Soft tissue tumors 2 2007


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Soft tissue tumors 2 2007

  1. 1. Oral & Maxillofacial Pathology II DB 3702 Topic: Soft Tissue Tumors Course Director: Dr. J. E. Bouquot Room 3.094b; 713-500-4420 Thursdays, 10:00 – 11:50 am Room DB 132
  2. 2. This presentation created by Dr. J. E. BouquotThis presentation is intended for students of Dr. Jerry Bouquot.Designated owners of the photographic images in this lectureretain the copyrights for those images but have agreed to allowtheir photos to be used for teaching. You are welcome to use thispresentation for your learning, alone or with other dental students,but permission is not given for the publication of these photos inelectronic or any other format. Disclaimer: Dr. Bouquot is Professor & Chair, Department of Diagnostic Sciences, University of Texas Dental Branch at Houston. The information and opinions provided herein are, however, his own and do not represent official opinion or policy of the University of Texas.
  3. 3. Fibrosarcoma
  4. 4. FibrosarcomaMalignant neoplasm of fibroblastsEtiology = unknownGALP:– None– Children, teenagers, young adults– Palate > tongue > buccal– 10% of all are in H&NPainless, firm massOften lobulatedMay have surface ulcerationSlow-growing in beginningModerate growth speed-- May be rapid
  5. 5. Fibrosarcoma HistopathologySpindle cells in collagenSpindle cells may be dysplasticGrade is important for prognosis-- Grades I - IVNot encapsulated Grade IMitotic figuresHerring bone pattern Grade III
  6. 6. FibrosarcomaPathophysiology, TreatmentCan grow rapidly toward end--Especially high grade lesionsDestroys underlying boneFibrosarcoma of bone-- Perforates through cortexTreatment:-- Radical surgical removal-- Including affected bone5-year survival = 50%
  7. 7. Malignant Fibrous Histiocytoma
  8. 8. Malignant Fibrous Histiocytoma Fibroxanthoma; DermatofibromaMalignant neoplasm of histiocytes-- With fibrous differentiationGALP:– None– Middle-age and older (but skin lesions: young adults)– Buccal< vestibule-- Rare in mouthPainless, firm massMay be lobulatedMay be ulcerated
  9. 9. Malignant Fibrous Histiocytoma Histopathology Numerous spindle cells Open nuclei (like histiocytes) Storiform pattern Maybe rounded histiocytic cells May look benign!
  10. 10. PyogenicGranuloma
  11. 11. Pyogenic GranulomaPyogenic Granuloma Type Hemangioma Lack of reduction of granulation tissue during normal healing process -- Not an infection, no pus but “pyogenic” = pus producing -- Not a granulomatous infection GALP: – None (although strong female predilection in biopsied cases) – Children & young adults – Gingiva (75%), lips, tongue, buccal – 50th most common mucosal lesion -- Prevalence = 1/10,000 adults “Proud flesh”
  12. 12. Pyogenic GranulomaEdematous granulation tissueNeovascularityChronic inflammatory cellsAcute inflammatory cellsSurface ulceration, oftenLobular (locular) capillary hemangioma Lobular hemangioma
  13. 13. Pyogenic Granuloma Painless erythematous mass Often hemorrhagic Often lobulated surface Often ulcerated Often pedunculated
  14. 14. Pyogenic Granuloma Special Variants Pregnancy tumor:-- PG of gingiva-- In pregnant woman Pregnancy tumor-- Papilla involved-- May be multiple-- Poor oral hygieneEpulis granulomatosum:-- PG within poorly healed Epulis granulomatosum extraction socket-- Curette thoroughlyParulis (gum boil):-- PG at opening of dental fistula-- Check for abscess in bone -- Treat the tooth Parulis
  15. 15. Pyogenic GranulomaMay shrink over timeMay become irritation fibroma -- Fibrotic pyogenic granulomaPregnancy tumor: -- Often disappears after birth of babyTreat: Surgical excision -- Remove causeFor pregnancy tumor: -- Wait until after birthMay recur -- If original cause is not removed -- More infection, trauma
  16. 16. Look-Alike: Traumatic Eosinophilic Ulcer Traumatic Ulcer with Stomal Eosinophilia May mimic pyogenic granuloma
  17. 17. PeripheralOssifying Fibroma
  18. 18. Peripheral Ossifying FibromaPeripheral Cementifying/Ossifying Fibroma Inflammatory proliferation of fibrous tissue From periodontal fibers Primitive stroma Bone or cementum GAL: – 2/3 females – Teenagers and young adults – Gingival papilla (must be in this location) -- Edentulous alveolus also
  19. 19. Peripheral Ossifying Fibroma Histopathology Primitive spindle cells in fibrous stroma Immature bone formation -- Often with active osteoblastsMaybe cementoid globules-- Few cementoblasts-- Almost no cementocytes
  20. 20. Peripheral Ossifying FibromaPainless mass of papillaFirm, red/pinkMay be lobulatedMay be ulceratedMay show radiopacitiesCan separate teethMay develop in socket
  21. 21. Peripheral Ossifying Fibroma Can Spread Teeth Apart
  22. 22. Peripheral Ossifying Fibroma Usually < 2 cm. -- Occasionally up to 3 cm. Treat: -- Conservative surgical excision -- With curettage of base – Cleaning/scaling adjacent teeth 15% recur
  23. 23. Peripheral Ossifying Fibroma (In Socket) Epulis Granulomatosum
  24. 24. Peripheral Ossifying FibromaCan (Rarely) Produce Massive Sclerosis Above the Crest
  25. 25. Peripheral Ossifying FibromaCan Occur on Edentulous Ridge (From Residual Periodontal Fibers)
  26. 26. Peripheral GiantCell Granuloma
  27. 27. Peripheral Giant Cell GranulomaPeripheral Giant Cell Lesion; Giant Cell Epulis Inflammatory proliferation of phagocytic cells from: – Irritation -- Trauma -- Infection GAL: – 60% in females – Fifth-sixth decades – Gingiva -- Alveolar mucosa
  28. 28. Peripheral Giant Cell Granuloma Histopathology Immature fibrous stroma Multinucleated giant cells Extravasated erythrocytes Spindled, oval mesenchymal cells
  29. 29. Peripheral Giant Cell Granuloma Clinical FeaturesPainless massPerhaps hemorrhagicOften red/bluish/brownSomewhat soft to palpationMay cup out underlying bony cortex-- Saucerization (from pressure)Maybe calcifications on radiograph-- Near lower borderOften ulceratedIn socket =epulis granulomatosum
  30. 30. Peripheral Giant Cell Granuloma Pathophysiology; Treatment Generally remain less than 2 cm. May become more than 4 cm. No malignant transformation Treat: Conservative surgical excision --With curettage of base – And cleaning/scaling of adjacent teeth 10% recur Caution: large or multiple or recurring lesions might be brown tumor of hyperparathyroidism
  31. 31. Hyperparathyroidism↑ PTH >> ↑ calcium taken from bonePrimary: ↑PTH from tumor-- 90%: from parathyroid adenoma-- 10% from parathyroid hyperplasia-- Rare: from parathyroid carcinoma Ground glass skullSecondary: chronic ↓ calcium >> ↑PTH-- Usually: chronic renal disease-- ↓ vitamin D made by kidney >>-- ↓ calcium GI absorption >>-- ↓ serum calcium (hypocalcaemia)-- Severe: renal osteodystrophyGALP:-- 1:4 male:female ratio-- >60 y/o Osteitis-- Kidneys, bone fibrosa cystica
  32. 32. Hyperparathyroidism“Bones, moans and abdominal groans”Renal calculi (kidney stones, nephrolithiasis) -- From ↑ serum calciumMetastatic calcification -- Dystrophic calcification of soft tissues -- From ↑ serum calciumSubperiosteal resorption of phalanges -- Index & middle fingersGround glass bone -- ↓ trabeculae -- Blurred radiographLoss of lamina dura (early sign)Brown tumorOsteitis fibrosa cystica -- Severe variant of bone change -- Marrow degeneration -- Fibrosis of brown tumors
  33. 33. HyperparathyroidismDuodenal ulcers (painful)WeaknessLethargyConfusionDementiaBrown tumor-- Multinucleated giant cells-- Extravasated RBCs-- Hemosiderin deposits-- Radiolucency (often multilocular)-- Bony expansion-- May be multiple-- Like central giant cell granuloma of jaws
  34. 34. HyperparathyroidismGround Glass Bone; Loss of Lamina Dura
  35. 35. Hemangioma
  36. 36. HemangiomaCavernous Hemangioma; Capillary Hemangioma Benign developmental growth of vessels Benign neoplasm of blood vessels GALP: – 3x females – Children and teenagers – Seldom congenital, but develop shortly after birth – Tongue > buccal > lips – 6th most common mucosal lesion – Prevalence = 6/1,000 adults – Head and neck: most common location
  37. 37. Hemangioma HistopathologyDilated vessels:cavernous hemangiomaSmall vessels:capillary hemangiomaEndothelium-lined channelsEndothelial nuclei are enlarged -- Plump; bulge into lumen -- If flat: inactive lesionBlood-filled luminaWithout blood: lymphangiomaNo encapsulationPort wine stain = capillary hemangioma
  38. 38. Capillary & Cavernous Hemangioma
  39. 39. Hemangioma Clinical CharacteristicsSessile, lobulatedSoft red massOften lobulatedPainlessSmooth-surfaceFluctuates and blanchesBlue color if venous bloodRed if arterialDeep lesions: no surface colorOn skin: port wine stain,-- Berry angioma-- Sturge-Weber syndrome
  40. 40. Deep HemangiomaDeep lesions may only discolor surface
  41. 41. Hemangioma PathophysiologyInfancy lesions:-- Often spontaneously regress-- Later lesions do notSome lesions continue to enlarge-- Until adulthood-- Perhaps even after– No cancer developmentProblems:-- Hemorrhage-- Clots (from stagnant blood)
  42. 42. Intramedullary Hemangioma Endosteal Hemangioma Central sunburst pattern
  43. 43. Hemangioma Treatment Often left aloneChildhood lesions: -- Corticosteroids -- Interferon-α-2aLaser therapy can be effectiveInjection of sclerosing solutions -- Sodium morulate -- 95% ethanol
  44. 44. Hemangioma Look-Alike Lesions HematomaLingual Varicosities (Does not Blanch)Kaposi’s Sarcoma Mucoepidermoid Carcinoma (AIDS) (Blue Color from Mucus)
  45. 45. TraumaticAngiomatous Lesion
  46. 46. Traumatic Angiomatous Lesion Venous Pool; Venous Lake; Venous Aneurysm Acute trauma to subepithelial vein -- With focal dilation or “aneurysm” GAL: – None -- Middle-aged and older -- Lips, buccal Small, painless red bleb – Blanches Micro: single dilated venous structure Perhaps with thrombus (may calcify) Remains indefinitely – Usually remains less than 4 mm – No malignant development Treat: conservative surgical removal OK to leave alone, except for esthetics
  47. 47. Sturge-WeberAngiomatosis
  48. 48. Sturge-Weber Angiomatosis Sturge-Weber Syndrome, Encephalotrigeminal AngiomatosisVascular plexus forms around cephalicpart of neural tube at six weeks-- Regresses after the ninth week-- Doesn’t regress with S-W syndrome– Not inheritedGALP:– None– Congenital– Face, buccal, maxilla-- Rare
  49. 49. Sturge-Weber Angiomatosis Sturge-Weber Syndrome, Encephalotrigeminal Angiomatosis Purple/red macule(s) of face -- Port wine stain -- Nevus flammeus -- Trigeminal nerve distribution, usually Often with involvement of oral mucosa Angiomas of ipsilateral leptomeninges -- May cause seizures --May cause mental retardation Calcifications of gyri
  50. 50. Angiosarcoma
  51. 51. Angiosarcoma Malignant HemangioendotheliomaVascular neoplasm of endotheliumLooks like hemangioma-- More rapid growthNo painDestroys adjacent structuresMets via blood (to lungs)Poor prognosis-- 10-year survival = 21% Hemangioendothelioma-- Histology may look OK-- Can’t predict from micro.
  52. 52. Kaposi Sarcoma
  53. 53. Kaposi Sarcoma In AIDSVascular proliferation (neoplasm?)-- Usually in AIDS-- Non-AIDS cases usually in old meStimulated by herpesvirus 8-- Kaposi’s sarcoma-associated herpesvirusGAL:– Strong male predilection– Young adults and middle-aged– Tongue, lips, gingivaSoft-to-firm red or purple nodule-- May be macular– Painless– Nonhemorrhagic-- May be multiple-- May be lobulated or granular
  54. 54. Kaposi SarcomaHistopathology, Pathophysiology, Treatment Combination of proliferating spindled &endothelial cells – Extravasated erythrocytes – Staghorn clefts (veins)Slowly enlargeNew lesions developing over timeTreat: lesions disappear withsuccessful AIDS treatment -- Protease inhibitors, antivirals, etc.
  55. 55. Kaposi Sarcoma
  56. 56. Lymphangioma
  57. 57. LymphangiomaBenign neoplasm of lymph vesselsHamartoma of lymph vesselsGAL: – None – Children and teenagers – Tongue (produces macroglossia)Soft painless cluster of clear blebsOften with outlying or satellite blebs-- Several mm from main massMay be scattered clear blebs
  58. 58. Lymphangioma HistopathologySame appearance as hemangioma,but without blood in the luminaCavernous type, usuallyPlump endothelial nuclei-- If flat: inactive lesionMay be admixed with blood vesselsNo encapsulation
  59. 59. Lymphangioma Pathophysiology, TreatmentSlowly enlarges with body growthNo spontaneous regression -- As with hemangiomaNo cancer developmentTreat: conservative surgical removal – Usually deliberately leave tumor behind (debulking)Repeat surgery is not uncommon-- Congenital cases: average = 4
  60. 60. Cystic HygromaDevelopmental Cavernous Lymphangioma
  61. 61. Developmental Lymphangioma
  62. 62. Lymphangioma Look-Alike LesionsInflammatory Papillary Hyperplasia (Early, Edematous Lesions) Benign Lymphoid Aggregates
  63. 63. Lymphangiosarcoma
  64. 64. LymphangiosarcomaMalignant neoplasm of lymph vesselsVery rareDysplastic endothelial cellsNo blood in vesselsTreat: radical surgeryPoor prognosis
  65. 65. Lipoma
  66. 66. LipomaBenign neoplasm of fat cellsSome are developmentalGALP:–None– Middle-aged– Buccal, vestibule– Most common soft tissue tumor in the body, but not so common in the mouth– 38th most common mucosal lesion in adults– Prevalence = 3/10,000
  67. 67. Lipoma Clinical FeaturesSessile, yellowish massVery softPainlessEncapsulated: freely movable
  68. 68. Lipoma HistopathologyMicro: mature adipocytes-- With collagen trabeculaeMay or may not be encapsulatedMay “infiltrate” great distancesinto surrounding stromaSometimes admixed with fibrous tissue (fibrolipoma)Problem: herniated buccal fat pad
  69. 69. Lipoma Pathophysiology, TreatmentSlowly enlargeUsually remain < 3 cm.No malignant transformationTreat: conservative surgical excision– Usually do not recur, except the infiltrating types
  70. 70. Familial LipomatosisPhoto: Dr. J. Bouquot, University of Texas, Houston, Texas
  71. 71. Traumatic Neuroma
  72. 72. Traumatic NeuromaReactive proliferation of neural tissue-- After nerve injuryGAL:-- None-- Middle-aged-- Mental foramenSmooth-surfaced noduleSoft, nonulceratedLess than half are tender or painful, may be burningMicro: Intertwining, tortuous nerve fibers in a fibrous stromaUsually remain less than 1 cm.; no malignant transformationTreat: conservative surgical excision-- With small part of affected nerveMay lead to paresthesia and painMay recur
  73. 73. Neurofibroma
  74. 74. NeurofibromaBenign neoplasm of Schwann cells-- And perineural fibroblastsGALP:– None– Young adults– Tongue, buccal– The most common peripheral nerve tumor-- 1/1,000 adultsSmooth-surfaced soft, nonulcerated nodulePainlessMay be huge and pendulous
  75. 75. Neurofibroma In Inferior Alveolar CanalPhoto: Dr. J. Bouquot, University of Texas, Houston, Texas
  76. 76. NeurofibromaWell circumscribed interlacing bundlesof spindle-shaped cells with wavy nuclei-- In a fibrous stromaUsually < 2 cm.-- May become hugeOral lesions seldom become malignant -- Less likely than skin lesionsTreat: conservative surgical excision– Recurrence is rare
  77. 77. Schwannoma
  78. 78. Schwannoma NeurilemmomaBenign neoplasm of Schwann cellsGALP:– None– Young adults and middle-aged– Tongue, hard palate– Up to half occur in head and neck areaSmooth, soft noduleNonulceratedPainlessMoveableNormal color or yellowish white
  79. 79. Schwannoma HistopathologyEncapsulatedTwo tissue types:– Antoni A: streaming fascicles of spindle Schwann cells forming Verocay bodies– Antoni B: disorganized neurites in loose fibrous stroma
  80. 80. Schwannoma Pathophysiology, TreatmentUsually remain less than 2 cmOral lesions seldom become malignantSkin lesions can but it is uncommonTreat: conservative surgical excision– Recurrence is rare
  81. 81. Neurofibrosarcoma
  82. 82. NeurofibrosarcomaMalignant Peripheral Nerve Sheath TumorDysplastic spindle cellsFew recognizable nervesTreat: radical surgery5-year survival = 40-50%
  83. 83. Neurofibromatosis
  84. 84. von Recklinghausen Neurofibromatosis Multiple Endocrine Neoplasia I (MEN I) Multiple neurofibromas -- Some schwannomas -- Throughout body -- Maybe hundreds -- Oral lesions in 1/4 of cases Autosomal dominant inheritance -- Gene is on chromosome 17
  85. 85. von Recklinghausen Neurofibromatosis Multiple Endocrine Neoplasia I (MEN I) Café au lait spots (brown skin patches) Abnormal bone development Lisch nodules (brown spots on iris) 5-10% chance of malignant development -- Usually neurofibrosarcoma (malignant peripheral nerve sheath tumor)
  86. 86. Multiple MucosalNeuroma Syndrome
  87. 87. Multiple Endocrine Neoplasia IIBMultiple Mucosal Neuroma Syndrome; MEN III Autosomal dominant inherited disease -- Multiple tumors or hyperplasias of neuroendocrine tissues Mutation of RET protooncogene -- On chromosome 10 GALP: – None – Teenagers and young adults – Tongue, lips -- Rare
  88. 88. Multiple Endocrine Neoplasia IIB Clinical Features Sessile, soft nodules -- Smooth-surfaced -- Painless -- Yellowish white -- Moveable Oral signs: often first evidence of disease Narrow face
  89. 89. Multiple Endocrine Neoplasia IIB Clinical Features Long extremities Abraham Lincoln appearance Weak muscles Pheochromocytomas (50%) Medullary thyroid carcinomas (90%) Elevated serum and urinary calcitonin -- From thyroid tumor Elevated urinary vanillylmandelic acid (VMA) Increased epinephrine-to-norepinephrine ratio -- From adrenal tumor
  90. 90. Multiple Endocrine Neoplasia IIBHistopathology, Pathophysiology, Treatment Micro: intertwining, tortuous nerve fibers -- Thick perineurium -- Spaces (artifactual) around nerves Oral neuromas remain small -- Less than 5 mm Oral neuromas do not become malignant Treat: no treatment needed for oral lesions -- Except for esthetics Treat systemic problems and tumors prn
  91. 91. NeuroectodermalTumor of Infancy
  92. 92. Neuroectodermal Tumor of Infancy Progonoma; Retinal Anlage Tumor Neoplasm of neural crest cells GALP: – None – Infancy; newborns – Anterior maxillary alveolus – Very rare Rapidly expanding blue/black painless mass Usually destroys underlying bone Elevated urinary vanillylmandelic acid (VMA) -- From oral tumor
  93. 93. Neuroectodermal Tumor of Infancy Histopathology Micro: two cell types: – Small dark round neuroblastic cells – Large epithelioid cells with melanin
  94. 94. Neuroectodermal Tumor of Infancy Pathophysiology, Treatment May reach alarming size May destroy anterior alveolar bone Malignant variants (very rare) Treat: Moderately severe surgical excision – 15% recurrence
  95. 95. Granular Cell Tumor
  96. 96. Granular Cell Tumor Granular Cell MyoblastomaBenign neoplasm of Schwann cellsOriginally thought to be fromstriated muscle cellsGALP:– 2x females– Fourth-sixth decades– Tongue-- 50% of all body cases are oralSessile mass-- Painless-- Firm-- Pale
  97. 97. Granular Cell TumorGranular Cell Myoblastoma (Schwann Cell Origin)
  98. 98. Granular Cell Tumor Histopathology Large, polygonal cells-- Like histiocytes-- Granular cytoplasm-- Small nucleiIn sheets and globulesMay be spindled cellsNot encapsulated
  99. 99. Granular Cell Tumor HistopathologyMay infiltrate between muscle fibersProblem:-- Pseudoepitheliomatous hyperplasia-- Mimics squamous cell carcinoma
  100. 100. Granular Cell Tumor Pathophysiology, TreatmentUsually remain 1-2 cm.Seldom enlarge after initial noticeNo malignant transformation riskTreat: conservative surgical excision-- Recurrence is very rare
  101. 101. Granular Cell Epulis
  102. 102. Granular Cell Epulis Congenital EpulisDevelopmental tumor of unknown histogenesisGAL: – 90% females – Newborn – Anterior maxillary alveolusPedunculated, soft, noduleSmooth-surfacedPink or pale
  103. 103. Granular Cell Epulis HistopathologyLarge, polygonal cells-- Granular cytoplasmLike cells in granular cell tumor-- But different immunohistochemistryAtrophic epithelium-- No pseudoepitheliomatous hyperplasia
  104. 104. Granular Cell Epulis Pathophysiology, TreatmentUsually remains less than 2 cm-- May become up to 9 cmTreat: conservative surgical excision-- As soon as baby can tolerate surgery– Does not recurIf left untreated: small lesions shrink-- Often disappear-- Does not interfere with tooth eruption
  105. 105. Leiomyoma
  106. 106. LeiomyomaBenign neoplasms ofsmooth muscleGALP:– None– Infancy or childhood– Tongue, lips– Very rareUsually sessile, firm, painless massNormal surface color and smooth surfaceMicro: cellular proliferations of smooth muscle cellsUsually encapsulatedUsually remain less than 2 cm.No cancer transformationTreat: conservative surgical removal – Few recurrences
  107. 107. Leiomyosarcoma
  108. 108. LeiomyosarcomaMalignant neoplasm ofsmooth muscleEtiology: unknownGALP:-- None-- Young adults & middle age-- No location predilection-- RareLobulated massRelatively firmMay be ulcerated
  109. 109. LeiomyosarcomaHistopathology, TreatmentDysplastic spindle cells-- blunt, cigar-shaped nucleiTreat: radical surgeryOverall: poor prognosisHigh grade = worse prognosis
  110. 110. Rhabdomyoma
  111. 111. RhabdomyomaBenign neoplasmof striated muscleEtiology: unknownGAL:– None– Infancy or childhood– Tongue, lips– Very rareUsually sessile, firm, painless massNormal surface color and smooth surface
  112. 112. RhabdomyomaMicro: cellular proliferationsof striated muscle cells-- Usually encapsulatedUsually remain less than 2 cm.No cancer transformationTreat: conservative surgical removal– Few recurrences
  113. 113. Rhabdomyosarcoma
  114. 114. RhabdomyosarcomaMalignant neoplasm ofstriated muscleGALP:-- None-- Childhood/young adults-- Tongue-- RareFirm massOften lobulatedSometimes ulcerated
  115. 115. Rhabdomyosarcoma HistopathologyDysplastic striate muscle cellsEmbryonal typeAlveolar typeTreat: radical surgery70% 5-year survival
  116. 116. Choristoma
  117. 117. Cartilaginous Choristoma Soft Tissue ChondromaTumor-like proliferation of normal cartilage-- But in wrong placeGAL:– None– Teens and young adults (probably started much earlier)– TongueSessile, firm, painless mass with normal surface color or pallorMicro: Normal cartilage (hyaline or fibrous) in a fibrous stroma
  118. 118. Cartilaginous Choristoma Soft Tissue Chondroma Usually remain 1-2 cm No cancer transformation Treat: conservative surgical removal– No recurrence Special variant: Cutright tumor:– Presumably secondary to continuing, low-level trauma– Older persons– Anterior maxillary alveolar midline– Firm, sessile nodule under denture– Treat: conservative surgical removal and fix denture (seldom recurs)
  119. 119. Osseous Choristoma Soft Tissue OsteomaTumor-like proliferation of normal bone -- But in wrong placeGALP:– None– Teens and young adults (probably started much earlier)– Tongue-- RareSessile, firm massNormal surface color or pallorPainlessMicro: Normal but immature bone-- Perhaps with marrow-- In fibrous stromaUsually remain 1-2 cmNo cancer transformationTreat: conservative surgical removal– No recurrence
  120. 120. Metastasisto the Mouth
  121. 121. Metastasis to the MouthMetastatic spread from extraoral source-- Almost always carcinomaUsually from lung, breast and GIGALP:– Moderate male predilection– Middle-aged and older– Gingiva, tongue-- 1-2% of all oral cancersFirm, smooth-surface nodule-- Often with normal colorOften ulceratedMay be painfulMay destroy bone
  122. 122. Metastasis to the MouthMicro: same appearance as primary cancerEnlarge rapidlyEventually with surface ulceration, painTreat:-- Radical surgical excision-- Radiotherapy-- Chemotherapy– Depends on condition of the primary tumor-- Depends on other metastases