NP is thought to be due to sensory neuropathy involving cutaneous branch of the posterior divisions of spinal sensory nerves.
The histological hallmark is of scattered single cell apoptosis in epidermis with secondary epidermal dyspigmentation and pigment incontinence. Crucially there is no primary dermal inflammatory, degenerative or neoplastic cause for dyspigmentation.
Notice although a normal lid has a large sebaceous gland it is actually beautifully elongated and compact to not distort the surface of the eyelid, so that the conjuntiva remains closely opposed to the eyeball. By contrast the eye las has relatively small sebaceous glands.
This small sebaceous trichofolliculoma was large enough to cause persistent irritation / conjunctivitis and clinical concern of a tumour (?BCC) resulting in a formal excision.
Squamoproliferative lesion was invented by some hotshot pathologist pretending its a diagnostic entity, but it actually means nothing more than an unspecified and unqualified proliferating squamous “lesion”.
CLYD cutaneous syndrome was first proposed by Rajan et al in 2009 (Arch Dermatol. 2009 Nov; 145(11): 1277–1284.). This brought together three syndromes caused by a mutation in the CYLD gene on the long arm of Chromosome 16.
@javiperezhisto @pembeoltulu So whats is my approach. Well I estimate the average curvature of flat epidermis (see the blue lines) ignoring any focal large deviations. This to the best of my estimation is the “average” level of flat skin ignoring physiological and tumour related undulations
@javiperezhisto @pembeoltulu Ignoring the focal abnormally large undulations / deviations, you can see that on average the epidermis maintains its level along the drawn lines with less than 0.5 mm of deviation. So thats my best guess for the “estimated deepest vertical cross section of tumour” in sampled sec