Identification of Basic Patterns - Skin - Fibrosing Dermatitis

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Identification of Basic Patterns: Skin: Fibrosing Dermatitis
See Fig. 5.350 A&B.
Figure 5.350: Fibrosing dermatitis. A. Early. B. Late (sclerosis).
Fibrosing dermatitis (as well as fibrosing peri-infundibulitis/perifolliculitis and fibrosing panniculitis) results, in every
instance, from injury to nonepithelial tissue, usually connective tissue, the assault coming either from outside or from
inside the skin. External injuries to skin generally take the form of wounds, i.e., erosions and/or ulcerations (Fig.
5.351 A&B) inflicted by fingernails as they are employed like talons in the act of animated excoriation, those defects
healing with a scar (Fig. 5.352 A&B). Injury also may be wrought by punctures, lacerations, burns of various kinds,
and surgical procedures (Fig. 5.353), as well as sustained pressure as occurs in chondrodermatitis nodularis helicis
(Fig. 5.354 A&B), those, too, resolving with fibrosing granulation tissue and, in time, a scar (Fig. 5.355 A&B). Injuries
that incite fibrosing inflammation from within the skin tend to be related to suppurative inflammation centered in
infundibular epidermis, such as pustular infundibulitis that typifies fulminant expressions of acne vulgaris, e.g.,
conglobata and keloidalis (Fig. 5.356 A&B), and analogues of them, to wit, perifolliculitis abscedens et suffodiens
(dissecting cellulitis of the scalp) and hidradenitis suppurativa. Those cataclysmic suppurative infundibulitides resolve
over many months with granulomatous and fibrosing inflammation (Fig. 5.357 A&B). The sequence of suppuration,
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granulomatous inflammation, and fibrosis also is played out dutifully in the aftermath of explosion of an infundibular
cyst, a phenomenon that occurs commonly (see Fig. 5.358 A&B). Fibrosing dermatitis may result from the effects on
fibrocytes of infiltrates of inflammatory cells of long standing, as occurs in diseases as different as lichen planus
(especially the infundibulo- and folliculocentric expression of that disease, i.e., lichen planopilaris (see Fig. 5.332
A&B), and the atrophic manifestation of it), discoid lupus erythematosus, granuloma faciale/erythema elevatum
diutinum, acrodermatitis chronica atrophicans, necrobiosis lipoidica (Fig. 3.359 A&B), and morphea (Fig. 5.360 A&B).
At a late stage in the life of a lesion of necrobiosis lipoidica, collagen bundles may be thickened and crowded in a
manner reminiscent highly of that of morphea at an autumnal stage.
Figure 5.351: A&B. A sign virtually diagnostic of the effects of excoriation: an ulcer the width of that of a
fingernail. The discrete superficial ulcer pictured is about the width of an adult fingernail, which is not
surprising considering that it came into being secondary to scratching furiously.
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Figure 5.352: A&B. A sign virtually diagnostic of excoriation: a small thin scar positioned just beneath the
epidermis. The changes shown bear testimony to an ulcer having been present at this site as a
consequence of scratching ferociously.
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Figure 5.353: A&B. A sign virtually diagnostic of trauma externally by curettage and electrodesiccation:
calcification in a zone of degenerated collagen situated just below the epidermis. Calcification at the base of
a zone of degenerated collagen is expected at times following injury by physical means, in this instance,
curettage and electrodesiccation several weeks previously at the very same site, the surgical procedure
having produced an ulcer that by now has repaired largely.
Figure 5.354: A&B. Signs indicative of the cause of chondrodermatitis nodularis helicis: external trauma.
What is called chondrodermatitis nodularis helicis simply is a response to injury by pressure sustained on a
helix, the result being ulceration and granulation tissue atop which are fibrin and crust, and at the side of
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which is pseudocarcinomatous (infundibular) proliferation of keratocytes.
Figure 5.355: A&B. Repair of chondrodermatitis nodularis helicis: fibroplasia characteristic of mending of an
ulcer inflicted by trauma externally. The ulcer and granulation tissue of chondrodermatitis nodularis helicis
are replaced by fibrosis of a scar.
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Figure 5.356: A&B. The life of a lesion of acne keloidalis: sequence chronologically from suppurative
infundibulitis to fibroplasia. The sequence, over a period of many years, of suppurative infundibulitis,
extrusion of neutrophils in large number from the infundibulum, granulomatous inflammation, and extensive
fibroplasia has resulted in a papule of acne keloidalis.
Figure 5.357: A&B. The "graveyard" of acne keloidalis: residua of a foreign body reaction and fibrosis. Once
the suppurative infundibulitis and suppurative dermatitis of acne keloidalis are no more, all that remains are
infundibulocystic structures, hair shafts surrounded by histiocytes, many of those macrophages being
multinucleate, and extensive fibroplasia.
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Figure 5.358: A&B. Signs of the cause of a particular scar: a hair shaft as evidence of an infundibular cyst
having ruptured at this site. The scar present throughout the dermis may be inferred to have resulted from
the effects of rupture of an infundibular cyst, the reason being that a hair shaft is enveloped by
multinucleate histiocytes in the fashion of a foreign body response (the space surrounded by histiocytes
housed a hair shaft).
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Figure 5.359: A&B. The similarity of collagen bundles in longstanding necrobiosis lipoidica and morphea:
crowded and thickened. The altered bundles of collagen and the arrangement of them in a longstanding
lesion of necrobiosis lipoidica, shown here, resemble closely those of morphea of many years' duration.
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Figure 5.360: A&B. The similarity of collagen bundles in longstanding morphea and necrobiosis lipoidica:
crowded and thickened. The character and arrangement of bundles of collagen in a longstanding lesion of
morphea, pictured here, are reminiscent of those in the longstanding lesion of necrobiosis lipoidica shown
in Figure 5.359.
A distinctive fibrosing process that qualifies as an inflammatory one because in some instances it is associated with
sparse perivascular infiltrates of lymphocytes, plasma cells, and eosinophils has been called to attention in the past
few years, namely, nephrogenic fibrosing dermopathy, a condition that, for practical purposes, comes into being only
in patients with chronic kidney disease, most of those persons having undergone renal dialysis. At scanning
magnification, the response at a glance of a knowledgeable dermatopathologist to findings in nephrogenic fibrosing
dermopathy is "morphea" (Fig. 5.361 A&B), the dermis being thickened, the septa in the subcutaneous fat being
widened markedly with resultant constriction of lobules, and the process also at times affecting the fascia and
skeletal muscle. Like morphea, the dermis may be spared entirely, only the subcutis being involved impressively, and
like morphea, an infiltrate of lymphocytes and plasma cells may be present around venules. But unlike morphea,
nephrogenic fibrosing dermopathy is marked early in its course by proliferation of fibrocytes floridly and in interstitial
fashion in the skin and subcutis (Fig. 5.362 A&B). Episodically, skeletal muscle is punctuated by plump oval,
monomorphous fibrocytes and in the same manner as is the dermis, septa of the subcutaneous fat, and fascia (Fig.
5.363 A&B). Some fibrocytes in those locales may be multinucleate. Because all patients who develop nephrogenic
fibrosing dermopathy have renal disease of some kind and the vast majority of them have been on dialysis, it seems
reasonable to infer that nephrogenic fibrosing dermopathy is analogous, if only vaguely, to tryptophane-myalgia
syndrome, toxic oil syndrome, and Shulman's syndrome (see Fig. 5.361 A&B), each of those conditions being
authentic morphea in response to a precipitating factor that is identifiable. In the case of nephrogenic fibrosing
dermopathy, the changes clinically are sclerodermatous, but the condition histopathologically is very different from
morphea, the most convincing difference being that in morphea, early, inflammatory cells are numerous, and, late, a
decreased number of fibrocytes is accompanied by collagen bundles that are crowded and thickened (Fig. 5.364
A&B), whereas in nephrogenic fibrosing dermopathy, inflammatory cells are paltry and fibrocytes are increased in
number and collagen bundles, although altered, are neither distinctly crowded nor thickened. Nephrogenic fibrosing
dermopathy is unrelated to morphea.
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Figure 5.361: A&B. The sweep of morphea on occasion: from the top of the reticular dermis through fascia.
Morphea, when fully formed, is typified by crowded, thickened bundles of collagen that may be present
throughout the reticular dermis, in markedly widened septa in the subcutaneous fat, in fascia, and, at times,
in skeletal muscle. What has been termed "eosinophilic fasciitis" and Shulman's syndrome is "morphea
profunda."
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Figure 5.362: A&B. Differentiation of nephrogenic fibrosing dermopathy from morphea: many more
fibrocytes in the former. At first glance, it is easy to misdiagnose nephrogenic fibrosing dermopathy as
morphea, the two conditions being so alike in silhouette, both in the dermis and in strikingly widened septa
in the subcutaneous fat. The number of fibrocytes in nephrogenic fibrosing dermopathy, at every stage in
the chronological sequence of it, is much greater than that in morphea at every stage in its course, near the
end of which fibrocytes actually are markedly decreased in number.
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Figure 5.363: A&B. Differentiation of nephrogenic fibrosing dermopathy from morphea: in the former, many
more fibrocytes, in a swath from dermis to skeletal muscle. The proliferation of fibrocytes in nephrogenic
fibrosing dermopathy sometimes affects not only the dermis, subcutaneous fat, and fascia, but skeletal
muscle, as shown here, findings that never are encountered in morphea, which is typified by decrease in
number of fibrocytes.
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Figure 5.364: A&B. Differentiation of morphea late in its course from nephrogenic fibrosing dermopathy late
in its course: in the former, a decrease in number of fibrocytes in the dermis. At a late stage of morphea,
not only is there no infiltrate of inflammatory cells, but fibrocytes in association with thickened bundles of
collagen are scant, a situation very different from that of nephrogenic fibrosing dermopathy at an
equivalent stage in which fibrocytes are increased markedly in number.
Fibrosis, literally, means a condition of fibers and, figuratively, as it is used in surgical pathology, a condition of
abnormal fibrous tissue that early in its sequence chronological tends to be accompanied by an increase in number of
fibrocytes, those cells producing altered bundles of collagen and often an increase in the amount of ground
substance. Later in its "life," fibrosis may take the form of sclerosis in which fibrocytes are decreased in number and
collagen bundles no longer are discernible as discrete units, a condition termed misleadingly "homogenization of
collagen." Fibroplasia is a synonym for fibrosis. It does not come to pass only in the course of an inflammatory
process; it may come into being in other pathologic processes, such as in the devolution of a verruca vulgaris (a
proliferation of epidermal keratocytes that fulfills the classic definition of "hyperplasia") located on a palm or a sole,
the residuum of that warty lesion being a kind of fibrotic papule; in a Clark's nevus (a "benign neoplasm" of abnormal
melanocytes) in which "lamellar"/"concentric" fibroplasia tends to develop immediately beneath the proliferation of
melanocytes situated at the dermoepidermal junction of thin, elongated rete ridges; in certain examples of an
intradermal Spitz's nevus (a benign neoplasm of abnormal melanocytes), they being marked by striking desmoplasia;
in melanoma (a malignant neoplasm of abnormal melanocytes) that also may be characterized episodically by
extensive desmoplasia, and in some carcinomas metastatic to skin in which desmoplasia may be rife.
Granulation tissue (Fig. 5.365 A&B), that quintessential inflammatory process characterized by an exuberant
proliferation of small blood vessels, edema, and a rich mixture of inflammatory cells, is followed inexorably by
fibroplasia in the form of a scar, keloid, or dermatofibroma, fibrosing inflammations all. Scars (Fig. 5.366 A&B),
keloids (Fig. 5.367 A&B), and dermatofibromas (Fig. 5.368 A&B) differ from one another clinically,
histopathologically, and biologically, but they are linked by having begun as granulation tissue and having resolved as
fibroplasia. It is important to know that a keloid at an early stage in its chronological course is devoid utterly of
bundles of collagen that are known, conventionally, as keloidal (Fig. 5.369 A&B). During the crescendo of each of
those types of fibrosing inflammation, granulation tissue becomes replete with fibrocytes, and during the diminuendo
of them, each displays a dearth of fibrocytes. Dermatofibromas take a different route from granulation tissue to
fibrosis than do scars and keloids, that is, progressing through a stage ("sclerosing hemangioma") in which
erythrocytes extravasated in large number are eyecatching (Fig. 5.370 A&B) and proceeding to a stage in which
siderophages and lipophages predominate (Fig. 5.371 A&B), those macrophages having been attracted to a site at
which the blood spilt from small blood vessels into the dermis secondary to the effects of trauma, which was initiating
at that locus, the lipid in serum not only being engulfed by macrophages but, at times, being represented by
cholesterol clefts (Fig. 5.372 A&B). Eventually, fibrocytes monopolize, there being no macrophages left, collagen
bundles associated with them in the bulk of the lesion in its center being coarse and at its periphery being thickened
markedly, all of those changes being accompanied by aberrations of surface epidermis, usually in the form of
acanthosis and hyperpigmentation (Fig. 5.373 A&B). That fully developed stage of the process is designated,
universally, dermatofibroma, a term that we advocate for the process at every stage in the course of it. When
fibrocytes of dermatofibroma are situated immediately beneath the epidermis, they are given to remind that surface
epithelium of the jolly time forebears of them had together in the embryo, where primitive mesenchymal cells induced
the future epidermis to give rise to hair follicles and sebaceous glands, those two structures being found often at the
summit of dermatofibroma during the period of evolution of it (Fig. 5.374 A&B). Some "ancient" dermatofibromas are
characterized by zones in which fibrocytes are scant and bundles of collagen seem to have become "homogenized"
(sclerotic), which explains the designation synonymously for a longstanding dermatofibroma characterized by that
particular change histopathologically, namely, "subepidermal nodular sclerosis." Fibroplasia in a longstanding
dermatofibroma may be so retracting that a dell comes into being (Fig. 5.375 A&B).
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Figure 5.365: A&B. The sequence chronological of granulation tissue: replacement invariably by fibroplasia.
Granulation tissue, the quintessential example of an inflammatory response to injury, is replaced,
invariably, by fibrosis.
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Figure 5.366: A&B. Signs diagnostic of a scar: fibrocytes and collagen bundles oriented parallel to the skin
surface, and venules perpendicular to it. A scar is a type of fibroplasia characterized, at its zenith, by
fibrocytes and fibrillary bundles of collagen oriented relatively parallel to the skin surface and venules
aligned somewhat perpendicular to it, those findings being evident here.
Figure 5.367: A&B. A sign diagnostic of a keloid: markedly thickened bundles of collagen in random array. A
keloid is a type of fibrosis characterized, at its apogee, by thick bundles of collagen arranged haphazardly.
Fibrocytes are aligned along the long axis of the thickened bundles.
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Figure 5.368: A&B. A sign virtually diagnostic of a dermatofibroma: fibrocytes (and, at times, histiocytes)
"splayed" between markedly thickened bundles of collagen at the periphery of the lesion. A dermatofibroma
is a type of fibrosis that, at its peak, is characterized centrally by fibrocytes in large number affiliated with
coarse bundles of collagen arrayed haphazardly, and, peripherally, by insinuation between greatly
thickened bundles.
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Figure 5.369: A&B. "Early" keloid: no keloidal bundles of collagen. During the development of a keloid, as
pictured here, fibroplasia is unassociated with bundles of keloidal collagen, that is, ones that are thickened
greatly and arranged haphazardly.
Figure 5.370: A&B. A stage relatively early in the sequence chronological of dermatofibroma: "sclerosing
hemangioma." At a relatively early stage in the evolution of dermatofibroma, extraordinary numbers of
extravasated erythrocytes and siderophages, consequent to the effects of trauma, are present in the
reticular dermis, at the periphery of the mass the macrophages being insinuated between markedly
thickened bundles of collagen.
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Figure 5.371: A&B. A more advanced stage in the sequence chronological of dermatofibroma:
"histiocytoma." As a dermatofibroma evolves, histiocytes that contain lipid in their cytoplasm (lipophages)
come to predominate, those foam cells sometimes being multinucleate and even of Touton type, as shown
here.
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Figure 5.372: A&B. A clue to a cause of dermatofibroma: "cholesterol clefts" in it. Cholesterol, delivered to
the dermis in blood extravasated secondary to trauma that initiated this dermatofibroma, has been
dissolved during processing of the tissue, only the residuum of it in the form of spindle-shaped clefts now
being apparent in the lower half of the fibrosing inflammatory process as it is viewed at scanning
magnification.
Figure 5.373: A&B. An advanced stage of the process known earlier in its course as "sclerosing
hemangioma" and "histiocytoma": dermatofibroma. When fully developed, a dermatofibroma is made up
overwhelmingly of fibrocytes in conjunction with coarse bundles of collagen. Keloidal collagen sometimes
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occurs near the surface. Fibrocytes at the periphery are interposed between strikingly thickened bundles of
collagen.
Figure 5.374: A&B. Induction of follicles by fibrocytes of dermatofibroma: recapitulation of dynamics in an

embryo between 11 and 13 weeks of intrauterine life. During the period of evolution of dermatofibroma,
fibrocytes may fool surface epidermis into acting as surface ectoderm and recapitulating events in an
embryo when primitive mesenchymal cells induced that future epidermis to generate hair follicles, as shown
here.
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Figure 5.375: A&B. A very late stage in the sequence chronological of dermatofibroma: a prominent dell.
Fibroplasia in a longstanding dermatofibroma may cause the skin to retract markedly, the result being a
dramatic dell in the center of the lesion, causing it to pucker.
Sclerosis in inflammatory diseases need not result only from resolution of granulation tissue by fibrosis. It may
supervene in longstanding lichenoid infiltrates of lymphocytes housed in a widened papillary dermis, as occurs in
lichen sclerosus et atrophicus (a superficial manifestation of morphea) and in late effects on the dermis and
subcutaneous fat of ionizing radiation, known as chronic radiodermatitis. As always is the case, irrespective of how it
comes to pass, sclerosis is typified by "homogenization" of collagen bundles and paucity of fibrocytes.
The definition of sclerosis just proffered pertains to findings in conditions such as lichen sclerosus et atrophicus (Fig.
5.376 A&B) and chronic radiation dermatitis (Fig. 5.377 A&B), but it does not obtain for the changes often said to be
"sclerotic" in morphea when that process affects the reticular dermis, the subcutaneous fat, and the fascia. Attributes
of morphea at those different anatomic sites do not fulfill criteria for "sclerosis" because bundles of collagen,
although crowded and thickened, remain distinct from one another (see Fig. 5.364); they are not effaced in the
manner of an amorphous structure, as is the case, for example, when morphea affects the papillary dermis where
then it is called lichen sclerosus et atrophicus, a condition of true sclerosis. Not unexpectedly, almost always the
uppermost part of the reticular dermis, at least, also is affected in lichen sclerosus et atrophicus, individual bundles
of collagen there being crowded and thickened in the conventional mode of morphea when it presents itself
stereotypically throughout the reticular dermis.
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Figure 5.376: A&B. Lichen sclerosus et atrophicus: a superficial expression of morphea and sclerotic truly.
Sclerosis in the upper part of the dermis is characteristic of that manifestation of morphea known as lichen
sclerosus et atrophicus. Findings typical of conventional morphea, to wit, crowded thickened bundles of
collagen, are found invariably in the upper part of the reticular dermis, beneath the zone of sclerosis in
lichen sclerosus et atrophicus.
Figure 5.377: A&B. Radiation sclerosis: sclerotic truly. Sclerosis, in the upper part of the dermis at least, in
conjunction with peculiar fibrocytes and telangiectases, as well as altered cornification, is characteristic of
chronic radiodermatitis (radiation sclerosis).
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Alterations markedly in the appearance of individual bundles of collagen and in their arrangement with respect to one
another occur in other longstanding lichenoid infiltrates in which lymphocytes monopolize, or nearly do, or are
accompanied by innumerable plasma cells, such as in diseases as unrelated as acrodermatitis chronica atrophicans
(Fig. 5.378 A&B), an inflammatory process caused by the borrelium named for Burgdorf and marked by countless
plasma cells, and mycosis fungoides, a lymphomatous process of unknown cause typified in the plaque stage by
lymphocytes in a persistent bandlike infiltrate that induce fibrocytes to produce wiry bundles of collagen that, in time,
come to be arrayed haphazardly (Fig. 5.379 A&B). Those distinctive bundles of collagen are a clue to a lichenoid
infiltrate of lymphocytes having been present for years in the upper part of the dermis. Similar changes may be
observed in some examples of long-sustained lesions of the lichenoid purpura of Gougerot and Blum, and even in
some longstanding lesions of lichen planus. Wiry bundles of collagen in random array in the upper part of the dermis
are analogous to other distinctive changes in collagen that direct attention to specific diagnoses, such as coarse
bundles of collagen arranged in vertical streaks in a thickened papillary dermis, a sign of lichen simplex chronicus;
thin bundles of collagen organized in short fascicles that interweave (Fig. 5.380 A&B), a finding characteristic in
resolving lesions of granuloma faciale/erythema elevatum diutinum; ribbon-like bundles of collagen in parallel to one
another but, from field to field, assuming peculiar geometric shapes, a pattern designated "sclerotic fibroma" (Fig.
5.381 A&B) and accompanying usually of a dermatofibroma or xanthogranuloma (Fig. 5.382 A&B) of many years
duration, and rims of collagen that surround blood vessels, findings expected in lupus profundus. When the distinctive
pattern of "sclerotic fibroma" occurs in a longstanding dermatofibroma (Fig. 5.383 A&B), findings of sclerosis may be
so striking that the condition, in former times, was called "subepidermal nodular sclerosis" (Fig. 5.384 A&B).
Figure 5.378: A&B. Abnormal collagen bundles in the upper part of the dermis: a result of the effects on
fibrocytes of a longstanding lichenoid infiltrate of an inflammatory process (acrodermatitis chronica
atrophicans). The broad lichenoid lymphoplasmacytic infiltrate of acrodermatitis chronica atrophicans of
long duration induces fibrocytes to manufacture distinctly thickened bundles of collagen arrayed
haphazardly, as illustrated here.
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Figure 5.379: A&B. Abnormal collagen bundles in the upper part of the dermis: a result of the effects on
fibrocytes of a longstanding lichenoid infiltrate of a neoplastic (lymphomatous) process (mycosis
fungoides). The patchy lichenoid infiltrate of lymphocytes of mycosis fungoides, after considerable
duration, induces fibrocytes to produce wiry bundles of collagen in haphazard array.
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Figure 5.380: A&B. Abnormal collagen bundles in the reticular dermis: a result of the effects on fibrocytes
of a longstanding infiltrate of a mix of inflammatory cells (granuloma faciale). A lesion of granuloma faciale
(and its identical twin, erythema elevatum diutinum) of long duration is typified by wiry bundles of collagen
arranged in fascicles that interweave and are joined by a mixed infiltrate of inflammatory cells.
Figure 5.381: A&B. The pattern of sclerotic fibroma: in a dermatofibroma. This dermatofibroma, which is
associated with slight acanthosis, is typified by ribbon-like bundles of collagen arranged in a particular
geometric design, this combination being known as sclerotic fibroma. In brief, what is termed sclerotic
fibroma is a distinctive pattern that is encountered most often in dermatofibroma.
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Figure 5.382: A&B. The pattern of sclerotic fibroma: in a xanthogranuloma. A longstanding infiltrate of an
inflammatory process (xanthogranuloma) confined largely to the reticular dermis results in production of
abnormal collagen bundles there, in this instance the pattern being that of sclerotic fibroma. A
xanthogranuloma resolves, after many months or years, with fibroplasia, the bundles sometimes assuming
the design of so-called sclerotic fibroma.
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Figure 5.383: A&B. The pattern of "sclerotic fibroma": devoid of specificity. The pattern of "sclerotic
fibroma" happens to be dominant in this dermatofibroma.
Figure 5.384: A&B. Implication of sclerosis in a dermatofibroma: lesion of many years' duration. Sclerosis is
so striking in this dermatofibroma that histopathologists of old termed such a lesion "subepidermal nodular
sclerosis."
The following algorithm shows the way to specific diagnosis of fibrosing dermatitides:
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ALGORITHM: Fibrosing Dermatitis
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Identification of Basic Patterns - Skin - Fibrosing Dermatitis

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Identification of Basic Patterns: Skin: Fibrosing Dermatitis

See Fig. 5.350 A&B.

Figure 5.350: Fibrosing dermatitis. A. Early. B. Late (sclerosis).

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which is pseudocarcinomatous (infundibular) proliferation of keratocytes.

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Figure 5.374: A&B. Induction of follicles by fibrocytes of dermatofibroma: recapitulation of dynamics in an

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ALGORITHM: Fibrosing Dermatitis

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