chap 2 legends

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Leukoplakia Figure 2.7. Speckled leukoplakia. This mixed white and red lesion of the buccal mucosa showed moderate epithelial dysplasia (Courtesy of: Dr Crispian Scully). Pg 127 Tobacco pouch keratosis Figure 2-10. Tobacco pouch keratosis. A white, wrinkled change of the mucosa in the mandibular buccal vestibule secondary to the use of chewing tobacco. Pg 136 (Courtesy of: Drs. Regazi JA, Sciubba JJ, Pogrel MA ) Oral submucous fibrosis (OSF) Figure 2-11. Advanced OSF with difficulty in mouth opening. Note the bilateral pouching in of cheek while opening mouth. Pg 137 Figure 2-12 A. Advanced OSF. Horizontal fibrosis traversing at the junction of hard and soft palate. Pg 137 Figure 2-12 B. Advanced OSF. Involvement of pterygomandibular raphae compounding the difficulty of mouth opening. Pg 137 Figure 12-2 C. Carcinoma developed on the palate. Pg 137 Figure 2-13. Advanced stage with fibrosis of lamina propria and submucosa Van-Gieson stain. Pg 139 Figure 2-14. Early OSF. Note the sparing of lamina propria from fibrosis Van-Gieson stain. Pg 139

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Page 1: CHAP 2 Legends

Leukoplakia

Figure 2.7. Speckled leukoplakia. This mixed white and red lesion of the buccal mucosa showed moderate epithelial dysplasia (Courtesy of: Dr Crispian Scully). Pg 127

Tobacco pouch keratosis

Figure 2-10. Tobacco pouch keratosis. A white, wrinkled change of the mucosa in the mandibular buccal vestibule secondary to the use of chewing tobacco. Pg 136(Courtesy of: Drs. Regazi JA, Sciubba JJ, Pogrel MA )

Oral submucous fibrosis (OSF)Figure 2-11. Advanced OSF with difficulty in mouth opening. Note the bilateral pouching in of cheek while opening mouth. Pg 137

Figure 2-12 A. Advanced OSF. Horizontal fibrosis traversing at the junction of hard and soft palate. Pg 137

Figure 2-12 B. Advanced OSF. Involvement of pterygomandibular raphae compounding the difficulty of mouth opening. Pg 137

Figure 12-2 C. Carcinoma developed on the palate. Pg 137

Figure 2-13. Advanced stage with fibrosis of lamina propria and submucosaVan-Gieson stain. Pg 139

Figure 2-14. Early OSF. Note the sparing of lamina propria from fibrosisVan-Gieson stain. Pg 139

Epidermoid carcinoma

Figure 2-21. Increased number of mitotic figures per field.(H&E stain). Pg 149

Figure 2-22. Squamous cell carcinoma with spindle metaplastic features. Pg 150

Figure 2-26 A to C. Epidermoid carcinoma of the tongue, early to advanced. Pg 157

Figure 2-27. Epidermoid carcinoma of the floor of the mouth. Pg 158

Figure 2-30. Epidermoid carcinoma of the palate. Pg 162

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Malignant melanoma

Figure 2-34 A to C. Typical lesions involve the palate and alveolar ridge. Pg 175

Figure 2-35. Advanced OSF withhigh Ag NOR count Pg 176

Giant cell tumor

Figure 2-45. Giant cell tumor.Typical appearance of a benign giant cell tumor. Giant cellswith varying numbers of nuclei are arranged more or lessuniformly within a background of mononuclear cells.(Courtesy of Dr KK Unni.) Pg 191

Nasopharyngeal angiofibroma

Figure 2-53. Sturge-Weber syndrome.A, The unilateral distribution of angiomatous malformations which never crosses the midline is pathognomic of the syndrome.B, Unilateral involvement of palate with angiomatous malformation. Pg 205

Figure 2-54. Nasopharyngeal angiofibroma.The dense fibrous quality of the stroma and the numerousthin-walled vessels are characteristic of this entity.(Courtesy of Dr Juan Rosai.) Pg 206

Osteoid Osteoma

Figure 2-59. Osteoid osteoma.This is the central nidus of an osteoid osteoma composedof irregular reactive new bone. Pg 215

Fibrosarcoma Figure 2-65. Low power appearance of well-differentiatedfibrosarcoma. The tumor has a monotonoushypercellular look with regimentation of nuclei. Mitoticfigures are common. Pg 221

Figure 2-66. Fibrosarcoma showing moderate degreeof nuclear pleomorphism. Pg 221

Benign fibrous histiocytoma Figure 2-67. Benign fibrous histiocytoma of cheek(intraoperative view).Pg 224

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Liposarcoma

Figure 2-68. Liposarcoma.Numerous tumor giant cells and malignant cells showingfeatures of lipoblasts. (Courtesy of Dr Juan Rosai.) Pg 227

HemangiopericytomaFigure 2-70. Dilated, thin-walled vessels as shown hereare common. These vessels simulate ‘stag horns’ thatare often associated with hemangiopericytoma. Pg 230

Kaposi’s sarcoma

Figure 2-71Kaposi’s sarcoma. Pg 232

Figure 2-72Immunoreactivity for Factor VIII-related antigen in Kaposi’s sarcoma(courtesy of: Dr Juan Rosai). Pg 233

Ewing's sarcoma

Figure 2-73Ewing's sarcoma is one of the "small round blue cell" tumors histologically. Note the many mitotic figures in the field. Pg 234

Chondrosarcoma Figure 2-76This is the low power microscopic appearance of a chondrosarcoma. The tissue is recognizable as cartilage, and there are chondrocytes in clear spaces, but there is no orderly pattern. At the bottom, this neoplasm can be seen invading and destroying bone. Pg 239

Osteosarcoma of the maxilla Figure 2-78Osteosarcoma of the maxilla.(courtesy of: Dr. Twinkle S. Prasad). Pg 242

Figure 2-80The neoplastic spindle cells of osteosarcoma are seen to be making pink osteoid here. Osteoid production by a sarcoma is diagnostic of osteosarcoma. Pg 244

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Non-Hodgkin’s lymphoma Figure 2-84Follicular non-Hodgkin’s lymphoma. Pg 251

Burkitt lymphoma Figure 2-87Burkitt lymphoma presenting as a large tumour of the jaw in an African child.(Courtesy of: WHO, World Cancer Report.2003) Pg 255

Figure 2-88“Starry sky” appearance of Burkitt’s lymphoma. (Courtesy of: K.W. Lee). Pg 256

Hodgkin's diseaseFigure 2-90. Reed-Sternberg cell.Cells with large, pale nuclei containing purple nucleoli atthe arrowheads. These are Reed-Sternberg cells that areindicative of Hodgkin’s disease. Most of the cellular contentof foci of Hodgkin’s disease consists of reactive lymphoidcells. Pg 258

Multiple Myeloma

Figure 2-92 AMultiple Myeloma: At low power, the abnormal plasma cells of multiple myeloma fill the marrow. Pg 262

Figure 2-92 BMultiple Myeloma: At medium power, the plasma cells of multiple myeloma here are very similar to normal plasma cells, but they may also be poorly differentiated. Usually, the plasma cells are differentiated enough to retain the function of immunoglobulin production. Thus, myelomas can be detected by an immunoglobulin "spike" on protein electrophoresis, or the presence of Bence-Jones proteins (light chains) in the urine. Immunoelectrophroesis characterizes the type of monoclonal immunoglobulin being produced. Pg 262

Figure 2-92 CMultiple Myeloma: Here is a smear of bone marrow aspirate from a patient with multiple myeloma. Note that there are numerous plasma cells with eccentric nuclei and a perinuclear halo of clearer cytoplasm. Pg 262

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Figure 2-92 DMultiple Myeloma:The rounded "punched out" lesions of multiple myeloma appear as lucent areas with this skull radiograph. Pg 262

Leiomyosarcoma

Figure 2-96Leiomyosarcoma of oral cavity. Note the prominent cytoplasmic vacuoles indenting to the nuclear poles. Pg 271(Courtesy of: Dr Juan Rosai)

Neurofibromas

Figure 2-101 CMultiple neurofibromas of the face. Pg 281

Figure 2-101 DNeurofibromatosis showing spindled, wavy nuclei in fascicular form. Pg 281

Figure 2-102. Plexiform neurofibroma of the gingiva.Abundant nerve tissue in fascicles and collagenous fibrousstroma in ordered arrangement. Pg 282

Malignant peripheral nerve sheath tumor

Figure 2-105Pigmented neuroectodermal tumour of infancy. The neoplastic islands located between the bone trabeculae contain abundant melanin pigment. Pg 287

Metastatic carcinoma of the lower jaw

Figure 2-107 A. Metastatic carcinoma of the lower alveolus. Pg 290

Figure 2-107 B. Primary from prostate. Pg 290

Figure 2-107 C. An osteolytic lesion of the mandible. Pg 290

Figure 2-107 D. Photomicrograph of metastatic carcinoma of the alveolus. Pg 290

Page 6: CHAP 2 Legends