Dermatofibroma pathophysiology: Difference between revisions

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==Overview==
==Overview==
The exact pathogenesis of [disease name] is not fully understood.
The exact pathogenesis of dermatofibroma is not fully understood. Although some mechanisms are suggested in the [[pathogenesis]] of this disease that include, reactive [[tissue]] changes, [[neoplastic]] [[proliferation]], the cell surface [[proteoglycan]], [[Syndecan 1|syndecan-1]], and [[fibroblast growth factor receptor 2]] may play a role in the [[growth]] of dermatofibromas, [[Transforming growth factor-β|transforming growth factor-beta]] ([[TGF-beta]]) [[Signaling pathway|signaling]] may be involved in the [[development]] of [[fibrosis]] in [[dermatofibroma]], and the presence of [[Factor XIII|factor XIIIa]] and [[CD]]168 suggests that dermatofibroma can originate from the [[dermal]] [[dendritic cell]]. On [[gross pathology]], firm yellowish [[papules]] which may have areas of [[hemorrhage]] and lipidization are characteristic findings of dermatofibroma. Microscopically dermatofibroma is characterized by localized [[nodular]] [[proliferation]] of [[spindle]]-shaped [[fibrous]] [[Cells (biology)|cells]] in a [[mixture]] of [[Histiocyte|histocytoid]] [[Cells (biology)|cells]] inside the [[dermis]], spiculated margin of cells, “Storiform” [[pattern]] which defines as whorls of elongated [[nuclei]], [[collagen]] bundles that usually seen inside and between the [[fascicles]] of [[Spindle|spindled]] [[fibrous]] [[cells]], "Grenz zone" which is an unaffected layer that separates the overlying [[epidermis]] from the [[dermis]], and [[epidermal]] [[hyperplasia]].
 
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==
==Pathophysiology==
===Pathogenesis===
===Pathogenesis===
*The exact pathogenesis of dermatofibroma is not completely understood.
*The exact [[pathogenesis]] of dermatofibroma is not completely understood.
 
*The mechanisms which are suggested in the pathogenesis of dermatofibroma include:
**Reactive tissue changes
**Neoplastic proliferation because of the clonality
**The cell surface proteoglycan, syndecan-1, and fibroblast growth factor receptor 2 may play a role in the growth of dermatofibromas.
**Transforming growth factor-beta (TGF-beta) signaling may be involved in the development of fibrosis in dermatofibroma
**The presence of factor factor XIIIa and CD168 suggests that dermatofibroma can originate from dermal dendritic cell.
* 
 
The precise mechanism for the development of dermatofibroma is unknown. Rather than a reactive tissue change, evidence that dermatofibroma may be a neoplastic process is demonstrated by its clonal proliferative growth. [2] Clonality, by itself, is not necessarily synonymous with a neoplastic process; it has been demonstrated in inflammatory conditions, including atopic dermatitis, lichen sclerosis, and psoriasis. Dermatofibroma tumorigenesis may be due to distorted protein kinase C activity. [3]


Results from immunohistochemical testing with antibodies to factor XIIIa, which label dermal dendritic cells, are frequently positive in dermatofibroma, while antibodies to MAC 387, which label monocyte-derived macrophages (histiocytes), show less consistent results. One study evaluated the expression in dermatofibroma of HSP47, a recently used marker for skin fibroblasts; CD68, a marker for histiocytes; and factor XIIIa. Most of the spindle-shaped cells in all 28 cases of dermatofibroma, irrespective of histologic variant, stained positively with HSP47, indicating that skin fibroblasts are a major constituent of dermatofibroma. Factor XIIIa–positive dendritic cells also are present, but the presence of CD68-positive histiocytes was inconsistent, especially between histologic variants. [4] CD14+ monocytes have been proposed as the cell of origin of dermatofibromas. [5]
*The mechanisms which are suggested in the [[pathogenesis]] of dermatofibroma include:<ref name="pmid10660130">{{cite journal| author=Chen TC, Kuo T, Chan HL| title=Dermatofibroma is a clonal proliferative disease. | journal=J Cutan Pathol | year= 2000 | volume= 27 | issue= 1 | pages= 36-9 | pmid=10660130 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10660130  }} </ref><ref name="pmid14501288">{{cite journal| author=Sellheyer K, Smoller BR| title=Dermatofibroma: upregulation of syndecan-1 expression in mesenchymal tissue. | journal=Am J Dermatopathol | year= 2003 | volume= 25 | issue= 5 | pages= 392-8 | pmid=14501288 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14501288  }} </ref><ref name="SkrozaRotolo2008">{{cite journal|last1=Skroza|first1=Nevena|last2=Rotolo|first2=Sabrina|last3=Ceccarelli|first3=Simona|last4=Romano|first4=Ferdinando|last5=Innocenzi|first5=Daniele|last6=Frati|first6=Luigi|last7=Angeloni|first7=Antonio|last8=Marchese|first8=Cinzia|title=Modulation of the expression of the FGFR2-IIIb and FGFR2-IIIc molecules in dermatofibroma|journal=Journal of Dermatological Science|volume=51|issue=1|year=2008|pages=53–57|issn=09231811|doi=10.1016/j.jdermsci.2008.02.004}}</ref><ref name="KuboIhn2006">{{cite journal|last1=Kubo|first1=M.|last2=Ihn|first2=H.|last3=Yamane|first3=K.|last4=Tamaki|first4=K.|title=The expression levels and the differential expression of transforming growth factor-beta receptors in dermatofibroma and dermatofibrosarcoma protuberans|journal=British Journal of Dermatology|volume=154|issue=5|year=2006|pages=919–925|issn=0007-0963|doi=10.1111/j.1365-2133.2005.06904.x}}</ref><ref name="CerioSpaull2006">{{cite journal|last1=Cerio|first1=R.|last2=Spaull|first2=J.|last3=Jones|first3=E.Wilson|title=Histiocytoma cutis: a tumour of dermal dendrocytes (dermal dendrocytoma)|journal=British Journal of Dermatology|volume=120|issue=2|year=2006|pages=197–206|issn=00070963|doi=10.1111/j.1365-2133.1989.tb07783.x}}</ref><ref name="TörőcsikBárdos2005">{{cite journal|last1=Törőcsik|first1=D.|last2=Bárdos|first2=H.|last3=Nagy|first3=L.|last4=Ádány|first4=R.|title=Identification of factor XIII-A as a marker of alternative macrophage activation|journal=Cellular and Molecular Life Sciences|volume=62|issue=18|year=2005|pages=2132–2139|issn=1420-682X|doi=10.1007/s00018-005-5242-9}}</ref><ref name="pmid1972317">{{cite journal| author=Cerio R, Spaull J, Oliver GF, Jones WE| title=A study of factor XIIIa and MAC 387 immunolabeling in normal and pathological skin. | journal=Am J Dermatopathol | year= 1990 | volume= 12 | issue= 3 | pages= 221-33 | pmid=1972317 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1972317  }} </ref>
 
**Reactive [[tissue]] changes
The cell surface proteoglycan, syndecan-1, [6] and fibroblast growth factor receptor 2, involved in epithelial-mesenchymal cross-talk, [7] may play a role in the growth of dermatofibromas. Transforming growth factor-beta (TGF-beta) signaling might be a trigger of the fibrosis seen in dermatofibromas. [8] TGF-beta, along with other fibrinogenic factors, may be produced by mast cells, which have been reported to occur in abnormally high numbers in dermatofibromas. [9]
**[[Neoplastic]] [[proliferation]] because of the [[clonality]]
 
**The cell surface [[proteoglycan]], [[Syndecan 1|syndecan-1]], and [[fibroblast growth factor receptor 2]] may play a role in the [[growth]] of dermatofibromas.
 
**[[Transforming growth factor-β|Transforming growth factor-beta]] ([[TGF-beta]]) [[Signaling pathway|signaling]] may be involved in the [[development]] of [[fibrosis]] in [[dermatofibroma]]
 
**The presence of [[Factor XIII|factor XIIIa]] and [[CD]]168 suggests that dermatofibroma can originate from the [[dermal]] [[dendritic cell]].
 
The precise cell of origin of dermatofibroma has long been
disputed. The contemporary hypothesis is that the tumor
originates from dermal dendritic cells (dendrocytes) of
monocyte/macrophage lineage.4,5,27,29,32,36e38 Whether a cell
adopts a dendritic or spindled configuration in the confines of
the extracellular matrix depends on the latter’s composition
and deformational capacity. The delicate dendritic processes
are outlined by factor XIIIa and CD168 immunostaining. The
monster cells are nonstaining, indicating that they may be
effete or degenerating forms. Cytoplasmic staining for factor
XIIIa has long been regarded as the preeminent hallmark of
the constituent dermal dendritic cells.4,5,35,37 Factor XIIIa is
synthesized, but not secreted, by monocytes of bone marrow
origin. It is not a property narrowly confined to dermal dendritic
cells, with which it is therefore not synonymous.
27,29,34,36,37 It is a transglutaminase heterotetramer
activated by thrombin that leads to the formation of an
insoluble clot conducive to a renewal of stromal assembly.
Factor XIIIa together with CD163 denote a lineage from
monocytes (bone marrow derived).Indeed, given the range of cellular morphologies in dermatofibromatous
lesions and the different immunophenotypes
of the participating cells, this diagnostic rubric probably
embraces lesions at different stages of, and with different
pathways for, their evolution. Included in these processes is
the recruitment of secondary inflammatory cells or their
activation through the effects of chemokines and cytokines.
The resultant cellular typologies are mixtures of plump polyhedral
histiocytoid cells/epithelioid cells, which in dermatofibromas
may have a heterogeneity of origins. The
coparticipation of myofibroblastic spindle cells can create a
storiform pattern. How lesions of different cellular phenotypes
are gathered together and governed architecturally remains
unknown. On the other hand, an almost totally
epithelioid cell proliferation devoid of a salient spindle/
fascicular cell component has been characterized among
dermatofibromas over the past 20 years.1,10,16,20,23,35 This
variant can simulate a Spitzoid melanoma or Spitz nevus,31
except for the absence of junctional nests. Melanocytic biomarkers
(MART-1, HMB45, MiTF) can assist in resolving this
diagnostic dilemma.
Dermal dendritic cells (dendrocytes) typically reside in a
close microanatomic relationship to the pericapillary space
(endothelium-related cells). They are thought to be the source
of many dermatofibromas23,32,35 and belong to the dermal microvascular unitda plexus in the upper reticular and
papillary dermis. The dendrocytes function as an adventitial
pool of reserve or stem cells. This complex microvascular
structure also includes monocytic/histiocytic cells. Nonproliferative
dermal dendritic cells are CD34þ, but this
biomarker expression is lost if the cells proliferate or differentiate.
This situation is also found in corneal stromal cells
(keratocytes), which are CD34þ in a resting phase but become
CD34 in corneal scar formation or fibrous downgrowth.14
The loss of CD34 expression which plays a role in intercellular
adhesion allows the cells to migrate.
Dendritic morphology alone, however, should not obscure
the fact that dendritiform cells offer a multiplicity of molecular/
biochemical phenotypes: some express factor XIIIa,
whereas others bear CD163þ monocyte/macrophage phenotypes29,37
or are CD1aþ Langerhans cells.35 The last cell type
together with indigenous dermal dendritic cells is example of
antigen-processing cells manifesting major histocompatibility
complex class-II molecules.26,35 In the lesion reported
herein, Langerhans cells and phagocytic histiocytes were
commingled, a feature also discovered in eyelid perilymphatic
granulomas of the Melkersson-Rosenthal syndrome.7 The
interplay of these disparate cells probably plays a central role
in the development of the lesions and may reflect a distinctive
organization and immunologic pattern of the eyelids. Some
have concluded that, rather than being a low-grade neoplasm,
dermatofibroma might well represent an abortive immunoreactive
process triggered by dermal dendrocytes.26
 
<br />


==Genetics==
==Genetics==
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  | pages = 901–903
  | pages = 901–903
  | year = 1995
  | year = 1995
| month = May
  | doi = 10.1016/0190-9622(95)91558-3
  | doi = 10.1016/0190-9622(95)91558-3
  | pmid = 7722054
  | pmid = 7722054
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  | pages = 266–270
  | pages = 266–270
  | year = 1991
  | year = 1991
| month = April
  | pmid = 2050454
  | pmid = 2050454
}}</ref><ref>{{Cite journal
}}</ref><ref>{{Cite journal
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  | pages = 1074–1076
  | pages = 1074–1076
  | year = 2017
  | year = 2017
| month = September
  | doi = 10.1111/1346-8138.13625
  | doi = 10.1111/1346-8138.13625
  | pmid = 27665731
  | pmid = 27665731
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  | pages = 59–60
  | pages = 59–60
  | year = 1994
  | year = 1994
| month = January
  | pmid = 8313640
  | pmid = 8313640
}}</ref><ref>{{Cite journal
}}</ref><ref>{{Cite journal
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  | pages = 319–321
  | pages = 319–321
  | year = 2003
  | year = 2003
| month =
  | doi = 10.1159/000073098
  | doi = 10.1159/000073098
  | pmid = 14571078
  | pmid = 14571078
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  | pages = 351–352
  | pages = 351–352
  | year = 1986
  | year = 1986
| month = February
  | doi = 10.1016/s0190-9622(86)70041-8
  | doi = 10.1016/s0190-9622(86)70041-8
  | pmid = 3950136
  | pmid = 3950136
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  | pages = 1062–1063
  | pages = 1062–1063
  | year = 2000
  | year = 2000
| month = May
  | doi = 10.1046/j.1365-2133.2000.03508.x
  | doi = 10.1046/j.1365-2133.2000.03508.x
  | pmid = 10809884
  | pmid = 10809884
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*[[Hematologic]] [[malignancies]]
*[[Hematologic]] [[malignancies]]
*[[Immunodeficiency|Immunodeficient]] [[Disease|diseases]] ([[HIV]])
*[[Immunodeficiency|Immunodeficient]] [[Disease|diseases]] ([[HIV]])
*[[Autoimmune diseases]] ([[myasthenia gravis]], [[Pemphigus vulgaris]], and [[systemic lupus erythematosus]])
*[[Autoimmune diseases]] ([[myasthenia gravis]], [[pemphigus vulgaris]], and [[systemic lupus erythematosus]])


==Gross Pathology==
==Gross Pathology==
Line 226: Line 110:
* "Grenz zone" which is an unaffected layer that separates the overlying [[epidermis]] from the [[dermis]]
* "Grenz zone" which is an unaffected layer that separates the overlying [[epidermis]] from the [[dermis]]
*[[Epidermal]] [[hyperplasia]]
*[[Epidermal]] [[hyperplasia]]
[[File:Proliferating histiocytic cells with foamy, granular cytoplasm.png|350px|thumb|https://openi.nlm.nih.gov/detailedresult?img=PMC3213176_1746-160X-7-20-3&query=&req=4|center]]
[[File:Spindle-shaped fibroblasts, arranged in a storiform pattern.png|350px|thumb|https://openi.nlm.nih.gov/detailedresult?img=PMC3213176_1746-160X-7-20-3&query=&req=4|center]]


==References==
==References==
{{Reflist|2}}
{{Reflist|2}}
[[Category:Medicine]]
[[Category:Medicine]]
[[Category:Oncology]]
[[Category:Oncology]]
[[Category:Up-To-Date]]
[[Category:Up-To-Date]]
[[Category:Primary care]]
[[Category:Dermatology]]
[[Category:Dermatology]]

Latest revision as of 21:18, 29 July 2020

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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

The exact pathogenesis of dermatofibroma is not fully understood. Although some mechanisms are suggested in the pathogenesis of this disease that include, reactive tissue changes, neoplastic proliferation, the cell surface proteoglycan, syndecan-1, and fibroblast growth factor receptor 2 may play a role in the growth of dermatofibromas, transforming growth factor-beta (TGF-beta) signaling may be involved in the development of fibrosis in dermatofibroma, and the presence of factor XIIIa and CD168 suggests that dermatofibroma can originate from the dermal dendritic cell. On gross pathology, firm yellowish papules which may have areas of hemorrhage and lipidization are characteristic findings of dermatofibroma. Microscopically dermatofibroma is characterized by localized nodular proliferation of spindle-shaped fibrous cells in a mixture of histocytoid cells inside the dermis, spiculated margin of cells, “Storiform” pattern which defines as whorls of elongated nuclei, collagen bundles that usually seen inside and between the fascicles of spindled fibrous cells, "Grenz zone" which is an unaffected layer that separates the overlying epidermis from the dermis, and epidermal hyperplasia.

Pathophysiology

Pathogenesis

  • The exact pathogenesis of dermatofibroma is not completely understood.

Genetics

Associated Conditions

Conditions associated with multiple dermatofibromas include:[8][9][10][11][12][13][14][15]

Gross Pathology

On gross pathology, firm yellowish papules which may have areas of hemorrhage and lipidization are characteristic findings of dermatofibroma.[16]

Microscopic Pathology

Microscopically dermatofibroma is characterized by: [17][18][19]

https://openi.nlm.nih.gov/detailedresult?img=PMC3213176_1746-160X-7-20-3&query=&req=4
https://openi.nlm.nih.gov/detailedresult?img=PMC3213176_1746-160X-7-20-3&query=&req=4

References

  1. ↑ Chen TC, Kuo T, Chan HL (2000). "Dermatofibroma is a clonal proliferative disease". J Cutan Pathol. 27 (1): 36–9. PMID 10660130.
  2. ↑ Sellheyer K, Smoller BR (2003). "Dermatofibroma: upregulation of syndecan-1 expression in mesenchymal tissue". Am J Dermatopathol. 25 (5): 392–8. PMID 14501288.
  3. ↑ Skroza, Nevena; Rotolo, Sabrina; Ceccarelli, Simona; Romano, Ferdinando; Innocenzi, Daniele; Frati, Luigi; Angeloni, Antonio; Marchese, Cinzia (2008). "Modulation of the expression of the FGFR2-IIIb and FGFR2-IIIc molecules in dermatofibroma". Journal of Dermatological Science. 51 (1): 53–57. doi:10.1016/j.jdermsci.2008.02.004. ISSN 0923-1811.
  4. ↑ Kubo, M.; Ihn, H.; Yamane, K.; Tamaki, K. (2006). "The expression levels and the differential expression of transforming growth factor-beta receptors in dermatofibroma and dermatofibrosarcoma protuberans". British Journal of Dermatology. 154 (5): 919–925. doi:10.1111/j.1365-2133.2005.06904.x. ISSN 0007-0963.
  5. ↑ Cerio, R.; Spaull, J.; Jones, E.Wilson (2006). "Histiocytoma cutis: a tumour of dermal dendrocytes (dermal dendrocytoma)". British Journal of Dermatology. 120 (2): 197–206. doi:10.1111/j.1365-2133.1989.tb07783.x. ISSN 0007-0963.
  6. ↑ Törőcsik, D.; Bárdos, H.; Nagy, L.; Ádány, R. (2005). "Identification of factor XIII-A as a marker of alternative macrophage activation". Cellular and Molecular Life Sciences. 62 (18): 2132–2139. doi:10.1007/s00018-005-5242-9. ISSN 1420-682X.
  7. ↑ Cerio R, Spaull J, Oliver GF, Jones WE (1990). "A study of factor XIIIa and MAC 387 immunolabeling in normal and pathological skin". Am J Dermatopathol. 12 (3): 221–33. PMID 1972317.
  8. ↑ Bhattacharjee, Pradip; Umar, Saleem; Fatteh, Shokat (2005). "Multiple Eruptive Dermatofibromas Occurring in a Patient with Myelodysplastic Syndrome". Acta Dermato-Venereologica. -1 (1): 1–1. doi:10.1080/00015550410024517. ISSN 0001-5555.
  9. ↑ I. Lu, P. R. Cohen & M. E. Grossman (1995). "Multiple dermatofibromas in a woman with HIV infection and systemic lupus erythematosus". Journal of the American Academy of Dermatology. 32 (5 Pt 2): 901–903. doi:10.1016/0190-9622(95)91558-3. PMID 7722054.
  10. ↑ P. R. Cohen (1991). "Multiple dermatofibromas in patients with autoimmune disorders receiving immunosuppressive therapy". International journal of dermatology. 30 (4): 266–270. PMID 2050454.
  11. ↑ Mayuri Tanaka, Toshihiko Hoashi, Naotaka Serizawa, Kyochika Okabe, Susumu Ichiyama, Rie Shinohara, Yoko Funasaka & Hidehisa Saeki (2017). "Multiple unilaterally localized dermatofibromas in a patient with Down syndrome". The Journal of dermatology. 44 (9): 1074–1076. doi:10.1111/1346-8138.13625. PMID 27665731.
  12. ↑ J. Stainforth & M. J. Goodfield (1994). "Multiple dermatofibromata developing during pregnancy". Clinical and experimental dermatology. 19 (1): 59–60. PMID 8313640.
  13. ↑ Yuichiro Tsunemi, Hironobu Ihn, Naoko Hattori, Hidehisa Saeki & Kunihiko Tamaki (2003). "Multiple eruptive dermatofibromas with CD34+ cells in a patient with hypertriglyceridemia". Dermatology (Basel, Switzerland). 207 (3): 319–321. doi:10.1159/000073098. PMID 14571078.
  14. ↑ H. B. Bargman & I. Fefferman (1986). "Multiple dermatofibromas in a patient with myasthenia gravis treated with prednisone and cyclophosphamide". Journal of the American Academy of Dermatology. 14 (2 Pt 2): 351–352. doi:10.1016/s0190-9622(86)70041-8. PMID 3950136.
  15. ↑ S. E. Chang, J. H. Choi, K. J. Sung, K. C. Moon & J. K. Koh (2000). "Multiple eruptive dermatofibromas occurring in a patient with acute myeloid leukaemia". The British journal of dermatology. 142 (5): 1062–1063. doi:10.1046/j.1365-2133.2000.03508.x. PMID 10809884.
  16. ↑ LeBoit, P. E. (2006). Pathology and genetics of skin tumours. Lyon: IARC Press. ISBN 9283224140.
  17. ↑ Lee, MiWoo; Lee, WooJin; Jung, JoonMin; Won, ChongHyun; Chang, SungEun; Choi, JeeHo; Moon, KeeChan (2015). "Clinical and histological patterns of dermatofibroma without gross skin surface change: A comparative study with conventional dermatofibroma". Indian Journal of Dermatology, Venereology, and Leprology. 81 (3): 263. doi:10.4103/0378-6323.154795. ISSN 0378-6323.
  18. ↑ Mentzel, Thomas; Wiesner, Thomas; Cerroni, Lorenzo; Hantschke, Markus; Kutzner, Heinz; Rütten, Arno; Häberle, Michael; Bisceglia, Michele; Chibon, Frederic; Coindre, Jean-Michel (2012). "Malignant dermatofibroma: clinicopathological, immunohistochemical, and molecular analysis of seven cases". Modern Pathology. 26 (2): 256–267. doi:10.1038/modpathol.2012.157. ISSN 0893-3952.
  19. ↑ Victor, Thomas A. (2003). "Neoplasms With Follicular Differentiation, 2nd ed. A. BERNARD ACKERMAN, VIJAYA B. REDDY, AND H. PETER SOYER, eds". Dermatologic Surgery. 29 (6): 641–641. doi:10.1046/j.1524-4725.2003.29153.x. ISSN 1076-0512.
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