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A palatal mass in an immunocompromised patient Jeffrey Hajibandeh and Louis Mandel JADA 2014;145(1):66-69 10.14219/jada.2013.5 The following resources related to this article are available online at jada.ada.org (this information is current as of June 28, 2014): Updated information and services including high-resolution figures, can be found in the online version of this article at: http://jada.ada.org/content/145/1/66
This article cites 10 articles, 1 of which can be accessed free: http://jada.ada.org/content/145/1/66/#BIBL Information about obtaining reprints of this article or about permission to reproduce this article in whole or in part can be found at: http://www.ada.org/990.aspx
Copyright © 2014 American Dental Association. All rights reserved. Reproduction or republication strictly prohibited without prior written permission of the American Dental Association.
Downloaded from jada.ada.org on June 28, 2014
ORIGINAL CONTRIBUTIONS
DIAGNOSTIC CHALLENGE
A palatal mass in an immunocompromised patient THE CHALLENGE
A
Jeffrey Hajibandeh, BS; Louis Mandel, DDS
53-year-old man visited the Division of Oral and Maxillofacial Surgery at Columbia University College of Dental Medicine because he had a seven-month history of a progressively enlarging growth on the left palate (Figure 1). The patient stated that the lesion caused some discomfort and occasionally bled. His medical history was significant only for the presence of human immunodeficiency virus (HIV) and hepatitis C, for which he inconsistently sought out antiretroviral therapy and medical care. When we examined the patient, his CD4 count was 139 cells per milliliter, and he had a viral load of 163,000 copies/mL. When we conducted an oral examination, we found a lobulated exophytic proliferation in the left palate that involved the maxillary molar area and measured approximately 5 × 3 centimeters. The growth was sessile, erythematous and had well-demarcated borders. When we conducted an oral examination, we found a lobulated exophytic proliferation on the left palate that involved the maxillary molar area and measured approximately 5 × 3 centimeters. The growth was sessile and erythematous and had well-demarcated borders. We also noted that the proliferative tissue involved the edentulous ridge in the maxillary left second molar area and the adjoining buccal soft tissues. Radiographically, alveolar bone loss was extensive in the maxillary left molar region (Figure 2). The maxillary left first and third molars were mobile, and the second molar was missing. We biopsied the lesion, and when we looked at the specimen microscopically, we saw masses of large monomorphic cells (Figure 3).
66 JADA 145(1)
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January 2014
Copyright © 2014 American Dental Association. All Rights Reserved.
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ORIGINAL CONTRIBUTIONS
Figure 1. Clinical view of proliferative lesion in maxillary left molar area.
Figure 2. Periapical radiograph showing extensive alveolar bone loss around maxillary left molars.
Figure 3. Microscopic appearance of the excised specimen. Intact surface epithelium covers a monomorphic mass of cells (hematoxylin-eosin, ×200 magnification).
Can you make the diagnosis? A. peripheral ossifying fibroma B. Kaposi sarcoma C. plasmablastic lymphoma
D. pyogenic granuloma E. squamous cell carcinoma
JADA 145(1)
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Copyright © 2014 American Dental Association. All Rights Reserved.
January 2014 67
Downloaded from jada.ada.org on June 28, 2014
ORIGINAL CONTRIBUTIONS
THE DIAGNOSIS
Malignant plasmablastic lymphoma (PBL), first described by Delecluse and colleagues,1 is an uncommon variant of a non-Hodgkin large B-cell lymphoma. PBL usually occurs in the oral cavity of immunosuppressed patients with HIV who have CD4 cell counts that are less than 200 cells/mL and serologic viral copies of more than 100,000 cells/mL.2 However, PBL also can occur extraorally in the gastrointestinal tract, skin, lungs and nasopharynx in immunosuppressed patients who have received a transplant and even in immunocompetent patients.3 PBL has a rapid and aggressive course, and 47 percent of people with PBL survive less than one year.4 Clinically, PBL usually involves the gingival or palatal mucosa of middle-aged HIV-positive men. The growth often infiltrates alveolar bone such that the resulting bone loss mimics periodontal disease. Surface mucosal ulceration of the rapidly growing exophytic mass may develop, and some pain may be present. The diagnosis of a PBL cannot be based only on its clinical features. The histopathologic study of a biopsy specimen combined with the results of a cellular immunohistochemistry study are essential elements in making a definitive diagnosis. Microscopically, PBL consists of large monomorphic round neoplastic cells that resemble B-cell immunoblasts, but the cells have a plasma cell phenotype. Individual cells have an abundant basophilic cytoplasm with eccentrically placed nuclei containing prominent centrally located nucleoli. Active mitosis and necrosis may be present. The critical element in diagnosing PBL is the identification of the cell’s surface markers by means of an immunohistochemistry study. Unlike the B-cell immunoblast, plasmablasts fail to express the leukocyte common antigen CD45 and the B-cell marker CD20.2 The plasmablasts, however, will stain positively for the plasma cell markers CD38, CD138 and MUM-1, thus indicating a phenotype compatible with plasma cells.2 This pattern of markers is exactly what we found in the results of an immunohistochemical study of our patient’s biopsy specimen and led to our making the final diagnosis. In addition, the tumor cells we biopsied from the patient demonstrated immunoreactivity for antibodies directed against the Epstein-Barr virus. The results of testing for Epstein-Barr virus are positive in 75 percent of patients who have PBL.4 We referred the patient to an oncologist for therapeutic attention, but we lost him to follow-up. Treatment outcomes for patients with PBL are poor. After excision of the oral mass, standard therapy involves the use of 68 JADA 145(1)
http://jada.ada.org
chemotherapeutic agents, radiotherapy or both. Some improvement in the patient’s life span may be obtained with the adjunctive use of highly active antiretroviral therapy. Regardless, the outcome is grim. DIFFERENTIAL DIAGNOSIS
Peripheral ossifying fibroma. Peripheral ossifying fibroma (POF) is a benign reactive inflammatory hyperplasia that causes a gingival enlargement and probably originates from chronic irritation of the labile periodontal ligament. The irritation may be caused by calculus, rough restorations, ill-fitting crowns or dental appliances. POF represents 9.6 percent of all biopsied gingival lesions; women between the ages of 25 and 35 years are most susceptible.5 More than 50 percent of POFs occur in the anterior maxilla and involve the interdental gingival papilla. An exophytic POF usually measures less than 1.5 cm; is slow growing, firm and painless; and has an intact overlying normal mucosa. Occasionally, painful ulcerations may develop. A POF can be either a sessile or a pedunculated growth. Calcified areas may be noted radiographically. Generally, no alveolar bone destruction is observed. A confirmatory diagnosis of POF can be made only by means of microscopic examination of excised tissue. The surface epithelium may be intact or ulcerated. The presence of a cellular fibrous tissue stroma, some inflammatory cells, a varying endothelial proliferation and most importantly mineralized material representing dystrophic calcification or bone deposition can be used to confirm the histologic diagnosis of POF. Kaposi sarcoma. Kaposi sarcoma (KS) is a multicentric angioproliferative disorder of vascular endothelial origin that affects primarily mucocutaneous tissue. AIDS-associated KS (AIDS-KS) is the most common variant of this disorder.6 Approximately 71 percent of patients with AIDS-KS will develop oral lesions in association with KS-related systemic lesions, whereas in 22 percent of patients, the disease initially develops in the mouth.7 There may be one or multiple oral lesions, and they usually begin as macules and progress to papules and nodules that eventually coalesce to form large exophytic masses. Characteristically, the lesion’s color varies from deep red to blue-purple. The sessile or pedunculated KS growths most frequently involve the hard palate and gingiva. They tend to be painless and bleed easily, and they can become ulcerated. Histologically, KS is recognized by the presence of spindle-shaped tumor cells, angiogenesis, an inflammatory infiltrate of
January 2014
Copyright © 2014 American Dental Association. All Rights Reserved.
Downloaded from jada.ada.org on June 28, 2014
ORIGINAL CONTRIBUTIONS
mononuclear cells, extravasated erythrocytes and edema. Because KS has a vascular origin, immunohistochemistry study results will feature endothelial markers rather than markers associated with PBL. Furthermore, human herpesvirus 8 is a common serologic finding in patients with AIDS-KS.8 Pyogenic granuloma. Pyogenic granuloma (PG) is an exuberant soft-tissue response and vascular proliferation resulting from a chronic low-grade inflammation caused by a chronic irritant, trauma or hormonal factors.9 In many instances, poor oral hygiene is a predisposing factor. The anterior maxillary gingiva in young females is the most frequent site of origin. A smooth or lobulated exophytic localized nodular lesion on a pedunculated or sessile base, measuring from a few millimeters to several centimeters, usually can be observed. PG has a soft consistency that can become firm when mature. It also can bleed easily and is reddish. Histologically, the surface epithelium usually is intact, but foci of ulceration may be noted. An edematous vascular stroma with capillary proliferation, hemorrhage and chronic inflammatory cells is present. Squamous cell carcinoma. Squamous cell carcinoma (SCC) is an epithelial malignancy that involves an invasion of altered squamous cells into the supporting connective tissue and adjacent structures. SCC represents approximately 90 percent of all oral carcinomas and occurs most frequently in men older than 45 years who have tobacco and alcohol risk factors.10 The floor of the mouth and tongue are common sites, whereas the hard palate is involved infrequently. There is a great variation in the appearance of SCC, but it usually manifests as an exophytic irregularly shaped fixated lesion with a rough pebbly surface that is pink or red with a varied interspersed amount of white keratin. Cellular proliferation may result in a centrally depressed ulceration with a peripheral rolled border. Histologically, sheets and nests of hyperchromatic cells with an apparent squamous epithelial origin are seen. Epithelial pearls, keratinized cells, large nuclei, nuclear pleomorphism and mitotic figures are evident.
CONCLUSION
We have presented a case of an immunocompromised patient with HIV who had a PBL. The diagnosis of this rare oral malignancy can be made only when its clinical and histologic features are considered along with the results of a cellular immunohistochemistry study showing the characteristic surface markers that identify the neoplastic cells as having plasma cell phenotypes. It is this microscopic appearance that differentiates PBL from clinically similar proliferations. n
doi:10.14219/jada.2013.5
Mr. Hajibandeh is a research assistant and a senior student, Columbia University College of Dental Medicine, New York City. Dr. Mandel is the director, Salivary Gland Center, and the associate dean and a professor, Division of Oral and Maxillofacial Surgery, Columbia University College of Dental Medicine, New York City. Address correspondence to Dr. Mandel at Columbia University College of Dental Medicine, 630 W. 168th St., New York, N.Y. 10032, e-mail [email protected]. Disclosure. Mr. Hajibandeh and Dr. Mandel did not report any disclosures. Diagnostic Challenge is published in collaboration with the American Academy of Oral and Maxillofacial Pathology and the American Academy of Oral Medicine. 1. Delecluse HJ, Anagostopoulos I, Dallenbach F, et al. Plasmablastic lymphomas of the oral cavity: a new entity associated with the human immunodeficiency virus infection. Blood 1997;89(4):1413-1420. 2. Bagul N, Mamatha GS, Mahalle A. Plasmablastic lymphoma of gingiva mimicking a reactive lesion: a case report (published online Sept. 13, 2012). Case Rep Dent 2012;2012:259307. doi:10.1155/2012/259307. 3. Rafaniello Raviele P, Pruneri G, Maiorano E. Plasmablastic lymphoma: a review. Oral Dis 2009;15(1):38-45. 4. Riedel DJ, Gonzalez-Cuyar LF, Zhao XF, Redfield RR, Gilliam BL. Plasmablastic lymphoma of the oral cavity: a rapidly progressive lymphoma associated with HIV infection. Lancet Infect Dis 2008;8(4):261-267. 5. Walters JD, Will JK, Hatfield RD, Cacchillo DA, Raabe DA. Excision and repair of the peripheral ossifying fibroma: a report of 3 cases. J Periodontol 2001;72(7):939-944. 6. Fatahzadeh M. Kaposi sarcoma: review and medical management update (published correction appears in Oral Surg Oral Med Oral Pathol Oral Radiol 2012;113[5]:708). Oral Surg Oral Med Oral Pathol Oral Radiol 2012;113(1):2-16. 7. Lager I, Altini M, Coleman H, Ali H. Oral Kaposi’s sarcoma: a clinicopathologic study from South Africa. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2003;96(6):701-710. 8. Pantanowitz L, Khammissa RA, Lemmer J, Feller L. Oral HIV-associated Kaposi sarcoma. J Oral Pathol Med 2013;42(3):201-207. 9. Gordón-Núñez MA, de Vasconcelos Carvalho M, Benevenuto TG, Lopes MF, Silva LM, Galvão HC. Oral pyogenic granuloma: a retrospective analysis of 293 cases in a Brazilian population. J Oral Maxillofac Surg 2010;68(9):2185-2188. 10. Ram H, Sarkar J, Kumar H, Konwar R, Bhatt ML, Mohammad S. Oral cancer: risk factors and molecular pathogenesis. J Oral Maxillofac Surg 2011;10(2):132-137.
JADA 145(1)
http://jada.ada.org
Copyright © 2014 American Dental Association. All Rights Reserved.
January 2014 69
A palatal mass in an immunocompromised patient Jeffrey Hajibandeh and Louis Mandel JADA 2014;145(1):66-69 10.14219/jada.2013.5 The following resources related to this article are available online at jada.ada.org (this information is current as of June 28, 2014): Updated information and services including high-resolution figures, can be found in the online version of this article at: http://jada.ada.org/content/145/1/66
This article cites 10 articles, 1 of which can be accessed free: http://jada.ada.org/content/145/1/66/#BIBL Information about obtaining reprints of this article or about permission to reproduce this article in whole or in part can be found at: http://www.ada.org/990.aspx
Copyright © 2014 American Dental Association. All rights reserved. Reproduction or republication strictly prohibited without prior written permission of the American Dental Association.
Downloaded from jada.ada.org on June 28, 2014
ORIGINAL CONTRIBUTIONS
DIAGNOSTIC CHALLENGE
A palatal mass in an immunocompromised patient THE CHALLENGE
A
Jeffrey Hajibandeh, BS; Louis Mandel, DDS
53-year-old man visited the Division of Oral and Maxillofacial Surgery at Columbia University College of Dental Medicine because he had a seven-month history of a progressively enlarging growth on the left palate (Figure 1). The patient stated that the lesion caused some discomfort and occasionally bled. His medical history was significant only for the presence of human immunodeficiency virus (HIV) and hepatitis C, for which he inconsistently sought out antiretroviral therapy and medical care. When we examined the patient, his CD4 count was 139 cells per milliliter, and he had a viral load of 163,000 copies/mL. When we conducted an oral examination, we found a lobulated exophytic proliferation in the left palate that involved the maxillary molar area and measured approximately 5 × 3 centimeters. The growth was sessile, erythematous and had well-demarcated borders. When we conducted an oral examination, we found a lobulated exophytic proliferation on the left palate that involved the maxillary molar area and measured approximately 5 × 3 centimeters. The growth was sessile and erythematous and had well-demarcated borders. We also noted that the proliferative tissue involved the edentulous ridge in the maxillary left second molar area and the adjoining buccal soft tissues. Radiographically, alveolar bone loss was extensive in the maxillary left molar region (Figure 2). The maxillary left first and third molars were mobile, and the second molar was missing. We biopsied the lesion, and when we looked at the specimen microscopically, we saw masses of large monomorphic cells (Figure 3).
66 JADA 145(1)
http://jada.ada.org
January 2014
Copyright © 2014 American Dental Association. All Rights Reserved.
Downloaded from jada.ada.org on June 28, 2014
ORIGINAL CONTRIBUTIONS
Figure 1. Clinical view of proliferative lesion in maxillary left molar area.
Figure 2. Periapical radiograph showing extensive alveolar bone loss around maxillary left molars.
Figure 3. Microscopic appearance of the excised specimen. Intact surface epithelium covers a monomorphic mass of cells (hematoxylin-eosin, ×200 magnification).
Can you make the diagnosis? A. peripheral ossifying fibroma B. Kaposi sarcoma C. plasmablastic lymphoma
D. pyogenic granuloma E. squamous cell carcinoma
JADA 145(1)
http://jada.ada.org
Copyright © 2014 American Dental Association. All Rights Reserved.
January 2014 67
Downloaded from jada.ada.org on June 28, 2014
ORIGINAL CONTRIBUTIONS
THE DIAGNOSIS
Malignant plasmablastic lymphoma (PBL), first described by Delecluse and colleagues,1 is an uncommon variant of a non-Hodgkin large B-cell lymphoma. PBL usually occurs in the oral cavity of immunosuppressed patients with HIV who have CD4 cell counts that are less than 200 cells/mL and serologic viral copies of more than 100,000 cells/mL.2 However, PBL also can occur extraorally in the gastrointestinal tract, skin, lungs and nasopharynx in immunosuppressed patients who have received a transplant and even in immunocompetent patients.3 PBL has a rapid and aggressive course, and 47 percent of people with PBL survive less than one year.4 Clinically, PBL usually involves the gingival or palatal mucosa of middle-aged HIV-positive men. The growth often infiltrates alveolar bone such that the resulting bone loss mimics periodontal disease. Surface mucosal ulceration of the rapidly growing exophytic mass may develop, and some pain may be present. The diagnosis of a PBL cannot be based only on its clinical features. The histopathologic study of a biopsy specimen combined with the results of a cellular immunohistochemistry study are essential elements in making a definitive diagnosis. Microscopically, PBL consists of large monomorphic round neoplastic cells that resemble B-cell immunoblasts, but the cells have a plasma cell phenotype. Individual cells have an abundant basophilic cytoplasm with eccentrically placed nuclei containing prominent centrally located nucleoli. Active mitosis and necrosis may be present. The critical element in diagnosing PBL is the identification of the cell’s surface markers by means of an immunohistochemistry study. Unlike the B-cell immunoblast, plasmablasts fail to express the leukocyte common antigen CD45 and the B-cell marker CD20.2 The plasmablasts, however, will stain positively for the plasma cell markers CD38, CD138 and MUM-1, thus indicating a phenotype compatible with plasma cells.2 This pattern of markers is exactly what we found in the results of an immunohistochemical study of our patient’s biopsy specimen and led to our making the final diagnosis. In addition, the tumor cells we biopsied from the patient demonstrated immunoreactivity for antibodies directed against the Epstein-Barr virus. The results of testing for Epstein-Barr virus are positive in 75 percent of patients who have PBL.4 We referred the patient to an oncologist for therapeutic attention, but we lost him to follow-up. Treatment outcomes for patients with PBL are poor. After excision of the oral mass, standard therapy involves the use of 68 JADA 145(1)
http://jada.ada.org
chemotherapeutic agents, radiotherapy or both. Some improvement in the patient’s life span may be obtained with the adjunctive use of highly active antiretroviral therapy. Regardless, the outcome is grim. DIFFERENTIAL DIAGNOSIS
Peripheral ossifying fibroma. Peripheral ossifying fibroma (POF) is a benign reactive inflammatory hyperplasia that causes a gingival enlargement and probably originates from chronic irritation of the labile periodontal ligament. The irritation may be caused by calculus, rough restorations, ill-fitting crowns or dental appliances. POF represents 9.6 percent of all biopsied gingival lesions; women between the ages of 25 and 35 years are most susceptible.5 More than 50 percent of POFs occur in the anterior maxilla and involve the interdental gingival papilla. An exophytic POF usually measures less than 1.5 cm; is slow growing, firm and painless; and has an intact overlying normal mucosa. Occasionally, painful ulcerations may develop. A POF can be either a sessile or a pedunculated growth. Calcified areas may be noted radiographically. Generally, no alveolar bone destruction is observed. A confirmatory diagnosis of POF can be made only by means of microscopic examination of excised tissue. The surface epithelium may be intact or ulcerated. The presence of a cellular fibrous tissue stroma, some inflammatory cells, a varying endothelial proliferation and most importantly mineralized material representing dystrophic calcification or bone deposition can be used to confirm the histologic diagnosis of POF. Kaposi sarcoma. Kaposi sarcoma (KS) is a multicentric angioproliferative disorder of vascular endothelial origin that affects primarily mucocutaneous tissue. AIDS-associated KS (AIDS-KS) is the most common variant of this disorder.6 Approximately 71 percent of patients with AIDS-KS will develop oral lesions in association with KS-related systemic lesions, whereas in 22 percent of patients, the disease initially develops in the mouth.7 There may be one or multiple oral lesions, and they usually begin as macules and progress to papules and nodules that eventually coalesce to form large exophytic masses. Characteristically, the lesion’s color varies from deep red to blue-purple. The sessile or pedunculated KS growths most frequently involve the hard palate and gingiva. They tend to be painless and bleed easily, and they can become ulcerated. Histologically, KS is recognized by the presence of spindle-shaped tumor cells, angiogenesis, an inflammatory infiltrate of
January 2014
Copyright © 2014 American Dental Association. All Rights Reserved.
Downloaded from jada.ada.org on June 28, 2014
ORIGINAL CONTRIBUTIONS
mononuclear cells, extravasated erythrocytes and edema. Because KS has a vascular origin, immunohistochemistry study results will feature endothelial markers rather than markers associated with PBL. Furthermore, human herpesvirus 8 is a common serologic finding in patients with AIDS-KS.8 Pyogenic granuloma. Pyogenic granuloma (PG) is an exuberant soft-tissue response and vascular proliferation resulting from a chronic low-grade inflammation caused by a chronic irritant, trauma or hormonal factors.9 In many instances, poor oral hygiene is a predisposing factor. The anterior maxillary gingiva in young females is the most frequent site of origin. A smooth or lobulated exophytic localized nodular lesion on a pedunculated or sessile base, measuring from a few millimeters to several centimeters, usually can be observed. PG has a soft consistency that can become firm when mature. It also can bleed easily and is reddish. Histologically, the surface epithelium usually is intact, but foci of ulceration may be noted. An edematous vascular stroma with capillary proliferation, hemorrhage and chronic inflammatory cells is present. Squamous cell carcinoma. Squamous cell carcinoma (SCC) is an epithelial malignancy that involves an invasion of altered squamous cells into the supporting connective tissue and adjacent structures. SCC represents approximately 90 percent of all oral carcinomas and occurs most frequently in men older than 45 years who have tobacco and alcohol risk factors.10 The floor of the mouth and tongue are common sites, whereas the hard palate is involved infrequently. There is a great variation in the appearance of SCC, but it usually manifests as an exophytic irregularly shaped fixated lesion with a rough pebbly surface that is pink or red with a varied interspersed amount of white keratin. Cellular proliferation may result in a centrally depressed ulceration with a peripheral rolled border. Histologically, sheets and nests of hyperchromatic cells with an apparent squamous epithelial origin are seen. Epithelial pearls, keratinized cells, large nuclei, nuclear pleomorphism and mitotic figures are evident.
CONCLUSION
We have presented a case of an immunocompromised patient with HIV who had a PBL. The diagnosis of this rare oral malignancy can be made only when its clinical and histologic features are considered along with the results of a cellular immunohistochemistry study showing the characteristic surface markers that identify the neoplastic cells as having plasma cell phenotypes. It is this microscopic appearance that differentiates PBL from clinically similar proliferations. n
doi:10.14219/jada.2013.5
Mr. Hajibandeh is a research assistant and a senior student, Columbia University College of Dental Medicine, New York City. Dr. Mandel is the director, Salivary Gland Center, and the associate dean and a professor, Division of Oral and Maxillofacial Surgery, Columbia University College of Dental Medicine, New York City. Address correspondence to Dr. Mandel at Columbia University College of Dental Medicine, 630 W. 168th St., New York, N.Y. 10032, e-mail [email protected]. Disclosure. Mr. Hajibandeh and Dr. Mandel did not report any disclosures. Diagnostic Challenge is published in collaboration with the American Academy of Oral and Maxillofacial Pathology and the American Academy of Oral Medicine. 1. Delecluse HJ, Anagostopoulos I, Dallenbach F, et al. Plasmablastic lymphomas of the oral cavity: a new entity associated with the human immunodeficiency virus infection. Blood 1997;89(4):1413-1420. 2. Bagul N, Mamatha GS, Mahalle A. Plasmablastic lymphoma of gingiva mimicking a reactive lesion: a case report (published online Sept. 13, 2012). Case Rep Dent 2012;2012:259307. doi:10.1155/2012/259307. 3. Rafaniello Raviele P, Pruneri G, Maiorano E. Plasmablastic lymphoma: a review. Oral Dis 2009;15(1):38-45. 4. Riedel DJ, Gonzalez-Cuyar LF, Zhao XF, Redfield RR, Gilliam BL. Plasmablastic lymphoma of the oral cavity: a rapidly progressive lymphoma associated with HIV infection. Lancet Infect Dis 2008;8(4):261-267. 5. Walters JD, Will JK, Hatfield RD, Cacchillo DA, Raabe DA. Excision and repair of the peripheral ossifying fibroma: a report of 3 cases. J Periodontol 2001;72(7):939-944. 6. Fatahzadeh M. Kaposi sarcoma: review and medical management update (published correction appears in Oral Surg Oral Med Oral Pathol Oral Radiol 2012;113[5]:708). Oral Surg Oral Med Oral Pathol Oral Radiol 2012;113(1):2-16. 7. Lager I, Altini M, Coleman H, Ali H. Oral Kaposi’s sarcoma: a clinicopathologic study from South Africa. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2003;96(6):701-710. 8. Pantanowitz L, Khammissa RA, Lemmer J, Feller L. Oral HIV-associated Kaposi sarcoma. J Oral Pathol Med 2013;42(3):201-207. 9. Gordón-Núñez MA, de Vasconcelos Carvalho M, Benevenuto TG, Lopes MF, Silva LM, Galvão HC. Oral pyogenic granuloma: a retrospective analysis of 293 cases in a Brazilian population. J Oral Maxillofac Surg 2010;68(9):2185-2188. 10. Ram H, Sarkar J, Kumar H, Konwar R, Bhatt ML, Mohammad S. Oral cancer: risk factors and molecular pathogenesis. J Oral Maxillofac Surg 2011;10(2):132-137.
JADA 145(1)
http://jada.ada.org
Copyright © 2014 American Dental Association. All Rights Reserved.
January 2014 69
