|
S3C1 - Lichen Planus, & misc. (tier 1)
SECTION 3
CHAPTER 1
(Home: Lichen Planus-like Reactions)
Richard J. Reed, M.D., New Orleans, LA
This is Section 3, Chapter 1. The section is in 3 tiers, including a HOME, a textual level, and a pictorial level. The conventions are the same as for all the other sections (with the
previously noted exceptions for Section 14). There are navigation bars in the MASTERBORDER to the left and at the end of each page. The blue first cluster of navigation
bars provides access to HOME and to textual chapters at level 2. The beige second cluster in the MASTERBORDER provides access to pictorials and relevant parent textual chapters (chapters marked with an “-X”). The third (mauve) cluster of horizontal bars at the end of each page provides access to all the sections of this site. An IMAGE MAP is the first page of the second tier; it is Chapter 2
of this section, and of all the succeeding sections (CLICK to go to the IMAGE MAP of this section). At the end of each page, there are three additional navigation aids. A click on one of these aids (NEXT) will take you to the next page in sequence at the level currently in the reader’s view (with the exception of HOME which is the only page of the first tier). In any group of pictorials - a grouping representative of children of a particular parent textual chapter (at level 2) - a click on this “SEQUENCE” or “NEXT” button will only allow the reader access, in a sequence, to children of the respective parent textual chapter; when the sequence is exhausted, additional clicks will simply repeat the cycle. The reader must seek out the next parent textual chapter in sequence in the beige cluster in the MASTERBORDER to the left. Having found the next parent textual chapter, he will then have access to the next group of pictorials; they follow in a downward sequence. A click on a second bar at the end of the page will take the reader UP to the next tier, and to a relevant parent textual page, if the reader is at the third (pictorial) tier. If the reader is at the second textual tier, a click on this bar will take the reader HOME (1st chapter, 1st tier). A third button, the BACK button, will take the reader back along the horizontal axis of the respective tier (in a spatial sequence); movement along tier 3 with this bar is restricted in the same manner as is movement with the NEXT button. Both the NEXT and the BACK buttons are inoperative at level 1. The reader’s browser also has utility in moving among the chapters, particularly in going back to the previous page or section (in a temporal sequence) with no limitation of directed movement along a tier, or from one tier to another.
The material on LICHEN STRIATUS was collected by a young Tom Meek.
Lichen Planus and Lichen Planus-like Reactions
Lichenoid reactions are immune-mediated, destructive processes affecting the basal layer and the basal unit of squamous epithelium of epidermis and of squamous
mucosae (the squamous epithelium of skin appendages also can be a target). In contrast to the immunoproliferative nature of the spongiotic and psoriasiform disorders, the basal layer of squamous epithelium is set
upon by lymphocytes and histiocytes; in the encounters, epithelial cells and clusters of epithelial cells (and in some cases, melanocytes) are damaged; they undergo lysis and coagulative necrosis (pathologic
apoptosis).
In the act, lytic defects often are produced in the target site. These defects contain histiocytes, lymphocytes, and dead keratinocytes; if found in the dermis, the dead keratinocytes are characterized as colloid bodies or Civatte bodies. The lymphoid infiltrates of some lichenoid reactions (i.e., lichen planus-like examples) tend to be band-like at the dermal-epidermal interface, but it is not the distribution, nor the apposition of the infiltrate to the basal layer of the epidermis that defines a lichenoid reaction. The requisite feature is an interplay between lymphoid cells and target cells. The target cells of a lichenoid reaction are keratinocytes of the epidermis, particularly those of the basal unit of the epidermis; effector cells are T lymphocytes.
Lichenoid reactions have a life history including an established and a senescent phase. For some variants, an initial (primary) stage might also be identified as
something histologically distinct from the established stage. By definition, the lichenoid reaction of lichen planus, as characterized in textbooks, is also the established phase; the process is defined by the
established pattern. If there is a primary stage, it has not been adequately documented, or, in its deviations from the classic histologic patterns, it will not be recognized as lichen planus.
The established lichenoid reaction of lichen planus is a chronic, erosive disorder affecting the dermal-epidermal interface (and, in addition, sometimes affecting,
in a similar manner, the basal unit of the epithelium of hair follicles, sweat ducts, and, on occasion, the epithelium of sweat glands). The erosive process of the established phase is fairly continuous along
a stretch at the dermal-epidermal interface; the diffuseness of the process at the interface is a characteristic of a lichenoid reaction. In contrast, in a spongiotic or psoriasiform process, lymphoid infiltrates
tend to be mostly perivascular in the dermis and to extend into the epidermis in focal patterns, often at the tips of rete ridges in areas of inter-cellular edema.
Within the confines of the area involved by diffuse infiltrates at the dermal-epidermal interface, the process, for some lichenoid reactions (i.e., lichen
planus-like variants), focally results in the formation of lytic clefts in the domain of the basal unit of the epidermis. The clefts contain loosely spaced, dead keratinocytes, lymphocytes and histiocytes, and
Langerhans cells. Occasional melanocytes may also be represented. The clefts form in the domain of the basal unit of the epidermis and usually are bordered on the dermal side by a damaged basement membrane. The
process is remittent in the sense that repair and erosions are sequential, in cycles, over the period of continued activity. In this manner, defects form and then are inlaid with fibrous tissue (accretive fibrosis).
A basal layer partially regenerates and a basement membrane is partially restructured; then the erosive process is repeated and another round of repair ensues. In this manner, the papillary dermis, in a process of
accretive fibrosis, becomes widened. A reduplication of basement membrane material provides a marker for the cyclic nature of the erosive process; dead keratinocytes, having been entrapped in the newly inlaid
fibrous tissue, become monuments for the alternating effects of the erosive process and the reparative processes; they become colloid bodies.
In the reparative process, the newly formed fibrous tissue, which is inlaid in the lytic defects, entraps the necrotic keratinocytes left behind by the erosive and
coagulative process. The entrapped, dead cells become colloid bodies. They are found in clusters in the altered “papillary dermis;” they are entrapped during the process of accretive fibrosis. Fibrous tissue in the
process of repair is inlaid in the defects about the dead keratinocytes. In time, with organization, the new fibrous tissue becomes an expansion of the papillary dermis, but is distinguished by the presence of
reduplicated lamina of basement membrane material.
The erosive process of lichen planus is most active along the margins of rete ridges; the erosive bites, being sequential, produce a shortening and a narrowing of
the affected rete. The rete ridges tend to be partially preserved with a broad base and a pointed extremity (qualities which generally are characterized as “saw-toothing” of the rete ridges).
Lichen planus and lichen planus-like reactions also are distinguished by hyperplasia of the superficial unit of the epidermis. The superficial unit of the epidermis
(i.e., the portion which manages to survive the assault on the basal unit) takes on the characteristics of a hyperplastic and hypertrophied superficial unit (with the granular layer participating in the changes). As
a consequence, the altered kinetics of the superficial unit find expression in an altered keratin layer, one that is compactly hyper-orthokeratotic.
In practice, many of the features, which we characterize as lichen planus-like, may, on occasion, be encountered in the setting of other lichenoid diseases, such as
lupus erythematosus, drug eruption, pityriasis lichenoides, and erythema multiforme. The process which we characterize as lichen planus is a common, but basic, reaction pattern.
|