{"id":8147,"date":"2016-08-21T08:48:11","date_gmt":"2016-08-21T08:48:11","guid":{"rendered":"http:\/\/biomedpharmajournal.org\/?p=8147"},"modified":"2018-01-29T05:11:38","modified_gmt":"2018-01-29T05:11:38","slug":"malignant-melanoma-of-oral-cavity","status":"publish","type":"post","link":"https:\/\/biomedpharmajournal.org\/staging\/vol9no2\/malignant-melanoma-of-oral-cavity\/","title":{"rendered":"Malignant Melanoma of Oral Cavity"},"content":{"rendered":"

Introduction\u00a0<\/strong><\/p>\n

Malignant melanoma (MM) is a neoplasm \u00a0of epidermal melanocytes, which are located primarily in the skin and mucosa .cutaneous melanomas are more common rather than the oral melanomas 2,3<\/sup><\/p>\n

It is more common on white skinned individuals than \u00a0the dark skinned ones \u00a0and the lesion accounts for 0.2 % of all melanomas \u00a0but it is extremely rare in united states .<\/p>\n

In oral cavity it represent less than 2% of all melanomas<\/p>\n

The\u00a0 Japanese, Black Africans, Native Americans, and Hispanics are most commonly affected by oral melanomas 13<\/sup><\/p>\n

Etiology<\/strong><\/p>\n

The factors affecting the cutaneous melanoma are environmental and genetic factors which may have a positive\u00a0 familial history 1,12<\/sup>. Etiology for oral mucosal melanomas was unknown\u00a0 and there was no relationship between any physical or chemical events 7 <\/sup>. But sometimes intraoral melanocytic proliferations (nevi) may be the source for oral malignant melanomas.\u00a0In 1975 clark postulated the\u00a0 2 growth pattern for melanoma .<\/p>\n

Radial growth phase\u00a0<\/strong><\/p>\n

In this phase \u00a0the neoplastic cells are limited only \u00a0to the epidermis and some may enter into the basement membrane destroying host cell immunologic response<\/p>\n

Vertical growth phase\u00a0<\/strong><\/p>\n

In this where neoplastic cells populate the underlying dermis metastasis is possible in this phase<\/p>\n

Types of melanomas<\/strong><\/p>\n

Cutaneous melanomas<\/strong><\/p>\n

superficial spreading melanoma , nodular melanoma , lentigo maligna melanoma and acral lentiginous melanoma<\/p>\n

ABCDE rule of melanoma\u00a0<\/strong><\/p>\n

asymmetry , border , color , diameter and elevation<\/p>\n

Clinical features<\/strong><\/p>\n

There are 5 clinical types –\u00a0 pigmented nodular , pigmented macular , pigmented mixed , nonpigmented nodular and nonpigmented mixed type.[14].<\/sup>Malignant melanoma may occur with or without radial growth phase[2]<\/sup> The color may be uniform and some lesions \u00a0appears as\u00a0 \u00a0black, grey, purple, or even reddish. The lesions are asymmetric, irregular in outline, and occasionally multiple. The surface architecture varies for oral melanomas ranging \u00a0from \u00a0nodular and macular to ulcerated.[4,5,7]\u00a0<\/sup>Amelanotic oral malignant melanoma (AOMM) : \u00a0some tumors are amelanotic which is of rare type . lesion is erythematous or pink ,sometimes it may be eroded or nodule . but the diagnosis of the lesion may be confused with other tumors , only by the histopathological examination the final diagnosis of the lesion can be made\u00a0 .[15]\u00a0<\/sup>Pain is an uncommon symptom of malignant melanoma, generally found in the advanced stages.[3,5,8]<\/sup> The tumor causes extensive destruction of\u00a0the underlying bone in 78% of cases.[5]<\/sup><\/p>\n

Histopathological features\u00a0<\/strong><\/p>\n

Abnormal melanocytes are seen in the epithelial and connective tissue junction and there is a \u00a0high density of melanocytes, atypical cells present in the\u00a0 oral melanotic lesion \u00a0which is diagnosed as oral malignant melanoma.6<\/sup><\/p>\n

In amelanotic melanoma , the melanoma cells have melanin granules but there is no production of melanin is seen . this less production causes difficulty in diagnosing as it may represent some other tumors<\/p>\n

Immunohistochemical studies shows\u00a0 S-100 protein, MART-1, and HMB-45 reactivity of the lesional cells in \u00a0melanomas from other malignancies.[6]<\/sup><\/p>\n

Diagnosis<\/strong><\/p>\n

Diagnosis of melanoma may be difficult because of its small biopsy size , lack of clinical or may be due to variety of reasons7<\/sup>. CT and MRI studies were\u00a0 done to know the metastases occurring in\u00a0 the cervical and submandibular \u00a0lymph nodes. Incisional biopsy is most common choice for diagnosis.[4]<\/sup><\/p>\n

Differential diagnosis<\/strong><\/p>\n

Differential diagnosis of oral melanomas are \u00a0oral melanotic macule, smoking-associated melanosis, medication-induced melanosis \u00a0melanocytic nevi of the oral mucosa, blue nevi, nevi of Spitz, Addisons disease, Peutz-Jeghers syndrome, amalgam tattoo and many other conditions .<\/p>\n

Management<\/strong><\/p>\n

Surgery excision is first line of\u00a0 treatment, but it is\u00a0 difficult due to\u00a0 anatomic restraints. Jaw resection and lymph node dissection is done when the bone or lymph nodes are involved .chemotherapy \u00a0and radio therapy were the other forms of treatment \u00a04-6<\/sup><\/p>\n

Prognosis and survival<\/strong><\/p>\n

Oral melanomas have poor prognosis than cutaneous melanomas. Cutaneous melanomas can be graded by Clark levels or the Breslow tumor thickness grading system. The clark classification assesss \u00a0the depth of invasion, whereas Breslow<\/p>\n

system measures the thickness of the tumor and depth of the tumor from the surface epidermis . \u00a0When the tumor thickness is increased there is a high risk for developing metastatic lesions.<\/p>\n

Both these system shows the 5 year survival rate . Factors that are significant in disease\u00a0 survival include high clinical stage at presentation, tumor thickness greater than 5 mm, , absence of melanosis, presence of vascular invasion,development of nodal and distant metastases.5,6,8<\/sup><\/p>\n

References<\/strong><\/p>\n

    \n
  1. Hicks MJ, Flaitz CM. Oral mucosal melanoma: Epidemiology and\u00a0pathobiology. Oral Oncol 2000;36:152-69.<\/li>\n
  2. Freedberg IM, Wolff K, Austen KF, et al. Dermatology in general\u00a0medicine. 5th ed. Mc Graw-Hill: United States; 1999. p. 981,1097.<\/li>\n
  3. Steidler NE, Reade PC, Radden BG. Malignant melanoma of the oral\u00a0mucosa. J Oral Maxillofac Surg 1984;42:333-6.<\/li>\n
  4. Greenberg MS, Glic KM. Burket\u2019s oral medicine. 9th ed. BC Decker:Hamilton; 2003. p. 131-2,214-5.<\/li>\n
  5. Prabhu SR, Wilson DF, Daftary DK. Oral diseases in the tropics. Oxford\u00a0University Press: New York; 1992. p. 460-1.<\/li>\n
  6. Neville BW, Damm D, Allenc R, Bouquot JE. Oral and maxillofacial\u00a0pathology. 2nd ed. W.B Saunders: Philadelphia; 2002. p. 334,376-80.<\/li>\n
  7. Silverman S. Oral cancer. 5th ed. BC Decker Inc: Hamilton, London;\u00a0p. 155-7.<\/li>\n
  8. van der Waal RI, Snow GB, Karim AB, Van der Waal I. Primary malignant melanoma of the oral cavity: A review of eight cases. Br Dent J 1994;176:185-8. 9.<\/li>\n
  9. Robertson GR, Defiebre BK, Firtell DN. Primary malignant melanoma of the mouth. J Oral Surg 1979;37:349-52.<\/li>\n
  10. Reddy CR, Ramachandra T, Ramulu C. Primary malignant melanoma of the hard palate. J Oral Surg 1976;34:937-9.2003;96:404-13.<\/li>\n
  11. Bina SH. Primary malignant melanoma of the oral cavity in Iranians\u00a0(review of 18 cases). J Oral Med 1979;34:51-2.<\/li>\n
  12. Tremblay JF, O\u2019Brien EA, Chauvin PJ. Melanoma in situ of the oral mucosa in an adolescent with dysplastic nevus syndrome. J Am Acad Dermatol\u00a0Tanaka N, Amagasa T, Iwaki H, Shioda S, Takeda M, Ohashi K, et al.Oral malignant melanoma in Japan. Oral Surg Oral Med Oral Pathol\u00a01994;78:81-90.<\/li>\n
  13. Tanaka N, Mimura M, Kimijima Y, Amagasa T. Clinical investigation of\u00a0amelanotic malignant melanoma in the oral region. J Oral Maxillofac\u00a0Surg 2004;62:933-7.<\/li>\n
  14. Rajendran R, Sivapada Sundaram B. Benign and malignant tumors of the oral cavity. Shafer, Hine, Lavy, editors Shafer’s Text book of Oral Pathology India: Elsevier2009:120-7.<\/li>\n<\/ol>\n","protected":false},"excerpt":{"rendered":"

    Introduction\u00a0 Malignant melanoma (MM) is a neoplasm \u00a0of epidermal melanocytes, […]<\/p>\n","protected":false},"author":9,"featured_media":0,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[32],"tags":[],"class_list":["post-8147","post","type-post","status-publish","format-standard","hentry","category-vol9no2"],"_links":{"self":[{"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/posts\/8147","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/users\/9"}],"replies":[{"embeddable":true,"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/comments?post=8147"}],"version-history":[{"count":7,"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/posts\/8147\/revisions"}],"predecessor-version":[{"id":18765,"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/posts\/8147\/revisions\/18765"}],"wp:attachment":[{"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/media?parent=8147"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/categories?post=8147"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/biomedpharmajournal.org\/staging\/wp-json\/wp\/v2\/tags?post=8147"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}