Skin colored papules are a common dermatological presentation, often benign but sometimes indicative of underlying conditions. These small, raised bumps on the skin can vary significantly in their appearance, cause, and clinical significance. This article provides a detailed overview of various skin lesions that manifest as skin colored papules, aiding in their differential diagnosis. Understanding the characteristics of each lesion is crucial for accurate identification and appropriate management.
Acrochordons (Skin Tags)
Acrochordons, commonly known as skin tags or fibroepithelial polyps, are extremely prevalent benign skin lesions, particularly in middle-aged and older adults. They frequently appear in areas such as the cervical region, axillae, upper trunk, and eyelids. While generally of low clinical concern, patients often seek information and reassurance about these growths.
Acrochordons are sometimes associated with specific conditions including pregnancy, diabetes mellitus, and intestinal polyposis syndromes. They can also develop following trauma. Characteristically, they are found in intertriginous zones like the axillae, groin, inframammary regions, and the low cervical area along the collar line. These lesions are soft, fleshy papules, often pedunculated, and can be single or multiple, ranging from 1 to 6 mm in diameter. Histologically, acrochordons consist of a thin squamous epithelium surrounding a fibrovascular core.
While treatment isn’t always necessary, acrochordons are often removed for reasons of bleeding, irritation, cosmetic concerns, or discomfort. In rare instances, a lesion may twist on its stalk, leading to pain, erythema, and necrosis. Removal methods include electrodesiccation, shaving, cryoablation, or surgical excision for larger lesions to achieve the best cosmetic outcome.
For more in-depth information, refer to Acrochordon.
Keratoacanthoma (KA)
Keratoacanthoma (KA) is a rapidly developing skin tumor often considered a variant of squamous cell carcinoma by many dermatologists. Its rapid growth rate is a key feature that helps distinguish it from other cutaneous malignancies. Typically, KA presents as a dome-shaped, skin colored papule or nodule featuring a central keratin-filled crater. It is more frequently observed in males, with a male-to-female ratio of approximately 3-4:1.
The clinical progression of keratoacanthoma follows a predictable pattern. It begins as a spontaneous, red to flesh-colored nodule. Over a few weeks, this nodule undergoes a rapid growth phase, evolving into a larger, crater-like nodule. In the subsequent months, the tumor may slowly resolve on its own.
Several subtypes of keratoacanthoma exist, including generalized eruptive keratoacanthomas (of Gryzbowski), multiple regressing keratoacanthomas of Ferguson-Smith, actinic keratoacanthomas, keratoacanthoma centrifugum marginatum, and giant and subungual variants. Various factors have been associated with KA development, including viral infections, exposure to mineral oil and tar products, but the most consistently linked factor is sun exposure.
Histologically, keratoacanthomas exhibit a hemispheric shape with a keratin-filled crater and overhanging edges. Mitotic figures are present due to rapid growth. Basaloid cells are found at the periphery, and eosinophils may also be common. While generally well-differentiated, slight pleomorphism can be observed. A pushing edge with an inflammatory rim extending into the muscle is characteristic at the margin. Immunohistochemical staining for filaggrin can aid in differentiating KA from other epidermal carcinomas.
Despite its self-limiting nature, intervention is often preferred due to potential cosmetic issues and the ongoing debate about whether KA is a squamous cell carcinoma variant. Common treatments include surgical excision, electrodesiccation, and curettage. Surgical excision is often favored as it allows for complete removal and provides a specimen for pathological examination.
For further reading, see Keratoacanthoma.
Pyogenic Granuloma
Pyogenic granuloma, also known as cutaneous ectasia, is a rapidly proliferating, solitary lesion characterized by disorganized vascular growth and a tendency to bleed. It is often linked to minor prior trauma to the affected area. Typically, these lesions are smaller than 1 cm and may have a collarette of scale around their base. Common locations include the face, fingers, and thorax. Clinically, it is important to differentiate pyogenic granuloma from melanoma. These lesions can become eroded, crusted, ulcerated, or occasionally infected, and they bleed easily with minor trauma.
Histologically, pyogenic granulomas show multiple dilated capillaries with prominent, swollen endothelial cells and edema in the stroma. They often have a pedunculated gross appearance.
Due to their tendency to bleed, pyogenic granulomas are typically treated. Preferred methods include shave removal or excision followed by electrodesiccation of the base. Repeated application of silver nitrate can also be an effective, simpler treatment. Recurrence is more common with therapies other than complete excision.
For comprehensive information, refer to Pyogenic Granuloma.
Cutaneous Horn
A cutaneous horn, or cornu cutaneum, is a skin lesion composed of compacted keratin that forms a conical, exophytic projection resembling a horn. These lesions are more common in fair-skinned individuals in their 60s and 70s. Cutaneous horns are clinical manifestations of underlying skin disorders rather than unique pathological entities themselves. They can arise from various hyperkeratotic lesions, such as actinic keratoses, seborrheic keratoses, benign verrucae, and squamous cell carcinomas. While most cutaneous horns are benign, malignancy, particularly squamous cell carcinoma, can be found at the base in approximately 20% of cases.
The exact cause of cutaneous horns is not clear, but they are secondary to underlying skin conditions. Histologically, they are composed of compact hyperkeratosis, which can be orthokeratotic or parakeratotic, often with associated acanthosis. The base reflects the pathology of the underlying lesion. Given the potential for malignancy at the base, excisional biopsy is recommended for cutaneous horns.
For detailed information, see Cutaneous Horn.
Keloid
Keloids are fibrotic papular lesions that develop as an abnormal healing response to skin injuries such as acne, trauma, surgery, and piercings. Common sites for keloids include earlobes, chest, lower legs, upper back, and jawline. Unlike hypertrophic scars, keloids extend beyond the boundaries of the original scar. They can be associated with pruritus, pain, and sometimes a burning sensation.
Keloids occur across all races, but are more prevalent in individuals with darker skin. Incidence rates are equal between men and women, and they can occur at almost any age, although they are rare in those over 65. The precise pathophysiology of keloids is not fully understood.
Keloid formation involves excessive fibroblast proliferation, leading to an overproduction of extracellular matrix (ECM) proteins like collagen and fibronectin. Transforming growth factor beta (TGF-β) plays a significant role in regulating fibroblast activity and upregulating metalloproteinases contributing to keloid development. Collagen type III production is significantly elevated in keloids, and overall collagen exhibits reduced crosslinking and a disorganized fibrillar pattern.
Treatment for keloids is challenging, and recurrence rates are high across all therapies. Prevention is the best approach. Individuals with a history of keloids are prone to developing new ones after skin trauma or surgery. However, different skin areas have varying propensities for keloid formation.
Intralesional steroids are a primary treatment. Corticosteroids reduce fibroblast collagen synthesis. Triamcinolone acetonide or diacetate injections are commonly used, with caution advised to start with lower concentrations to avoid dermal atrophy and hypopigmentation. Silicone gel or occlusive sheeting is also used to reduce keloid size and prevent further development. Surgical excision alone is not recommended due to high recurrence rates, but combined with steroid injections or radiation therapy, it can be more effective. Cryotherapy and laser surgery are other modalities with variable success.
For further information, consult Wound Healing, Widened and Hypertrophic Scar and Keloid and Hypertrophic Scars.
Nevus Sebaceus of Jadassohn
Nevus sebaceus of Jadassohn is a congenital, yellowish plaque usually found on the head and neck. While often classified with skin adnexal tumors, it is actually an epithelial nevus. Histopathologically, it shows papillomatosis, acanthosis, sebaceous hyperplasia, and often a lack of hair follicles. The lesion tends to enlarge and become more wart-like with age.
Tumors can arise within a nevus sebaceus over time, mostly benign ones like syringocystadenoma papilliferum and trichoblastoma. Rarely, malignant tumors, primarily basal cell carcinoma, can develop. Nevus sebaceus lesions are typically yellowish-orange, waxy, hairless plaques. An accelerated growth phase may occur during adolescence due to hormonal changes. The lesion’s natural progression includes evolving from a smooth lesion to a verrucous, thickened plaque with crusting and ulceration. Complete surgical excision is the recommended treatment.
Seborrheic Keratosis (SK)
Seborrheic keratosis (SK), also known as seborrheic wart, senile keratosis, or basal cell papilloma, is a common benign, noninvasive, hyperplastic epidermal lesion. Despite its name, it has no relation to sebaceous gland function. The term “seborrheic” refers to its greasy appearance and prevalence in areas with high sebaceous gland concentration, such as the face, shoulder, chest, and back. SKs are the most common benign skin tumors in middle-aged and elderly populations.
Seborrheic keratoses typically present as small, flesh-colored, waxy papules with a characteristic “stuck-on” appearance. They can exhibit epidermal hyperplasia and exophytic growth, becoming raised and resembling a cutaneous horn or wart. They can also become pedunculated. SKs can be solitary or multiple. Stucco keratosis is a variant presenting as multiple keratotic papules on the hands, feet, and legs.
In individuals with darker skin, dermatosis papulosa nigra, a variant characterized by multiple small black or dark-brown waxy papules on the forehead, malar, and neck regions, may develop. Older SK lesions can darken, mimicking melanoma, but their elevated position, distinct borders, and greasy texture often indicate their benign nature.
Seborrheic keratoses may be mildly pruritic or asymptomatic. Sudden eruption of multiple lesions, known as the sign of Leser-Trelat, may indicate internal malignancy, particularly gastrointestinal neoplasms.
The etiology of seborrheic keratosis is unknown. Histologically, SKs are exophytic with a flat base at the epidermis level, showing an increased number of basal cells forming cords or sheets with keratin cysts (horn cysts). Varying degrees of acanthosis, papillomatosis, and hyperkeratosis are present. Hyperpigmentation of basal cells can further complicate diagnosis.
Treatment for seborrheic keratosis is often unnecessary. However, for removal, curettage and cryoablation are common methods. Topical 40% hydrogen peroxide solution has also shown effectiveness, particularly for facial keratoses. Rarely, malignant lesions can arise within SKs, or malignancies like melanoma may mimic SKs, necessitating excision biopsy when malignancy is suspected.
For more information, see Seborrheic Keratosis.
Actinic Keratosis (AK)
Actinic keratoses (AK), also known as solar or senile keratoses, are scaly papules, patches, or plaques on sun-damaged skin. They are most common in fair-skinned individuals with a history of chronic sun exposure and typically appear after age 50, although they can present as early as 20 years old. Men are more frequently affected than women. Immunosuppressed individuals are at higher risk of developing AKs and malignant transformation to squamous cell carcinoma.
Actinic keratoses can present with keratin excrescences, referred to as cutaneous horns. They have a rough, sandpaper-like texture and can be red, pink, yellow, brown, or gray. Clinically, AKs may resemble psoriasis, Bowen disease, or Paget disease. The most significant concern with AKs is their premalignant potential, with an annual malignant transformation rate to squamous cell carcinoma estimated at less than 1% per lesion.
Ultraviolet solar damage to epidermal keratinocytes is the primary cause of actinic keratoses. Other causes include artificial UV light, x-ray irradiation, and exposure to aromatic hydrocarbons. Histologically, actinic changes are limited to the interfollicular epidermis, sparing follicles. The lower epidermal layers are most affected, and the stratum corneum exhibits parakeratosis.
Prevention through sun avoidance and habitual use of high-factor sunscreen is crucial. Treatment options for AKs include cryoablation, curettage, electrodesiccation for isolated lesions, and topical 5-fluorouracil for multiple lesions. Laser resurfacing and dermabrasion are also used. Topical therapy is advantageous for treating subclinical AKs surrounding visible lesions. Excision is generally not necessary unless malignancy is suspected.
For comprehensive details, refer to Actinic Keratosis.
Bowen Disease and Bowenoid Papulosis
Bowen disease is essentially squamous cell carcinoma in situ. Bowenoid papulosis describes similar histologic changes found within genital warts. Bowenoid papulosis is generally considered benign, unlike Bowen disease, which has malignant potential. Itching is a common symptom in bowenoid papulosis, and lesions are often scaly, crusted, erythematous plaques, possibly linked to HPV-16 or 18 infection.
In Bowen disease, a scaly red plaque on sun-damaged skin carries a risk of progressing to invasive squamous cell carcinoma. Squamous cell carcinoma arising from Bowen disease tends to be more aggressive than those from actinic keratoses, with a higher metastasis rate. Bowen disease on the penis is termed erythroplasia of Queyrat.
Histologically, Bowen disease shows atypical epithelial changes, including cytoplasmic vacuolization, nuclear hyperchromasia, dyskeratosis, increased mitoses, and acanthosis, while maintaining an intact dermal-epidermal interface.
Treatment for Bowen disease traditionally includes curettage and electrodesiccation for small lesions, though recurrence rates can be high. Surgical excision is often considered the standard treatment. Cryoablation and irradiation are also used. Immunosuppression is a significant risk factor for recurrence.
For further reading, see Bowen Disease.
Sebaceous Adenoma (SA)
Sebaceous adenoma (SA), also known as sebaceous epithelioma or sebaceoma, is a benign nodular and lobulated skin adnexal tumor with sebaceous differentiation. It occurs primarily in areas rich in sebaceous glands, mainly the head and neck, but can appear anywhere hair-bearing. These are typically small (2-10 mm), tan, reddish-brown, or yellowish papules, sometimes with central speckles. Sebaceous adenoma can be challenging to differentiate from basal cell carcinoma, often requiring biopsy.
Multiple eruptive sebaceous adenomas can be associated with visceral carcinoma, specifically Muir-Torre syndrome, linked to adenocarcinomas of the colon, stomach, and other organs. Muir-Torre syndrome is related to genetic mutations in DNA mismatch repair genes.
Histologically, sebaceous adenoma is multilobulated and connected to the surface epidermis. It is composed of sebaceous lobules with mature sebocytes, undifferentiated basaloid cells, and transitional cells. Sebocytes have pale cytoplasm and central nuclei, while germinative cells have basophilic cytoplasm. Sebaceous adenoma is defined by having 50% or more sebocytes. It is benign, with no malignant potential, but excisional biopsy is recommended to rule out basal cell carcinoma.
For more detailed information, consult Sebaceous Adenoma.
Conclusion
Differential diagnosis of skin colored papules encompasses a wide range of benign and potentially malignant conditions. Careful clinical examination, consideration of lesion characteristics, patient history, and when necessary, histological evaluation are essential for accurate diagnosis and appropriate management. This overview serves as a guide to understanding the key features of common skin colored papules and aids in the process of differential diagnosis. It is important to consult with a dermatologist for definitive diagnosis and treatment of any skin lesions.
