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Ameloblastoma pathophysiology

Introduction

Overview

Overview

Ameloblastoma arise from remnants of ameloblast or dental lamina, dentigerous cysts, or basal layer of oral mucosa. There is evidence that suppression of matrix metalloproteinase-2 may inhibit the local invasiveness of ameloblastoma. On gross pathology, the characteristic findings of ameloblastoma may include solid and cystic, multicystic and intraosseous or extraosseous, or rarely unicystic. On microscopic histopathological analysis, stellate reticulum, giant cells, subepithelial hyalinization, and columnar basal cells in palisading arrangement with vacuolated cytoplasm are characteristic findings of ameloblastoma. The exact pathophysiology of ameloblastoma is not fully understood. It is thought that ameloblastoma is the result of either suppression of matrix metalloproteinase-2 that may inhibit the local invasiveness of ameloblastoma, or there is also some research suggesting that Ξ±5Ξ²1 integrin may participate in the local invasiveness of ameloblastoma. Genes involved in the pathogenesis of ameloblastoma include BRAF V600E.

Pathophysiology

Pathophysiology

Pathogenesis

Genetics

Genetics

Genes involved in the pathogenesis of ameloblastoma include:

Gross Pathology

Gross Pathology

On gross pathology the following are the characteristic findings of ameloblastoma:[7][8][9]

Microscopic Pathology

Microscopic Pathology

On microscopic examination, the following characteristic findings of ameloblastoma are present:

  • Stellate reticulum – star-shaped cells, found in a developing tooth[10][11]
  • Giant cells may or may not be present
  • Subepithelial hyalinization may or may not be present
  • Seen deep to the basement membrane
  • Suprabasal cells loosely textured and noncohesive, resembling stellate reticulum
  • The plexiform type has epithelium that proliferates in a “Fish Net Pattern”
  • The follicular type will have outer arrangement of columnar or palisaded ameloblast like cells and inner zone of triangular shaped cells resembling stellate reticulum in bell stage. The central cells sometimes degenerate to form central microcysts
  • No enamel or dentin formation
  • Tall columnar cells
    • Palisaded nuclei with reverse polarization
      • Reverse polarization of nuclei = nuclei distant from the basement membrane/nuclei at pole opposite of basement membrane
      • Palisaded nuclei = picket fence appearance; columnar-shaped nuclei with long axis perpendicular to the basement membrane (key feature)
    • Subnuclear vacuolation
  • The following are the different histopathological variants of ameloblastoma:[2][1]
    • Intraosseous (follicular, plexiform, acanthomatous, multicystic, unicystic, granular cell [lysosomes by EM], basal cell, desmoplastic)
    • Extraosseous (follicular, plexiform, basal cell)

The image shows the characteristic features:[12]

  • Subnuclear vacuolation in palisading cell – vacuoles at the basement membrane aspect
  • Loose stroma around the islands of cells
  • Star-like cells at the centre of the islands of cells (stellate reticulum)

Video

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References

References

  1. ↑ 1.0 1.1 Ameloblastoma. Wikipedia(2015) https://en.wikipedia.org/wiki/Ameloblastoma Accessed on December 25, 2015
  2. ↑ 2.0 2.1 Ameloblastoma. Libre pathology(2015) http://librepathology.org/wiki/index.php/Ameloblastoma Accessed on December 25, 2015
  3. ↑ Pandya NJ, Stuteville OH (1972). “Treatment of ameloblastoma”. Plast Reconstr Surg. 50 (3): 242–8. PMIDΒ 4115148.
  4. ↑ Masthan KM, Anitha N, Krupaa J, Manikkam S (April 2015). “Ameloblastoma”. J Pharm Bioallied Sci. 7 (Suppl 1): S167–70. doi:10.4103/0975-7406.155891. PMCΒ 4439660. PMIDΒ 26015700.
  5. ↑ Brazis PW, Miller NR, Lee AG, Holliday MJ (1995). “Neuro-ophthalmologic Aspects of Ameloblastoma”. Skull Base Surg. 5 (4): 233–44. PMCΒ 1656531. PMIDΒ 17170964.
  6. ↑ McClary, Andrew C.; West, Robert B.; McClary, Ashley C.; Pollack, Jonathan R.; Fischbein, Nancy J.; Holsinger, Christopher F.; Sunwoo, John; Colevas, A. Dimitrios; Sirjani, Davud (2015). “Ameloblastoma: a clinical review and trends in management”. European Archives of Oto-Rhino-Laryngology. 273 (7): 1649–1661. doi:10.1007/s00405-015-3631-8. ISSNΒ 0937-4477.
  7. ↑ Mendenhall WM, Werning JW, Fernandes R, Malyapa RS, Mendenhall NP (December 2007). “Ameloblastoma”. Am. J. Clin. Oncol. 30 (6): 645–8. doi:10.1097/COC.0b013e3181573e59. PMIDΒ 18091060.
  8. ↑ Dunfee BL, Sakai O, Pistey R, Gohel A (2006). “Radiologic and pathologic characteristics of benign and malignant lesions of the mandible”. Radiographics. 26 (6): 1751–68. doi:10.1148/rg.266055189. PMIDΒ 17102048.
  9. ↑ McClary, Andrew C.; West, Robert B.; McClary, Ashley C.; Pollack, Jonathan R.; Fischbein, Nancy J.; Holsinger, Christopher F.; Sunwoo, John; Colevas, A. Dimitrios; Sirjani, Davud (2015). “Ameloblastoma: a clinical review and trends in management”. European Archives of Oto-Rhino-Laryngology. 273 (7): 1649–1661. doi:10.1007/s00405-015-3631-8. ISSNΒ 0937-4477.
  10. ↑ Gardner DG, Corio RL (April 1984). “Plexiform unicystic ameloblastoma. A variant of ameloblastoma with a low-recurrence rate after enucleation”. Cancer. 53 (8): 1730–5. PMIDΒ 6697311.
  11. ↑ McClary, Andrew C.; West, Robert B.; McClary, Ashley C.; Pollack, Jonathan R.; Fischbein, Nancy J.; Holsinger, Christopher F.; Sunwoo, John; Colevas, A. Dimitrios; Sirjani, Davud (2015). “Ameloblastoma: a clinical review and trends in management”. European Archives of Oto-Rhino-Laryngology. 273 (7): 1649–1661. doi:10.1007/s00405-015-3631-8. ISSNΒ 0937-4477.
  12. ↑ Gruica B, Stauffer E, Buser D, Bornstein M. (2003). “Ameloblastoma of the follicular, plexiform, and acanthomatous type in the maxillary sinus: a case report”. Quintessence International. 34 (4): 311–4. PMIDΒ 12731620. Unknown parameter |month= ignored (help)

Editor-In-Chief:
C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Shivali Marketkar, M.B.B.S. [2], Vamsikrishna Gunnam M.B.B.S [3]