|
DERMATITIS
The designation, dermatitis, gives recognition to inflammation of the skin; clinically, the designation embraces lesions with the classic signs of inflammation, namely rubor (redness), dolor (pain), calor (heat), and
tumor (swelling). Histologically, the designation embraces those processes which are characterized by inflammatory infiltrates in the skin. It is a most general term, embracing a variety of patterns, and cell-types.
Many of the clinical characteristics of inflammation can be appreciated on histologic sections of the affected areas; the histologic correlates include telangiectasia and edema. The most common pattern of
inflammation in the skin is characterized by infiltrates along the vessels of the papillary dermis and inflammatory changes in the overlying epidermis. This limited distribution of infiltrates forms the basis for a
characterization of a reactive unit; the reactive superficial unit is composed of the epidermis and the adventitial dermis; it is composed of the epithelial components (the epidermis, and the follicular epithelium),
the papillary dermis, the perivascular spaces, and the perifollicular connective tissue sheaths; this functioning unit is involved to varying degrees in the spongiotic, the pityriasic, and psoriasiform dermatitides.
When we speak of a psoriasiform, or spongiotic process, we usually are giving recognition to a dermatitis. In point of fact, we usually are giving recognition to an immune process mediated at the level of the
Langerhans’ cell.
A lichenoid reaction is a specific immune, cytolytic process mediated by lymphocytes and histiocytes with keratinocytes as target cells; it is a dermatitis because it is manifested in association with signs of inflammation, whether at the clinical, or the histologic level. Interstitial infiltrates of the reticular dermis, that cannot be characterized as neoplastic, also are likely to be characterized as some type of dermatitis; they, and the associated perivenular infiltrates of similar cells, are likely to be grouped together as dermatitis. Perivascular and interstitial infiltrates of neutrophils, if associated with the breakdown of nuclei (leukocytoclasia), are likely to be characterized as a vasculitis. On the other hand by the criteria of some observers, perivenular infiltrates of lymphoid cells, in a distribution similar to those of the leukocytoclastic angiitides, are likely to be assigned to the category of the lymphocytic infiltrates; we do this because we have been told, and many of us are willing to accept, the admonitions, that such lesions are not to be classified as a form of vasculitis. Prominent, interstitial infiltrates of neutrophils are likely to be classified as “neutrophilic dermatitis.” On the other hand, similar infiltrates, if relatively limited in distribution, but associated with perivenular infiltrates of similar cells and with evidence of fibrinoid necrosis of the wall of the affected vessel, are likely to be characterized as a vasculitis; the interstitial infiltrates are ignored. To compound the confusion, similar combinations of changes involving the interstitium of the dermis and neighboring vessels, if extensive and suppurative, are to be characterized as a pyoderma. Pyodermas are commonly associated with necrosis of the walls of vessels in the adjacent dermis; distinctions become arbitrary; they find “specificity” in clinicopathologic correlations.
Some of the interface disorders are vesicular or bullous; the process is initiated in the region of the basement membrane; they are inflammatory processes; for these disorders, we go to great lengths to define the
precise level of basement membrane involvement; from one perspective, the process is a “membranitis.” We characterize some of these processes as bullous dermatoses; we cannot even bring ourselves to classify
them as dermatitides. Some of these disorders are remarkably cell poor but, clearly, the damage is mediated at the level of an inflammatory process. Some are mediated at the level of the neutrophil (dermatitis
herpetiformis) and are classified as “dermatitis.” Some of the bullous disorders are genetically determined, but are expressed in cellular alterations that are remarkably similar to immune mediated processes. A
lesion of a bullous disease, encountered early in its evolution, is likely to be characterized as “interface” dermatitis. In all this confusion, we are asked to make accommodations for variations in histologic
patterns, type of immune response, clinical presentations, and most of all personal prejudices, often of an archaic nature.
In dermatopathology, in the realm of the inflammatory disorders, pathologists must interpret many variables including: cellular infiltrates; the cytopathic effects of the activated inflammatory cells; the cytopathic
effects of immune complexes; the relationships between the age of lesions and variations in histologic patterns; the significance of the patterns produced by dying cells (and the type of cell death); and the effects
of repair. Often, all this is to be accomplished under the constraints of archaic clinical terminology.
The disorders, which are relatively confined in their cutaneous manifestations to the superficial reactive unit, are an appropriate topic for an introduction to specific inflammatory diseases of the skin. In
addition, it seems appropriate to first consider those disorders that have an immunostimulatory effect (they are associated with hyperplasia of the basal unit of the epidermis) on the epidermis; this would include
the spongiotic and psoriasiform disorders.
The epidermis is divisible into a basal unit and a superficial unit; there are histologic correlates for these two functioning units. Normally, there are about as many cell layers in the basal unit as the superficial
unit. Those of the basal unit tend to have basophilic cytoplasm and to be elongated with the long axis perpendicular to the surface of the skin. The superficial unit is concerned with terminal differentiation; its
cells are committed to a distinctive form of cell death - in the process an impermeable layer is formed at the surface of the skin. The cells of the superficial unit are polygonal and acidophilic; their long axes
tend to parallel the surface to the skin.
|
