: 1668 : 567 
Punctate porokeratosis is a skin condition associated with either classic porokeratosis or linear porokeratosis types of porokeratosis, and is characterized by multiple, minute, and discrete punctate, hyperkeratotic, seed-like skin lesions surrounded by a thin, raised margin on the palms and soles. : 535 : 1668 
Porokeratosis plantaris discreta is a skin condition that occurs in adults, with a 4:1 female preponderance, characterized by a sharply marginated, rubbery, wide-based papules. : 213   It is also known as "Steinbergs lesion". It was characterized in 1970. Genetics
Linear porokeratosis has been associated with mutations in the PMVK and MVD genes. The PMVK gene encodes the enzyme phosphomevalonate kinase and the MVD gene encodes the enzyme diphosphomevalonate decarboxylase. Diagnosis
Pathology
Porokeratosis has a characteristic histomorphologic feature known as a cornoid lamella. Treatment
Dermabrasion

See also
List of cutaneous conditions
List of cutaneous conditions associated with increased risk of nonmelanoma skin cancer

References
External links

Database of rare diseases at Orphanet
NIHs Genetic and Rare Diseases Information Center
The fibrils are, however, far from innocuous, as they keep the protein homeostasis network engaged, release oligomers, cause the formation of toxic oligomers via secondary nucleation, grow indefinitely spreading from district to district and, in some cases, may be toxic themselves.Calcium dysregulation has been observed to occur early in cells exposed to protein oligomers. These small aggregates can form ion channels through lipid bilayer membranes and activate NMDA and AMPA receptors. Channel formation has been hypothesized to account for calcium dysregulation and mitochondrial dysfunction by allowing indiscriminate leakage of ions across cell membranes. Studies have shown that amyloid deposition is associated with mitochondrial dysfunction and a resulting generation of reactive oxygen species (ROS), which can initiate a signalling pathway leading to apoptosis. There are reports that indicate amyloid polymers (such as those of huntingtin, associated with Huntingtons disease) can induce the polymerization of essential amyloidogenic proteins, which should be deleterious to cells. Also, interaction partners of these essential proteins can also be sequestered.All these mechanisms of toxicity are likely to play a role. In fact, the aggregation of a protein generates a variety of aggregates, all of which are likely to be toxic to some degree. A wide variety of biochemical, physiological and cytological perturbations has been identified following the exposure of cells and animals to such species, independently of their identity. The oligomers have also been reported to interact with a variety of molecular targets. Hence, it is unlikely that there is a unique mechanism of toxicity or a unique cascade of cellular events.