Dysplastic Nevi: Clinical and Macroscopic Presentation
Dysplastic nevi often present during adolescence and are predominantly localized on the upper trunk. A single patient may have up to a hundred lesions, and the condition can be sporadic or inherited.
Clinical diagnosis relies on 5 main criteria:
- Lesion size greater than 5 mm.
- Irregular borders.
- Asymmetrical shape.
- Variable pigmentation.
- Presence of a pink or 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 forms also occur. A mandatory feature is the presence of a macular component with indistinct borders. If a papule rises in the center of such a macule, the lesion acquires a specific appearance often compared to a "fried-egg".
Histological Features of Dysplasia
Microscopically, the lesion size exceeds 4 mm. Lentiginous melanocytic hyperplasia develops: nests of melanocytes are unevenly distributed along the dermal-epidermal junction and coalesce into bridges.
A key architectural feature is the "shoulder" phenomenon. This means that the epidermal component of the nevus extends peripherally beyond the dermal component by at least three epidermal rete ridges.
In the papillary dermis, stromal reactions occur in the form of eosinophilic fibroplasia and perivascular lymphocytic infiltrates.
Clinically important rule: according to WHO guidelines, pathologists do not routinely grade the degree of dysplasia in standard reports. However, the presence of severe cellular atypia must be explicitly noted, 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 within pre-existing nevi.
The primary precipitating factor is ultraviolet radiation. The cumulative UV dose received during the first 5 years of life and childhood sunburns are of critical importance. Individuals with fair skin, red or light-colored hair, and numerous freckles are at the highest risk.
Approximately 10% of cases have a genetic basis. 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 type, which accounts for over 2/3 of cases) is divided into two stages:
- Radial growth phase: the tumor grows slowly (over years) within the epidermis through the proliferation of atypical cells. Macroscopically, this presents as an asymmetric macule with irregular pigmentation.
- Vertical growth phase: begins with the breaching of the basement membrane. A distinct nodule forms in the dermis. The tumor surface becomes irregular, crusts over, bleeds easily, and its pigmentation shifts to dark 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, this rule performs poorly for nodular, small, and amelanotic forms.
Assessing Invasion: Clark and Breslow
Prognosis depends directly on the depth of tumor penetration. Pathology utilizes two staging scales:
Clark Levels of Invasion (anatomical layers):
- Level I — tumor limited to the epidermis (melanoma in situ).
- Level II — invasion into the papillary dermis (without filling it).
- Level III — filling and expansion of the papillary dermis.
- Level IV — infiltration into the reticular dermis.
- Level V — invasion into the subcutaneous adipose tissue.
Breslow Thickness: measured in millimeters from the granular cell layer of the epidermis to the deepest invasive tumor cell. It is considered a more objective prognostic criterion.
In some cases, the immune system attacks the tumor, causing partial or complete regression (clinically visible as depigmented zones, histologically as fibrosis and inflammation). Paradoxically, this process is associated with an unfavorable prognosis and frequent metastasis.