Dermatofibroma (superficial benign fibrous histiocytoma) is a common cutaneous nodule of unknown etiology that occurs more often in women. Dermatofibroma frequently develops on the extremities (mostly the lower legs) and is usually asymptomatic, although pruritus and tenderness can be present. It is actually the most common painful skin tumor.[1] A number of well-described, histologic subtypes of dermatofibroma have been reported. Removal of the tumor is usually not typically required unless diagnostic uncertainty exists or particularly troubling symptoms are present.

This article discusses primarily cutaneous (superficial) dermatofibroma. Subcutaneous (deep) benign fibrous histiocytomas are also well documented and may have a more aggressive clinical course, as can tumors displaying cellular, aneurysmal (hemosiderotic), and atypical histologic variants of dermatofibroma.

In addition, benign fibrous histiocytomas are reported in bone, orbital, airway, gastrointestinal, splenic, genitourinary, and intracranial locations.


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 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]

Gene fusions have been described in dermatofibroma tumorigenesis.[10, 11] ALK gene rearrangement and overexpression has been demonstrated in the epithelioid and atypical dermatofibroma variants.[12, 13]


Historically attributed to be a reactive process to some traumatic insult to the skin (eg, arthropod bite, skin tattooing, tuberculin skin testing, prior folliculitis),[14, 15, 16, 17] the cause of dermatofibroma is unknown. Clonal analysis suggest it may represent a true neoplasm.[2]

Altered immunity likely plays a role in many cases of multiple eruptive dermatofibromas associated with various underlying conditions and medications (see History).

A study of eruptive dermatofibromas in a kindred suggests that a genetic component may exist.[18]



Dermatofibromas are relatively common.


Frequency of dermatofibroma appears to be similar in all races.


Females are affected by dermatofibroma more commonly than males, with a male-to-female ratio of 1:2, or higher.[19, 20]


Dermatofibroma can occur in patients of any age. In one series, 80% of biopsy specimens were from patients aged 20-49 years,[19] and in another the mean age of the patients was 42.18±13.72 years.[20]


Typical superficial dermatofibromas are considered benign lesions, and the prognosis for patients with this condition is excellent. However, discomfort from pain or itching may be significant.

Deep, cellular, aneurysmal (hemosiderotic), and atypical variants, which are notoriously more locally recurrent (≤20% of cases), can rarely metastasize.[21, 22, 23] (The deep subset of dermatofibroma that arises in the subcutaneous or deep soft tissue may undergo further classification.[22] ) Such variants, or any indeterminant dermatofibroma, might be regarded as potentially malignant lesions.[24] In these exceptional cases, pulmonary and nodal metastases were most commonly seen, some patients developed multiple satellite nodules, and deaths have occurred.[25] The primary tumors tended to be large and cellular, but aggressive behavior is not entirely predictable, although early or frequent recurrences of the tumor should raise concern.[25] Array-based comparative genomic hybridization (CGH) may prove useful in identifying these higher-risk variants.[26, 27, 22]

The epithelioid variant has also been reported to metastasize, although demonstration of ALK gene rearrangement may indicate it is a biologically distinct tumor.[12]

In a study of common dermatofibromas with an increased mitotic rate but no other worrisome features, none recurred or metastasized.[28]

Spontaneous regression has been reported,[29] and this may yield postinflammatory hypopigmentation, although this appears to be quite rare.

Patient Education

For patient education resources, see the Procedures Center, as well as Mole Removal.


Dermatofibromas typically arise slowly and most often occur as a solitary nodule on an extremity, particularly the lower leg, but any cutaneous site is possible. Dermatofibromas are usually asymptomatic, but itching and pain often are noted. They are the most common of all painful skin tumors.[1] Women who shave their legs may be bothered by the razor traumatizing the lesion in that region, causing pain, bleeding, erosive changes, and ulceration. Although cases of unusually rapid growth exist, most dermatofibromas remain static for decades or persist indefinitely. Patients may describe a hard mole or unusual scar and are often concerned about the possibility of skin cancer.

Several lesions may be present, but rarely are numerous (ie, ≥15) tumors found. This multiple eruptive variant occurs in less than 1% of patients, approximately 60% of whom have an underlying systemic condition, such as HIV infection or systemic lupus erythematosus.[30, 31, 32] However, dermatomyositis,[33] Graves disease,[34] Hashimoto thyroiditis,[35] myasthenia gravis,[35] Down syndrome,[36] leukemia,[37] myelodysplastic syndrome,[38] cutaneous T-cell lymphoma,[39] multiple myeloma,[39] atopic dermatitis,[40] Crohn disease,[41] and ulcerative colitis[42] have all been reported in association with the phenomenon. In addition, antiretroviral agents,[43] the biologic agent efalizumab,[44] antitumor necrosis factor-alpha agents,[45] and the tyrosine kinase inhibitor imatinib[46] have been linked to their appearance.

Both congenital[47] and acquired[48] cases of multiple clustered dermatofibromas have been reported.

Physical Examination

Typically, the clinical appearance of dermatofibroma is a solitary, 0.5- to 1-cm nodule. A sizable minority of patients may have several lesions, but rarely (< 1% of cases) are more than 15 lesions present. (See History) The overlying skin can range from flesh to gray, yellow, orange, pink, red, purple, blue, brown, or black, or a combination of hues (see the image below). On palpation, the hard nodule may feel like a small pebble fixed to the skin surface and is freely movable over the subcutis. Tenderness may be elicited with manipulation of the lesion.

View Image

Erythematous, slightly hyperpigmented nodule on the leg. Courtesy of David Barnette, MD.

The characteristic tethering of the overlying epidermis to the underlying lesion with lateral compression (pinching), called the dimple sign, may be a useful clinical sign for diagnosis.[49] However, presence of the dimple sign does not always assure the lesion is dermatofibroma,[50] and dermatoscopy may be useful in supporting the clinical impression.[51]

The extremities are the most common sites of involvement, particularly the legs.[19, 20] Although any cutaneous site can be seen, palm, sole, digital, oral, and genital involvement is relatively rare. Giant (>5 cm in diameter),[52] atrophic,[53] polypoid,[54] and dermatofibroma with spreading satellitosis[55] variants have been reported. The largest reported tumor was 17 x 9 x 4 cm.[56]

Multiple clustered dermatofibromas[48] are rare and can mimic dermatofibrosarcoma protuberans. This phenomenon has been reported in a segmental distribution.[57]

A halo of dermatitis (Meyerson phenomenon) surrounding a dermatofibroma occurred in one patient.[58]

Imaging Studies

A study of localized lesions of the skin imaged via variable-frequency ultrasound included the image of a hypoechoic solid nodule created by a dermatofibroma.[59] Dermatofibromas have been analyzed by high-definition optical coherent tomography.[60]

Dermatofibroma can mimic a malignant lesion on fluorodeoxyglucose positron-emission tomography (FDG-PET) scans.[61]


For those trained in dermoscopy, this may be a useful adjunctive diagnostic technique for dermatofibromas. The most common pattern seen is a peripheral pigment network with a central white area.[62] Dermoscopy of a xanthomatous dermatofibroma shows a homogeneous pattern with shades of yellow and a peripheral pigment network.[63] A green color may indicate the hemosiderotic variant.[64] If a suggestive melanocytic or atypical pattern is noted with dermoscopy, a diagnostic biopsy is warranted.[65]

Confocal laser scanning microscopy findings have been described.[66]

If any diagnostic uncertainty exists, excisional biopsy into the subcutaneous fat is advised.

Histologic Findings

The overlying epidermis is usually acanthotic. Pseudoepitheliomatous hyperplasia and a basaloid proliferation may be noted. The hyperplasia may be caused by the action of fibroblasts on epidermal keratinocytes.[67] Increased pigment may be seen, which may be iron or melanin. Most lesions display a grenz zone of normal papillary dermis overlying the tumor.

The bulk of the tumor is within the mid dermis where no capsule is present and the periphery of the lesion blends with the surrounding tissue. Whorling fascicles of a spindle cell proliferation with excessive collagen deposition are characteristic. At the periphery, the spindle cells characteristically wrap around normal collagen bundles (see the images below). Occasionally, melanocytes have been reported to be interspersed amongst the spindle cells.[68]

View Image

Acanthotic epithelium with basilar hyperpigmentation (dirty feet) over a dermal spindle cell proliferation (X10). Courtesy of David Barnette, MD.

View Image

Collagen trapping by the dermal fibrohistiocytic infiltrate (X40). Courtesy of David Barnette, MD.

The subcutis typically is preserved, but if involved (especially when a storiform [cartwheel] pattern is observed), be alert to the possibility of the lesion being a dermatofibrosarcoma protuberans (DFSP).[69]  

Antibodies toward factor XIIIa and CD34 are useful in distinguishing the two tumors, with the former suggesting dermatofibroma and the latter suggesting DFSP.[70] However, occasional CD34 positivity occurs in the cellular variant of dermatofibroma.[71, 72] Dermatofibromas retain elastic fibers, while these are fragmented or displaced in DFSP. This can be assessed with fluorescence microscopy of hematoxylin and eosin (H&E) sections or with an elastic stain.[73]

Stromelysin-3 (ST-3) expression of dermatofibroma by immunohistochemical staining may also be useful in differentiation from DFSP.[74]

Transforming growth factor-beta type I and type II receptor expression patterns may also help distinguish between dermatofibroma and DFSP.[8] Thrombospondin-1 (TSP-1) mediates TGF-beta I activation, and its elevated expression in DFSP may aid in the differential diagnosis.[75]

Immunostaining with insulinlike growth factor–binding protein 7 (IGFBP7) is positive more frequently in dermatofibroma and aids in the differentiation from DFSP.[76]

Nestin, expressed in only 13% of dermatofibroma, but 94% of DFSP, could be a useful marker to distinguish between these two tumors.[77]

Collagen triple helix repeat containing-1 (Cthrc1) staining is positive much more frequently in DFSP and is another potential discriminating test.[78]

D2-40 immunostain appears to be a sensitive marker for dermatofibromas, including the cellular variant, can aid in differentiation from DFSP.[79]

Cathepsin K expression[80] and immunohistochemical analysis of chemokine receptor CXCR4[81] are other possible tools in delineating the two tumors.

Indeterminate tumors that share histologic and immunohistochemical features of dermatofibroma and DFSP have been described[82] ; however, those studied do not harbor the COL1A1-PDGFB chimeric transcripts of DFSP.[83]

Expression of FGFR3/FOXN1 and FGF2/FGFR4 in dermatofibroma pathogenesis may also help differentiate from DFSP.[84]

CD99 has been used alone or in combination with factor XIIIa and CD34 to differentiate dermatofibroma from DFSP.[85, 86, 87]

Leukocyte-specific protein 1 (LSP1) may aid in differentiation of dermatofibroma from DFSP.[5]

5-Hydroxymethylcytosine (5-hmC) may be a useful marker to distinguish dermatofibroma from DFSP.[88]

Fluorescence in situ hybridization (FISH) analysis may be helpful in differentiating dermatofibroma from DFSP.[89]

B-cell lymphoma 2 (Bcl-2) expression may help distinguish subcutaneous dermatofibroma from DFSP.[90]

One clinicopathologic classification scheme[91] describes the following four categories of dermatofibroma:

Of the variants listed above, keep in mind that the uncommon sclerotic fibromalike dermatofibroma should be differentiated from sclerotic fibroma. One study[94] showed 7 of 7 of the former lesions to be negative for CD34 and CD99, while 3 of 3 solitary fibromas were positive for CD34 and CD99. For comparison, 14 of 14 "common-type" dermatofibromas in this study were negative for CD34, while 4 demonstrated positivity with CD99.

A histologic review of 192 dermatofibromas found 80% common type, 5.7% aneurysmal, 5.7% hemosiderotic, 2.6% epithelioid, 2.1% cellular, 2.1% lipidized, 1% atrophic, and 0.5% clear cell.[95]

Immunoperoxidase staining is consistently positive for both CD10 and actin in dermatofibromas.[96] CD10 was positive in 11 of 11 dermatofibromas and only positive in 1 of 7 epithelioid dermatofibromas, so it was postulated that epithelioid dermatofibroma may be a distinct entity.[97]

Lichenoid dermatofibroma,[98] ulcerated dermatofibroma,[98] erosive dermatofibroma,[98] dermatofibroma with diffuse eosinophilic infiltrate,[99] dermatofibroma accompanied by perforating dermatosis,[100] and one showing perforating dermatosis with floret-type multinucleated giant cells have been described.[101] Dermatofibromas with overlying sebaceous hyperplasia,[102] with intracytoplasmic eosinophilic globules,[103] signet-ring cells,[104] amyloid light chain deposition,[105] and incidental acantholysis[106] have also been reported. A case of an apocrine gland cyst with a hemosiderotic dermatofibroma was termed an apocrine hemosiderotic dermatofibroma.[107] Cutaneous adenodermatofibroma (entrapped apocrine structures without hemosiderotic changes), keloidal, collapsing angiokeloidal, and dermatofibromas with dystrophic calcification variants have been reported.[108, 109, 110, 111] Blue nevus associated with dermatofibroma has been reported, as has coexisting leukemia cutis.[112, 113]

One case of mycosis fungoides showed histologic features of dermatofibroma.[114]

Induction of hyperplasia in nearby structures by dermatofibroma is frequently described. In a study of over 10,000 dermatofibromas, associated induction (where follicular germinative and sebaceous glandular induction were seen in 6% of cases), cellular alterations, and stromal alterations are outlined with their attributes.[96] Dermatofibromas of the shoulder have a high incidence of sebaceous induction with seborrheic keratosis‒like hyperplasia.[115]

A case series[116] reported the uncommon occurrence of dermatofibroma and melanocytic lesions in the same biopsy specimen. Four of 14 specimens showed the 2 processes to seemingly merge imperceptibly. The lesions included junctional, dermal, and compound nevi, as well as a single case of melanoma in situ. Knowledge of this relationship can help prevent rendering the wrong diagnosis and is facilitated by the use of immunohistochemistry, with the melanocytic lesions showing S-100 and Mart-1 positivity with FXIIIa negativity and the dermatofibroma showing S-100 and Mart-1 negativity and FXIIIa positivity. Another tool is Sox10 immunoreactivity, which is positive in melanocytic lesions, but not fibrohistiocytic proliferations.[117] A case report[118] documenting an invasive melanoma occurring in association with a dermatofibroma underscores the role of these immunohistochemical stains.

INI-1, present in 100% of dermatofibromas, but decreased or absent in the vast majority of epithelioid sarcomas in one study, can help distinguish between the 2 lesions.[119]

Approach Considerations

No treatment is usually necessary for dermatofibromas. Simple reassurance that the lesion is benign may be indicated, unless one of the aggressive subtypes is suspected or diagnosed.

Intralesional steroid injections have been attempted with variable results.

Surgical Care

For cosmetically unacceptable lesions, those that are particularly symptomatic, if there is any diagnostic uncertainty, or when one of the aggressive subtypes is suspected, complete excision, including the subcutaneous fat, is the ideal procedure. Obtaining a 3-mm margin has been shown to completely remove typical dermatofibromas.[120] One of the aggressive histologic subtypes, aneurysmal dermatofibroma, has been successfully treated via Mohs micrographic surgery.[121]

An inverted pyramidal biopsy technique may allow for an aesthetically pleasing result, while still providing adequate tissue for histologic findings.[122]

Superficially shaving the lesion or cryosurgery can be attempted for cosmesis or to decrease the symptoms; however, recurrences are more likely.

Carbon dioxide and pulsed-dye laser treatments have been used in the treatment of dermatofibromas.[123, 124]

Long-Term Monitoring

If the dermatofibroma is not removed and significant change occurs in the color, size, border, or symptoms, the patient should seek follow-up evaluation.

If complete removal has been previously attempted, patients with lesions that recur should seek follow-up evaluation. An aggressive subtype or another diagnosis should be ruled out.

If multiple eruptive lesions develop, screening for a family history of such and for underlying associated diseases and medications is warranted (See History).

What is a dermatofibroma?What is the pathophysiology of dermatofibroma?What causes dermatofibroma?How common are dermatofibromas?What is the racial distribution of dermatofibroma?Are dermatofibromas more common in males or females?What are the age-related demographics of dermatofibroma?What is the prognosis of dermatofibroma?What patient education resources are available on dermatofibroma?What is the clinical history of dermatofibroma?What are the physical exam findings in dermatofibroma?Which conditions should be considered in the diagnosis of dermatofibroma?What are the differential diagnoses for Dermatofibroma?Which imaging studies are indicated in the workup of dermatofibroma?Which clinical procedures are indicated in the workup of dermatofibroma?What are the histologic characteristics of a dermatofibroma?What are the histologic findings in dermatofibroma?How are dermatofibromas classified?What are the histologic characteristics of dermatofibromas?How are dermatofibromas treated?When is surgical care indicated in the treatment of a dermatofibroma?When is follow-up evaluation indicated in dermatofibroma?


Joseph C Pierson, MD, Dermatology Residency Program Director, University of Vermont College of Medicine

Disclosure: Nothing to disclose.


Christine C Tam, MD, Managing Member, Certified Dermatologists

Disclosure: Nothing to disclose.

Specialty Editors

David F Butler, MD, Former Section Chief of Dermatology, Central Texas Veterans Healthcare System; Professor of Dermatology, Texas A&M University College of Medicine; Founding Chair, Department of Dermatology, Scott and White Clinic

Disclosure: Nothing to disclose.

Edward F Chan, MD, Clinical Assistant Professor, Department of Dermatology, University of Pennsylvania School of Medicine

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD, Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

Disclosure: Nothing to disclose.


The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author, Diane Pierson, DO, to the development and writing of this article.


  1. Naversen DN, Trask DM, Watson FH, Burket JM. Painful tumors of the skin: "LEND AN EGG". J Am Acad Dermatol. 1993 Feb. 28(2 Pt 2):298-300. [View Abstract]
  2. Chen TC, Kuo T, Chan HL. Dermatofibroma is a clonal proliferative disease. J Cutan Pathol. 2000 Jan. 27(1):36-9. [View Abstract]
  3. Plaszczyca A, Nilsson J, Magnusson L, Brosjö O, Larsson O, Vult von Steyern F, et al. Fusions involving protein kinase C and membrane-associated proteins in benign fibrous histiocytoma. Int J Biochem Cell Biol. 2014 Apr 8. [View Abstract]
  4. Kuroda K, Tajima S. Proliferation of HSP47-positive skin fibroblasts in dermatofibroma. J Cutan Pathol. 2008 Jan. 35(1):21-6. [View Abstract]
  5. Jin SY, Choi JS, Choi YL, Choi YL, Kim do H, Lee SH. Identification of leukocyte-specific protein 1-positive cells: a clue to the cell of origin and a marker for the diagnosis of dermatofibroma. Ann Dermatol. 2015 Apr. 27 (2):157-62. [View Abstract]
  6. Sellheyer K, Smoller BR. Dermatofibroma: upregulation of syndecan-1 expression in mesenchymal tissue. Am J Dermatopathol. 2003 Oct. 25(5):392-8. [View Abstract]
  7. Skroza N, Rotolo S, Ceccarelli S, et al. Modulation of the expression of the FGFR2-IIIb and FGFR2-IIIc molecules in dermatofibroma. J Dermatol Sci. 2008 Jul. 51(1):53-7. [View Abstract]
  8. Kubo M, Ihn H, Yamane K, Tamaki K. The expression levels and the differential expression of transforming growth factor-beta receptors in dermatofibroma and dermatofibrosarcoma protuberans. Br J Dermatol. 2006 May. 154(5):919-25. [View Abstract]
  9. Yamamoto T. Dermatofibroma: a possible model of local fibrosis with epithelial/mesenchymal cell interaction. J Eur Acad Dermatol Venereol. 2009 Apr. 23(4):371-5. [View Abstract]
  10. Walther C, Hofvander J, Nilsson J, Magnusson L, Domanski HA, Gisselsson D, et al. Gene fusion detection in formalin-fixed paraffin-embedded benign fibrous histiocytomas using fluorescence in situ hybridization and RNA sequencing. Lab Invest. 2015 Sep. 95 (9):1071-6. [View Abstract]
  11. Panagopoulos I, Gorunova L, Bjerkehagen B, Lobmaier I, Heim S. LAMTOR1-PRKCD and NUMA1-SFMBT1 fusion genes identified by RNA sequencing in aneurysmal benign fibrous histiocytoma with t(3;11)(p21;q13). Cancer Genet. 2015 Nov. 208 (11):545-51. [View Abstract]
  12. Doyle LA, Mariño-Enriquez A, Fletcher CD, Hornick JL. ALK rearrangement and overexpression in epithelioid fibrous histiocytoma. Mod Pathol. 2015 Jul. 28 (7):904-12. [View Abstract]
  13. Szablewski V, Laurent-Roussel S, Rethers L, Rommel A, Van Eeckhout P, Camboni A, et al. Atypical fibrous histiocytoma of the skin with CD30 and p80/ALK1 positivity and ALK gene rearrangement. J Cutan Pathol. 2014 Sep. 41 (9):715-9. [View Abstract]
  14. Evans J, Clarke T, Mattacks CA, Pond CM. Dermatofibromas and arthropod bites: is there any evidence to link the two?. Lancet. 1989 Jul 1. 2(8653):36-7. [View Abstract]
  15. Lobato-Berezo A, Churruca-Grijelmo M, Martínez-Pérez M, Imbernón-Moya A, Vargas-Laguna ME, Fernández-Cogolludo E, et al. Dermatofibroma Arising within a Black Tattoo. Case Rep Dermatol Med. 2014. 2014:745304. [View Abstract]
  16. Watanabe K, Fukuda H, Niiyama S, Oharasaki T, Mukai H. Multiple dermatofibromas subsequent to folliculitis. Eur J Dermatol. 2013 Nov-Dec. 23 (6):890-1. [View Abstract]
  17. Nomura E, Yamamoto T. Photoletter to the editor: Fibrous histiocytoma developing at the site of tuberculin skin test. J Dermatol Case Rep. 2012 Dec 31. 6 (4):130-1. [View Abstract]
  18. Samlaska C, Bennion S. Eruptive dermatofibromas in a kindred. Cutis. 2002 Mar. 69(3):187-8, 190. [View Abstract]
  19. Han TY, Chang HS, Lee JH, Lee WM, Son SJ. A clinical and histopathological study of 122 cases of dermatofibroma (benign fibrous histiocytoma). Ann Dermatol. 2011 May. 23(2):185-92. [View Abstract]
  20. Şenel E, Yuyucu Karabulut Y, Doğruer Şenel S. Clinical, histopathological, dermatoscopic and digital microscopic features of dermatofibroma: a retrospective analysis of 200 lesions. J Eur Acad Dermatol Venereol. 2015 Oct. 29 (10):1958-66. [View Abstract]
  21. Kaddu S, McMenamin ME, Fletcher CD. Atypical fibrous histiocytoma of the skin: clinicopathologic analysis of 59 cases with evidence of infrequent metastasis. Am J Surg Pathol. 2002 Jan. 26(1):35-46. [View Abstract]
  22. Gleason BC, Fletcher CD. Deep "benign" fibrous histiocytoma: clinicopathologic analysis of 69 cases of a rare tumor indicating occasional metastatic potential. Am J Surg Pathol. 2008 Mar. 32(3):354-62. [View Abstract]
  23. Szumera-Cieckiewicz A, Ptaszynski K. Benign fibrous histiocytoma of the skin metastasizing to the inguinal lymph node. Pol J Pathol. 2011 Sep. 62(3):183-6. [View Abstract]
  24. Kimyai-Asadi A, Goldberg LH, Greenberg C, et al. Cellular, atypical, and indeterminate dermatofibromas: benign or malignant?. Dermatol Surg. 2008 Sep. 34(9):1264-71; discussion 1271-2. [View Abstract]
  25. Doyle LA, Fletcher CD. Metastasizing "benign" cutaneous fibrous histiocytoma: a clinicopathologic analysis of 16 cases. Am J Surg Pathol. 2013 Apr. 37 (4):484-95. [View Abstract]
  26. Charli-Joseph Y, Saggini A, Doyle LA, Fletcher CD, Weier J, Mirza S, et al. DNA copy number changes in tumors within the spectrum of cellular, atypical, and metastasizing fibrous histiocytoma. J Am Acad Dermatol. 2014 Apr 19. [View Abstract]
  27. Mentzel T, Wiesner T, Cerroni L, Hantschke M, Kutzner H, Rütten A, et al. Malignant dermatofibroma: clinicopathological, immunohistochemical, and molecular analysis of seven cases. Mod Pathol. 2013 Feb. 26 (2):256-67. [View Abstract]
  28. Fernandez-Flores A, Manjon JA. Mitosis in dermatofibroma: a worrisome histopathologic sign that does not necessarily equal recurrence. J Cutan Pathol. 2008 Sep. 35(9):839-42. [View Abstract]
  29. Niemi KM. The benign fibrohistiocytic tumours of the skin. Acta Derm Venereol Suppl (Stockh). 1970. 50(63):Suppl 63:1-66. [View Abstract]
  30. Massone C, Parodi A, Virno G, Rebora A. Multiple eruptive dermatofibromas in patients with systemic lupus erythematosus treated with prednisone. Int J Dermatol. 2002 May. 41(5):279-81. [View Abstract]
  31. García-Millán C, Aldanondo I, Fernández-Lorente M, Carrillo R, Jaén P. [Multiple eruptive dermatofibromas in 2 patients infected with the human immunodeficiency virus]. Actas Dermosifiliogr. 2007 Dec. 98(10):702-6. [View Abstract]
  32. Marque M, Pallure V, Huet P, Bessis D, Guillot B. [Multiple familial "eruptive" dermatofibromas]. Ann Dermatol Venereol. 2013 Jun-Jul. 140 (6-7):452-4. [View Abstract]
  33. Huang PY, Chu CY, Hsiao CH. Multiple eruptive dermatofibromas in a patient with dermatomyositis taking prednisolone and methotrexate. J Am Acad Dermatol. 2007 Nov. 57(5 Suppl):S81-4. [View Abstract]
  34. Lopez N, Fernandez A, Bosch RJ, Herrera E. Multiple eruptive dermatofibromas in a patient with Graves-Basedow disease. J Eur Acad Dermatol Venereol. 2008 Mar. 22(3):402-3. [View Abstract]
  35. Kimura Y, Kaneko T, Akasaka E, Nakajima K, Aizu T, Nakano H, et al. Multiple eruptive dermatofibromas associated with Hashimoto's thyroiditis and myasthenia gravis. Eur J Dermatol. 2010 Jul-Aug. 20(4):538-9. [View Abstract]
  36. Monteagudo B, Suarez-Amor O, Cabanillas M, et al. [Down syndrome: another cause of immunosuppression associated with multiple eruptive dermatofibromas?]. Dermatol Online J. 2009 Sep 15. 15(9):15. [View Abstract]
  37. Alexandrescu DT, Wiernik PH. Multiple eruptive dermatofibromas occurring in a patient with chronic myelogenous leukemia. Arch Dermatol. 2005 Mar. 141(3):397-8. [View Abstract]
  38. Bhattacharjee P, Umar SA, Fatteh SM. Multiple eruptive dermatofibromas occurring in a patient with myelodysplastic syndrome. Acta Derm Venereol. 2005. 85(3):270-1. [View Abstract]
  39. Zaccaria E, Rebora A, Rongioletti F. Multiple eruptive dermatofibromas and immunosuppression: report of two cases and review of the literature. Int J Dermatol. 2008 Jul. 47(7):723-7. [View Abstract]
  40. Yazici AC, Baz K, Ikizoglu G, Koca A, Kokturk A, Apa DD. Familial eruptive dermatofibromas in atopic dermatitis. J Eur Acad Dermatol Venereol. 2006 Jan. 20(1):90-2. [View Abstract]
  41. Beyazit Y, Caner S, Kurt M, Kekilli M, Aydog G, Ibis M. Dermatofibroma in a patient with Crohn's disease: a novel clinical manifestation. J Crohns Colitis. 2010 Oct. 4(4):490-1. [View Abstract]
  42. Hiraiwa T, Hanami Y, Yamamoto T. Hidradenitis suppurativa and multiple dermatofibromas in a patient with ulcerative colitis. J Dermatol. 2013 Dec. 40 (12):1071-2. [View Abstract]
  43. Bachmeyer C, Cordier F, Blum L, Cazier A, Vérola O, Aractingi S. Multiple eruptive dermatofibromas after highly active antiretroviral therapy. Br J Dermatol. 2000 Dec. 143(6):1336-7. [View Abstract]
  44. Santos-Juanes J, Coto-Segura P, Mallo S, Galache C, Soto J. Multiple eruptive dermatofibromas in a patient receiving efalizumab. Dermatology. 2008. 216(4):363. [View Abstract]
  45. Caldarola G, Bisceglia M, Pellicano R. Multiple eruptive plaque-like dermatofibromas during anti-TNFa treatment. Int J Dermatol. 2013 May. 52(5):638-41. [View Abstract]
  46. Llamas-Velasco M, Fraga J, Solano-López GE, Steegmann JL, García Diez A, Requena L. Multiple eruptive dermatofibromas related to imatinib treatment. J Eur Acad Dermatol Venereol. 2014 Jul. 28 (7):979-81. [View Abstract]
  47. Finch J, Berke A, McCusker M, Chang MW. Congenital Multiple Clustered Dermatofibroma in a 12-Year-Old Girl. Pediatr Dermatol. 2011 Dec 30. [View Abstract]
  48. Gershtenson PC, Krunic AL, Chen HM. Multiple clustered dermatofibroma: case report and review of the literature. J Cutan Pathol. 2010 Sep. 37(9):e42-5. [View Abstract]
  49. Fitzpatrick TB, Gilchrest BA. Dimple sign to differentiate benign from malignant pigmented cutaneous lesions. N Engl J Med. 1977 Jun 30. 296(26):1518. [View Abstract]
  50. Lookingbill DP. A malignant dimple. N Engl J Med. 1977 Oct 13. 297(15):841-2. [View Abstract]
  51. Meffert JJ, Peake MF, Wilde JL. Dimpling' is not unique to dermatofibromas. Dermatology. 1997. 195(4):384-6. [View Abstract]
  52. Requena L, Farina MC, Fuente C, et al. Giant dermatofibroma. A little-known clinical variant of dermatofibroma. J Am Acad Dermatol. 1994 May. 30(5 Pt 1):714-8. [View Abstract]
  53. Ohnishi T, Sasaki M, Nakai K, Watanabe S. Atrophic dermatofibroma. J Eur Acad Dermatol Venereol. 2004 Sep. 18(5):580-3. [View Abstract]
  54. Kai H, Fujita H, Yamamoto M, Asahina A. Letter: Polypoid dermatofibroma with a slim pedicle: A case report. Dermatol Online J. 2012 Mar 15. 18(3):16. [View Abstract]
  55. Curco N, Jucgla A, Bordas X, Moreno A. Dermatofibroma with spreading satellitosis. J Am Acad Dermatol. 1992 Dec. 27(6 Pt 1):1017-9. [View Abstract]
  56. Kalsi H, Rahman A, Harbol T, Sidhu J. Giant Hemosiderotic Dermatofibroma: The Largest Giant Dermatofibroma Reported to Date. Am J Dermatopathol. 2015 Oct. 37 (10):778-82. [View Abstract]
  57. Bhabha FK, Magee J, Ng SY, Grills CE, Su J, Orchard D. Multiple clustered dermatofibroma presenting in a segmental distribution. Australas J Dermatol. 2016 Feb. 57 (1):e20-2. [View Abstract]
  58. Schofield C, Weedon D, Kumar S. Dermatofibroma and halo dermatitis. Australas J Dermatol. 2012 May. 53(2):145-7. [View Abstract]
  59. Wortsman X, Wortsman J. Clinical usefulness of variable-frequency ultrasound in localized lesions of the skin. J Am Acad Dermatol. 2010 Feb. 62(2):247-56. [View Abstract]
  60. Picard A, Long-Mira E, Chuah SY, Passeron T, Lacour JP, Bahadoran P. Interest of high-definition optical coherent tomography (HD-OCT) for non-invasive imaging of dermatofibroma: a pilot study. J Eur Acad Dermatol Venereol. 2016 Mar. 30 (3):485-7. [View Abstract]
  61. Demir MK, Ozdemir H, Genchallaç H, Altaner S, Kartal O. Dermatofibroma mimicking malignancy on integrated F-18 fluorodeoxyglucose PET-CT. Diagn Interv Radiol. 2009 Mar. 15(1):61-3. [View Abstract]
  62. Zaballos P, Puig S, Llambrich A, Malvehy J. Dermoscopy of dermatofibromas: a prospective morphological study of 412 cases. Arch Dermatol. 2008 Jan. 144(1):75-83. [View Abstract]
  63. Cavicchini S, Tourlaki A, Tanzi C, Alessi E. Dermoscopy of solitary yellow lesions in adults. Arch Dermatol. 2008 Oct. 144(10):1412. [View Abstract]
  64. Roldán-Marín R, Barreiro-Capurro A, García-Herrera A, Puig S, Alarcón-Salazar I, Carrera C, et al. Green colour as a novel dermoscopic finding in the diagnosis of haemosiderotic dermatofibroma. Australas J Dermatol. 2013 Jul 19. [View Abstract]
  65. Ferrari A, Argenziano G, Buccini P, Cota C, Sperduti I, De Simone P, et al. Typical and atypical dermoscopic presentations of dermatofibroma. J Eur Acad Dermatol Venereol. 2013 Nov. 27(11):1375-80. [View Abstract]
  66. Pereira Guedes RV, Noronha de Menezes NM, Leite IB, Baptista MA. Benign fibrous histiocytoma: Particular aspects on confocal laser scanning microscopy. Eur J Dermatol. 2012 Mar-Apr. 22(2):288-9. [View Abstract]
  67. Kideryova L, Lacina L, Dvorankova B, et al. Phenotypic characterization of human keratinocytes in coculture reveals differential effects of fibroblasts from benign fibrous histiocytoma (dermatofibroma) as compared to cells from its malignant form and to normal fibroblasts. J Dermatol Sci. 2009 Jul. 55(1):18-26. [View Abstract]
  68. Nair V, Weinreb I, MacNeil N, Szollosi Z, Chetty R, Ghazarian D. A unique biphasic variant of cutaneous fibrous histiocytoma with a storiform pattern and intralesional pigmented melanocytes: "storiform melano-fibrous histiocytoma". Eur J Dermatol. 2008 May-Jun. 18(3):332-6. [View Abstract]
  69. Wick MR, Ritter JH, Lind AC, Swanson PE. The pathological distinction between "deep penetrating" dermatofibroma and dermatofibrosarcoma protuberans. Semin Cutan Med Surg. 1999 Mar. 18(1):91-8. [View Abstract]
  70. Goldblum JR, Tuthill RJ. CD34 and factor-XIIIa immunoreactivity in dermatofibrosarcoma protuberans and dermatofibroma. Am J Dermatopathol. 1997 Apr. 19(2):147-53. [View Abstract]
  71. Volpicelli ER, Fletcher CD. Desmin and CD34 positivity in cellular fibrous histiocytoma: an immunohistochemical analysis of 100 cases. J Cutan Pathol. 2012 Aug. 39 (8):747-52. [View Abstract]
  72. John AM, Holahan HH, Singh P, Handler MZ, Lambert WC. When Immunohistochemistry Deceives Us: The Pitfalls of CD34 and Factor XIIIa Stains in Dermatofibroma and Dermatofibrosarcoma Protuberans. Skinmed. 2017. 15 (1):53-55. [View Abstract]
  73. Borucki R, Perry DM, Lopez-Garcia DR, Kazlouskaya V, Elston DM. Fluorescence microscopy for the evaluation of elastic tissue patterns within fibrous proliferations of the skin on hematoxylin-eosin-stained slides. J Am Acad Dermatol. 2018 Jan 5. [View Abstract]
  74. Kim HJ, Lee JY, Kim SH, et al. Stromelysin-3 expression in the differential diagnosis of dermatofibroma and dermatofibrosarcoma protuberans: comparison with factor XIIIa and CD34. Br J Dermatol. 2007 Aug. 157(2):319-24. [View Abstract]
  75. Maekawa T, Jinnin M, Ihn H. The expression levels of thrombospondin-1 in dermatofibroma and dermatofibrosarcoma protuberans. Eur J Dermatol. 2011 Jul-Aug. 21(4):534-8. [View Abstract]
  76. Li J, Yu Y, Yang Y, Wang L, Cao J, Liang X, et al. IGFBP7, a novel immunohistochemical marker in differentiating dermatofibroma from dermatofibrosarcoma protuberans. J Eur Acad Dermatol Venereol. 2012 Mar. 26(3):382-5. [View Abstract]
  77. Mori T, Misago N, Yamamoto O, Toda S, Narisawa Y. Expression of nestin in dermatofibrosarcoma protuberans in comparison to dermatofibroma. J Dermatol. 2008 Jul. 35(7):419-25. [View Abstract]
  78. Wang L, Xiang YN, Zhang YH, Tu YT, Chen HX. Collagen triple helix repeat containing-1 in the differential diagnosis of dermatofibrosarcoma protuberans and dermatofibroma. Br J Dermatol. 2011 Jan. 164(1):135-40. [View Abstract]
  79. Bandarchi B, Ma L, Marginean C, Hafezi S, Zubovits J, Rasty G. D2-40, a novel immunohistochemical marker in differentiating dermatofibroma from dermatofibrosarcoma protuberans. Mod Pathol. 2010 Mar. 23(3):434-8. [View Abstract]
  80. Yan X, Takahara M, Xie L, Tu Y, Furue M. Cathepsin K expression: a useful marker for the differential diagnosis of dermatofibroma and dermatofibrosarcoma protuberans. Histopathology. 2010 Sep. 57(3):486-8. [View Abstract]
  81. Toyozawa S, Yamamoto Y, Ishida Y, Kondo T, Nakamura Y, Furukawa F. Immunohistochemical analysis of CXCR4 expression in fibrohistiocytic tumors. Acta Histochem Cytochem. 2010 May 1. 43(2):45-50. [View Abstract]
  82. Horenstein MG, Prieto VG, Nuckols JD, Burchette JL, Shea CR. Indeterminate fibrohistiocytic lesions of the skin: is there a spectrum between dermatofibroma and dermatofibrosarcoma protuberans?. Am J Surg Pathol. 2000 Jul. 24(7):996-1003. [View Abstract]
  83. Wang WL, Patel KU, Coleman NM, et al. COL1A1:PDGFB chimeric transcripts are not present in indeterminate fibrohistiocytic lesions of the skin. Am J Dermatopathol. 2010 Apr. 32(2):149-53. [View Abstract]
  84. Ishigami T, Hida Y, Matsudate Y, Murao K, Kubo Y. The involvement of fibroblast growth factor receptor signaling pathways in dermatofibroma and dermatofibrosarcoma protuberans. J Med Invest. 2013. 60(1-2):106-13. [View Abstract]
  85. Kazlouskaya V, Malhotra S, Kabigting FD, Lal K, Elston DM. CD99 expression in dermatofibrosarcoma protuberans and dermatofibroma. Am J Dermatopathol. 2014 May. 36(5):392-6. [View Abstract]
  86. Mentzel T. Cutaneous mesenchymal tumours: an update. Pathology. 2014 Feb. 46(2):149-59. [View Abstract]
  87. West KL, Cardona DM, Su Z, Puri PK. Immunohistochemical markers in fibrohistiocytic lesions: factor XIIIa, CD34, S-100 and p75. Am J Dermatopathol. 2014 May. 36(5):414-9. [View Abstract]
  88. Mikoshiba Y, Ogawa E, Uchiyama R, Uchiyama A, Uhara H, Okuyama R. 5-Hydroxymethylcytosine is a useful marker to differentiate between dermatofibrosarcoma protuberans and dermatofibroma. J Eur Acad Dermatol Venereol. 2016 Jan. 30 (1):130-1. [View Abstract]
  89. Karanian M, Pérot G, Coindre JM, Chibon F, Pedeutour F, Neuville A. Fluorescence in situ hybridization analysis is a helpful test for the diagnosis of dermatofibrosarcoma protuberans. Mod Pathol. 2015 Feb. 28 (2):230-7. [View Abstract]
  90. Kaur H, Kaur J, Gill KS, Mannan R, Arora S. Subcutaneous dermatofibroma: a rare case report with review of literature. J Clin Diagn Res. 2014 Apr. 8 (4):FD01-2. [View Abstract]
  91. Zelger BG, Zelger B. [Dermatofibroma. A clinico-pathologic classification scheme]. Pathologe. 1998 Nov. 19(6):412-9. [View Abstract]
  92. Deguchi M, Aiba S. Cholesterotic Fibrous Histiocytoma in a Patient with Metabolic Syndrome. Case Rep Dermatol. 2017 May-Aug. 9 (2):136-140. [View Abstract]
  93. Zelger BG, Sidoroff A, Zelger B. Combined dermatofibroma: co-existence of two or more variant patterns in a single lesion. Histopathology. 2000 Jun. 36(6):529-39. [View Abstract]
  94. Gonzalez-Vela MC, Val-Bernal JF, Martino M, Gonzalez-Lopez MA, Garcia-Alberdi E, Hermana S. Sclerotic fibroma-like dermatofibroma: an uncommon distinctive variant of dermatofibroma. Histol Histopathol. 2005 Jul. 20(3):801-6. [View Abstract]
  95. Alves JV, Matos DM, Barreiros HF, Bártolo EA. Variants of dermatofibroma - a histopathological study. An Bras Dermatol. 2014 Jun. 89(3):472-7. [View Abstract]
  96. McCalmont TH. Everything you wanted to know about dermatofibroma but were afraid to ask. J Cutan Pathol. 2014 Jan. 41(1):5-8. [View Abstract]
  97. de Feraudy S, Mar N, McCalmont TH. Evaluation of CD10 and procollagen 1 expression in atypical fibroxanthoma and dermatofibroma. Am J Surg Pathol. 2008 Aug. 32(8):1111-22. [View Abstract]
  98. Sanchez Yus E, Soria L, de Eusebio E, Requena L. Lichenoid, erosive and ulcerated dermatofibromas. Three additional clinico-pathologic variants. J Cutan Pathol. 2000 Mar. 27(3):112-7. [View Abstract]
  99. Aiba S, Terui T, Tagami H. Dermatofibroma with diffuse eosinophilic infiltrate. Am J Dermatopathol. 2000 Jun. 22(3):281-4. [View Abstract]
  100. Aydin E, Vardareli OS, Bilezikci B, Ozgirgin ON. [Dermatofibroma accompanied by perforating dermatosis in the auricle: a case report]. Kulak Burun Bogaz Ihtis Derg. 2005. 15(3-4):83-6. [View Abstract]
  101. Kim EJ, Park HS, Yoon HS, Cho S. A case of perforating dermatofibroma with floret-like giant cells. Clin Exp Dermatol. 2015 Apr. 40 (3):305-8. [View Abstract]
  102. Fuciarelli K, Cohen PR. Sebaceous hyperplasia: a clue to the diagnosis of dermatofibroma. J Am Acad Dermatol. 2001 Jan. 44(1):94-5. [View Abstract]
  103. Spaun E, Zelger B. Dermatofibroma with intracytoplasmic eosinophilic globules: an unusual phenomenon. J Cutan Pathol. 2009 Jul. 36(7):796-8. [View Abstract]
  104. Garrido-Ruiz MC, Carrillo R, Enguita AB, Peralto JL. Signet-ring cell dermatofibroma. Am J Dermatopathol. 2009 Feb. 31(1):84-7. [View Abstract]
  105. Quigley BC, Ricciuti J, Morgan MB. Amyloid Light Chain Deposition Associated with Dermatofibroma: Serendipity or Association?. Am J Dermatopathol. 2010 Jan 23. [View Abstract]
  106. Yamamoto T. Incidental acantholysis of the overlying epidermis of dermatofibroma. J Eur Acad Dermatol Venereol. 2009 Jun. 23(6):735-6. [View Abstract]
  107. Gonzalez S. Regarding the case report of Dr Phillip W. Allen on apocrine gland cyst with hemosiderotic dermatofibroma. Adv Anat Pathol. 2008 Nov. 15(6):376; author reply 376. [View Abstract]
  108. Santos-Briz A, Llamas-Velasco M, Arango L, Yuste M, Paredes BE, Kutzner H. Cutaneous adenodermatofibroma: report of 2 cases. Am J Dermatopathol. 2013 Aug. 35(6):e103-5. [View Abstract]
  109. Kanitakis J. Keloidal dermatofibroma: report of a rare dermatofibroma variant in a young white woman. Am J Dermatopathol. 2013 May. 35(3):400-1. [View Abstract]
  110. Schnebelen AM, Brown JA, Cheung WL, Hiatt KM, Smoller BR. Collapsing angiokeloidal dermatofibroma. Am J Dermatopathol. 2012 Oct. 34(7):e103-5. [View Abstract]
  111. Famenini S, Cassarino DS. Dermatofibroma-associated dystrophic calcification. J Cutan Pathol. 2014 Jan. 41(1):68-70. [View Abstract]
  112. Baderca F, Mates I, Solovan C. Unusual variant of blue nevus associated with dermatofibromas. Rom J Morphol Embryol. 2013. 54(2):413-7. [View Abstract]
  113. Maughan C, Kolker S, Markus B, Young J. Leukemia cutis coexisting with dermatofibroma as the initial presentation of B-cell chronic lymphocytic leukemia/small lymphocytic lymphoma. Am J Dermatopathol. 2014 Jan. 36(1):e14-5. [View Abstract]
  114. Morcos SM, Girardi M, Subtil A, Wilson LD, Cowper SE. Mycosis fungoides exhibiting features of a dermatofibroma: a case report and review of the literature. J Cutan Pathol. 2012 Jan. 39(1):40-6. [View Abstract]
  115. Zeidi M, North JP. Sebaceous induction in dermatofibroma: a common feature of dermatofibromas on the shoulder. J Cutan Pathol. 2015 Jun. 42 (6):400-5. [View Abstract]
  116. King R, Googe PB, Page RN, Mihm MC Jr. Melanocytic lesions associated with dermatofibromas: a spectrum of lesions ranging from junctional nevus to malignant melanoma in situ. Mod Pathol. 2005 Aug. 18(8):1043-7. [View Abstract]
  117. Shin J, Vincent JG, Cuda JD, Xu H, Kang S, Kim J, et al. Sox10 is expressed in primary melanocytic neoplasms of various histologies but not in fibrohistiocytic proliferations and histiocytoses. J Am Acad Dermatol. 2012 Oct. 67(4):717-26. [View Abstract]
  118. Kovach BT, Boyd AS. Melanoma associated with a dermatofibroma. J Cutan Pathol. 2007 May. 34(5):420-2. [View Abstract]
  119. Orrock JM, Abbott JJ, Gibson LE, Folpe AL. INI1 and GLUT-1 expression in epithelioid sarcoma and its cutaneous neoplastic and nonneoplastic mimics. Am J Dermatopathol. 2009 Apr. 31(2):152-6. [View Abstract]
  120. Kim HJ, Kim IH. A 3-mm margin completely removes dermatofibromas: a study of 151 cases. Dermatol Surg. 2015 Feb. 41 (2):283-6. [View Abstract]
  121. Halim K, Karia PS, Schmults CD. Aneurysmal dermatofibroma successfully treated with Mohs micrographic surgery. Dermatol Surg. 2015 Jan. 41 (1):168-70. [View Abstract]
  122. Weber PJ, Moody BR, Foster JA. Inverted pyramidal biopsy. Dermatol Surg. 2001 Jul. 27(7):681-4. [View Abstract]
  123. Krupa Shankar DS, Kushalappa AA, Suma KS, Pai SA. Multiple dermatofibromas on face treated with carbon dioxide laser. Indian J Dermatol Venereol Leprol. 2007 May-Jun. 73(3):194-5. [View Abstract]
  124. Alonso-Castro L, Boixeda P, Segura-Palacios JM, de Daniel-Rodríguez C, Jiménez-Gómez N, Ballester-Martínez A. Dermatofibromas treated with pulsed dye laser: Clinical and dermoscopic outcomes. J Cosmet Laser Ther. 2012 Apr. 14(2):98-101. [View Abstract]

Erythematous, slightly hyperpigmented nodule on the leg. Courtesy of David Barnette, MD.

Acanthotic epithelium with basilar hyperpigmentation (dirty feet) over a dermal spindle cell proliferation (X10). Courtesy of David Barnette, MD.

Collagen trapping by the dermal fibrohistiocytic infiltrate (X40). Courtesy of David Barnette, MD.

Erythematous, slightly hyperpigmented nodule on the leg. Courtesy of David Barnette, MD.

Acanthotic epithelium with basilar hyperpigmentation (dirty feet) over a dermal spindle cell proliferation (X10). Courtesy of David Barnette, MD.

Collagen trapping by the dermal fibrohistiocytic infiltrate (X40). Courtesy of David Barnette, MD.