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 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.

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]

The cell surface proteoglycan, syndecan-1,[5] and fibroblast growth factor receptor 2, involved in epithelial-mesenchymal cross-talk,[6] 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.[7] 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.[8]



United States

Dermatofibromas are relatively common.


Incidence of dermatofibroma is probably similar to that in the United States.


Simple dermatofibromas are regarded as benign lesions; however, discomfort from pain or itching may be significant.

Cellular, aneurysmal, and atypical variants, which are notoriously more locally recurrent, can rarely metastasize.[9] Such variants, and indeterminant dermatofibromas, might be regarded as potentially malignant lesions.[10] In these exceptional cases, indolent nodal and pulmonary metastases were typically seen.[11]

Fatal metastases of large (>5 cm), deep, fibrous histiocytomas (a subset of dermatofibroma that arises in the subcutaneous or deep soft tissue, the classification of which may undergo further evolution) has been reported. Like the more aggressive cellular, aneurysmal, and atypical variants, local recurrence rates can approach 20%.[12]


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 1:4.


Dermatofibroma can occur in patients of any age. In one series, 80% of biopsy specimens were from patients aged 20-49 years.[13]


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 or more) tumors found. A multiple eruptive variant occurs in only 0.3% of patients, many of whom have an alteration in their immune status, classically, HIV infection and systemic lupus erythematosus.[14, 15] However, dermatomyositis,[16] Graves disease,[17] Hashimoto thyroiditis,[18] myasthenia gravis,[18] Down syndrome,[19] leukemia,[20] myelodysplastic syndrome,[21] cutaneous T-cell lymphoma,[22] multiple myeloma,[22] atopic dermatitis,[23] and Crohn disease[24] have all been reported in association with the phenomenon. In addition, antiretroviral agents,[25] the biologic agent efalizumab,[26] and antitumor necrosis factor alpha agents[27] have been linked to their appearance.

Both congenital[28] and acquired[29] cases of multiple clustered dermatofibromas have been reported.


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 (0.3% 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.[30] However, presence of the dimple sign does not always assure the lesion is dermatofibroma,[31] and dermatoscopy may be useful in supporting the clinical impression.[32]

The extremities are the most common sites of involvement, particularly the lower legs. Although any cutaneous site can be seen, palm, sole, digital, oral, and genital involvement is relatively rare. Giant (>5 cm in diameter),[33] atrophic,[34] polypoid,[35] and dermatofibroma with spreading satellitosis[36] variants have been reported.

Multiple clustered dermatofibromas[29] are rare but can mimic dermatofibrosarcoma protuberans.

A halo of dermatitis (Meyerson phenomenon) surrounding a dermatofibroma occurred in one patient.[37]


Historically attributed to be a reactive process to some traumatic insult to the skin (eg, arthropod bite),[38] 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.[39]

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.[40]

Dermatofibroma can mimic a malignant lesion on fluorodeoxyglucose positron-emission tomography (FDG-PET) scans.[41]


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.[42] Dermoscopy of a xanthomatous dermatofibroma shows a homogeneous pattern with shades of yellow and a peripheral pigment network.[43] A green color may indicate the hemosiderotic variant.[44] If a suggestive melanocytic or atypical pattern is noted with dermoscopy, a diagnostic biopsy is warranted.[45]

Confocal laser scanning microscopy findings have been described.[46]

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.[47] 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.[48]

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).[49]

One clinicopathologic classification scheme[65] describes the following 4 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[67] 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.[68]

Immunoperoxidase staining is consistently positive for both CD10 and actin in dermatofibromas.[69] 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.[70]

Lichenoid dermatofibroma,[71] ulcerated dermatofibroma,[71] erosive dermatofibroma,[71] dermatofibroma with diffuse eosinophilic infiltrate,[72] and dermatofibroma accompanied by perforating dermatosis[73] have been described. Dermatofibromas with overlying sebaceous hyperplasia,[74] with intracytoplasmic eosinophilic globules,[75] signet-ring cells,[76] amyloid light chain deposition,[77] and incidental acantholysis[78] have also been reported. A case of an apocrine gland cyst with a hemosiderotic dermatofibroma was termed an apocrine hemosiderotic dermatofibroma.[79] Cutaneous adenodermatofibroma (entrapped apocrine structures without hemosiderotic changes), keloidal, collapsing angiokeloidal, and dermatofibromas with dystrophic calcification variants have been reported.[80, 81, 82, 83] Blue nevus associated with dermatofibroma has been reported, as has coexisting leukemia cutis.[84, 85]

One case of mycosis fungoides showed histologic features of dermatofibroma.[86]

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.[69]

A case series[87] 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.[88] A case report[89] 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.[90]

Medical Care

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.

An inverted pyramidal biopsy technique may allow for an aesthetically pleasing result, while still providing adequate tissue for histologic findings.[91]

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

Carbon dioxide laser treatment of multiple facial dermatofibroma has been reported.[92] More recently, pulsed-dye laser has been used with success.[93]

Further Outpatient Care

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 autoimmune disease or altered immunity is warranted.


Simple dermatofibromas are considered a benign lesion, and the prognosis for patients with this condition is excellent.

Aggressive subtypes (cellular, aneurysmal, atypical, and deep/subcutaneous) locally recur in up to 20% of cases and can rarely metastasize. Array-based comparative genomic hybridization may prove useful in identifying these higher risk variants.[94]

In a study of common dermatofibromas with an increased mitotic rate but no other worrisome features, none recurred or metastasized.[95]

Spontaneous regression has been reported,[96] and this may yield postinflammatory hypopigmentation, although this appears to be quite rare.


Joseph C Pierson, MD, Dermatology Residency Program Director, University of Vermont College of Medicine, Fletcher Allen Health Care

Disclosure: Nothing to disclose.


Christine C Tam, MD, Resident Physician, Department of Dermatology, University of Cincinnati College of Medicine

Disclosure: Nothing to disclose.

Specialty Editors

Terry L Barrett, MD, Clinical Professor of Dermatology and Pathology, University of Texas Southwestern School of Medicine; Director, ProPath Dermatopathology, Dallas, Texas

Disclosure: Nothing to disclose.

David F Butler, MD, 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.

Catherine M Quirk, MD, Clinical Assistant Professor, Department of Dermatology, University of Pennsylvania

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD, Director, Ackerman Academy of Dermatopathology, New York

Disclosure: Nothing to disclose.

Additional Contributors

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. Feb 1993;28(2 Pt 2):298-300. [View Abstract]
  2. Chen TC, Kuo T, Chan HL. Dermatofibroma is a clonal proliferative disease. J Cutan Pathol. Jan 2000;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. Apr 8 2014;[View Abstract]
  4. Kuroda K, Tajima S. Proliferation of HSP47-positive skin fibroblasts in dermatofibroma. J Cutan Pathol. Jan 2008;35(1):21-6. [View Abstract]
  5. Sellheyer K, Smoller BR. Dermatofibroma: upregulation of syndecan-1 expression in mesenchymal tissue. Am J Dermatopathol. Oct 2003;25(5):392-8. [View Abstract]
  6. 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. Jul 2008;51(1):53-7. [View Abstract]
  7. 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. May 2006;154(5):919-25. [View Abstract]
  8. Yamamoto T. Dermatofibroma: a possible model of local fibrosis with epithelial/mesenchymal cell interaction. J Eur Acad Dermatol Venereol. Apr 2009;23(4):371-5. [View Abstract]
  9. 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. Jan 2002;26(1):35-46. [View Abstract]
  10. Kimyai-Asadi A, Goldberg LH, Greenberg C, et al. Cellular, atypical, and indeterminate dermatofibromas: benign or malignant?. Dermatol Surg. Sep 2008;34(9):1264-71; discussion 1271-2. [View Abstract]
  11. Szumera-Cieckiewicz A, Ptaszynski K. Benign fibrous histiocytoma of the skin metastasizing to the inguinal lymph node. Pol J Pathol. Sep 2011;62(3):183-6. [View Abstract]
  12. 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. Mar 2008;32(3):354-62. [View Abstract]
  13. 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. May 2011;23(2):185-92. [View Abstract]
  14. Massone C, Parodi A, Virno G, Rebora A. Multiple eruptive dermatofibromas in patients with systemic lupus erythematosus treated with prednisone. Int J Dermatol. May 2002;41(5):279-81. [View Abstract]
  15. 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. Dec 2007;98(10):702-6. [View Abstract]
  16. Huang PY, Chu CY, Hsiao CH. Multiple eruptive dermatofibromas in a patient with dermatomyositis taking prednisolone and methotrexate. J Am Acad Dermatol. Nov 2007;57(5 Suppl):S81-4. [View Abstract]
  17. Lopez N, Fernandez A, Bosch RJ, Herrera E. Multiple eruptive dermatofibromas in a patient with Graves-Basedow disease. J Eur Acad Dermatol Venereol. Mar 2008;22(3):402-3. [View Abstract]
  18. 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. Jul-Aug 2010;20(4):538-9. [View Abstract]
  19. Monteagudo B, Suarez-Amor O, Cabanillas M, et al. [Down syndrome: another cause of immunosuppression associated with multiple eruptive dermatofibromas?]. Dermatol Online J. Sep 15 2009;15(9):15. [View Abstract]
  20. Alexandrescu DT, Wiernik PH. Multiple eruptive dermatofibromas occurring in a patient with chronic myelogenous leukemia. Arch Dermatol. Mar 2005;141(3):397-8. [View Abstract]
  21. 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]
  22. Zaccaria E, Rebora A, Rongioletti F. Multiple eruptive dermatofibromas and immunosuppression: report of two cases and review of the literature. Int J Dermatol. Jul 2008;47(7):723-7. [View Abstract]
  23. Yazici AC, Baz K, Ikizoglu G, Koca A, Kokturk A, Apa DD. Familial eruptive dermatofibromas in atopic dermatitis. J Eur Acad Dermatol Venereol. Jan 2006;20(1):90-2. [View Abstract]
  24. 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. Oct 2010;4(4):490-1. [View Abstract]
  25. Bachmeyer C, Cordier F, Blum L, Cazier A, Vérola O, Aractingi S. Multiple eruptive dermatofibromas after highly active antiretroviral therapy. Br J Dermatol. Dec 2000;143(6):1336-7. [View Abstract]
  26. 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]
  27. Caldarola G, Bisceglia M, Pellicano R. Multiple eruptive plaque-like dermatofibromas during anti-TNFa treatment. Int J Dermatol. May 2013;52(5):638-41. [View Abstract]
  28. Finch J, Berke A, McCusker M, Chang MW. Congenital Multiple Clustered Dermatofibroma in a 12-Year-Old Girl. Pediatr Dermatol. Dec 30 2011;[View Abstract]
  29. Gershtenson PC, Krunic AL, Chen HM. Multiple clustered dermatofibroma: case report and review of the literature. J Cutan Pathol. Sep 2010;37(9):e42-5. [View Abstract]
  30. Fitzpatrick TB, Gilchrest BA. Dimple sign to differentiate benign from malignant pigmented cutaneous lesions. N Engl J Med. Jun 30 1977;296(26):1518. [View Abstract]
  31. Lookingbill DP. A malignant dimple. N Engl J Med. Oct 13 1977;297(15):841-2. [View Abstract]
  32. Meffert JJ, Peake MF, Wilde JL. 'Dimpling' is not unique to dermatofibromas. Dermatology. 1997;195(4):384-6. [View Abstract]
  33. Requena L, Farina MC, Fuente C, et al. Giant dermatofibroma. A little-known clinical variant of dermatofibroma. J Am Acad Dermatol. May 1994;30(5 Pt 1):714-8. [View Abstract]
  34. Ohnishi T, Sasaki M, Nakai K, Watanabe S. Atrophic dermatofibroma. J Eur Acad Dermatol Venereol. Sep 2004;18(5):580-3. [View Abstract]
  35. Kai H, Fujita H, Yamamoto M, Asahina A. Letter: Polypoid dermatofibroma with a slim pedicle: A case report. Dermatol Online J. Mar 15 2012;18(3):16. [View Abstract]
  36. Curco N, Jucgla A, Bordas X, Moreno A. Dermatofibroma with spreading satellitosis. J Am Acad Dermatol. Dec 1992;27(6 Pt 1):1017-9. [View Abstract]
  37. Schofield C, Weedon D, Kumar S. Dermatofibroma and halo dermatitis. Australas J Dermatol. May 2012;53(2):145-7. [View Abstract]
  38. Evans J, Clarke T, Mattacks CA, Pond CM. Dermatofibromas and arthropod bites: is there any evidence to link the two?. Lancet. Jul 1 1989;2(8653):36-7. [View Abstract]
  39. Samlaska C, Bennion S. Eruptive dermatofibromas in a kindred. Cutis. Mar 2002;69(3):187-8, 190. [View Abstract]
  40. Wortsman X, Wortsman J. Clinical usefulness of variable-frequency ultrasound in localized lesions of the skin. J Am Acad Dermatol. Feb 2010;62(2):247-56. [View Abstract]
  41. Demir MK, Ozdemir H, Genchallaç H, Altaner S, Kartal O. Dermatofibroma mimicking malignancy on integrated F-18 fluorodeoxyglucose PET-CT. Diagn Interv Radiol. Mar 2009;15(1):61-3. [View Abstract]
  42. Zaballos P, Puig S, Llambrich A, Malvehy J. Dermoscopy of dermatofibromas: a prospective morphological study of 412 cases. Arch Dermatol. Jan 2008;144(1):75-83. [View Abstract]
  43. Cavicchini S, Tourlaki A, Tanzi C, Alessi E. Dermoscopy of solitary yellow lesions in adults. Arch Dermatol. Oct 2008;144(10):1412. [View Abstract]
  44. 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. Jul 19 2013;[View Abstract]
  45. 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. Nov 2013;27(11):1375-80. [View Abstract]
  46. Pereira Guedes RV, Noronha de Menezes NM, Leite IB, Baptista MA. Benign fibrous histiocytoma: Particular aspects on confocal laser scanning microscopy. Eur J Dermatol. Mar-Apr 2012;22(2):288-9. [View Abstract]
  47. 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. Jul 2009;55(1):18-26. [View Abstract]
  48. 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. May-Jun 2008;18(3):332-6. [View Abstract]
  49. Wick MR, Ritter JH, Lind AC, Swanson PE. The pathological distinction between "deep penetrating" dermatofibroma and dermatofibrosarcoma protuberans. Semin Cutan Med Surg. Mar 1999;18(1):91-8. [View Abstract]
  50. Goldblum JR, Tuthill RJ. CD34 and factor-XIIIa immunoreactivity in dermatofibrosarcoma protuberans and dermatofibroma. Am J Dermatopathol. Apr 1997;19(2):147-53. [View Abstract]
  51. 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. Aug 2007;157(2):319-24. [View Abstract]
  52. Maekawa T, Jinnin M, Ihn H. The expression levels of thrombospondin-1 in dermatofibroma and dermatofibrosarcoma protuberans. Eur J Dermatol. Jul-Aug 2011;21(4):534-8. [View Abstract]
  53. 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. Mar 2012;26(3):382-5. [View Abstract]
  54. Mori T, Misago N, Yamamoto O, Toda S, Narisawa Y. Expression of nestin in dermatofibrosarcoma protuberans in comparison to dermatofibroma. J Dermatol. Jul 2008;35(7):419-25. [View Abstract]
  55. 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. Jan 2011;164(1):135-40. [View Abstract]
  56. 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. Mar 2010;23(3):434-8. [View Abstract]
  57. 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. Sep 2010;57(3):486-8. [View Abstract]
  58. Toyozawa S, Yamamoto Y, Ishida Y, Kondo T, Nakamura Y, Furukawa F. Immunohistochemical analysis of CXCR4 expression in fibrohistiocytic tumors. Acta Histochem Cytochem. May 1 2010;43(2):45-50. [View Abstract]
  59. 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. Jul 2000;24(7):996-1003. [View Abstract]
  60. 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. Apr 2010;32(2):149-53. [View Abstract]
  61. 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]
  62. Kazlouskaya V, Malhotra S, Kabigting FD, Lal K, Elston DM. CD99 expression in dermatofibrosarcoma protuberans and dermatofibroma. Am J Dermatopathol. May 2014;36(5):392-6. [View Abstract]
  63. Mentzel T. Cutaneous mesenchymal tumours: an update. Pathology. Feb 2014;46(2):149-59. [View Abstract]
  64. West KL, Cardona DM, Su Z, Puri PK. Immunohistochemical markers in fibrohistiocytic lesions: factor XIIIa, CD34, S-100 and p75. Am J Dermatopathol. May 2014;36(5):414-9. [View Abstract]
  65. Zelger BG, Zelger B. [Dermatofibroma. A clinico-pathologic classification scheme]. Pathologe. Nov 1998;19(6):412-9. [View Abstract]
  66. Zelger BG, Sidoroff A, Zelger B. Combined dermatofibroma: co-existence of two or more variant patterns in a single lesion. Histopathology. Jun 2000;36(6):529-39. [View Abstract]
  67. 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. Jul 2005;20(3):801-6. [View Abstract]
  68. Alves JV, Matos DM, Barreiros HF, Bártolo EA. Variants of dermatofibroma - a histopathological study. An Bras Dermatol. Jun 2014;89(3):472-7. [View Abstract]
  69. McCalmont TH. Everything you wanted to know about dermatofibroma but were afraid to ask. J Cutan Pathol. Jan 2014;41(1):5-8. [View Abstract]
  70. de Feraudy S, Mar N, McCalmont TH. Evaluation of CD10 and procollagen 1 expression in atypical fibroxanthoma and dermatofibroma. Am J Surg Pathol. Aug 2008;32(8):1111-22. [View Abstract]
  71. Sanchez Yus E, Soria L, de Eusebio E, Requena L. Lichenoid, erosive and ulcerated dermatofibromas. Three additional clinico-pathologic variants. J Cutan Pathol. Mar 2000;27(3):112-7. [View Abstract]
  72. Aiba S, Terui T, Tagami H. Dermatofibroma with diffuse eosinophilic infiltrate. Am J Dermatopathol. Jun 2000;22(3):281-4. [View Abstract]
  73. 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]
  74. Fuciarelli K, Cohen PR. Sebaceous hyperplasia: a clue to the diagnosis of dermatofibroma. J Am Acad Dermatol. Jan 2001;44(1):94-5. [View Abstract]
  75. Spaun E, Zelger B. Dermatofibroma with intracytoplasmic eosinophilic globules: an unusual phenomenon. J Cutan Pathol. Jul 2009;36(7):796-8. [View Abstract]
  76. Garrido-Ruiz MC, Carrillo R, Enguita AB, Peralto JL. Signet-ring cell dermatofibroma. Am J Dermatopathol. Feb 2009;31(1):84-7. [View Abstract]
  77. Quigley BC, Ricciuti J, Morgan MB. Amyloid Light Chain Deposition Associated with Dermatofibroma: Serendipity or Association?. Am J Dermatopathol. Jan 23 2010;[View Abstract]
  78. Yamamoto T. Incidental acantholysis of the overlying epidermis of dermatofibroma. J Eur Acad Dermatol Venereol. Jun 2009;23(6):735-6. [View Abstract]
  79. Gonzalez S. Regarding the case report of Dr Phillip W. Allen on apocrine gland cyst with hemosiderotic dermatofibroma. Adv Anat Pathol. Nov 2008;15(6):376; author reply 376. [View Abstract]
  80. Santos-Briz A, Llamas-Velasco M, Arango L, Yuste M, Paredes BE, Kutzner H. Cutaneous adenodermatofibroma: report of 2 cases. Am J Dermatopathol. Aug 2013;35(6):e103-5. [View Abstract]
  81. Kanitakis J. Keloidal dermatofibroma: report of a rare dermatofibroma variant in a young white woman. Am J Dermatopathol. May 2013;35(3):400-1. [View Abstract]
  82. Schnebelen AM, Brown JA, Cheung WL, Hiatt KM, Smoller BR. Collapsing angiokeloidal dermatofibroma. Am J Dermatopathol. Oct 2012;34(7):e103-5. [View Abstract]
  83. Famenini S, Cassarino DS. Dermatofibroma-associated dystrophic calcification. J Cutan Pathol. Jan 2014;41(1):68-70. [View Abstract]
  84. 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]
  85. 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. Jan 2014;36(1):e14-5. [View Abstract]
  86. 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. Jan 2012;39(1):40-6. [View Abstract]
  87. 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. Aug 2005;18(8):1043-7. [View Abstract]
  88. 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. Oct 2012;67(4):717-26. [View Abstract]
  89. Kovach BT, Boyd AS. Melanoma associated with a dermatofibroma. J Cutan Pathol. May 2007;34(5):420-2. [View Abstract]
  90. 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. Apr 2009;31(2):152-6. [View Abstract]
  91. Weber PJ, Moody BR, Foster JA. Inverted pyramidal biopsy. Dermatol Surg. Jul 2001;27(7):681-4. [View Abstract]
  92. Krupa Shankar DS, Kushalappa AA, Suma KS, Pai SA. Multiple dermatofibromas on face treated with carbon dioxide laser. Indian J Dermatol Venereol Leprol. May-Jun 2007;73(3):194-5. [View Abstract]
  93. 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. Apr 2012;14(2):98-101. [View Abstract]
  94. 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. Apr 19 2014;[View Abstract]
  95. Fernandez-Flores A, Manjon JA. Mitosis in dermatofibroma: a worrisome histopathologic sign that does not necessarily equal recurrence. J Cutan Pathol. Sep 2008;35(9):839-42. [View Abstract]
  96. Niemi KM. The benign fibrohistiocytic tumours of the skin. Acta Derm Venereol Suppl (Stockh). 1970;50(63):Suppl 63:1-66. [View Abstract]
  97. Troxel DB. An insurer's perspective on error and loss in pathology. Arch Pathol Lab Med. Oct 2005;129(10):1234-6. [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.