Solar lentigines / seborrheic keratoses / lichen planus-like keratosis (full text)
|Description||This chapter provides the full text of all previous chapters on dermoscopy of Solar lentigines / seborrheic keratoses / lichen planus-like keratosis (full text)|
|Author(s)||Ralph P. Braun · Stephanie Nouveau|
|Responsible author||Ralph Braun → send e-mail|
|Status update||July 25, 2018|
|Status by||Ralph P. Braun|
- 1 Solar lentigo
- 2 Seborrheic keratoses
- 3 Milia-like cysts:
- 4 Comedo-like openings:
- 5 Fissures and ridges:
- 6 Network-like structures:
- 7 Cerebriform pattern:
- 8 Fat-fingers:
- 9 Sharply demarcated borders:
- 10 Typical hairpin blood vessels :
- 11 Wobble test:
- 12 Lichen Planus-like Keratosis
Solar lentigines, Solar lentigo, Seborrheic keratoses, Seborrheic keratosis, Lichen planus like keratosis Solar lentigines / seborrheic keratoses – cite! Solar lentigines (message) Solar lentigines / seborrheic keratoses – participate!
Solar lentigines are sharply circumscribed, uniformly pigmented macules that are located predominantly on the sun-exposed areas of the skin, such as the dorsum of the hands, the shoulders, and the scalp. Lentigines are a result of hyperplasia of keratinocytes and melanocytes, with increased accumulation of melanin in the keratinocytes. They are induced by ultraviolet light exposure.
Unlike freckles, solar lentigines persist indefinitely. Nearly 90% of Caucasians over the age of 60 years have these lesions. Due to the increased prevalence of lentigines in the elderly, these lesions are sometimes referred to as “lentigo senilis”. However, younger individuals who tend to burn after ultraviolet exposure can also develop lentigines after acute or prolonged ultraviolet light exposure. Clinically, solar lentigines may be oval, round, or irregular in shape and can vary from a few millimeters to a few centimeters in diameter. Most lesions have a uniform light brown color; however, there are instances when they vary from dark brown to black. One variant of solar lentigo, “ink-spot” lentigo, has a jet-black color. Actinic purpura or other signs of solar damage can frequently be found in the skin surrounding solar lentigines. Solar lentigines are benign lesions that can evolve to a pigmented seborrheic keratosis. Histologically, it is characterized by club-shaped rete ridges with small nub-like extensions. In addition, there is an increased number of melanocytes and increased pigmentation in the basal keratinocytes. Although most solar lentigines are easily recognized on clinical examination, some lesions pose diagnostic challenges because their clinical appearance resembles that of melanoma. Dermoscopy can be helpful in correctly differentiating a solar lentigo from melanoma. The key dermoscopic features of solar lentigines are as follows:
The presence of a sharply demarcated and irregularly curved border is characteristic of solar lentigines. Often, portions of the border are scalloped, giving a motheaten appearance
Homogenous light brown pigmentation
Many lesions have no structures or networks, only containing light brown and structureless areas; the term “jelly sign” had been proposed to describe the pigment quality of these lesions. The pigment appears as if jelly had been smeared on the skin surface.
There may be an area of faint, reticulation. This correlates with the presence of melanocytes and melanin-filled keratinocytes in the rete ridges.
They are areas consisting of fine parallel running lines of light brown to dark brown colors. They resemble the dermatoglyphics of a human fingerprint.
Lentigines located on the scalp and face share features of pigmented melanocytic lesions in this special location revealing a pseudonetwork pattern. This is created when a diffusely pigmented area is interrupted by nonpigmented adnexal openings .
Symmetric brown follicular pigmentation
In a solar lentigo the pigment around hair follicles is distributed in a symmetric fashion creating small brown circles. The pigment is usually light brown in color and similar to the color of the rest of the lesion. While the pigment is usually distributed symmetrically around the follicle, some follicles may appear asymmetrically pigmented. These asymmetrically pigmented follicles appear as brown crescent shaped structures. However, these asymmetric follicles will also have a brown color like the rest of the lesion. If the color of the pigment around the follicle, whether symmetric or asymmetric, is of a grayish hue or differs from the rest of the lesion then melanoma needs to enter the differential diagnosis.
Ink-spot lentigines have their own distinct dermoscopic pattern.These lesions have a very prominent blackpigmented network, which has an almost three-dimensional quality under dermoscopy. The network lines can be either thin or thick in width, and the network ends abruptly at the edge of the lesion
Seborrheic keratoses are benign epithelial lesions that can appear on any part of the body except for the mucous membranes, palms, and soles. The lesions are quite prevalent in people older than 30 years. The etiology of seborrheic keratoses remains unclear. Ultraviolet light exposure may be responsible for the development of some seborrheic keratoses because they appear to evolve from solar lentigines; however, many develop in areas of the skin naturally protected from ultraviolet light exposure, such as the inframammary (intertriginous) areas. Clinically, early seborrheic keratoses are light- to dark brown oval macules with sharply demarcated borders (solar lentigo). As the lesions progress, they transform into plaques with a waxy or stuck-on appearance.
The surfaces of these lesions have a warty and keratotic appearance. Often, the lesions have follicular plugs scattered over their surfaces. The size of the lesions varies from a few millimeters to a few centimeters. Histologically, there are several distinct forms of seborrheic keratoses. In general, the lesions are characterized by papillomatous epidermal hyperplasia of uniform and monotonous keratinocytes and the presence of pseudocysts. The diagnosis of most seborrheic keratoses is straightforward. However, some seborrheic keratoses, especially the deeply pigmented variant, can simulate malignant melanomas. Thin, early lesions have moth-eaten borders and fingerprint-like structures as described for solar lentigines. Thicker pigmented seborrheic keratoses have the typical dermoscopy features as follows :
They are white-to-yellow, round structures that appear very bright when contrasted with their dark brown or black surroundings. The presence of multiple milia-like cysts in pigmented seborrheic keratoses conjures up an image of “stars in the sky.” Milia-like cysts can also be seen in non-pigmented seborrheic keratosis and other lesions such as basal cell carcinoma and melanocytic lesions including congenital nevi and melanoma. However, if the lesion is non-melanocytic and is not a basal cell carcinoma then the presence of milia-like cyst is diagnostic of seborrheic keratoses specially if more then three are seen. It is interesting to note that the quality of milia-like cysts appear somewhat different in seborrheic keratosis and melanocytic lesions. In melanoma and congenital nevi the cysts appear “starry”, which is defined as small, bright and sharp. In seborrheic keratosis they appear “cloudy”, defined as larger and hazier in appearance. Histologically, the cysts correspond to intraepidermal, keratin-filled cysts. It is important to be aware that milia-like cysts are more conspicuous with non-polarized dermoscopy and are often difficult to visualize with polarized dermoscopy.
They are round to ovoid craters that have black or brown comedo like plugs. Histologically, they correlate with keratin-filled invaginations of the skin surface.
Fissures and ridges:
Fissures (sulci) are comedo-like openings, which are not round but rather linear and appear as dark brown to black linear to curvilinear structures within the lesion. The presence of numerous fissures and ridges can result in the formation of network-like structures or result in a cerebriform pattern. Histologically, they represent deep invaginations of the epidermis, filled with keratin.
Interlacing fissures and ridges can create an appearance of network-like structures. The quality of the grid of network-like structures in a seborrheic keratosis differs from the network grid seen in melanocytic nevi by being significantly larger. However, at times the network-like structure in a seborrheic keratosis can look very similar to that of a nevus. Clinical examination of the lesion via side lighting can make the ridges more evident, thereby making it easier to differentiate network-like ridges in seborrheic keratosis and pigment network in melanocytic lesions.
Multiple fissures (sulci) and ridges (gyri) may produce a cerebriform pattern, where the structures resemble sulci and gyri of the brain (brain-like appearance). These features are generally associated with an acanthotic seborrheic keratosis.
Fat fingers are linear and wide dermoscopic structures corresponding to ridges. They often appear as short sausage-shaped structures. Their colors vary from tan/brown, blue to hypopigmented. They are named fat-fingers because their shapes can resemble a straight finger (linear), bent finger (curvi-linear), or finger tip (oval–circular).
Sharply demarcated borders:
As known from clinical examination, seborrheic keratosis often have sharply demarcated borders.
Typical hairpin blood vessels :
Some seborrheic keratoses are associated with hairpin vessels. These hairpin vessels can appear as perfect “U”-shaped vessels of as “U”-shaped vessels that are twisted upon themselves. Typical hairpin blood vessels have a whitish halo around the blood vessel corresponding to the surrounding keratin. It is important to note that some melanomas can have hairpin vessels, but these vessels generally do not have the surrounding white halo but rather have a pink halo. Similar hairpin vessels on a pink background can be seen in irritated seborrheic keratosis.
This is a dynamic test that can only be performed with a contact dermoscopy device. The test is performed as follows: once the contact plate of the dermoscope is firmly pressed down (pressure in vertical direction) against the lesion, it is then moved slightly back and forth in the horizontal plane (parallel to the skin surface). Seborrheic keratosis will appear to stick to the glass plate and move en bloc with the movement of the dermoscopic face plate. In other words, they will slide back and forth. In contrast, nevi will not move en bloc but, rather roll back and forth. In other words, intradermal nevi will wobble. Knowledge of the above-described dermoscopic features and patterns seen in seborrheic keratosis will often prove valuable in differentiating seborrheic keratoses from other lesions, including melanoma. However, irritated or traumatized seborrheic keratoses can mimic melanoma or squamous cell carcinoma. In these cases the history of trauma or the presence of typical criteria for seborrheic keratoses in another part of the lesion might be comforting. However, it is important to remember that skin cancer can develop within a seborrheic keratosis, and thus a biopsy is justified for atypical appearing seborrheic keratosis.
Lichen Planus-like Keratosis
Lichen planus-like keratosis, also known as LPLK and lichenoid keratosis, is one of the common benign neoplasms of the skin. It is believed to be either a seborrheic keratosis or a solar lentigo that is undergoing regression. Supporting evidence has been published beginning with Mehregan’s findings of the presence of lentiginous epidermal hyperplasia in lesions interpreted as LPLK. Further supporting evidence can be found by Laur, et al who in 1981 published a detailed clinical-histopathologic correlation in the JAAD . In addition, Goldenhersh et al , described performing biopsies of lentigines on two instances. The first being a biopsy of a solar lentigo and 5 years later, after the lesion had demonstrated a clinical change into a solitary lichen planus‐like keratosis.
Clinical and Histologic Appearance
Lichen planus-like keratosis is a great masquerader with a differential diagnosis including basal cell carcinoma, squamous cell carcinoma and melanoma. The wide differential diagnosis is due to the extreme variability in characteristic appearance with many pigmentation and morphologic possibilities. The clinical appearance depends on its stage of evolution.
The lesion can appear as a macule or papule that is pink, pinkish brown, pinkish orange, rust colored, purplish brown, dusky violaceous or blue-gray to black. Some lesions are characterized by a velvety appearance, some have a fine scale, while others have accentuated skin markings. Lesions can be solitary or in some cases multiple.
The histologic features of early stage of LPLK include hypergranulosis, epidermal hyperplasia, a few necrotic keratinocytes and a superficial, bandlike lichenoid infiltrate. Clinically these lesions appear as pink macules or papules and may be difficult to distinguish from basal cell carcinoma or squamous cell carcinoma.
Histologically intermediate stage LPLK is characterized by melanophages, inflammatory cells and fibrosis, with features consistent with either a lentigo or a seborrheic keratosis. In some cases, clinically, the lesion may be difficult to distinguish from melanoma (melanoma on sun-damaged skin, lentiginous melanoma, lentigo maligna melanoma).
Late stage LPLK is characterized histologically by papillary fibrosis, telangiectasias, and melanophages. The lesions have a more blue-gray to black clinical appearance and may be difficult to distinguish from melanoma.
Dermoscopy allows the detailed visualization of the structures found within the epidermis, dermoepidermal junction and papillary dermis. This information creates a bridge between the clinical and histologic correlates, thus narrowing the differential and allowing for a more accurate assessment of the lesion.
Early Stage LPLK
Lichen planus-like keratosis in its early stage is characterized by polymorphous vessels: dotted vessels and short thin vessels that are either linear, slightly curved or serpentine in appearance. The lesions may appear structureless, pink-white with an orange or yellow hue, colors that are not bright nor saturated, borders that are scalloped and a scale. Shiny white structures (SWS, or crystalline structures) are commonly seen with LPLK, that appear as white strands or blotches. Rosettes can also be seen with LPLKs that coincide with actinically damaged skin.
Here are two examples of early stage LPLKs:
Intermediate Stage LPL
Lichen planus-like keratosis in the intermediate phase is characterized by two patterns. The first pattern depicts the dermoscopic features of a solar lentigo (fine lines parallel; straight, slightly curved, long or short, with sharply demarcated and scalloped borders) with the addition of regression structures: focal gray dots/granules.
The second pattern portrays the features of a seborrheic keratosis (borders sharply demarcated, milia-like cysts, comedo-like openings, fissures, ridges, looped vessels and fine vessels surrounded by a halo) with the addition of regression structures: focal gray dots/granules.
Late Stage LPLK
Lichen planus-like keratosis in the late phase is characterized by scattered clumps of pigment with diffuse gray dots/granules or gray dots/granules that form what is known as a diffuse granular pattern, and borders that are often scalloped or have a moth-eaten appearance.
In a recent study for the US  LPLKs were compared with non-LPLK cutaneous lesions. LPLKs had the clinical differential diagnosis of basal cell carcinoma, squamous cell carcinoma, neavus, melanoma, seborrehic keratosis, lentigo, and actinic keratosis. Dermoscopic features that were found to distinguish LPLKs from other lesions include: Overall organized dermoscopic structures, scale, orange color, coarse +/- fine granules and peppering as the only feature present. LPLKs were less likely to have moth-eaten borders and irregular dots compared to the other lesions.
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- Liopyris et al.: Clinical and dermoscopic features associated with lichen planus-like keratoses that undergo skin biopsy: A single-center, observational study. Australas. J. Dermatol. 2018;. PMID: 30450536. DOI.