Sunday, August 29, 2010


Lines take precedence over other structures and lines reticular is a common structure because we look at a lot of nevi. Remember it is made up of the arrangement of pigmented cells over the dermal papillae (clear holes) and along the sides of the rete ridges (pigmented network).

View these YouTube videos on the different types of lines. Click on the arrow and when it starts go to the bottom of the screen and change the 360 resolution to 1080 and then click on the box with the arrows pointing out to enlarge to full screen. These videos are recorded in high definition. Press ESC on your keyboard to return to normal size.

View this YouTube video.

View this YouTube video on Lines Parallel

White Lines

White lines are seen in mainly BCCs, invasive melanomas and in Dermatofibromas. They are best seen with a polarising dermatoscope. They may cross each other at right angles.  Below is an extract from a recent article on the topic . 

Superficial spreading melanoma begins as in situ melanoma and progresses by dermal invasion with subsequent metastases. The functional interaction of melanoma cells with surrounding neoplastic cells, tumoral stoma, inflammatory milieu, and growth factors is critical, and fibroblasts serve as the major source of extracellular matrix and contribute to melanoma progression. Basic fibroblast growth factor (bFGF) appears to play a critical role in the ability of melanoma cells to invade and proliferate in the papillary dermis. In primary invasive melanomas, the greatest expression of bFGF is along the advancing front of the neoplasm, adjacent to the fibrotic changes in the dermis, and it is usually not detectable in definitive in situ lesions.Melanocyte-fibroblast interactions and tumor-induced collagen turn-over appear to play a critical role in melanoma evolution through both radial and vertical growth phases. Melanocytes in the radial and early vertical growth phases have been shown to induce de novo type I collagen synthesis by fibroblasts juxtaposed to microinvasive nests in the papillary dermis; staining with Sirius red can identify tightly woven collagen bundles encircling these melanoma nests at the dermoepidermal junction. In contrast, this has not been demonstrated in dysplastic nevi. Evidence of stromal remodeling can also be identified with reflectance confocal microscopy by visualizing bundles of collagen fibers that histopathologically correspond to fibroplasia and to regression structures on dermatoscopy. Type I collagen with extracellular matrix glycoproteins, such as tenascin C and fibronectin, have been shown to facilitate dermal invasion during the more advanced vertical growth phase by forming tubular channels that ensheath and isolate invading melanoma cells. Based on the available preclinical data, we hypothesize that CS may reflect de novo synthesis or remodeling of type I collagen in the papillary dermis, signifying changes in the extracellular matrix induced by tumor progression and dermal invasion.