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The Mutual Interdependence of the Basal Epidermal Unit and the Adventitial Dermis
(epidermal kinetics and blood supply)
The surface of the skin is a relatively finite expanse. There are constraints on the number of cell layers in the epidermis that can be supported by a vessel of a dermal papilla. A short papilla with a limited
capillary surface for the exchange of metabolites has a limited capacity to support significant increases in the number of cells per unit area. In some inflammatory disorders of the skin, the basal unit of the
epidermis is preferentially expanded. One available accommodation which allows for a significant increase in the epidermal domain, particularly the basal unit, is lengthening of dermal papillae, with elongation and
tortuosity of the vessel of each papilla. The corresponding rete ridges are also elongated. An elongation of the capillaries of dermal papillae, in a localized expanse of skin, greatly augments the surface area of
the vessels; it facilitates the exchange of metabolites and catabolic products across the vessel wall. Expansion of the surface area of capillaries in dermal papillae would accommodate an expansion of the basal unit
of the epidermis; such changes in vessels are basic to the response of both the epidermis and the papillary dermis in psoriasiform epidermal hyperplasias.
RAPID TURNOVER OF BASAL KERATINOCYTES: The rate at which cells of the basal unit replicate influences the cell density in the basal unit. The configuration of the rete ridges is a direct consequence of the rate at
which the basal unit is replicating. The shape and length of rete ridges expresses the inter-relationships between dermal papillae, vascularity, and cellular activity in both the papillary dermis, and the basal unit
of the epidermis. It is possible to have elongated, club-shaped rete ridges (an expansion of the basal unit) alternating with suprapapillary expanses in which the basal unit is thin with an even less conspicuous
superficial epidermal unit over the thin basal unit (i.e., this combination of features is basic to the epidermal patterns that are characterized as psoriasiform). A lesion showing such features
is likely to also show parakeratosis along its surface (the altered keratin layer in which pyknotic nuclei are represented is a parakeratotic layer). As a barrier at the skin surface, a parakeratotic layer will be less resistant than a orthokeratotic layer; inflammatory cells are likely to weep into it.
TURNOVER OF BASAL KERATINOCYTES: A thin basal unit may thwart normal epidermal kinetics and, in turn, compromise the maturation of cells in the superficial unit. If the process of terminal differentiation has been
altered in a manner that accelerates the delivery of cells to the surface, the kinetics of terminal differentiation of cells will be altered in a manner that interferes with: 1.) contraction of the dying cells, 2.)
obliteration of the intercellular spaces by a lipid membrane, and 3.) the contraction and lysis of nuclei of the dying cells.
A compromise in blood supply may in part explain the basal unit atrophy of some lichenoid disorders, such as lupus erythematosus.
An alteration in epidermal kinetics by which the turnover of epidermal keratinocytes of the basal unit is retarded would favor terminal differentiation of cells of the superficial unit. As a result, the formation of
a compact layer of orthokeratin at the surface would be favored.
THE CHARACTER OF KERATINIZED DEBRIS: Alternating zones of compact orthokeratosis and parakeratosis are common in inflammatory diseases, including contact dermatitides, and ezematous dermatitides. In the latter two
disorders, external irritants or allergens often are the initiators of the inflammatory reactions. If the response of the body to inflammation is an increased in the rate of turnover of cells of the superficial
unit, the product at the skin surface may not provide adequate protection; the response of the superficial unit of the epidermis determines the character of alterations in the prime barrier along the surface of the
skin.
The granular layer of the epidermis is basic to the formation of a normal keratin layer. The phenomena of keratinization, and the formation of a granular layer would appear to be time-dependent; if in response to
inflammation the process is accelerated, the formation of keratohyalin granules, and the release of Odland bodies would appear to be compromised. The keratin layer would then be compromised, being both parakeratotic
and deficient in intercellular lipid material. These alterations would tend to promote the absorption of irritants and allergens from the surface of the skin.
BASEMENT MEMBRANES
(INTERFACE DISORDERS)
Some nidi, that are preferential as sites for common patterns of inflammation, are remarkably specific. For example, the structural components of the basement membrane are antigen-specific sites; in some disorders,
these specific sites determine the localization of inflammatory infiltrates.
INFLAMMATION AND THE RETICULAR DERMIS
INTRODUCTION: Not all inflammatory diseases of the skin are concentrated in the environs of the epidermis and the papillary dermis. Some examples are concentrated in the dermis. The response to inflammation is
mediated at the level of the vascular plexus with contributions from native mesenchymal cells, including fibroblasts, dendritic histiocytes, and mast cells. The response of fibroblasts influences not only the
character of the fibrous component of the dermis but also the character of the interstitial matrix. The possible responses include mucinous alterations of the interstitium, sclerosis, and alterations in the quantity
and quality of the elastic component.
THE MUCINOUS INTERSTITIUM: The mucinous interstitium of the reticular dermis seems to be universally indiscriminate in regard to the distribution of antigens or antigen-antibody complexes, and the localization of
inflammatory infiltrates. The influence of hydrodynamics, and the character of blood vessels at various levels of the dermis provide some specificity for the localization of inflammatory infiltrates in the mucinous
interstitium of the dermis. In the reticular dermis, post-capillary venules in the upper portion of the reticular dermis are functionally important in allowing the egress of inflammatory cells, and the leakage of
antigens, and immune complexes from vessels into the interstitium of the dermis. In turn, inflammatory infiltrates are often localized to the perivascular spaces of the upper portion of the reticular dermis.
FIBRINOID: Currently, fibrinoid is seldom emphasized in descriptions of inflammatory processes of the skin but, at a time when the connective tissue (collagen-vascular) diseases were first being defined, fibrinoid
received great emphasis. The designation, fibrinoid, has application to a variety of acidophilic alterations in connective tissue, but is most appropriate for disorders in which alterations in connective tissue are
associated with the deposits of fibrin. In this context, fibrinoid generally has a fibrillar quality but, in some examples, the fibrils may be compacted into homogenous deposits. The fibrinoid of the necrotic wall
of a vessel in the area of a vasculitis probably consists of necrotic smooth muscle as well as deposits of fibrin. The fibrinoid at the dermal-epidermal interface in a lesion of lupus erythematosus is in part
fibrin, but also includes deposits of immunoglobins, and perhaps basement membrane material. The fibrinoid in soft tissue in lesions such as lupus erythematosus, rheumatic fever, rheumatoid arthritis, and granuloma
annulare consists in large part of fibrin (often in a mucinous matrix).
THE COLLAGENOSES (INTERSTITIAL INFLAMMATION AND ALTERATIONS IN THE QUANTITY AND QUALITY OF CONNECTIVE TISSUE)
DISORDERS AFFECTING NON-CELLULAR COMPONENTS: In the reticular dermis, interstitial infiltrates of inflammatory cells among the collagen bundles are common, particularly in association with perivenular infiltrates of
inflammatory cells. Infiltrates of lymphocytes and histiocytes are most common, but some examples are characterized by interstitial infiltrates of neutrophils. Interstitial infiltrates of inflammatory cells commonly
are associated with changes in the dermal connective tissue, including alterations in the mucinous interstitium (mucinoses), the collagenous component (collagenoses), and even the elastic component (elastoses).
These alterations of connective tissue may be additionally qualified as to the character of the inflammatory infiltrates. Thus, it is possible to speak of lymphohistiocytic, histiocytic, granulomatous, or even
neutrophilic collagenoses. A lymphohistiocytic mucinosis is a common finding in the dermis in collagen-vascular diseases, and is a prominent feature of lesions of lupus erythematosus and dermatomyositis.
Lymphohistiocytic collagenosis is a common feature of scleroderma. In scleroderma, the perivascular infiltrates usually contain plasma cells. A lymphohistiocytic collagenosis with plasmacytosis is also a feature of
lesions of lupus profundus and necrobiosis lipoidica dibeticorum.
A granulomatous collagenosis is the characteristic response in the dermis in lesions of granuloma annulare. It is a feature of both rheumatoid nodule and necrobiotic xanthogranuloma. A granulomatous elastolysis is
characteristic of lesions of actinic granuloma, and is manifested in more striking patterns in granulomatous lax skin. A neutrophilic collagenosis is the characteristic dermal response in lesions of Sweet's
syndrome, and the pyodermas. In nasal biopsies of lesions of Wegener's syndrome, a pattern of reactive fibroplasia with infiltrates of neutrophils may be a feature. A neutrophilic and histiocytic collagenosis
(neutrophilic dermatitis) is sometimes a feature of skin lesions of rheumatoid arthritis. A neutrophilic and granulomatous collagenosis is likely to be characterized by a central zone of necrosis that is distinctly
basophilic. An eosinophilic collagenosis is the characteristic response in lesions of Well's syndrome (eosinophilic cellulitis). The allergic granuloma is an eosinophilic and granulomatous collagenosis. Mast cells,
in increased numbers among the collagen bundles of the reticular dermis, could be characterized as a mast cell collagenosis or mucinosis.
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