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HISTOGENETIC APPROACH
In the histopathogenetic approach to histologic patterns, an understanding of only the most basic priniciples of immune reactions
is required. To depend too greatly on detailed immunological interactions in defining pathogenetic relationships would divert attention from significant morphologic features; the usefulness of the interpretation of
histologic patterns would be compromised. This becomes evident when the nature of contributions to current pathology journals are searched, and evaluated, for morphologic details rather than for the results of
batteries of immunoreactions, and other specialized laboratory procedures; in the current literature, the emphasis on histopathology is directly related to the size and quality of the respective photomicrographs of
H&E stained sections.
A variety of clinical settings can serve as the basis for the grouping of clinical disorders of diverse types. With only the most
basic knowledge of the nature of immune mechanisms, and the related cellular responses, it is possible to structure basic reaction patterns (parcels of structured virtual images) for the classification of
inflammatory diseases of the skin. For cutaneous inflammatory diseases, the relationships between reactions affecting particular microanatomic compartments, and histopathogenesis can be manipulated to define
categories of inflammatory diseases of the skin. The imposition of specificity on one of the basic histologic reaction patterns affecting a particular microanatomic compartment usually requires attention to
historical, clinical, histologic and laboratory findings; clinicopathologic correlations are required.
BASIC REACTION PATTERNS
Some basic features, and reaction patterns to be factored into the histologic interpretation of inflammatory diseases of the skin
include:
1. epidermal response
a. hyperplasia or atrophy of functioning units (i.e., the basal unit and/or the superficial unit)
b. epidermal infiltrates of either neutrophils or lymphocytes, and alterations in the fluidity of the epidermal interstitium
c. spongiotic changes
d. psoriasiform hyperplasia
e. erosive effects of a lichenoid reaction (interface reaction)
f. lytic effects, including lysis of cells, necrosis of individual cells (apoptosis), lysis of membranes of adherence (including
extracellular membranes and the cytoplasm of cells in apposition to those membranes),
g. dyskeratosis and acantholysis
h. immunostimulation (epidermal)
2. dermal response
a. alterations in the amount, and the quality of interstitial matrix (including both watery and mucinous matrices)
b. alterations in the patterns of collagenous tissue, and in the relationships between fibrous and fluid components
c. alterations in the patterns of elastic tissue in, or as a consequence of, inflammatory diseases
d. immunostimulation (dermal): productive of mucinous or fibrous matrices
e. lymphoepithelial lesions
f. eosinophils and eosinophilic necrosis
g. plasma cells (secretory products, Dutcher bodies, etc.)
h. neutrophils (collagenosis and suppuration)
i. fibrinoid
INFLAMMATION AND ANATOMIC COMPARTMENTS
In general, and by current standards, chronic inflammation usually is a manifestation of an immune reaction; reactions to physical
trauma are exceptions. In response to a local antigen, or in response to a localized deposition of immune complexes in the skin, lymphocytes find their way into the dermis by egress from the lumina, and through the
walls, of blood vessels. They may be prominently represented in the perivascular spaces in the papillary dermis and, in this context, are also likely to find their way into the epidermis, generally in areas in which
the interstitial spaces among the epidermal keratinocytes have been widened (and the nature of the mucinous interstitium altered) (spongiotic patterns). They may also produce lytic defects in the epidermal domain
(lichenoid patterns). The epidermal reactions in response to inflammatory diseases involving the epidermis include edema (spongiosis), lysis and death of keratinocytes (lichenoid reaction), and proliferative changes
(acanthosis, hyperplasia of the epidermal basal unit, hyperplasia of the superficial epidermal unit, hypergranulosis, hyperkeratosis, and parakeratosis [i.e., psoriasiform patterns]). The epidermal changes are also
dependent on the age of the reaction. Lichenoid and psoriasiform reactions are not mutually exclusive; for some disorders, such combinations qualify as pityriasic patterns. In late stages of inflammatory disorders,
the changes may include some degree of epidermal atrophy with depletion of cells of the basal epidermal unit, including effacement of the rete patterns. Alternately, there may be hyperplasia with elongated rete
ridges, and widening and fibrosis of papillary dermis.
DERMATITIS AND ANATOMIC COMPARTMENTS: Dermatitis is a general designation for inflammation of the skin. It has more utility as a
clinical than as a histologic term. As a histologic term, it provides no distinctions between perivenular infiltrates, interstitial infiltrates, or epidermal infiltrates. Limits, implicit in the term, offer
restrictions on neither cell types nor localization of infiltrates.
PREFERENTIAL SITES OF INFLAMMATION
(IMPLICATIONS RELEVANT TO SELECTED MICROANATOMIC SITES):
Some antigens are native to the host; they are a structural or functional constituents. They lend a specificity to the amalgam of
real and virtual images by determining the sites in which immune deposits either first form, or in which they are deposited. In the act, some sites of tissue damage are identified as being both antigen-specific and
site-specific. The interstitial spaces of the epidermis are a favored site for the deposition of site-sensitive, antigen-specific antibodies. An antigen-antibody reaction affecting keratinocytes at their cell
membrane level is characteristic of pemphigus; acantholysis and dyskeratosis are the results. Of the commonly selected anatomic sites in the reactive superficial unit of the epidermis, the basement membrane zone of
the epidermis is often preferentially involved; the respective immune diseases are generally characterized as interface disorders. The basement membrane zone consists of lamina lucida, lamina densa, collagens,
anchoring fibrils and the cell surfaces of neighboring basal keratinocytes. This detailed composition is evident only at the level of ultrastructure, as augmented with immunohistochemistry. The site specificity of
some antibodies, which are attracted to the region of the basement membrane, is mind-boggling. The limited physicality of immune deposits, in which antibodies are attached to specific antigens of a lamina, or in the
lucent or dense zone in the basement membrane area of the epidermis, is, in its impact on the integrity of the attachment of the epidermis to the dermis, a consequential enormity. In the interface disorders, the
inflammatory reaction may be lymphocytic and histiocytic but, in contrast to the patterns in common lichenoid reactions (as seen in the lichen planus-like categories), it is less likely to be densely cell-rich.
In the lymphocytic infiltrates of the dermis (infiltrates of lymphocytes along vessels of the reticular dermis), traceries of
histiocytes and lymphocytes in the reticular dermis among collagen bundles are a common feature (i.e., lymphohistiocytic collagenosis), but variable in intensity. As an explanation for these associations, it might
be proposed that antigens in the interstitium of the dermis have initiated an immune reaction, or that immune complexes have leaked into, or formed in, the interstitium of the reticular dermis. In response to these
deposits, reacting cells, in their migration through the vessel wall, will induce the changes of a lymphocytic vasculitis. The interstitial infiltrates associated with lymphocytic infiltrates of the dermis are an
indication of injurious agents among collagen bundles of the reticular dermis. The interstitium of the reticular dermis, with its hydrophilic glycoproteins, may be predisposed in a manner that favors the deposition
of antigens, or immune complexes (the epidermis, and its interstitium seem to have a similar proclivity).
SPECIFICITY OF TISSUE RESPONSE
Experimentally, it is convenient to compartmentalize immune responses; they are either cell-mediated, or humorally mediated. In
practice, the preponderant cells in most inflammatory reactions are T lymphocytes, regardless of the nature of the basic immune response. Once an injury to tissue has produced damage, the morphologic differences
between a humoral and a cell-mediated reaction usually are obscure, with the exception that neutrophils are unlikely to be a manifestation of a pure, uncomplicated cell-mediated response. Once a tissue response is
well-developed, the patterns may reflect a mixed reaction in which both humoral and cellular responses are intermingled. In some of these mixed patterns, a humoral reaction may have secondarily elicited a
cell-mediated response. Distinctions cannot be accurately defined on the basis of pure morphologic patterns.
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