eMedicine Specialties > Plastic Surgery > Skin

Skin, Benign Skin Lesions

Author: Ginard I Henry, MD, Assistant Professor of Surgery, Section of Plastic Surgery, Medical Student Faculty Coordinator, University of Chicago Pritzker School of Medicine; Plastic Surgeon, Weiss Memorial Hospital
Coauthor(s): Mark A Grevious, MD, FACS, Assistant Professor of Surgery, Associate Program Director, Division of Plastic and Reconstructive Surgery, University of Illinois at Chicago; Todd A Morton, MD, FACS, Consulting Staff, Department of Plastic Surgery, Kaiser Permanente; Wayne Karl Stadelmann, MD, Stadelmann Plastic Surgery, PC
Contributor Information and Disclosures

Updated: May 19, 2009

Introduction

Most skin lesions presented by patients are benign; however, some concern has caused the patient to make an inquiry, and a correct diagnosis is important. The plethora of dermatologic conditions makes a correct diagnosis challenging. To combat this, the clinician must approach the evaluation of the lesion in a systematic way. In addition to the physical characteristics of the lesion, the patient’s demographics, presence of associated symptoms, related systemic disorders, and location and growth patterns of the lesion all give clues to adequately diagnose and treat. The accurate diagnosis of any skin lesions can be made by histological examination of a skin biopsy. However, clinicians must gain the clinical acumen to correctly identify common benign skin lesions and to distinguish those skin conditions that do need a biopsy and possible further treatment.

Initially, benign lesions must be differentiated from malignant lesions. This is best done by being familiar with characteristics of common malignant lesions. (For more information, see the articles in the Skin section of eMedicine's Plastic Surgery journal.) The clinician should try to categorize any skin lesion presented with as most likely benign, most likely malignant. and unclear. The latter 2 categories receive full-thickness skin biopsies. However, surgical procedures can be avoided in the presence of many benign skin lesions. Once the benign nature of the lesions is assumed, the diagnosis must be made accurately in order to assess any future malignant potential. A critical caveat is that all benign lesions must be surveilled by the patient and examined by a clinician should any changes occur.

This article reviews many of the most common conditions and acquaints the reader with the clinical significance and treatment options.

Defining the Lesion

The following 3 general categories of characteristics must been considered when defining a benign lesion:

• Characteristics outside of the lesion
• Physical characteristics of the lesion
• Intralesional characteristics

Gross morphologic terms describe the exterior physical appearance of the lesion visible with the naked eye. Histiologic terms primarily refer to characteristics seen with microscopic pathology examinations but can also be used to describe more specific exterior findings. Understanding of histiologic terms requires knowledge of the anatomical layout of skin and the associated cells and extracellular matrix content that populate each layer. For more information, see eMedicine article Skin, Anatomy.

• Blister - Nonspecific term for fluid-filled lesion (see vesicle or bulla)
• Bulla - Fluid-filled lesion >5 mm in greatest dimension
• Excoriation - Lesion of traumatic nature with epidermal loss in a generally linear shape
• Lichenification * - Grossly thickened, leathery, hyperpigmented skin with hyperkeratosis and deep, widely-spaced skin markings
• Macule - Flat circumscribed area demarcated by color from surrounding tissue
• Nodule - Solid raised discrete lesion >5 mm in greatest dimension
• Onycholysis - Loosening or loss of nail substance resulting in loss of integrity
• Papule - Solid raised discrete lesion £ 5 mm
• Pedunculated - Attached to its base by a stalklike structure
• Plaque - Flat but elevated area, usually >5 mm
• Pustule - Small pus-filled elevated area of the skin with discrete borders
• Seborrheic - Related to excessive secretion of sebum
• Sebum - Thick, greasy substance secreted by sebaceous glands that consists of fat and cellular debris
• Sessile - Attached directly to the skin by a broad base; not pedunculated
• Vesicle - Fluid-filled lesion £ 5 mm

• Acantholysis - Dissolution of intercellular integrity with fragmentation of epidermis
• Acanthosis - Hyperplasia of epidermal layer
• Dyskeratosis - Abnormal keratinization occurring prematurely in cells below the stratum granulosum
• Erosion - Loss of epidermis
• Exocytosis - Infiltration of epidermis by inflammatory cells
• Hyperkeratosis (keratosis) - Thickening of the stratum corneum (the outermost layer of the epidermis) with excess abnormal keratin
• Lichenification * - Hyperplasia of all compartments of the epidermis with acantholysis and papillomatosis
• Papillomatosis - Hyperplasia of the papillary dermis and lengthening and/or widening of the dermal papillae
• Parakeratosis - Persistence of the nuclei within the cells of the stratum corneum of the epidermis as seen in psoriasis
• Spongiosis - Edema limited to the epidermis
• Ulceration - Loss of epidermis with variable partial-to-complete loss of dermis

Other terms

• Acral - Related to the extremities and the more distal parts of the body
• Actinic – Relating to biochemical changes in the skin produced by sunlight energy from both the visible and ultraviolet rays

Benign Nodular Lesions

Papular Lesions

Acrochordon

• Skin tag
• Fibroepithelial polyp
• Fibroma mole
• Fibroepithelial papilloma

Clinical presentation

Acrochordons are common tumors found in middle-aged and older persons. They are commonly found on the cervical region, axilla, upper trunk and eyelids. These skin tags are of low clinical significance but for the questions and concerns they can generate for the patient. These lesions have been observed to follow warts, seborrheic keratoses (SKs), and inflammatory skin conditions. Acrochordons occasionally are associated with pregnancy, diabetes mellitus, and intestinal polyposis syndromes. 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.

Etiology

Whether this is a specific entity or a common pathway in healing and recovery of several nonspecific inflammatory conditions of the skin is debatable.

Histology

Acrochordons all consist of a thin squamous epithelium surrounding a fibrovascular core.

Treatment

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. Surgical excision provides the most cosmetic result and is necessary for removal of larger lesions.

Keratoacanthoma

Synonym

• Molluscum sebaceum

Clinical presentation

Keratoacanthoma (KA) is a well-known self-healing skin tumor. It is most well known for its rapid growth rate. In fact, this rate of growth is frequently adequate to allow the clinician to distinguish keratoacanthoma from malignancy because it grows much more quickly than carcinoma. The lesion is classically a dome-shaped mound 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. Keratoacanthoma appears to be a product of the infundibulum of the hair follicle.

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 approximately 1-2 weeks. It reaches approximately 1-2 cm and grows much faster than skin cancers, as previously mentioned. Keratoacanthoma develops a central keratin plug, followed by either a static or an involutional period.

Subtypes have been described. A Gryzbowski-type keratoacanthoma presents with multiple lesions simultaneously. When lesions present in a typical distribution, again with multiple locations, keratoacanthoma tends to be referred to as a Ferguson-Smith type. When the lesion is observed in sun-exposed skin associated with actinic keratoses, it is referred to as an actinic keratoacanthoma. Further associations have been noticed, particularly with certain inflammatory dermatoses, certain congenital lesions, certain genetic diseases, scarring, and actinic keratoses. The keratoacanthoma actually may represent a highly or very well-differentiated squamous cell carcinoma. The continued growth and the clinical finding of regional lymph node metastasis in rare occasions support this belief.

Etiology

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

Histology

Keratoacanthoma is determined easily when a number of its critical elements are demonstrated. A lesion with an overall hemispheric shape with a keratin-filled crater and overhanging edges is highly characteristic of keratoacanthoma. 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 rind with extension into the muscle. Perineural and vascular invasion also can be observed.

These features make this lesion occasionally difficult to discern from an epidermal carcinoma. Immunohistochemical staining can help differentiate the two. Filaggrin is a histidine-rich protein that is found in the horny and granule layers of the dermis. It is ubiquitous in keratoacanthoma but is apparently uncommon in carcinoma. When the biopsy specimen lacks the central keratin plug and the other characteristic anatomy is difficult to determine, this lesion may be confused with squamous cell carcinoma. The biopsy findings, clinical history, and a description of the gross physical appearance greatly facilitate making this diagnosis.

Treatment

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. Surgical excision, curettage, and electrodesiccation have been the traditional approaches to this lesion. Because keratoacanthoma can be removed in total with surgical excision, which provides an adequate pathologic specimen, this is generally the treatment of choice.

Pyogenic Granuloma

• Granuloma telangiectaticum

Clinical presentation

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. 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.

Histology

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

Treatment

The approach varies but excision is the mainstay of treatment. Frequently, biopsy is performed to confirm the diagnosis. Performing curettage and electrodesiccation is another option. Application of silver nitrate repeatedly can also be a simple yet effective therapy. Recurrence is common with therapies other than complete excision.

Cutaneous Horn

Synonym

• Cornu cutaneum

Clinical presentation

A cutaneous horn is skin lesion made of compacted keratin that forms an exophytic conical projection that becomes curved and resembles a French horn. This lesion is a clinical finding related to other skin disorders but not its own unique pathologic entity. Cutaneous horns can occur from other hyperkeratotic lesions such as actinic keratoses, seborrheic keratoses, benign verrucae, inverted follicular keratoses, and epidermoid carcinomas. Although most cutaneous horns are benign, malignant lesions have been reported found at the base of 20% of horns. The most common malignancy is squamous cell carcinoma.

Patients with cutaneous horns tend to be fair-skinned individuals in their sixties and seventies.

Etiology

The etiology of the cutaneous horn itself is unclear; the underlying skin disorder associated is the precipitating factor.

Histology

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.

Treatment

Because of the potential of malignancy at the base of a cutaneous horn, excisional biopsy is recommended.

Keloid

• Crab claw
• See dedicated eMedicine articles (Wound Healing, Widened and Hypertrophic Scars and Wound Healing, Keloids)

Macular Skin-Colored Lesions

Nevus Sebaceus of Jadassohn

• Verrucous epidermal nevi (some consider a variant)

Clinical presentation

While this lesion often is included in tumors of the skin adnexum, it is actually an epithelial nevus. Nevus sebaceus of Jadassohn 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.

The malignant potential of this lesion has been estimated at 10-50%. Degeneration into basal cell carcinoma is most common; however, other malignancies include adnexal tumors and squamous 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.

Histology

Microscopically, many sebaceous glands in a vascular stroma with abortive hair follicles are observed. Some of the sebaceous glands communicate with the surface directly.

Treatment

Complete surgical excision is the treatment of choice.

Seborrheic Keratosis

• Seborrheic wart
• Senile wart
• Basal cell papilloma

Clinical presentation

Seborrheic keratosis (SK) 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.

Histology

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.

Treatment

Most patients require no specific treatment. 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 (such as 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.

Actinic Keratosis

Synonyms

• Solar keratoses
• Senile keratoses

Clinical presentation

Actinic keratoses (AK) 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 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 a high risk for developing actinic keratoses and malignant transformation into squamous cell carcinoma with higher rates of metastasis.

These lesions may demonstrate certain excrescences of keratin, referred to as cutaneous horns. The rough texture of the lesion imparts to the skin a sandpaperlike 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.

Etiology

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.

Histology

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. Also, 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.

Treatment

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 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.

Bowen Disease

Synonyms

• Carcinoma in situ
• Squamous intraepidermoid neoplasia

Clinical presentation

Originally described by Bowen in 1912, these lesions predominantly involve skin that is not exposed to the sun (ie, protected). Classically, Bowen disease 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.

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.

Etiology

Efforts have been made to correlate arsenic and Bowen disease. The results have been inconclusive at best.

Histology

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

Treatment

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.

Sebaceous Adenoma

Synonyms

• Sebaceous epithelioma (sebaceoma)⁵
• Sebocrine adenoma

Clinical presentation

Sebaceous adenoma (SA) 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.

New eruptions of multiple sebaceous adenoma can sometimes be associated with a visceral carcinoma. Adenocarcinomas of the colon, stomach, duodenum, or 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.

Etiology

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.

Histology

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.

Treatment

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

Pigmented Lesions

Dermatofibroma

Synonyms

• Histiocytoma
• Sclerosing hemangioma

Clinical presentation

Dermatofibromas present as firm, raised, pigmented lesions that range in color from brown to red, purple, and pink. They are usually small lesions, frequently found on the lower extremities. Frequently, patients had previous insect bites in the region. A common finding of dermatofibroma is the Fitzpatrick sign—dimpling of the skin of the lesion when lateral pressure (squeezing the lesion) is applied. They are occasionally tender and usually round in shape.

Etiology

The etiology of a dermatofibroma is unclear, and some controversy remains over whether a dermatofibroma represents a true neoplasm or a fibrous reaction to some minor trauma.

Histology

A dermatofibroma has a variable histological appearance but is comprised mainly of irregularly distributed spindle cells dispersed among abundant collagen fibrils. This fibrotic mass usually occupies the reticular dermis and exhibits indistinct peripheral borders.

Treatment

Asymptomatic dermatofibromas do not require any treatment. However, dermatofibromas can become challenging to differentiate from melanomas. When clinical confusion arises, an excisional biopsy of the lesion is warranted.

Nevus

General

The definition of a nevus can be expanded to include any congenital lesion that is circumscribed to well-defined. The term also occasionally has been used as a synonym for mole. A mole is defined as a shapeless mass. Most nevi appear when individuals are aged 2-60 years. They have a predictable evolution. They rarely undergo activation or malignant degeneration. Nevi tend to be more common on the head, neck, and trunk. However, a great deal of variability exists with regard to size, shape, and even amount of hair present.

Nevomelanocytic nevi, which are the most common, are categorized classically and clinically in 3 different ways: junctional, compound, and intradermal subtypes.

• Junctional nevi: Junctional nevi are characterized by a melanocytic proliferation, which is limited to the basal epidermis only. Minimal elevation is found, and absence of hairy appendageal components is noticeable. Histologically, a nest of melanocytes on the epidermal side of the junction only is observed.
• Compound nevi: Compound nevi are believed to represent an intermediate step in the evolution of the melanocytic nevus. Components of both dermal and junctional nevi are found simultaneously. The incidence of junctional nevi decreases with age as the nevus evolves through the compound stage to intradermal histology. Glabrous surfaces have a privileged relationship with junctional nevi, and they may remain on palms and soles for a lifetime without undergoing evolutionary change to an intradermal type.
• Intradermal nevi: These represent the most common type of adult nevus. These may be papillary, pedunculated, or flat. They often have components of hairy change. They commonly can be multiple. The melanocytes in this lesion are entirely within the dermis, with irregular margins. These lesions also are notable for their variable degrees of pigmentation. When the lesion is observed histologically, the lower one half of the lesion tends to be slightly less cellular with bundles of spindle cells, which are related to their presumed Schwann cell derivatives.

Other morphologic findings are associated with intradermal nevi, including amyloid, bone, folliculitis, abscesses, and psammoma bodies. While the junctional nevus can have a reputation for degeneration into malignant melanoma, the intradermal nevus does not.

Special variances and subtypes of nevi exist. The first of these is the blue nevus. The blue nevus tends to be a small discrete lesion, typically located in the head and neck and, occasionally, on the upper extremity. A variant form of this has manifestation on the buttock and sacrococcygeal areas. In general, the blue nevus has abundant melanin pigment. It is located entirely within the dermis. No epidermal or junctional component is present. If the pigment is misinterpreted as hemosiderin, blue nevus occasionally can be misdiagnosed as a benign fibrous histiocytoma.

Two predominant types of blue nevi exist, the common and the cellular blue nevus. The cellular blue nevus is a special variety characterized by larger size and more intense pigmentation. Its distribution tends to be in the buttock and sacrococcygeal areas. Its subtypical import is that it must be distinguished from a malignant melanoma. The confusion surrounds the increased degree of pigmentation. After the sacrococcygeal and buttock areas, other regions of expression include the scalp, face, and backs of the hands and feet.

Histologically, it is distinguished from melanoma by the absence of peripheral reaction and stigmata of invasion and by the lack of atypical junctional activity or mitotic figures. The natural history is that of a benign course, which is occasionally recurrent locally. Regional lymph node involvement has been demonstrated and is of concern; however, patients generally are cured by primary excision. Additionally, a malignant variant of the blue nevus exists.

Subepidermal Lesions

Keratinous Cyst

Synonyms

• Sebaceous cyst⁶
• Wen
• Atheroma
• Steatoma
• Epidermoid/epidermal inclusion cyst (EIC)
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    Subepidermal lesion: Keratinous cyst (epidermal inclusion cyst).

    [ CLOSE WINDOW ]

    

    Subepidermal lesion: Keratinous cyst (epidermal inclusion cyst).

• Pilar cyst
• Trichilemmal cyst

Clinical presentation

For many years, keratinous cysts have been misnamed and referred to incorrectly as sebaceous cysts. Historically, 2 essential types have been identified. The most common type is known as an epidermoid or epidermal inclusion cyst. This represents approximately 90% of keratinous cysts. The second most common type is termed a pilar or trichilemmal cyst. Cornified epithelium, a very well-demarcated granular layer, and multiple lamellae of keratin without calcification characterize the epidermoid cysts.

These lesions can be found in almost any location. Variations found in 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.

Treatment

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

The cyst wall is comprised 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 three primary embryonic germ layers: skin, hair or teeth.

Treatment

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.

Neurofibroma

Treatment

Schwannoma

Synonyms

• Neurilemmoma

Etiology

The pathogenesis of schwannomas is unclear.

Histology

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.

Treatment

Lipoma

Lipomas are the most common subcutaneous soft tissue tumors with an annual incidence of nearly one in 1,000 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.

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.

Etiology

Lipoma etiology 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 that 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.

Histology

Treatment

Hair-Related Lesions

Inverted Follicular Keratosis

Clinical presentation

Inverted follicular keratosis is believed to be an inflammatory variant of seborrheic keratosis. It commonly is found on the faces 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.

Etiology

This is an acquired lesion, similar to seborrheic keratosis.

Histology

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

Treatment

Since this lesion is benign, simple excision is adequate.

Trichoepithelioma

Clinical presentation

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 face and scalp and, less commonly, the trunk and neck. A certain familial incidence exists. While these lesions tend to be multiple, a solitary presentation also can be observed. In general, all the lesions are less than 8-10 mm.

Histology

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.

Treatment

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

Clinical presentation

Trichilemmoma is a benign tumor with a pattern of globular glycogen-rich clear cells. Occasionally, keratinization in the center is identified grossly. These lesions have some unique and interesting associations, specifically papillomas of the oral mucosa, acrokeratoses, and, most significantly, tumors of the breast, thyroid, and GI tract. This is a condition known as Cowden disease, which is a multiple hamartomatous syndrome. Additionally, a rare carcinoma variant of trichilemmoma is known as trichilemmal carcinoma.

Pilomatrixoma

Pilomatrixoma is also known as pilomatricoma and the calcified epithelioma of Malherbe.

Clinical presentation

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

Histology

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.

Treatment

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.

Miscellaneous Lesions

Pseudoepitheliomatous Hyperplasia

Synonym

• Pseudocarcinomatous hyperplasia

Clinical presentation

This lesion is believed to be a reparative process characterized by tongues of squamous epithelium growing downward into the dermis. It can be difficult to distinguish from squamous carcinoma. Certain conditions and infections also have been implicated, such as North American blastomycosis, bromoderma, pyoderma vegetans, tuberculosis, syphilis, granular cell tumor, Spitz and other melanocytic nevi, and granuloma inguinale.

Etiology

The presence of this lesion is a feature of trauma and irritation. History of these predisposing conditions may be critical to distinguishing and interpreting the histology to discriminate carcinoma from the benign lesion.

Histology

As mentioned, invading tongues of squamous epithelium extend into the dermis as thin anastomosing strands. One of the most significant discriminators from squamous carcinoma is the profound chronic inflammatory infiltrate, which accompanies the epithelium. Another important finding is the lack of anaplasia.

Treatment

A conservative approach is warranted. If the lesion cannot be determined to be benign, then treat it as a squamous carcinoma with appropriate margins.

Benign Dermatoses

Psoriasis

Psoriasis is one of the most common dermatoses.⁸

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 in intercellular spaces. Munro microabscesses are intracorneal collections of 4 or more neutrophils.

Psoriasis occasionally is associated with other systemic illnesses, particularly psoriatic arthritis. Psoriatic arthritis occurs in approximately 5-10% of patients with psoriasis. A clinical entity known as psoriasis vulgaris may occur anywhere on the skin, including the extensor surfaces, lumbosacral areas, intergluteal cleft, and glans of the penis. Males may be affected in approximately one third of cases. Typically, mucosal surfaces are spared. A plaquelike salmon-colored lesion is the most common finding clinically.

Changes of the nails include dimpling, onycholysis, pitting, thickening, 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 systemic and topical forms and phototherapy.^9,10,8,11 Prior to elective procedures, psoriasis should be clinically optimized.

Discoid lupus erythematosus

Discoid lupus erythematosus and systemic lupus erythematosus are clinically distinct entities. Discoid lupus is a chronic, relatively common dermatitis with clinical presentation more common in women than in men. It presents with erythematous plaques that vary from an atrophic to hyperkeratotic appearance in the region of the face, scalp, neck, extremities, and trunk.¹² These may be exacerbated by sunlight.¹³

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 particularly 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 commonly 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 lupus band test. This occurs predominantly in the basement membrane and is found in the clinically uninvolved non–sun-exposed skin in patients with this autoimmune process. Topical treatment of this occurrence has involved a combination of steroid and antimalarial drugs such as hydroxychloroquine.^13,14

Despite efforts to control the disease topically, scarring and healing 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. As with most dermatoses, daily protection from solar exposure is essential.¹³

Scleroderma circumscriptum

These lesions often are defined on the trunk or an extremity in a dermatome. A particular manifestation of this is the face and paramedian forehead. These lesions appear to be violations that are lilac-colored and isolated. Occasionally, pruritus is associated. Scleroderma circumscriptum may be widespread and chronic, and it may involve the digits of the hand. Clinically, it almost always is distinguished from the systemic form of scleroderma, also known as progressive systemic sclerosis. 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.

A special situation known as scleroderma en coup de sabre is associated with progressive hemifacial atrophy in children. This is manifest with atrophy of the skin, subcutaneous tissues, muscle, and bone. Occasionally, the process resolves spontaneously. It can be unpredictable in its clinical course. While it remains destructive and progressive, this condition is observed. In its burnout quiescent phase, the treatment of choice is self-tissue augmentation.

In systemic scleroderma, the classic acrosclerotic form is observed generally in women aged 20-50 years. This can be associated with vasospastic or Raynaud phenomenon of the hand. These hand lesions are remarkable for a fixed partial flexion with extreme limitation of motion. Skin becomes inelastic and bound with ulcerations over fingertip and joint surfaces. Because of its progressive and incurable nature, conservation and therapy are recommended.

Some medical regimen approaches include medical sympathetic block and episodic steroids with systemic effect, although neither has been shown to be beneficial. A patient with scleroderma requiring an operation requires great concern in planning. The wound healing conditions are tenuous at best. Ulcers should be managed with careful debridement and skin grafting as permitted.

Neurofibromatosis

Also known as Von Recklinghausen disease, this is a relatively common disorder with a frequency of approximately 1 in 3000.¹⁵ Nearly 50% of patients with neurofibromatosis have a definable autosomal dominant transmission pattern.¹⁵ 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. Numerous pigmented skin lesions occur. The classic café au lait spots predominate. Additionally, pigmented iris hamartomas (ie, Lisch nodules) are common. Bone lesions and intracranial and GI lesions and symptoms may be identified. While pigmentary changes may occur at birth, the tumor formation is most aggressive during puberty. The severity of the disease is associated loosely with the age at which symptoms or tumors are found. Central and peripheral neurologic deficiency may follow the progressive growth of these lesions in their mass effect.

With respect to surgery, the most common indications are 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. While café au lait spots may be found in the healthy population, the presence of 6 or more spots in an aggregate of more than 1.5 cm in greatest dimension establishes the diagnosis of neurofibromatosis.

Clinical course is difficult to predict. An association of severity with youthful onset appears to exist. 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 seldom is 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.¹⁶ Its most obvious clinical characteristic is a bullous formation in the skin following essentially minimal trauma.^16,17 This heals with scarring and aggressive contracture. The incidence is approximately 1 in 300,000 live births. One half of the physiobiologic mechanisms that have been discovered include an excessive activity of a particular epidermal collagenase and fibroblasts with supranormal contractile abilities.

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. A pathognomonic sign of this is the appearance of blisters with minimal trauma referred to as the Nikolsky sign.

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.¹⁸ Two types have been recognized. One is autosomal dominant and manifests only in the skin. The other type has a recessive inheritance pattern and is associated with fascial deficiencies in the inguinal and ventral areas.

Other 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 it to literally hang in sheets of loose folds. 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.¹⁹ Some of the 8-10 forms that are described are recessive and some are dominant in their inheritance. The basic defects in these patterns tend to be a defect in the synthesis of type 3 collagen, a deficiency of the lysyl hydroxylase enzyme preventing cross-linkage, or the procollagen-N -peptidase enzyme deficiency, which impairs the aggregation of collagen fibers. An X-linked recessive form is the result of a possible deficiency in the lysyl-oxidase enzyme.

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.

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 some experience with acne.²¹ Clinically significant lesions consist of an open comedone, which corresponds to the term blackhead.²¹ Closed comedones correspond to whiteheads. Additional inflammatory lesions include pustules and papules.²¹ The most aggressive forms of acne have chronic scarring coexisting with active inflammatory foci.

The fundamental unit of involvement is the diseased 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 P acnes 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.²² 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.²¹ The pustular and papular forms respond better to these antibiotics than the cystic or comedonal forms. Tetracycline and erythromycin share similar efficacy in the systemic sense because both are concentrated in the sebaceous gland and follicle. Both also limit leukocyte chemotaxis to decrease the inflammatory milieu.

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

The scarring of acne tends to be of two 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 is associated with ulcerative colitis, 50% of the time it occurs without inflammatory bowel disease.²³

Topical antimicrobials and those with systemic effect 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 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.

Treatment

Biopsy and surgical therapy

Surgical treatment of skin lesion 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 surgical 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.

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. The resultant open area is treated with antibiotic ointment applied daily after the area is washed. Re-epithelialization 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 do not required 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, 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 which, 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 is applied to a benign skin lesion to facilitate 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. 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. Re-epithelialization usually is complete for most small wounds within 72 hours. Hypopigmentation and dysesthesia may complicate cryosurgery but usually are self-limited.

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.²⁴

To take consistent photographs that document well the physical characteristics in question, some guideline 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 1) a direct light flash (the built-in camera flash or an attached ring flash); 2) natural light (if available); and 3) 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.

Multimedia

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Media file 1: Papular benign skin lesion: Acrochordon (skin tag).

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Media file 2: Papular benign skin lesion: Pyogenic granuloma.

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Media file 3: Papular lesions: Keloids developed from back acne.

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Media file 4: Macular benign skin lesions: Seborrheic keratoses of back and trunk.

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Media file 5: Macular benign skin lesions: Seborrheic keratoses of the face.

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Media file 6: Macular benign skin lesion: Nevus sebaceous of Jadassohn.

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Media file 7: Subepidermal lesion: Keratinous cyst (epidermal inclusion cyst).

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Media file 8: Subepidermal benign lesion: Lipoma of posterior neck.

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Media file 9: Benign pigmented lesion: Dermatosis papulosa nigra.

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Media file 10: Psoriasis.

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Media file 11: Necrobiosis lipoidica diabeticorum.

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Media file 12: Pyoderma gangrenosum.

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Media file 13: Common benign skin lesion algorithm.

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Media file 14: Papular lesions.

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Media file 15: Macular skin-colored lesions.

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Media file 16: Pigmented lesions.

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Media file 17: Subepidermal lesions.

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Media file 18: Anatomy of the skin.

Keywords

benign skin lesions, skin disorders, skin lesion, dermatoses, acantholysis, acanthosis, dyskeratosis, erosion, exocytosis, hyperkeratosis, papillomatosis, spongiosis, ulceration, seborrheic keratosis, acrochordon, actinic keratosis, cutaneous horn, bowen disease, pseudoepitheliomatous hyperplasia, nevus sebaceus, Jadassohn, sebaceous adenoma, inverted follicular keratosis, trichoepithelioma, trichilemmoma, keratoacanthoma, keratinous cyst, dermoid cyst, pilomatrixoma, nevus, junctional nevi, compound nevi, intradermal nevi, blue nevus, pyogenic granuloma, psoriasis, discoid lupus erythematosus, scleroderma circumscriptum, neurofibromatosis, xeroderma pigmentosum, dystrophic epidermolysis bullosa, cutis laxa, cutis hyperelastica, Ehlers-Danlos syndrome, necrobiosis lipoidica diabeticorum, acne vulgaris, pyoderma gangrenosum

Acknowledgement and grateful thanks are owed to Scott Bangs, MD, of Owatonna Clinic - Mayo Health System for the benign lesion algorithm concept and its original organization.

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