Dermatofibroma pathophysiology
|
Dermatofibroma Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Dermatofibroma pathophysiology On the Web |
|
American Roentgen Ray Society Images of Dermatofibroma pathophysiology |
|
Risk calculators and risk factors for Dermatofibroma pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1], Associate Editor(s)-in-Chief: Homa Najafi, M.D.[2]Faizan Sheraz, M.D. [3]
Overview
Dermatofibromas are composed of disordered collagen laid down by fibroblasts.
Pathophysiology
Dermatofibromas form as a reaction to previous injuries such as insect bites or thorn pricks. Dermatofibromas are composed of disordered collagen laid down by fibroblasts.
Immunohistochemical staining
| Neoplasm | CD34 | Stromelysin-3[1] | Factor XIIIa |
|---|---|---|---|
| Dermatofibroma | + | + | + |
| Dermatofibrosarcoma protuberans | + | - | - |
Video
{{#ev:youtube|tq4xFLIw1TA}}
Overview
The exact pathogenesis of [disease name] is not fully understood.
OR
It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
OR
[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
OR
Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
OR
[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
OR
The progression to [disease name] usually involves the [molecular pathway].
OR
The pathophysiology of [disease/malignancy] depends on the histological subtype.
Pathophysiology
Physiology
The normal physiology of [name of process] can be understood as follows:
Pathogenesis
- The exact pathogenesis of [disease name] is not completely understood.
OR
- It is understood that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
- [Pathogen name] is usually transmitted via the [transmission route] route to the human host.
- Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
- [Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
- The progression to [disease name] usually involves the [molecular pathway].
- The pathophysiology of [disease/malignancy] depends on the histological subtype.
Dermatofibromas have many histologic variants including cellular, epithelioid, lipidized, aneurysmal, monster cell, and atypical (to name only a few); but the most frequently diagnosed is the common fibrous histiocytoma or common dermatofibroma.
The common dermatofibroma is characterized histopathologically by a localized proliferation of spindle-shaped fibrous cells admixed with histiocytoid cells within the dermis. This proliferation is usually nodular in appearance, with spiculated, but moderately defined, borders that may have a pushing appearance in regards to the surrounding tissue. The spindle cells will form focally what is referred to as a “storiform” pattern, which describes a multi-centric whorling appearance of the elongated nuclei. There may be intermixed capillaries and lymphocytes or multinucleated giant cells. These proliferations are usually contained within the dermis, but it is not uncommon to observe a small portion of the lesion dipping down into the subcutaneous tissue along septal lines. A helpful and distinguishing characteristic is the presence of trapped collagen bundles or “collagen balls” within and between the fascicles of spindled fibrous cells. These entrapped collagen collections are more commonly found forming at the periphery of the lesion.
The overlying epidermis is usually separated by a clearly delineated and unaffected zone of separation, the "Grenz zone." Typical reactive epidermis changes include hyperkeratosis and acanthosis. The epidermis also will often exhibit elongated rete ridges diving into the dermis with hyperpigmented basal keratinocytes, which is referred to as the “dirty feet” sign.
Arguably the most important entity to distinguish dermatofibromas from is the similar appearing, but much more worrisome, dermatofibrosarcoma protuberans (DFSP). These lesions are more typically much more cellular, have a more marked development of the storiform pattern, and will invade and involve the subcutis much more deeply, often entrapping fat as it dives and proliferates along the subcutaneous septae
Genetics
[Disease name] is transmitted in [mode of genetic transmission] pattern.
OR
Genes involved in the pathogenesis of [disease name] include:
- [Gene1]
- [Gene2]
- [Gene3]
OR
The development of [disease name] is the result of multiple genetic mutations such as:
- [Mutation 1]
- [Mutation 2]
- [Mutation 3]
Associated Conditions
Conditions associated with [disease name] include:
- [Condition 1]
- [Condition 2]
- [Condition 3]
Gross Pathology
On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Microscopic Pathology
On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
- ↑ Kim HJ, Lee JY, Kim SH; et al. (2007). "Stromelysin-3 expression in the differential diagnosis of dermatofibroma and dermatofibrosarcoma protuberans: comparison with factor XIIIa and CD34". Br. J. Dermatol. 157 (2): 319–24. doi:10.1111/j.1365-2133.2007.08033.x. PMID 17596171. Unknown parameter
|month=ignored (help)