Dysplastic nevi: clinical and macroscopic presentation
Dysplastic nevi often debut in adolescence and are predominantly localized on the upper half of the trunk. A single patient may have up to a hundred of them, and the condition can be either sporadic or hereditary.
Clinical diagnosis is based on 5 main criteria:
- Lesion size greater than 5 mm.
- Indistinct borders.
- Asymmetrical shape.
- Irregular pigmentation.
- Presence of a red hue.
Macroscopically, dysplastic nevi are larger than common nevi (up to 1.2 cm) with bizarre outlines. Color ranges from light brown to black, and amelanotic (amelanotic) forms also occur. A mandatory feature is the presence of a mottled macular component with blurred edges. If a papule rises in the center of such a macule, the lesion acquires a specific appearance compared to a «fried-egg».
Histological signs of dysplasia
Microscopically, the lesion size exceeds 4 mm. Lentiginous melanocytic hyperplasia develops: nests of melanocytes are unevenly distributed along the dermoepidermal junction and coalesce into bridges.
A key architectural feature is the «shoulder» sign. This means that the epidermal component of the nevus extends beyond the dermal component peripherally by at least three epidermal rete ridges.
Stromal reactions appear in the papillary dermis as eosinophilic fibroplasia and perivascular lymphocytic infiltrates.
Clinically important rule: according to the WHO classification, the pathologist does not indicate the grade of dysplasia in a routine report. However, the presence of marked cellular atypia must be recorded, as this condition dramatically increases the risk of developing melanoma.
Malignant melanoma: pathogenesis and risk factors
Melanoma is a highly malignant tumor originating from atypical melanocytes. It arises de novo or on the background of pre-existing nevi.
The main triggering factor is ultraviolet radiation. The cumulative dose of UV received in the first 5 years of life, as well as childhood sunburns, is of critical importance. Individuals with fair skin, red or light hair, and numerous freckles are in the highest risk group.
About 10% of cases are genetic in origin. A family history (multiple nevi and melanoma) reveals autosomal dominant mutations in tumor suppressor genes: $p16$ (locus $9p21$) and $CDK$ (locus $12q13$).
Growth phases and diagnosis
The progression of most melanomas (especially the superficial spreading form, which accounts for more than 2/3 of cases) is divided into two stages:
- Horizontal growth phase: the tumor grows slowly (over years) within the epidermis through the proliferation of atypical cells. Macroscopically, this is an asymmetrical macule with uneven pigmentation.
- Vertical growth phase: begins with the breach of the basement membrane. A bulky nodule forms in the dermis. The tumor surface becomes uneven, crusts over, bleeds easily, and the pigmentation becomes blue-black.
For early clinical evaluation, the ABCD rule is applied: A — asymmetry, B — border irregularity, C — color variation, D — diameter greater than 6 mm. However, it performs poorly for nodular, small, and amelanotic forms.
Assessment of invasion: Clark and Breslow
The prognosis of the disease directly depends on the depth of tumor invasion. Two scales are used in pathomorphology:
Clark levels of invasion (assessment of anatomical layers):
- I — tumor confined to the epidermis (melanoma in situ).
- II — invasion into the papillary dermis (without expansion).
- III — complete filling of the papillary dermis.
- IV — infiltration of the reticular dermis.
- V — invasion into the subcutaneous adipose tissue.
Breslow thickness: measured in millimeters and considered a more objective prognostic criterion.
In some cases, the immune system attacks the tumor, causing its partial or complete regression (clinically visible as depigmentation zones, histologically as fibrosis and inflammation). Paradoxically, this process is associated with a poor prognosis and frequent metastasis.
Briefly: answers to topical questions
What are the main histological types of melanoma distinguished in pathomorphology?
The provided sources distinguish four main forms of cutaneous melanoma:
- Superficial spreading — the most frequent form (75%); also classified in the classification as melanoma on skin with low cumulative sun damage.
- Nodular — accounts for 15% of cases.
- Lentigo maligna melanoma — occurs in 5% of cases.
- Acral lentiginous — accounts for 2–3%.
How exactly is melanoma thickness measured according to Breslow?
Breslow thickness of melanoma is measured in millimeters from the upper granular cell layer of the epidermis to the deepest point of tumor cell invasion. This indicator is a significant and reproducible prognostic parameter.
The following tumor thickness gradations are distinguished:
- Up to 0.76 mm.
- From 0.76 to 1.5 mm.
- From 1.5 to 4 mm.
- Greater than 4 mm.
What are the main pathways of metastasis of malignant melanoma?
The main pathways of malignant melanoma metastasis are lymphogenous and hematogenous.
- Lymphogenous pathway — predominantly occurs in the early stages, with the first metastases appearing in regional lymph nodes.
- Hematogenous pathway — responsible for distant metastasis. Melanoma exhibits a pronounced tendency toward early hematogenous metastasis to the lungs, liver, brain, and bones, even with a small primary tumor thickness.
What types of common melanocytic nevi exist according to their histological structure?
Based on the histological structure and location of nevus cell nests, three main types of common melanocytic nevi are distinguished.
| Nevus type | Localization of nevus cells |
|---|---|
| Junctional | Epidermal-dermal junction zone |
| Compound (mixed) | Cell nests in both the epidermis and the dermis simultaneously |
| Dermal (intradermal) | In the dermis only |
These types reflect the dynamics of maturation: a junctional nevus evolves over time into a compound one and then sinks deeper, becoming intradermal.
For rapid clinical assessment during an appointment, use the ABCD rule: A (Asymmetry), B (Border irregularity), C (Color variation), D (Diameter greater than 6 mm).
Class and exam questions
What is the "shoulder" sign in the histological examination of a nevus?
This is a sign of a dysplastic nevus, in which the epidermal component exceeds the dermal one in extent and extends peripherally beyond it by at least 3 epidermal ridges.
Should the degree of dysplasia be indicated in the histological report?
No, according to the WHO classification (2006), the degree of dysplasia is not routinely specified. The only clinically significant exception is the presence of pronounced cellular atypia, which must be reported to the physician.
What does spontaneous focal regression of melanoma indicate?
Clinically, it manifests as foci of depigmentation, and histologically as fibrosis and an inflammatory infiltrate. Despite being an immune response, the presence of regression is a sign of an unfavorable prognosis and is associated with metastasis.
What else to study on this topic
- Rare melanocytic nevi: plexiform spindle cell and combined nevi
- Cytological features of atypical melanocytes and the use of immunohistochemistry (IHC)
- Limitations of the ABCD rule in nodular melanoma
- Relationship between skin phototype and melanoma risk
Master the entire topic in the "Pathological Anatomy" course
This is a summary. The course covers everything tested in classes and exams.
- Complete study guide on "Melanocytic nevi" and 4,414 more pages on the subject
- Assignments and quizzes after every topic — just like in a colloquium
- AI tutor answers questions on the topic anytime
- 153 video lessons on the subject
Other topics in "Chapter 23. Skin Diseases"
Free video lessons: pathological anatomyShort lessons with study notes — no registration required.
Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.