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Ulcerated Nodule on the Scalp
Author(s)
Craig J. Garofola, DO
Mariana A. Phillips, MD
Aleksandra Brown, DO
Douglas J. Grider, MD

The Diagnosis: Proliferating Pilar Tumor  

Proliferating pilar tumor (PPT), or cyst, is a neoplasm of trichilemmal keratinization first described by Wilson-Jones1 in 1966. Proliferating pilar tumors lie on a spectrum with malignant PPT, which is a rare adnexal neoplasm first described by Saida et al2 in 1983. The incidence of PPT is unknown given the paucity of cases and the possible misdiagnosis as squamous cell carcinoma (SCC). Proliferating pilar tumors tend to present on the head and neck of older females as a multilobular and sometimes ulcerating nodule.3 Although PPT can occur de novo, the majority of cases are thought to develop progressively from a benign pilar cyst. Histopathologically, PPT is characterized by cords and nests of squamous cells that display trichilemmal keratinization (quiz images).  

Classification of PPT as benign or malignant is challenging, though criteria have been proposed.3-7 Lesions with minimal infiltration into the surrounding dermis and scant mitosis typically behave in a benign manner, while lesions showing nuclear atypia, atypical mitosis, and irregular infiltration into the surrounding dermis can have up to a 50% locoregional recurrence rate.3 In addition, distinguishing a PPT from an SCC or trichilemmal carcinoma also can be difficult; however, SCC is favored when there is a lack of trichilemmal keratinization or when squamous atypia is present in the adjacent epidermis.8 Trichilemmal carcinoma is a rare tumor that has been questioned as a distinct entity.9-12  

Pilomatricoma, also known as calcifying epithelioma of Malherbe, is a benign pilar tumor that presents as a slowly growing nodule on the head or neck area or arms.13,14 Most pilomatricomas develop by the second decade of life. Multiple lesions may be present in association with myotonic dystrophy or Gardner syndrome among other syndromes.15-17 Similar to PPT, pilomatricomas present as large dermal nodules; however, they tend to be circumscribed and have a trabecular network that consists of basophilic cells and eosinophilic keratinized shadow cells (Figure 1).18 Calcification may be seen and bone formation subsequently may occur.19  

Figure 1. Pilomatricoma. Dermal tumor with peripheral basaloid cells, ghost cells, focal keratin debris, and focal multinucleated foreign body giant cells (H&E, original magnification ×100).

Most sources now consider keratoacanthoma (KA) as a well-differentiated SCC.20 The typical presentation consists of a rapidly growing erythematous to flesh-colored nodule with a central keratinous plug that develops over a period of weeks. If untreated, KAs may resolve over a period of months and leave a depressed scar. Local destruction can result from KAs, and they have the potential to transform into a more aggressive SCC. Accordingly, most clinicians use tissue destructive methods, excision, or Mohs micrographic surgery for treatment based on location. Histologically, a well-circumscribed proliferation of glassy cytoplasm is noted. A depressed keratin-filled center is surrounded by a lip of epithelium extending over the lesion (Figure 2).20,21 Pseudoepitheliomatous hyperplasia accompanied by hypergranulosis is seen in the center of KAs rather than at the periphery, which is typical of non-KA SCCs. Typical KAs lack acantholysis, a feature suggesting a non-KA type of SCC. Neutrophilic microabscesses and eosinophils commonly are seen in KAs.20,21  

Figure 2. Keratoacanthoma. Crateriform squamous proliferation with keratin debris in the center of the cystic spaces and squamous cells toward the periphery with eosinophilic and glassy cytoplasm (H&E, original magnification ×40).

Inverted follicular keratosis is a benign tumor that gained traction as its own entity in the 1960s.22 These lesions typically develop from the follicular infundibulum, but some consider them a version of a wart or seborrheic keratosis.23 They generally are flesh-colored nodules on the upper cutaneous lip or face. Treatment usually consists of complete excision. There are many different growth patterns described, but they typically are endophytic tumors with eosinophilic squamous cells in the center and more basophilic cells at the periphery (Figure 3).24 Characteristically, there are squamous eddies throughout the tumor (Figure 3 [inset]). There also may be a scant lymphohistiocytic infiltrate within the dermis surrounding the lesion.  

Figure 3. Inverted follicular keratosis. Endophytic, slightly verrucous squamous proliferation with central cyst formation and keratin debris (H&E, original magnification ×20). Squamous eddies and dendritic melanocytes can be seen on higher magnification (H&E, original magnification ×100 [inset]). 

 

 

 

 

 

Trichilemmomas are flesh-colored adnexal neoplasms that may present as a solitary lesion or in clusters on the face. They have been reported to occur on all nonglabrous skin sites.25 Multiple lesions may occur in association with Cowden syndrome or with nevus sebaceous.26 A desmoplastic variant of trichilemmomas has been reported.27 Desmoplastic trichilemmomas appear as well-circumscribed tumors of outer root sheath differentiation with lobules extending down into the dermis.28 Vacuolated glycogen-filled keratinocytes are scattered throughout the lesion but are most prominent at the base. At the periphery of the lobules, peripheral palisading of basaloid cells is accompanied by a thickened eosinophilic basement membrane that is periodic acid-Schiff positive. Typical trichilemmomas also can display these features; however, the main differentiating feature of a desmoplastic trichilemmoma is the pink hyalinized stroma separating small islets of basophilic cells (Figure 4). Differentiation from an invasive malignant carcinoma sometimes can be challenging without a focus of typical trichilemmoma or if the biopsy specimen is too superficial.29 

Figure 4. Desmoplastic trichilemmoma. Proliferation of lobules of squamous cells with clear cytoplasm, peripheral palisading of more basaloid keratinocytes, and a thickened basement membrane (H&E, original magnification ×100).

Pilar cysts are common tumors that typically arise on the scalp and sometimes are proliferating. Proliferating pilar tumor should be kept on the differential when secondary changes such as ulceration occur in the primary lesion of the scalp. Microscopically, and sometimes clinically, PPT can be difficult to differentiate from other mimickers.  

References
  1. Wilson-Jones E. Proliferating epidermoid cysts. Arch Dermatol. 1966;94:11-19. 
  2. Saida T, Oohara K, Hori Y, et al. Development of a malignant proliferating trichilemmal cyst in a patient with multiple trichilemmal cysts. Dermatologica. 1983;166:203-208. 
  3. Ye J, Nappi O, Swanson PE, et al. Proliferating pilar tumours: a clinicopathological study of 76 cases with a proposal for definition of benign and malignant variants. Am J Clin Pathol. 2004;122:566-574. 
  4. Garg PK, Dangi A, Khurana N, et al. Malignant proliferating trichilemmal cyst: a case report with review of literature. Malaysian J Pathol. 2009;31:71-76. 
  5. Herrero J, Monteagudo C, Ruiz A, et al. Malignant proliferating trichilemmal tumors: a histopathological and immunohistochemical study of three cases with DNA ploidy and morphometric evaluation. Histopathology. 1998;33:542-546.  
  6. Haas N, Audring H, Sterry W. Carcinoma arising in a proliferating trichilemmal cyst expresses fetal and trichilemmal hair phenotype. Am J Dermatopathol. 2002;24:340-344.  
  7. Rutty GN, Richman PI, Laing JH. Malignant change in trichilemmal cysts: a study of cell proliferation and DNA content. Histopathology. 1992;21:465-468.  
  8. Brownstein MH, Arluk DJ. Proliferating trichilemmal cyst: a simulant of squamous cell carcinoma. Cancer. 1981;48:1207-1214.  
  9. Misago N, Ackerman AB. Tricholemmal carcinoma? Dermatopathol Pract Concept. 1999;5:205-206. 
  10. Misago N, Narisawa Y. Tricholemmal carcinoma in continuity with trichoblastoma within nevus sebaceous. Am J Dermatopathol. 2002;24:149-155. 
  11. Liang H, Wu H, Giorgadze TA, et al. Podoplanin is a highly sensitive and specific marker to distinguish primary skin adnexal carcinomas from adenocarcinomas metastatic to skin. Am J Surg Pathol. 2007;31:304-310. 
  12. Swanson PE, Marrogi AJ, Williams DJ, et al. Trichilemmal carcinoma: clinicopathologic study of 10 cases. J Cutan Pathol. 1992;19:100-109. 
  13. Mehregan AH. Hair follicle tumors of the skin. J Cutan Pathol. 1985;12:189-195.  
  14. Julian CG, Bowers PW. A clinical review of 209 pilomatricomas. J Am Acad Dermatol. 1998;39:191-195.  
  15. Marrogi AJ, Wick MR, Dehner LP. Pilomatrical neoplasms in children and young adults. Am J Dermatopathol. 1992;14:87-94.  
  16. Berberian BJ, Colonna TM, Battaglia M, et al. Multiple pilomatricomas in association with myotonic dystrophy and a family history of melanoma. J Am Acad Dermatol. 1997;37:268-269.  
  17. Cooper PH, Fechner RE. Pilomatricoma-like changes in the epidermal cysts of Gardner's syndrome. J Am Acad Dermatol. 1983;8:639-644.  
  18. Kaddu S, Soyer HP, Cerroni L, et al. Clinical and histopathologic spectrum of pilomatricomas in adults. Int J Dermatol. 1994;33:705-708.  
  19. Sano Y, Mihara M, Miyamoto T, et al. Simultaneous occurrence of calcification and amyloid deposit in pilomatricoma. Acta Derm Venereol. 1990;70:256-259.  
  20. Schwartz RA. Keratoacanthoma. J Am Acad Dermatol. 1994;30:1-19.  
  21. Kwiek B, Schwartz RA. Keratoacanthoma (KA): an update and review. J Am Acad Dermatol. 2016;74:1220-1233. 
  22. Mehregan AH. Inverted follicular keratosis. Arch Dermatol. 1964;89:117-123. 
  23. Spielvogel RL, Austin C, Ackerman AB. Inverted follicular keratosis is not a specific keratosis but a verruca vulgaris (or seborrheic keratosis) with squamous eddies. Am J Dermatopathol. 1983;5:427-445. 
  24. Mehregan AH. Inverted follicular keratosis is a distinct follicular tumor. Am J Dermatopathol. 1983;5:467-470. 
  25. Brownstein MH. Trichilemmoma. benign follicular tumor or viral wart? Am J Dermatopathol. 1980;2:229-231. 
  26. Brownstein MH. Multiple trichilemmomas in Cowden's syndrome. Arch Dermatol. 1979;115:111. 
  27. Roson E, Gomez Centeno P, Sanchez Aguilar D, et al. Desmoplastic trichilemmoma arising within a nevus sebaceous. Am J Dermatopathol. 1998;20:495-497. 
  28. Tellechea O, Reis JP, Baptista AP. Desmoplastic trichilemmoma. Am J Dermatopathol. 1992;14:107-114. 
  29. Sharma R, Sirohi D, Sengupta P, et al. Desmoplastic trichilemmoma of the facial region mimicking invasive carcinoma. J Maxillofac Oral Surg. 2010;10:71-73. 
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Garofola CT105001021.PDF
Author and Disclosure Information

Drs. Garofola and Brown are from the Department of Dermatology, LewisGale Hospital Montgomery, Blacksburg, Virginia. Drs. Phillips and Grider are from the Dermatology Section, Department of Internal Medicine, Virginia Tech Carilion School of Medicine, Roanoke. Dr. Grider also is from the Department of Basic Science Education, Virginia Tech Carilion School of Medicine.

The authors report no conflict of interest.

Correspondence: Craig J. Garofola, DO, 3700 S Main St, Blacksburg, VA 24060 (cgarofola@vcom.vt.edu)

Issue
Cutis - 105(1)
Publications
MDedge Dermatology
Cutis
Topics
Dermatopathology
Page Number
21-23
Sections
Dermpath Diagnosis
Author(s)
Craig J. Garofola, DO
Mariana A. Phillips, MD
Aleksandra Brown, DO
Douglas J. Grider, MD
Author(s)
Craig J. Garofola, DO
Mariana A. Phillips, MD
Aleksandra Brown, DO
Douglas J. Grider, MD
Author and Disclosure Information

Drs. Garofola and Brown are from the Department of Dermatology, LewisGale Hospital Montgomery, Blacksburg, Virginia. Drs. Phillips and Grider are from the Dermatology Section, Department of Internal Medicine, Virginia Tech Carilion School of Medicine, Roanoke. Dr. Grider also is from the Department of Basic Science Education, Virginia Tech Carilion School of Medicine.

The authors report no conflict of interest.

Correspondence: Craig J. Garofola, DO, 3700 S Main St, Blacksburg, VA 24060 (cgarofola@vcom.vt.edu)

Author and Disclosure Information

Drs. Garofola and Brown are from the Department of Dermatology, LewisGale Hospital Montgomery, Blacksburg, Virginia. Drs. Phillips and Grider are from the Dermatology Section, Department of Internal Medicine, Virginia Tech Carilion School of Medicine, Roanoke. Dr. Grider also is from the Department of Basic Science Education, Virginia Tech Carilion School of Medicine.

The authors report no conflict of interest.

Correspondence: Craig J. Garofola, DO, 3700 S Main St, Blacksburg, VA 24060 (cgarofola@vcom.vt.edu)

Article PDF
Garofola CT105001021.PDF
Article PDF
Garofola CT105001021.PDF
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The Diagnosis: Proliferating Pilar Tumor  

Proliferating pilar tumor (PPT), or cyst, is a neoplasm of trichilemmal keratinization first described by Wilson-Jones1 in 1966. Proliferating pilar tumors lie on a spectrum with malignant PPT, which is a rare adnexal neoplasm first described by Saida et al2 in 1983. The incidence of PPT is unknown given the paucity of cases and the possible misdiagnosis as squamous cell carcinoma (SCC). Proliferating pilar tumors tend to present on the head and neck of older females as a multilobular and sometimes ulcerating nodule.3 Although PPT can occur de novo, the majority of cases are thought to develop progressively from a benign pilar cyst. Histopathologically, PPT is characterized by cords and nests of squamous cells that display trichilemmal keratinization (quiz images).  

Classification of PPT as benign or malignant is challenging, though criteria have been proposed.3-7 Lesions with minimal infiltration into the surrounding dermis and scant mitosis typically behave in a benign manner, while lesions showing nuclear atypia, atypical mitosis, and irregular infiltration into the surrounding dermis can have up to a 50% locoregional recurrence rate.3 In addition, distinguishing a PPT from an SCC or trichilemmal carcinoma also can be difficult; however, SCC is favored when there is a lack of trichilemmal keratinization or when squamous atypia is present in the adjacent epidermis.8 Trichilemmal carcinoma is a rare tumor that has been questioned as a distinct entity.9-12  

Pilomatricoma, also known as calcifying epithelioma of Malherbe, is a benign pilar tumor that presents as a slowly growing nodule on the head or neck area or arms.13,14 Most pilomatricomas develop by the second decade of life. Multiple lesions may be present in association with myotonic dystrophy or Gardner syndrome among other syndromes.15-17 Similar to PPT, pilomatricomas present as large dermal nodules; however, they tend to be circumscribed and have a trabecular network that consists of basophilic cells and eosinophilic keratinized shadow cells (Figure 1).18 Calcification may be seen and bone formation subsequently may occur.19  

Figure 1. Pilomatricoma. Dermal tumor with peripheral basaloid cells, ghost cells, focal keratin debris, and focal multinucleated foreign body giant cells (H&E, original magnification ×100).

Most sources now consider keratoacanthoma (KA) as a well-differentiated SCC.20 The typical presentation consists of a rapidly growing erythematous to flesh-colored nodule with a central keratinous plug that develops over a period of weeks. If untreated, KAs may resolve over a period of months and leave a depressed scar. Local destruction can result from KAs, and they have the potential to transform into a more aggressive SCC. Accordingly, most clinicians use tissue destructive methods, excision, or Mohs micrographic surgery for treatment based on location. Histologically, a well-circumscribed proliferation of glassy cytoplasm is noted. A depressed keratin-filled center is surrounded by a lip of epithelium extending over the lesion (Figure 2).20,21 Pseudoepitheliomatous hyperplasia accompanied by hypergranulosis is seen in the center of KAs rather than at the periphery, which is typical of non-KA SCCs. Typical KAs lack acantholysis, a feature suggesting a non-KA type of SCC. Neutrophilic microabscesses and eosinophils commonly are seen in KAs.20,21  

Figure 2. Keratoacanthoma. Crateriform squamous proliferation with keratin debris in the center of the cystic spaces and squamous cells toward the periphery with eosinophilic and glassy cytoplasm (H&E, original magnification ×40).

Inverted follicular keratosis is a benign tumor that gained traction as its own entity in the 1960s.22 These lesions typically develop from the follicular infundibulum, but some consider them a version of a wart or seborrheic keratosis.23 They generally are flesh-colored nodules on the upper cutaneous lip or face. Treatment usually consists of complete excision. There are many different growth patterns described, but they typically are endophytic tumors with eosinophilic squamous cells in the center and more basophilic cells at the periphery (Figure 3).24 Characteristically, there are squamous eddies throughout the tumor (Figure 3 [inset]). There also may be a scant lymphohistiocytic infiltrate within the dermis surrounding the lesion.  

Figure 3. Inverted follicular keratosis. Endophytic, slightly verrucous squamous proliferation with central cyst formation and keratin debris (H&E, original magnification ×20). Squamous eddies and dendritic melanocytes can be seen on higher magnification (H&E, original magnification ×100 [inset]). 

 

 

 

 

 

Trichilemmomas are flesh-colored adnexal neoplasms that may present as a solitary lesion or in clusters on the face. They have been reported to occur on all nonglabrous skin sites.25 Multiple lesions may occur in association with Cowden syndrome or with nevus sebaceous.26 A desmoplastic variant of trichilemmomas has been reported.27 Desmoplastic trichilemmomas appear as well-circumscribed tumors of outer root sheath differentiation with lobules extending down into the dermis.28 Vacuolated glycogen-filled keratinocytes are scattered throughout the lesion but are most prominent at the base. At the periphery of the lobules, peripheral palisading of basaloid cells is accompanied by a thickened eosinophilic basement membrane that is periodic acid-Schiff positive. Typical trichilemmomas also can display these features; however, the main differentiating feature of a desmoplastic trichilemmoma is the pink hyalinized stroma separating small islets of basophilic cells (Figure 4). Differentiation from an invasive malignant carcinoma sometimes can be challenging without a focus of typical trichilemmoma or if the biopsy specimen is too superficial.29 

Figure 4. Desmoplastic trichilemmoma. Proliferation of lobules of squamous cells with clear cytoplasm, peripheral palisading of more basaloid keratinocytes, and a thickened basement membrane (H&E, original magnification ×100).

Pilar cysts are common tumors that typically arise on the scalp and sometimes are proliferating. Proliferating pilar tumor should be kept on the differential when secondary changes such as ulceration occur in the primary lesion of the scalp. Microscopically, and sometimes clinically, PPT can be difficult to differentiate from other mimickers.  

The Diagnosis: Proliferating Pilar Tumor  

Proliferating pilar tumor (PPT), or cyst, is a neoplasm of trichilemmal keratinization first described by Wilson-Jones1 in 1966. Proliferating pilar tumors lie on a spectrum with malignant PPT, which is a rare adnexal neoplasm first described by Saida et al2 in 1983. The incidence of PPT is unknown given the paucity of cases and the possible misdiagnosis as squamous cell carcinoma (SCC). Proliferating pilar tumors tend to present on the head and neck of older females as a multilobular and sometimes ulcerating nodule.3 Although PPT can occur de novo, the majority of cases are thought to develop progressively from a benign pilar cyst. Histopathologically, PPT is characterized by cords and nests of squamous cells that display trichilemmal keratinization (quiz images).  

Classification of PPT as benign or malignant is challenging, though criteria have been proposed.3-7 Lesions with minimal infiltration into the surrounding dermis and scant mitosis typically behave in a benign manner, while lesions showing nuclear atypia, atypical mitosis, and irregular infiltration into the surrounding dermis can have up to a 50% locoregional recurrence rate.3 In addition, distinguishing a PPT from an SCC or trichilemmal carcinoma also can be difficult; however, SCC is favored when there is a lack of trichilemmal keratinization or when squamous atypia is present in the adjacent epidermis.8 Trichilemmal carcinoma is a rare tumor that has been questioned as a distinct entity.9-12  

Pilomatricoma, also known as calcifying epithelioma of Malherbe, is a benign pilar tumor that presents as a slowly growing nodule on the head or neck area or arms.13,14 Most pilomatricomas develop by the second decade of life. Multiple lesions may be present in association with myotonic dystrophy or Gardner syndrome among other syndromes.15-17 Similar to PPT, pilomatricomas present as large dermal nodules; however, they tend to be circumscribed and have a trabecular network that consists of basophilic cells and eosinophilic keratinized shadow cells (Figure 1).18 Calcification may be seen and bone formation subsequently may occur.19  

Figure 1. Pilomatricoma. Dermal tumor with peripheral basaloid cells, ghost cells, focal keratin debris, and focal multinucleated foreign body giant cells (H&E, original magnification ×100).

Most sources now consider keratoacanthoma (KA) as a well-differentiated SCC.20 The typical presentation consists of a rapidly growing erythematous to flesh-colored nodule with a central keratinous plug that develops over a period of weeks. If untreated, KAs may resolve over a period of months and leave a depressed scar. Local destruction can result from KAs, and they have the potential to transform into a more aggressive SCC. Accordingly, most clinicians use tissue destructive methods, excision, or Mohs micrographic surgery for treatment based on location. Histologically, a well-circumscribed proliferation of glassy cytoplasm is noted. A depressed keratin-filled center is surrounded by a lip of epithelium extending over the lesion (Figure 2).20,21 Pseudoepitheliomatous hyperplasia accompanied by hypergranulosis is seen in the center of KAs rather than at the periphery, which is typical of non-KA SCCs. Typical KAs lack acantholysis, a feature suggesting a non-KA type of SCC. Neutrophilic microabscesses and eosinophils commonly are seen in KAs.20,21  

Figure 2. Keratoacanthoma. Crateriform squamous proliferation with keratin debris in the center of the cystic spaces and squamous cells toward the periphery with eosinophilic and glassy cytoplasm (H&E, original magnification ×40).

Inverted follicular keratosis is a benign tumor that gained traction as its own entity in the 1960s.22 These lesions typically develop from the follicular infundibulum, but some consider them a version of a wart or seborrheic keratosis.23 They generally are flesh-colored nodules on the upper cutaneous lip or face. Treatment usually consists of complete excision. There are many different growth patterns described, but they typically are endophytic tumors with eosinophilic squamous cells in the center and more basophilic cells at the periphery (Figure 3).24 Characteristically, there are squamous eddies throughout the tumor (Figure 3 [inset]). There also may be a scant lymphohistiocytic infiltrate within the dermis surrounding the lesion.  

Figure 3. Inverted follicular keratosis. Endophytic, slightly verrucous squamous proliferation with central cyst formation and keratin debris (H&E, original magnification ×20). Squamous eddies and dendritic melanocytes can be seen on higher magnification (H&E, original magnification ×100 [inset]). 

 

 

 

 

 

Trichilemmomas are flesh-colored adnexal neoplasms that may present as a solitary lesion or in clusters on the face. They have been reported to occur on all nonglabrous skin sites.25 Multiple lesions may occur in association with Cowden syndrome or with nevus sebaceous.26 A desmoplastic variant of trichilemmomas has been reported.27 Desmoplastic trichilemmomas appear as well-circumscribed tumors of outer root sheath differentiation with lobules extending down into the dermis.28 Vacuolated glycogen-filled keratinocytes are scattered throughout the lesion but are most prominent at the base. At the periphery of the lobules, peripheral palisading of basaloid cells is accompanied by a thickened eosinophilic basement membrane that is periodic acid-Schiff positive. Typical trichilemmomas also can display these features; however, the main differentiating feature of a desmoplastic trichilemmoma is the pink hyalinized stroma separating small islets of basophilic cells (Figure 4). Differentiation from an invasive malignant carcinoma sometimes can be challenging without a focus of typical trichilemmoma or if the biopsy specimen is too superficial.29 

Figure 4. Desmoplastic trichilemmoma. Proliferation of lobules of squamous cells with clear cytoplasm, peripheral palisading of more basaloid keratinocytes, and a thickened basement membrane (H&E, original magnification ×100).

Pilar cysts are common tumors that typically arise on the scalp and sometimes are proliferating. Proliferating pilar tumor should be kept on the differential when secondary changes such as ulceration occur in the primary lesion of the scalp. Microscopically, and sometimes clinically, PPT can be difficult to differentiate from other mimickers.  

References
  1. Wilson-Jones E. Proliferating epidermoid cysts. Arch Dermatol. 1966;94:11-19. 
  2. Saida T, Oohara K, Hori Y, et al. Development of a malignant proliferating trichilemmal cyst in a patient with multiple trichilemmal cysts. Dermatologica. 1983;166:203-208. 
  3. Ye J, Nappi O, Swanson PE, et al. Proliferating pilar tumours: a clinicopathological study of 76 cases with a proposal for definition of benign and malignant variants. Am J Clin Pathol. 2004;122:566-574. 
  4. Garg PK, Dangi A, Khurana N, et al. Malignant proliferating trichilemmal cyst: a case report with review of literature. Malaysian J Pathol. 2009;31:71-76. 
  5. Herrero J, Monteagudo C, Ruiz A, et al. Malignant proliferating trichilemmal tumors: a histopathological and immunohistochemical study of three cases with DNA ploidy and morphometric evaluation. Histopathology. 1998;33:542-546.  
  6. Haas N, Audring H, Sterry W. Carcinoma arising in a proliferating trichilemmal cyst expresses fetal and trichilemmal hair phenotype. Am J Dermatopathol. 2002;24:340-344.  
  7. Rutty GN, Richman PI, Laing JH. Malignant change in trichilemmal cysts: a study of cell proliferation and DNA content. Histopathology. 1992;21:465-468.  
  8. Brownstein MH, Arluk DJ. Proliferating trichilemmal cyst: a simulant of squamous cell carcinoma. Cancer. 1981;48:1207-1214.  
  9. Misago N, Ackerman AB. Tricholemmal carcinoma? Dermatopathol Pract Concept. 1999;5:205-206. 
  10. Misago N, Narisawa Y. Tricholemmal carcinoma in continuity with trichoblastoma within nevus sebaceous. Am J Dermatopathol. 2002;24:149-155. 
  11. Liang H, Wu H, Giorgadze TA, et al. Podoplanin is a highly sensitive and specific marker to distinguish primary skin adnexal carcinomas from adenocarcinomas metastatic to skin. Am J Surg Pathol. 2007;31:304-310. 
  12. Swanson PE, Marrogi AJ, Williams DJ, et al. Trichilemmal carcinoma: clinicopathologic study of 10 cases. J Cutan Pathol. 1992;19:100-109. 
  13. Mehregan AH. Hair follicle tumors of the skin. J Cutan Pathol. 1985;12:189-195.  
  14. Julian CG, Bowers PW. A clinical review of 209 pilomatricomas. J Am Acad Dermatol. 1998;39:191-195.  
  15. Marrogi AJ, Wick MR, Dehner LP. Pilomatrical neoplasms in children and young adults. Am J Dermatopathol. 1992;14:87-94.  
  16. Berberian BJ, Colonna TM, Battaglia M, et al. Multiple pilomatricomas in association with myotonic dystrophy and a family history of melanoma. J Am Acad Dermatol. 1997;37:268-269.  
  17. Cooper PH, Fechner RE. Pilomatricoma-like changes in the epidermal cysts of Gardner's syndrome. J Am Acad Dermatol. 1983;8:639-644.  
  18. Kaddu S, Soyer HP, Cerroni L, et al. Clinical and histopathologic spectrum of pilomatricomas in adults. Int J Dermatol. 1994;33:705-708.  
  19. Sano Y, Mihara M, Miyamoto T, et al. Simultaneous occurrence of calcification and amyloid deposit in pilomatricoma. Acta Derm Venereol. 1990;70:256-259.  
  20. Schwartz RA. Keratoacanthoma. J Am Acad Dermatol. 1994;30:1-19.  
  21. Kwiek B, Schwartz RA. Keratoacanthoma (KA): an update and review. J Am Acad Dermatol. 2016;74:1220-1233. 
  22. Mehregan AH. Inverted follicular keratosis. Arch Dermatol. 1964;89:117-123. 
  23. Spielvogel RL, Austin C, Ackerman AB. Inverted follicular keratosis is not a specific keratosis but a verruca vulgaris (or seborrheic keratosis) with squamous eddies. Am J Dermatopathol. 1983;5:427-445. 
  24. Mehregan AH. Inverted follicular keratosis is a distinct follicular tumor. Am J Dermatopathol. 1983;5:467-470. 
  25. Brownstein MH. Trichilemmoma. benign follicular tumor or viral wart? Am J Dermatopathol. 1980;2:229-231. 
  26. Brownstein MH. Multiple trichilemmomas in Cowden's syndrome. Arch Dermatol. 1979;115:111. 
  27. Roson E, Gomez Centeno P, Sanchez Aguilar D, et al. Desmoplastic trichilemmoma arising within a nevus sebaceous. Am J Dermatopathol. 1998;20:495-497. 
  28. Tellechea O, Reis JP, Baptista AP. Desmoplastic trichilemmoma. Am J Dermatopathol. 1992;14:107-114. 
  29. Sharma R, Sirohi D, Sengupta P, et al. Desmoplastic trichilemmoma of the facial region mimicking invasive carcinoma. J Maxillofac Oral Surg. 2010;10:71-73. 
References
  1. Wilson-Jones E. Proliferating epidermoid cysts. Arch Dermatol. 1966;94:11-19. 
  2. Saida T, Oohara K, Hori Y, et al. Development of a malignant proliferating trichilemmal cyst in a patient with multiple trichilemmal cysts. Dermatologica. 1983;166:203-208. 
  3. Ye J, Nappi O, Swanson PE, et al. Proliferating pilar tumours: a clinicopathological study of 76 cases with a proposal for definition of benign and malignant variants. Am J Clin Pathol. 2004;122:566-574. 
  4. Garg PK, Dangi A, Khurana N, et al. Malignant proliferating trichilemmal cyst: a case report with review of literature. Malaysian J Pathol. 2009;31:71-76. 
  5. Herrero J, Monteagudo C, Ruiz A, et al. Malignant proliferating trichilemmal tumors: a histopathological and immunohistochemical study of three cases with DNA ploidy and morphometric evaluation. Histopathology. 1998;33:542-546.  
  6. Haas N, Audring H, Sterry W. Carcinoma arising in a proliferating trichilemmal cyst expresses fetal and trichilemmal hair phenotype. Am J Dermatopathol. 2002;24:340-344.  
  7. Rutty GN, Richman PI, Laing JH. Malignant change in trichilemmal cysts: a study of cell proliferation and DNA content. Histopathology. 1992;21:465-468.  
  8. Brownstein MH, Arluk DJ. Proliferating trichilemmal cyst: a simulant of squamous cell carcinoma. Cancer. 1981;48:1207-1214.  
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Issue
Cutis - 105(1)
Issue
Cutis - 105(1)
Page Number
21-23
Page Number
21-23
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MDedge Dermatology
Cutis
Publications
MDedge Dermatology
Cutis
Topics
Dermatopathology
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Article
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Ulcerated Nodule on the Scalp
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Ulcerated Nodule on the Scalp
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Dermpath Diagnosis
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A 66-year-old woman presented to the dermatology clinic with a rapidly enlarging, draining lesion on the scalp. The lesion seemed to enlarge over the last 3 months from a lesion that had been there for years. Physical examination revealed a 2.2-cm ulcerated nodule on the right parietal scalp. A shave biopsy was obtained. 

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