S9C12P5Morphea


S9C12P5-1: The lymphohistiocytic collagenosis of morphea has a perivascular component, but the sclerosing effects are almost certainly related to the effects of lymphokines on dermal fibroblasts. The sclerosing process is something more than a simple addition of collagen fibrils. It is a coordinated process which includes alterations to the mucinous matrices, not only to those of the inter-bundle domain, but also to the matrix of the individual collagen bundles. In certain stages, and in focal areas, fibrillation and clefting of collagen bundles (unbundling) is a precursory change, allowing for the addition of new fibrils to the bundles. The process seems to be more than simple accretive growth at the periphery of individual bundles. Accretive growth may occasionally be manifested in patterns of ring-binding of collagen bundles (S9C16P8-5). At the bottom of the field, lymphoid infiltrates are represented among lipocytes; they might be characterized as anticipatory of a change in the interstitial matrix of lipocytes; the change might be a promotion of a environment into which migratory fibroblasts are first attracted and then activated. In such a manner, substitutive fibrosis could begin and progress at the interface between the reticular dermis and the subcutaneous fat; the domain of dermal-type collagenous tissue of the reticular dermis, in the process of substitutive fibrosis, would be expanded at the expense of the domain of the adipose tissue (see S9C14VA1-1).


S9C12P5-2: The lymphohistiocytic collagenosis of morphea is represented. There are occasional plasma cells in the infiltrates; this contrasts with the rarity of plasma cells in the infiltrates of discoid LE. On the other hand, plasma cells are as common in the deep infiltrates of LE profundus as they are in the dermal and subcutaneous infiltrates of morphea. In this field, the collagen bundles show variations in tinctorial qualities (pale areas alternating with brightly acidophilic areas) and many of the bundles are fibrillated (partitioned longitudinally by defects). Some are not only fibrillated, but are also reduced in size; the increase in number, and the reduction in size, of collagen bundles could be a result of clefting. The collagenosis of morphea (as a disease manifested in a formation of an abnormal collagenous product) is both quantitative and qualitative; the pallor may represent a degree of collagenolysis which facilitates the widening of the spaces among collagen bundles. Histiocytes probably have a role in the unbundling of collagen bundles. Activated fibroblasts probably are the effector cells in the alterations of the collagen bundles (the alterations allow for the incorporation of new fibrils in the interstices of, and among, the altered collagen bundles).

S9C12P5-3: It is in the domain of the interstitial infiltrates, as seen in this field, that the substitutive fibrosis of morphea will first make an appearance; the infiltrates prepare a stroma and form a community that later favors an ingrowth, or proliferation, of fibroblasts and a deposition of a newly formed, fibrous matrix.

S9C12P5-4: As the sclerosis advances, the lymphohistiocytis infiltrates of the collagenosis of morphea become less conspicuous. Below the center of the field, some of the widened interstitial spaces contain pale, delicate collagen fibers. Some of the bundles are fissured, clefted, or pock-marked (i.e., collagenolysis as the preparatory stage for the deposition of new collagen fibrils).

S9C12P5-5: The epidermal pattern of this lesion has psoriasiform qualities. Rete ridges are elongated; there are mild vacuolar changes at the dermal-epidermal interface. The papillary dermis is widened and hyalinized; it has a homogeneous quality rather than a coarsely bundled quality. The infiltrates of lymphocytes and histiocytes are confined to the interface between the zone of hyalinized dermis (altered papillary dermis and perhaps a portion of the neighboring reticular dermis); substitutive fibrosis has altered the quality and quantity of the papillary dermis. The process has extended from the papillary dermis into the reticular dermis. As the process of fibrosis expands its domain, the lymphoid infiltrates are denied access to the zones of sclerosis and hyalinization. The fibrosing process acquires the qualities of an immunologic barrier confining the cellular infiltrates beyond the domain of the altered fibrous tissue. This restriction might be characterized as having the qualities of a “defense” ( LS&A-like sclerosis of superficial morphea).

S9C12P5-6: Even in a late stage of evolution, the deep, dermal sclerosis of morphea shows not only coarsening of collagen bundles, but also fissuring and fibrillation of the bundles.

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