humans.

Additionally, P acnes may have complement activation contributions, further increasing the inflammation. Additionally, a pathophysiologic cycle occurs with respect to the keratinized layer of the sebaceous duct. In normal uninflamed ducts, the keratinized epithelium is loosely adherent and easily separates up to the skin surface as it is regenerated from deeper layers. In the acne condition, these follicular cells are cohesive and coalesce to form retention hyperkeratosis, a physical obstruction to the pilosebaceous unit. This leads to back pressure and the leakage of sebum and bacteria into the dermis across the epithelialized surface, stimulating the inflammatory response.

Clinically, the features of acne can have many forms. Closed comedones are approximately 1-3 mm in diameter. Open comedones are approximately 2-5 mm in diameter, and this dark core is a packed combination of melanin, oxidized lipids, keratin, and bacteria. Occasionally, several adjacent units may coalesce and create deep dermal abscesses.

The treatment objectives are decreasing the count of P acnes, decreasing the hyperkeratosis, and decreasing the sebum production. Topical antibiotic preparations and those with systemic effect have been used, as have sebum antagonists. Benzoyl peroxide is a common bactericidal with a free oxygen radical moiety as its active mechanism. It simultaneously decreases the organism concentration and the amount of free fatty acids available on the surface. Because it is a keratolytic, enhanced global skin blood flow is recognized. Transretinoic acid (tretinoin) is a topical preparation with established efficacy.^[35]The primary mechanism is to decrease retention hyperkeratosis by limiting cohesiveness of the keratinized layer. This regimen results in the thinning of the stratum corneum to approximately one half of its usual thickness.

Topical tetracycline, erythromycin, and clindamycin also have been used.^[34]The pustular and papular forms respond better to these antibiotics than the cystic or comedonal forms. An oral tetracycline is also very efficacious.

Isotretinoin (13-cis -retinoic acid) has revolutionized treatment for severe cystic or scarring acne. This compound reduces sebaceous gland size by 50% and function by more than 90%. It inhibits keratinocyte proliferation and permits thinning of the epidermis. During a regimen, serum lipoproteins should be monitored, since as many as 25% of patients may develop hypertriglyceridemia. Isotretinoin is a known teratogen, and adherence to the government controlled iPledge program is necessary to prescribe isotretinoin .

The scarring of acne tends to be of 2 different types, either the broad-based depression or the ice-pick lesion. Treatment usually centers on making the scar borders less distinct with techniques such as dermabrasion, laser abrasion, and chemical peeling. Subcutaneous collagen injections can be a useful adjunct. Frequently, it is best to excise ice-pick lesions. Because of the significant changes in epidermal thickness by isotretinoin therapy, efforts to resurface by dermabrasion or laser should be deferred for at least 1 year to afford the skin the opportunity to recover.

Pyoderma gangrenosum

While pyoderma gangrenosum (see the image below) is associated with ulcerative colitis, 50% of the time it occurs without inflammatory bowel disease.^[36]

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Pyoderma gangrenosum.

Other associations include ulcer diathesis, diverticular disease, rheumatoid arthritis, pulmonary and hematologic illnesses, and carcinoid tumors. The lesions typically are ulcers with rolled borders. Physiologically, the wound is more like a progressive vasculitis than an infection. However, gram-positive and gram-negative bacteria species have been cultured from these chronic wounds. Streptococcal and Proteus species appear to be involved frequently.

Topical antimicrobials and those with systemic effects are effective to some degree in controlling the disease. The mainstay of management appears to be anti-inflammatory regimens of steroids with local and systemic effect, as well as steroid-sparing regiments such as cyclosporine or azathioprine. Surgical caveats remain minimal debridement and limitation of all forms of skin trauma and irritation. The slightest cutaneous injury may evolve into a disastrous area of necrosis.

References

Surgical Treatment and Biopsy

Excisional and incisional

Surgical treatment of skin lesions primarily consists of total excision of the mass (with a variable amount of ‘normal’ skin periphery depending on the indications) or a partial tissue sampling of the lesion (with variability in regard to depth, location, and percentage of total lesion). Excision of a presumed benign lesion accomplishes 2 goals: accurate tissue diagnosis and removal of visual insult to the patient.

Small benign lesions of the skin can be excised easily. If the lesions are small (generally < 2 cm) and are not located in an anatomically sensitive area (ie, periorbita, ear, white roll of the lip), they can be surgically excised by a practitioner without an extensive surgical background. Good surgical technique gives the best chance of avoiding recurrence and a favorable aesthetic outcome.

Incisions should be made in an oval-shape excision with at least a 1-mm margin around the lesion. The incisions must be made throughout the entire depth of the dermis and include any visible subdermal extension. Primary closure is usually required, although some excisions (eg, < 1-cm circular incisions on the back) are best left to heal by secondary intention. This yields the most appealing-looking scar on the back. In all other areas, nonabsorbable suture is commonly used to close these wounds. As a general rule, the sutures are left in 5-6 days for facial areas; 10-14 days on the extremities and scalp, which receive more daily trauma; and 7-10 days for all other areas.

When total excision of a skin lesion is not feasible, an incisional biopsy can be performed for tissue diagnosis. A biopsy refers to a sampling of the tissue for diagnosis purposes. A complete removal of the lesion is also termed an excisional biopsy; any biopsy less than complete is referred to as an incisional biopsy.

Shave and punch biopsy

An incisional biopsy on a benign skin lesion can be performed in several different ways, including shave biopsy and punch biopsy. A shave biopsy consists of simple tangential excision of the raised aspect of the lesion at the same level of the peripheral skin plane. Sutures are not necessary and reepithelialization should occur within a few days.

A punch biopsy is usually performed with a specialized trephine (ie, biopsy punch) that is a device with a knife conformed into a complete circle that is slightly tapered at the end. After local anesthesia is administered, the trephine is twisted in a back-and-forth motion and pushed down through the skin to incise the entire thickness of the dermis. The circular segment of skin is removed; optimally, a small amount of subcutaneous fat is included.

Biopsy punches usually have a diameter that ranges from 2-12 mm. Biopsy devices 2-5 mm in size are most common, and the resultant wounds often do not require suture closure. The round shape facilitates quick wound contracture and spontaneous closure. A biopsy diameter greater than 5 mm usually needs a simple suture to adequately close the wound. When a biopsy punch is not available, a similar amount of tissue may be incised freehand with a scalpel.

Curettage, electrosurgery, cryosurgery

Curettage, electrosurgery, and cryosurgery (additional techniques for removing simple benign lesions) are all simple procedures that can be performed in the clinic setting with minimal patient preparation. The procedures are primarily ablative techniques; they cannot be used for tissue diagnosis.

Curettage is a simple technique used for removing small benign lesions. Using a curette (a cutting instrument with a circular or loop-shaped cutting edge), the practitioner is able to scoop out the skin lesion. Normal skin is more resilient to the action of the curette and, therefore, is not easily included in the removal process. The lesion is typically more friable than normal skin and is removed more easily. Repeated passes are usually needed to remove the entire lesion. In the process, the excised lesion becomes too fragmented and distorted to be adequately used for a pathological sample. However, if the initial pass does result in an intact section of the lesion, the section should be seen for pathological examination.

Electrosurgery is technique wherein a high-frequency, alternating current is produced at the tip of an electrode that, when applied to the skin lesion, causes high resistance at the contact point and generates heat that destroys the surrounding tissue. This principle of electrosurgery can be applied in several different ways, usually from a small unit that can be stored in a clinic room. This technique is completely ablative and leaves no usable tissue for pathological examination.

Electrodessication is when the electrode tip is applied directly in contact with the lesion through a monoterminal unit. When the electrode needle tip is held a short distance away from the lesion, a spark is emitted and the current that emanates causes tissues destruction; this monoterminal electrocautery modification is called electrofulguration. If the patient is grounded, the electrosurgical technique is now bi-terminal; a higher amperage used at the electrode tip conducts a high current in the tissue, and the resultant resistance causes heat that cauterizes the lesion. This modification is called electrocoagulation (or electrocautery).

Another electrosurgical tool is a completely handheld battery-operated device. This device uses battery current to pass through a high-resistance wire to produce a red-hot electrode tip, which cauterizes any tissue by the application of intense heat. This can be used for ablating small lesions in the clinic as well as assisting in hemostasis for office-based procedures.

Cryosurgery is another ablative technique, in which repeated application of freezing agents to a benign skin lesion facilitates its destruction and a separation of the epidermal-dermal junction at the basement membrane. Various agents such as Freon, ethyl chloride, Freederm and liquid nitrogen can be used. Liquid nitrogen is the most widely used and most readily available. A disadvantage of liquid nitrogen is user variability. One method includes using a cotton-tipped applicator, liquid nitrogen is applied 4 times within 60 seconds to freeze the skin. The rapid process of freezing and thawing of the lesion causes the most damage. Erythema and swelling result, and the superficial surface of the lesion spontaneously sloughs. Reepithelialization usually is complete for most small wounds within 72 hours. Hypopigmentation and dysesthesia may complicate cryosurgery but usually are self-limited.

References

Surveillance and Follow-up

Photographic documentation

In this age of digital photography, the advantages of storage and reproduction of digital photographs clearly demonstrate its utility in the diagnosis and care of skin lesions. Most clinic and hospital filing systems do not yet have an easy way to store and reproduce digital photographs of lesions, but this technology is fast approaching.

Patients themselves can be an extremely useful source of a photographic history of a skin lesion progression over time. The advantage of using the patients as a source of skin lesion documentation is that compliance with HIPPA edicts is simpler; the disadvantages are possible poor photographic quality and imprecise interval recording. Nevertheless, photographic documentation of the lesion should be obtained whenever possible. In a randomized trial of nearly 1100 patients, photographic surveillance of skin lesions was shown to increase the early detection of melanoma and decrease biopsies of benign skin lesions.^[37]

To take consistent photographs that document well the physical characteristics in question, some guidelines should be followed. When shooting small objects, photographs must be taken up close. If using a digital camera, select the macro setting for close shots (a camera without this function will provide inferior pictures). Nondigital cameras require a macro lens for the clearest pictures. Wide angle is needed occasionally (eg, taking pictures of the entire back of a patient who has multiple neurofibromatosis lesions).

Lighting is critical in all photography, and skin lesions are no exception. What is captured by the camera can differ dramatically, depending on the lighting source. The best approach is to take photographs of the same lesions using multiple lighting sources. One should attempt to photograph each lesion in question using a direct light flash (the built-in camera flash or an attached ring flash); natural light (if available); and indirect light (light angled to the skin lesion not directly in front or overhead). To accomplish this, first take a photograph without examination light (just camera flash); second, take a photograph with the camera flash disabled; and third, take a photograph with camera flash on but examination light directed at the lesions from the side. This gives a wide range of appearances of the lesions, which highlight different characteristics and allow better future comparison.

References

What are benign skin lesions and how are they diagnosed?How is an accurate diagnosis of benign skin lesions made?How are benign skin lesions differentiated from malignant lesions?How are benign skin lesions characterized?Which characteristics outside a lesion should be assessed in the evaluation of a benign skin lesion?What are the physical characteristics of a benign skin lesion?What terms are used to describe morphologic findings of benign skin lesions?What terms are used to describe histologic findings of benign skin lesions?How are acral and actinic defined in benign skin lesion?What is a keratoacanthoma (KA)?What is a pyogenic granuloma?What are keloids?What is seborrheic keratosis (SK)?How is actinic keratosis (AK) characterized?What are acrochordons (skin tags)?What is the clinical sequence of keratoacanthoma (KA)?What are subtypes of keratoacanthoma (KA)?What causes keratoacanthoma (KA)?What are histologic features of keratoacanthoma (KA)?What are the treatment options for keratoacanthoma (KA)?How is keratoacanthoma (KA) classified?How is a pyogenic granuloma diagnosed and treated?What is a cutaneous horn?What causes a cutaneous horn?Which patients are at highest risk for keloids?What is the pathogenesis of keloids?What are the treatment options for keloids?What is the mainstay of treatment for keloids?What is the role of silicone gel or occlusive sheeting in the treatment of keloids?What is the role of surgery in the treatment of keloids?What is the efficacy of cryotherapy in the treatment of keloids?What is the efficacy of extracorporeal shock wave therapy in the treatment of keloids?What is nevus sebaceus of Jadassohn?What is the clinical progression of nevus sebaceus of Jadassohn?What are the signs and symptoms of seborrheic keratosis (SK)?What causes seborrheic keratosis (SK)?How is irritated seborrheic keratosis (SK) characterized?What is an inverted follicular keratosis?How is verruca plana (VP) differentiated from VP-like seborrheic keratosis?What are the treatment options for seborrheic keratosis (SK)?What is actinic keratosis (AK)?What is the prevalence of actinic keratosis (AK)?What causes actinic keratosis (AK)?What are the treatment options for actinic keratosis (AK)?What is bowenoid papulosis?What is Bowen disease?How is Bowen disease characterized?What are the treatment options for Bowen disease?Which factor increases the risk for recurrence of Bowen disease?What is sebaceous adenoma (SA)?What is Muir-Torre syndrome?What causes sebaceous adenoma (SA)?How is sebaceous adenoma (SA) characterized?What is the malignant potential of sebaceous adenoma (SA)?What are the different types of pigmented benign skin lesions?How is nevus sebaceus of Jadassohn characterized?What are the clinical manifestations of seborrheic keratosis (SK)?What is the malignant potential of a nevus sebaceus of Jadassohn?What is the clinical progression of nevus sebaceus of Jadassohn?What is a seborrheic keratosis (SK)?What are the signs and symptoms of seborrheic keratosis (SK)?What causes seborrheic keratosis (SK)?How is irritated seborrheic keratosis (SK) characterized?What is an inverted follicular keratosis?How are verruca plana (VP) and VP-like seborrheic keratosis differentiated?What are the treatment options for seborrheic keratosis (SK)?What is actinic keratosis (AK)?Which patients are at increased risk for actinic keratosis (AK)?How is actinic keratosis (AK) characterized?What is the pathogenesis of actinic keratoses (AK)?What are the treatment options for actinic keratosis (AK)?What is Bowen disease?How are the lesions of Bowen disease characterized?What are the hallmarks of Bowen disease?What are the treatment options for Bowen disease?What are the risk factors for recurrence of Bowen disease?What is sebaceous adenoma (SA)?Which malignancies are associated with sebaceous adenoma (SA)?What causes sebaceous adenoma (SA)?How are sebaceous adenoma (SA) lesions characterized?What is the malignant potential of sebaceous adenoma (SA)?What are the types of subepidermal benign skin lesions?What are lipomas?What is a keratinous cyst?How are keratinous cysts differentiated from other benign skin lesions?What are the treatment options for keratinous cysts?What are dermoid cysts?How are craniofacial dermoid cysts differentiated from encephaloceles?What are treatment options for dermoid cysts?What are neurofibromas?What is the presentation of neurofibromas?What is the composition of neurofibromas?What are the treatment options for cutaneous neurofibromas?What is the malignancy risk of neurofibromas?What are schwannomas?What are the histologic characteristics of schwannomas?What are the indications for resection of schwannomas?What is the presentation of lipomas?What causes lipomas?What is the composition of lipomas?What are the treatment options for lipomas?What is inverted follicular keratosis?What is the hallmark of inverted follicular keratosis?What is trichoepithelioma?How is a trichoepithelioma characterized?What are the treatment options for a trichoepithelioma?What is a trichilemmoma?What is a pilomatrixoma?How is pilomatrixoma treated?What is psoriasis?What is discoid lupus erythematosus?What is the characteristic presentation of psoriasis?What is the prevalence of psoriatic arthritis in psoriasis?What nail changes may be present in patients with psoriasis?What are the treatment options for psoriasis?What are histological features of discoid lupus erythematosus?What are the treatment options for discoid lupus erythematosus?What follow-up care may be needed for discoid lupus erythematosus?What is cutaneous morphea?What is the prevalence of neurofibromatosis (Von Recklinghausen disease)?What is the presentation of neurofibromatosis?What are the treatment options for neurofibromatosis?What is the clinical course of neurofibromatosis?What is xeroderma pigmentosum?What are the treatment options for xeroderma pigmentosum?What is the prevalence of dystrophic epidermolysis bullosa?What is the presentation and clinical progression of dystrophic epidermolysis bullosa?What are treatment options for dystrophic epidermolysis bullosa?What is cutis laxa?What are the non-cutaneous manifestations of cutis laxa?How is cutis laxa characterized and how is it treated?What is the prevalence of cutis hyperelastica (Ehlers-Danlos syndrome)?What is the presentation of cutis hyperelastica (Ehlers-Danlos syndrome)?How is cutis hyperelastica (Ehlers-Danlos syndrome) differentiated from cutis laxa?What is necrobiosis lipoidica diabeticorum?What is acne vulgaris?How does the pilosebaceous system determine the location of acne vulgaris?What is the pathogenesis of acne vulgaris?What are the clinical features of acne vulgaris?What are the goals of treatment for acne vulgaris?What is the role of isotretinoin (13-cis -retinoic acid) in the treatment of acne vulgaris?What are the treatment options for acne vulgaris scarring?What is pyoderma gangrenosum?What are the treatment options for pyoderma gangrenosum?What are the surgical options for benign skin lesions?What are best practices for incisions to treat benign skin lesions?When is an incisional biopsy indicated for benign skin lesions?What is a shave and punch biopsy for benign skin lesions?What are best practices for a punch biopsy in the treatment of benign skin lesions?Which simple surgical techniques are used to remove benign skin lesions?How is curettage performed in the treatment of benign skin lesions?How is electrosurgery performed in the treatment of benign skin lesions?How is electrodessication performed in the treatment of benign skin lesions?How is cryosurgery performed in the treatment of benign skin lesions?What is the role of photographic documentation of benign skin lesions?What are guidelines for photographic documentation of benign skin lesions?

References

Benign Skin Lesions

Overview

Common benign skin lesion algorithm. (Concept and original organization courtesy of Scott Bangs, MD, Owatonna Clinic - Mayo Health System)

Papular benign skin lesion: Acrochordon (skin tag).

Papular benign skin lesion: Pyogenic granuloma.

Papular lesions: Keloids developed from back acne.

Macular benign skin lesions: Seborrheic keratoses of back and trunk.

Macular benign skin lesions: Seborrheic keratoses of the face.

Macular benign skin lesion: Nevus sebaceous of Jadassohn.

Subepidermal lesion: Keratinous cyst (epidermal inclusion cyst).

Subepidermal benign lesion: Lipoma of posterior neck.

Benign pigmented lesion: Dermatosis papulosa nigra.

Psoriasis.

Necrobiosis lipoidica diabeticorum.

Pyoderma gangrenosum.

Defining the Lesion

Characteristics outside the lesion

Physical characteristics of lesion

Anatomy of the skin.

Gross morphologic terms

Histologic terms

Other terms

Papules and Plaques

Acrochordon

Papular benign skin lesion: Acrochordon (skin tag).

Keratoacanthoma

Keratoacanthoma

Keratoacanthoma

Keratoacanthoma

Pyogenic granuloma

Papular benign skin lesion: Pyogenic granuloma.

Cutaneous horn

Keloid

Papular lesions: Keloids developed from back acne.

Nevus sebaceus of Jadassohn

Macular benign skin lesion: Nevus sebaceous of Jadassohn.

Seborrheic keratosis

Macular benign skin lesions: Seborrheic keratoses of back and trunk.

Macular benign skin lesions: Seborrheic keratoses of the face.

Actinic keratosis

Bowen disease and Bowenoid papulosis

Sebaceous adenoma

Pigmented Lesions

Macular skin-colored lesions.

Nevus sebaceus of Jadassohn

Macular benign skin lesion: Nevus sebaceous of Jadassohn.

Seborrheic keratosis

Macular benign skin lesions: Seborrheic keratoses of back and trunk.

Macular benign skin lesions: Seborrheic keratoses of the face.

Actinic keratosis

Bowen disease

Sebaceous adenoma

Subepidermal Lesions

Subepidermal lesions.

Keratinous cyst

Subepidermal lesion: Keratinous cyst (epidermal inclusion cyst).

Dermoid cyst

Neurofibroma

Schwannoma

Lipoma

Subepidermal benign lesion: Lipoma of posterior neck.

Inverted follicular keratosis

Trichoepithelioma

Trichilemmoma

Pilomatrixoma

Benign Dermatoses

Psoriasis

Psoriasis.

Discoid lupus erythematosus

Morphea

Neurofibromatosis

Xeroderma pigmentosum

Dystrophic epidermolysis bullosa

Cutis laxa

Cutis hyperelastica (Ehlers-Danlos syndrome)

Necrobiosis lipoidica diabeticorum

Necrobiosis lipoidica diabeticorum.

Acne vulgaris

Pyoderma gangrenosum

Pyoderma gangrenosum.