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Asymptomatic bilateral facial swelling
CLINICAL
PRACTICE
DIAGNOSTIC
CHALLENGE
Asymptomatic bilateral facial swelling Louis Mandel, DDS; Renata Khelemsky, DDS THE CHALLENGE
72-year-old man sought treatment at the Salivary Gland Center at Columbia University (New York City) for a painless and persistent bilateral facial swelling that he had noticed six months previously (Figure 1). A friend of the patient had called the swellings to the patient’s attention and commented on his “chubby” face. At no time did the patient experience pain, nor were there any fluctuations in the size of the swelling before and after eating. The patient’s medical history indicated that he had received treatment for hypertension for the preceding 22 years, and his type 2 diabetes mellitus (DM) had been diagnosed seven years previous. The medications he took for his hypertension included metoprolol, quinipril, doxazosin, amlodipine and hydrochlorothiazide. The patient took insulin daily and initiated dietary control to treat his type 2 DM. He successfully maintained his blood pressure at 135/70 millimeters of mercury. His insulin therapy kept his glucose level in the range of 100 to 120 milligrams per 100 milliliters. He reported that his
A
Figure 1. Clinical view of bilateral facial swelling.
glycosylated hemoglobin level was consistently lower than 6. Extraorally, we noticed a striking bilateral facial swelling in the region of the parotid glands. When we palpated the area, we noted that each soft-tissue swelling was normal in tone and painless. There was no cervical lymphadenopathy. Intraorally, the mucosa was normally moist. Adequate and clear saliva exited from each patent parotid duct orifice when we aggressively massaged the respective parotid glands. A computed tomographic (CT) scan obtained without use of contrast material showed bilaterally enlarged parotid glands exhibiting uniformly increased density (Figure 2). No other radiographic abnormalities were visible on the CT scans. We performed fine-needle aspiration (FNA) biopsies on both of the patient’s parotid glands. We observed a normal cellular population; however, we also noted enlarged serous acini with basally placed nuclei (Figure 3). Measurements indicated that each acinus was approximately 80 micrometers or more in diameter. In addition, an extensive influx of fine granules distended each cell’s cytoplasm.
Figure. 2. Axial computed tomographic scan obtained without use of contrast material showing bilateral enlargement of the parotid salivary glands (boldfaced Ps). An increase in parotid gland density is shown.
Figure 3. Photomicrograph of a fineneedle aspiration biopsy specimen (DiffQuick, ×200 magnification). An enlarged serous acinus (80 micrometers or more in diameter) was present in a field of erythrocytes (arrow). No other cytologic abnormalities were present.
Can you make the diagnosis? A. masseteric muscle hypertrophy D. diabetic sialosis B. Sjögren syndrome E. sarcoidosis C. epidemic parotitis (mumps) JADA 143(11)
http://jada.ada.org
Copyright © 2012 American Dental Association. All rights reserved.
November 2012
1205
CLINICAL
PRACTICE
DIAGNOSTIC
CHALLENGE
THE DIAGNOSIS
D. diabetic sialosis normal parotid gland will have multiple irregular We made a diagnosis of diabetic sialosis on areas of radiolucency, reflecting the gland’s fatty the basis of the patient’s history, the clinical content. As the diameter of each acinus increases, examination, the CT findings and the results of the FNA biopsies. Sialosis, or sialadenosis, is the gland’s normally present adipose tissue is discharacterized by asymptomatic persistent, painplaced and the CT scan shows increased density less, bilateral parotid gland enlargement and in the gland. Consequently, our patient’s CT scan occasional submandibular gland involvement revealed a glandular density that approached that can develop in people who have DM.1-6 In that of the masseter muscle (Figure 2). some instances, sialosis may precede the clinical We notified the patient’s physician regarding diagnosis of DM or it may occur in patients the etiology of the parotid gland swellings. Diawhose type 2 DM is controlled.1-3 Sialosis does betic care and control result only in minimal not appear to be influenced by the duration, improvement in gland size. The use of piloseverity or control of this metabolic disease. carpine has been advocated to decrease parotSialosis also occurs in people with alcoholism idomegaly, but its success has been reported who have hepatic disease,5,6 in only once.12 Surgical reduction people who experience chronic rarely is warranted. Regardless, A demyelinating malnutrition5,7 and in people in the known benign course of diawhom there is no known assobetic sialosis mandates a conserautonomic ciated systemic disease.7,8 vative no-treatment option, tincneuropathy seems A demyelinating autonomic tured with a dose of reassurance to be the common neuropathy seems to be the comfor the patient. denominator that mon denominator that unites diaDIFFERENTIAL DIAGNOSIS unites diabetes, betes, alcoholism and malnutrition with the manifestations of Masseteric muscle hyperalcoholism and sialosis.5,8-10 The autonomic nerve trophy. Masseter muscle hypermalnutrition with supply to the parotid glands introphy (MMH), which frequently the manifestations volves both parasympathetic and is mistaken for parotid gland of sialosis. sympathetic innervation. Parahypertrophy, creates an asymptosympathetic activity results in fluid and electrolyte secretion, whereas sympathetic innervation is associated with intracellular protein synthesis and secretion. With the onset of autonomic neuropathy, a sympathetic deregulation of protein synthesis, its secretion or both results. Cellular engorgement from intracytoplasmic zymogen granules ensues and causes cell enlargement.9-11 Parenchymal acini are formed from groups of seven to 10 individual acinar cells. The acini, which normally are 56 μm in diameter,11 can expand up to become as large as 100 μm.3,5,7,11 The visible extraoral parotid gland swelling is the end product of the process. The results from the FNA biopsies of our patient’s parotid glands indicated no inflammatory or neoplastic cells. The results did show enlarged serous acini measuring 80 μm or more in diameter. In addition, an extensive influx of fine granules, which probably were zymogen, distended each cell’s cytoplasm. The enlargement of individual cells as a result of their increased protein content can cause parenchymal acinar hypertrophy. On a CT scan, a 1206 JADA 143(11)
http://jada.ada.org
matic persistent facial enlargement that usually involves both masseter muscles. The masseter muscle is near the parotid gland. Although the muscle has some anatomical overlap with the parotid gland, the bulk of it is located primarily anterior to the parotid gland. Classically, a patient’s constantly clenching, bruxing or chewing gum initiates MMH, and MMH is unusual in older patients. In patients with MMH, their faces take on a characteristic rectangular configuration because of the increased masseter muscle bulk that develops in the mandibular angle area. In comparison, parotid gland hypertrophy is distinguished by its ability to increase facial ovality. Furthermore, augmented masseter muscle tension causes a bony hyperplasia in the mandibular angle area that often is visible radiographically. When a patient clenches, the previously flaccid masseter muscles become firm and display their discrete and prominent diagnostic anatomical outlines. Sjögren syndrome. Sjögren syndrome (SS) is a chronic autoimmune disease characterized by mononuclear infiltrations that create
November 2012
Copyright © 2012 American Dental Association. All rights reserved.
CLINICAL
destructive lesions in exocrine glands, primarily the salivary and lacrimal glands.13 Primary SS involves the lacrimal and salivary glands, whereas secondary SS also is associated with a systemic autoimmune disease, usually rheumatoid arthritis. Intraorally, a major concern for patients is xerostomia. The hyposalivation can cause burning mucosal sensations, difficulty with eating and swallowing, rampant caries and altered taste. The tongue is smooth or has a cobblestone appearance. Acute suppurative parotid gland swellings with pain may occur that result from the ascent of oral bacteria into the duct, facilitated by decreased salivary lavage. Bilateral parotid gland swellings in SS also may develop from a benign lymphoproliferation or from a true neoplasm such as mucosaassociated lymphoid tissue lymphoma.14 These kinds of swellings tend to be long-standing and painless, and they do not fluctuate in size or suppurate. Diagnosis of SS primarily is based on decreased lacrimation and salivation, serologic evidence of SS antibodies and labial salivary gland biopsy results that indicate pathognomonic focal aggregates of lymphocytes and parenchymal atrophy. Epidemic parotitis (mumps). Epidemic parotitis is an acute viral contagious disease that affects primarily children. After a person has contact with airborne saliva droplets from an infected person, the virus enters the nose or mouth, proliferates in the salivary glands or respiratory tissues and causes a generalized infection. In the usual case of epidemic parotitis, bilateral firm painful parotid gland swelling develops after a 16- to 18-day viral incubation period. The enlarged parotid glands gradually decrease in size during the next three to seven days. Additional features of epidemic parotitis, particularly in adults, include orchitis in male patients and pancreatitis, thyroiditis and mastitis in patients of both sexes. Mumps is diagnosed on the basis of a patient’s history of never having had mumps, a recent exposure to the virus and a compatible clinical picture of parotitis. Serologic testing for the virus is available. Mumps is a self-limiting disease whose exposure confers immunity. Treatment primarily is aimed at symptomatic care. The prognosis usually is favorable. Vaccination with a live attenuated virus is the standard preventive measure. Sarcoidosis. Sarcoidosis is a chronic multisystem granulomatous disease of unknown origin that has a specific predilection for the lungs and hilar lymph nodes. Most patients with sarcoidosis have respiratory symptoms such as coughing, dyspnea or chest pain. Bilateral
PRACTICE
DIAGNOSTIC
CHALLENGE
parotid gland sialadenopathy occurs in many patients with sarcoidosis.15 The glands tend to be firm and slightly painful, but they do not fluctuate in size during eating. Because sarcoidal granulomas replace parenchymal cells, a moderate decrease in salivary production occurs. The results of incisional and FNA biopsies can be used to identify noncaseating granulomas, and chest radiographs can show a distinctive lung infiltrate and hilar lymphadenopathy. The results of blood tests often indicate elevated calcium and alkaline phosphatase levels, increased angiotensin-converting enzyme levels and hypergammaglobulinemia. Because spontaneous resolution can be expected, treatment generally is symptomatic. In severe cases, the use of corticosteroids can help. CONCLUSION
Because sialosis may develop before diabetes is diagnosed, practitioners need to consider that patients might have an underlying diabetic condition. To facilitate diagnosing diabetic sialosis, we have described its differentiation from MMH, SS, epidemic parotitis and sarcoidosis. ■ Dr. Mandel is the director, Salivary Gland Center, and the associate dean and a clinical professor, Division of Oral and Maxillofacial Surgery, Columbia University College of Dental Medicine, 630 W. 168th St., New York, N.Y. 10032, e-mail [email protected]. Address reprint requests to Dr. Mandel. Dr. Khelemsky was a research assistant, Salivary Gland Center; and a fourth-year student, Columbia University College of Dental Medicine, New York City, when this article was written. She now is a resident in oral and maxillofacial surgery, Beth Israel Medical Center, New York City. Disclosure. Drs. Mandel and Khelemsky 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. Russotto SB. Asymptomatic parotid gland enlargement in diabetes mellitus. Oral Surg Oral Med Oral Pathol 1981;52(6):594-598. 2. Quirino MR, Birman EG, Paula CR. Oral manifestations of diabetes mellitus in controlled and uncontrolled patients. Braz Dent J 1995;6(2):131-136. 3. Mandel L, Patel S. Sialadenosis associated with diabetes mellitus: a case report. J Oral Maxillofac Surg 2002;60(6):696-698. 4. Carda C, Mosquera-Lloreda N, Salom L, Gomez de Ferraris ME, Peydró A. Structural and functional salivary disorders in type 2 diabetic patients. Med Oral Patol Oral Cir Bucal 2006;11(4):E 309-E314. 5. Scully C, Bagán JV, Eveson JW, Barnard N, Turner FM. Sialosis: 35 cases of persistent parotid swelling from two countries (published online ahead of print March 17, 2008). Br J Oral Maxillofac Surg 2008;46(6):468-472. doi:10.1016/j.bjoms.2008.01.014. 6. Merlo C, Bohl L, Carda C, Gómez de Ferraris ME, Carranza M. Parotid sialosis: morphometrical analysis of the glandular parenchyme and stroma among diabetic and alcoholic patients (published online ahead of print July 19, 2009). J Oral Pathol Med 2010;39(1):10-15. doi:10.1111/j.1600-0714.2009.00806.x. 7. Henry-Stanley MJ, Beneke J, Bardales RH, Stanley MW. Fineneedle aspiration of normal tissue from enlarged salivary glands: sialosis or missed target? Diagn Cytopathol 1995;13(4):300-303. 8. Ino C, Matsuyama K, Ino M, Yamashita T, Kumazawa T. Approach to the diagnosis of sialadenosis using sialography. Acta Otolaryngol Suppl 1993;500:121-125.
JADA 143(11)
http://jada.ada.org
Copyright © 2012 American Dental Association. All rights reserved.
November 2012
1207
CLINICAL
PRACTICE
DIAGNOSTIC
CHALLENGE
9. Chilla R. Sialadenosis of the salivary glands of the head: studies on the physiology and pathophysiology of parotid secretion. Adv Otorhinolaryngol 1981;26:1-38. 10. Donath K, Seifert G. Ultrastructural studies of the parotid glands in sialadenosis. Virchows Arch A Pathol Anat Histol 1975; 365(2):119-135. 11. Ascoli V, Albedi FM, De Blasiis R, Nardi F. Sialadenosis of the parotid gland: report of four cases diagnosed by fine-needle aspiration cytology. Diagn Cytopathol 1993;9(2):151-155. 12. Coleman H, Altini M, Nayler S, Richards A. Sialadenosis: a presenting sign in bulimia. Head Neck 1998;20(8):758-762.
1208 JADA 143(11)
http://jada.ada.org
13. Vitali C, Bombardieri S, Jonsson R, et al; European Study Group on Classification Criteria for Sjögren’s Syndrome. Classification criteria for Sjögren’s syndrome: a revised version of the European criteria proposed by the American-European Consensus Group. Ann Rheum Dis 2002;61(6):554-558. 14. Harris NL. Lymphoid proliferations of the salivary glands. Am J Clin Pathol 1999;111(1 suppl 1):S94-S103. 15. Batsakis JG. Tumors of the Head and Neck: Clinical and Pathological Considerations. 2nd ed. Baltimore: Williams and Wilkins; 1979:101-103.
November 2012
Copyright © 2012 American Dental Association. All rights reserved.
PRACTICE
DIAGNOSTIC
CHALLENGE
Asymptomatic bilateral facial swelling Louis Mandel, DDS; Renata Khelemsky, DDS THE CHALLENGE
72-year-old man sought treatment at the Salivary Gland Center at Columbia University (New York City) for a painless and persistent bilateral facial swelling that he had noticed six months previously (Figure 1). A friend of the patient had called the swellings to the patient’s attention and commented on his “chubby” face. At no time did the patient experience pain, nor were there any fluctuations in the size of the swelling before and after eating. The patient’s medical history indicated that he had received treatment for hypertension for the preceding 22 years, and his type 2 diabetes mellitus (DM) had been diagnosed seven years previous. The medications he took for his hypertension included metoprolol, quinipril, doxazosin, amlodipine and hydrochlorothiazide. The patient took insulin daily and initiated dietary control to treat his type 2 DM. He successfully maintained his blood pressure at 135/70 millimeters of mercury. His insulin therapy kept his glucose level in the range of 100 to 120 milligrams per 100 milliliters. He reported that his
A
Figure 1. Clinical view of bilateral facial swelling.
glycosylated hemoglobin level was consistently lower than 6. Extraorally, we noticed a striking bilateral facial swelling in the region of the parotid glands. When we palpated the area, we noted that each soft-tissue swelling was normal in tone and painless. There was no cervical lymphadenopathy. Intraorally, the mucosa was normally moist. Adequate and clear saliva exited from each patent parotid duct orifice when we aggressively massaged the respective parotid glands. A computed tomographic (CT) scan obtained without use of contrast material showed bilaterally enlarged parotid glands exhibiting uniformly increased density (Figure 2). No other radiographic abnormalities were visible on the CT scans. We performed fine-needle aspiration (FNA) biopsies on both of the patient’s parotid glands. We observed a normal cellular population; however, we also noted enlarged serous acini with basally placed nuclei (Figure 3). Measurements indicated that each acinus was approximately 80 micrometers or more in diameter. In addition, an extensive influx of fine granules distended each cell’s cytoplasm.
Figure. 2. Axial computed tomographic scan obtained without use of contrast material showing bilateral enlargement of the parotid salivary glands (boldfaced Ps). An increase in parotid gland density is shown.
Figure 3. Photomicrograph of a fineneedle aspiration biopsy specimen (DiffQuick, ×200 magnification). An enlarged serous acinus (80 micrometers or more in diameter) was present in a field of erythrocytes (arrow). No other cytologic abnormalities were present.
Can you make the diagnosis? A. masseteric muscle hypertrophy D. diabetic sialosis B. Sjögren syndrome E. sarcoidosis C. epidemic parotitis (mumps) JADA 143(11)
http://jada.ada.org
Copyright © 2012 American Dental Association. All rights reserved.
November 2012
1205
CLINICAL
PRACTICE
DIAGNOSTIC
CHALLENGE
THE DIAGNOSIS
D. diabetic sialosis normal parotid gland will have multiple irregular We made a diagnosis of diabetic sialosis on areas of radiolucency, reflecting the gland’s fatty the basis of the patient’s history, the clinical content. As the diameter of each acinus increases, examination, the CT findings and the results of the FNA biopsies. Sialosis, or sialadenosis, is the gland’s normally present adipose tissue is discharacterized by asymptomatic persistent, painplaced and the CT scan shows increased density less, bilateral parotid gland enlargement and in the gland. Consequently, our patient’s CT scan occasional submandibular gland involvement revealed a glandular density that approached that can develop in people who have DM.1-6 In that of the masseter muscle (Figure 2). some instances, sialosis may precede the clinical We notified the patient’s physician regarding diagnosis of DM or it may occur in patients the etiology of the parotid gland swellings. Diawhose type 2 DM is controlled.1-3 Sialosis does betic care and control result only in minimal not appear to be influenced by the duration, improvement in gland size. The use of piloseverity or control of this metabolic disease. carpine has been advocated to decrease parotSialosis also occurs in people with alcoholism idomegaly, but its success has been reported who have hepatic disease,5,6 in only once.12 Surgical reduction people who experience chronic rarely is warranted. Regardless, A demyelinating malnutrition5,7 and in people in the known benign course of diawhom there is no known assobetic sialosis mandates a conserautonomic ciated systemic disease.7,8 vative no-treatment option, tincneuropathy seems A demyelinating autonomic tured with a dose of reassurance to be the common neuropathy seems to be the comfor the patient. denominator that mon denominator that unites diaDIFFERENTIAL DIAGNOSIS unites diabetes, betes, alcoholism and malnutrition with the manifestations of Masseteric muscle hyperalcoholism and sialosis.5,8-10 The autonomic nerve trophy. Masseter muscle hypermalnutrition with supply to the parotid glands introphy (MMH), which frequently the manifestations volves both parasympathetic and is mistaken for parotid gland of sialosis. sympathetic innervation. Parahypertrophy, creates an asymptosympathetic activity results in fluid and electrolyte secretion, whereas sympathetic innervation is associated with intracellular protein synthesis and secretion. With the onset of autonomic neuropathy, a sympathetic deregulation of protein synthesis, its secretion or both results. Cellular engorgement from intracytoplasmic zymogen granules ensues and causes cell enlargement.9-11 Parenchymal acini are formed from groups of seven to 10 individual acinar cells. The acini, which normally are 56 μm in diameter,11 can expand up to become as large as 100 μm.3,5,7,11 The visible extraoral parotid gland swelling is the end product of the process. The results from the FNA biopsies of our patient’s parotid glands indicated no inflammatory or neoplastic cells. The results did show enlarged serous acini measuring 80 μm or more in diameter. In addition, an extensive influx of fine granules, which probably were zymogen, distended each cell’s cytoplasm. The enlargement of individual cells as a result of their increased protein content can cause parenchymal acinar hypertrophy. On a CT scan, a 1206 JADA 143(11)
http://jada.ada.org
matic persistent facial enlargement that usually involves both masseter muscles. The masseter muscle is near the parotid gland. Although the muscle has some anatomical overlap with the parotid gland, the bulk of it is located primarily anterior to the parotid gland. Classically, a patient’s constantly clenching, bruxing or chewing gum initiates MMH, and MMH is unusual in older patients. In patients with MMH, their faces take on a characteristic rectangular configuration because of the increased masseter muscle bulk that develops in the mandibular angle area. In comparison, parotid gland hypertrophy is distinguished by its ability to increase facial ovality. Furthermore, augmented masseter muscle tension causes a bony hyperplasia in the mandibular angle area that often is visible radiographically. When a patient clenches, the previously flaccid masseter muscles become firm and display their discrete and prominent diagnostic anatomical outlines. Sjögren syndrome. Sjögren syndrome (SS) is a chronic autoimmune disease characterized by mononuclear infiltrations that create
November 2012
Copyright © 2012 American Dental Association. All rights reserved.
CLINICAL
destructive lesions in exocrine glands, primarily the salivary and lacrimal glands.13 Primary SS involves the lacrimal and salivary glands, whereas secondary SS also is associated with a systemic autoimmune disease, usually rheumatoid arthritis. Intraorally, a major concern for patients is xerostomia. The hyposalivation can cause burning mucosal sensations, difficulty with eating and swallowing, rampant caries and altered taste. The tongue is smooth or has a cobblestone appearance. Acute suppurative parotid gland swellings with pain may occur that result from the ascent of oral bacteria into the duct, facilitated by decreased salivary lavage. Bilateral parotid gland swellings in SS also may develop from a benign lymphoproliferation or from a true neoplasm such as mucosaassociated lymphoid tissue lymphoma.14 These kinds of swellings tend to be long-standing and painless, and they do not fluctuate in size or suppurate. Diagnosis of SS primarily is based on decreased lacrimation and salivation, serologic evidence of SS antibodies and labial salivary gland biopsy results that indicate pathognomonic focal aggregates of lymphocytes and parenchymal atrophy. Epidemic parotitis (mumps). Epidemic parotitis is an acute viral contagious disease that affects primarily children. After a person has contact with airborne saliva droplets from an infected person, the virus enters the nose or mouth, proliferates in the salivary glands or respiratory tissues and causes a generalized infection. In the usual case of epidemic parotitis, bilateral firm painful parotid gland swelling develops after a 16- to 18-day viral incubation period. The enlarged parotid glands gradually decrease in size during the next three to seven days. Additional features of epidemic parotitis, particularly in adults, include orchitis in male patients and pancreatitis, thyroiditis and mastitis in patients of both sexes. Mumps is diagnosed on the basis of a patient’s history of never having had mumps, a recent exposure to the virus and a compatible clinical picture of parotitis. Serologic testing for the virus is available. Mumps is a self-limiting disease whose exposure confers immunity. Treatment primarily is aimed at symptomatic care. The prognosis usually is favorable. Vaccination with a live attenuated virus is the standard preventive measure. Sarcoidosis. Sarcoidosis is a chronic multisystem granulomatous disease of unknown origin that has a specific predilection for the lungs and hilar lymph nodes. Most patients with sarcoidosis have respiratory symptoms such as coughing, dyspnea or chest pain. Bilateral
PRACTICE
DIAGNOSTIC
CHALLENGE
parotid gland sialadenopathy occurs in many patients with sarcoidosis.15 The glands tend to be firm and slightly painful, but they do not fluctuate in size during eating. Because sarcoidal granulomas replace parenchymal cells, a moderate decrease in salivary production occurs. The results of incisional and FNA biopsies can be used to identify noncaseating granulomas, and chest radiographs can show a distinctive lung infiltrate and hilar lymphadenopathy. The results of blood tests often indicate elevated calcium and alkaline phosphatase levels, increased angiotensin-converting enzyme levels and hypergammaglobulinemia. Because spontaneous resolution can be expected, treatment generally is symptomatic. In severe cases, the use of corticosteroids can help. CONCLUSION
Because sialosis may develop before diabetes is diagnosed, practitioners need to consider that patients might have an underlying diabetic condition. To facilitate diagnosing diabetic sialosis, we have described its differentiation from MMH, SS, epidemic parotitis and sarcoidosis. ■ Dr. Mandel is the director, Salivary Gland Center, and the associate dean and a clinical professor, Division of Oral and Maxillofacial Surgery, Columbia University College of Dental Medicine, 630 W. 168th St., New York, N.Y. 10032, e-mail [email protected]. Address reprint requests to Dr. Mandel. Dr. Khelemsky was a research assistant, Salivary Gland Center; and a fourth-year student, Columbia University College of Dental Medicine, New York City, when this article was written. She now is a resident in oral and maxillofacial surgery, Beth Israel Medical Center, New York City. Disclosure. Drs. Mandel and Khelemsky 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. Russotto SB. Asymptomatic parotid gland enlargement in diabetes mellitus. Oral Surg Oral Med Oral Pathol 1981;52(6):594-598. 2. Quirino MR, Birman EG, Paula CR. Oral manifestations of diabetes mellitus in controlled and uncontrolled patients. Braz Dent J 1995;6(2):131-136. 3. Mandel L, Patel S. Sialadenosis associated with diabetes mellitus: a case report. J Oral Maxillofac Surg 2002;60(6):696-698. 4. Carda C, Mosquera-Lloreda N, Salom L, Gomez de Ferraris ME, Peydró A. Structural and functional salivary disorders in type 2 diabetic patients. Med Oral Patol Oral Cir Bucal 2006;11(4):E 309-E314. 5. Scully C, Bagán JV, Eveson JW, Barnard N, Turner FM. Sialosis: 35 cases of persistent parotid swelling from two countries (published online ahead of print March 17, 2008). Br J Oral Maxillofac Surg 2008;46(6):468-472. doi:10.1016/j.bjoms.2008.01.014. 6. Merlo C, Bohl L, Carda C, Gómez de Ferraris ME, Carranza M. Parotid sialosis: morphometrical analysis of the glandular parenchyme and stroma among diabetic and alcoholic patients (published online ahead of print July 19, 2009). J Oral Pathol Med 2010;39(1):10-15. doi:10.1111/j.1600-0714.2009.00806.x. 7. Henry-Stanley MJ, Beneke J, Bardales RH, Stanley MW. Fineneedle aspiration of normal tissue from enlarged salivary glands: sialosis or missed target? Diagn Cytopathol 1995;13(4):300-303. 8. Ino C, Matsuyama K, Ino M, Yamashita T, Kumazawa T. Approach to the diagnosis of sialadenosis using sialography. Acta Otolaryngol Suppl 1993;500:121-125.
JADA 143(11)
http://jada.ada.org
Copyright © 2012 American Dental Association. All rights reserved.
November 2012
1207
CLINICAL
PRACTICE
DIAGNOSTIC
CHALLENGE
9. Chilla R. Sialadenosis of the salivary glands of the head: studies on the physiology and pathophysiology of parotid secretion. Adv Otorhinolaryngol 1981;26:1-38. 10. Donath K, Seifert G. Ultrastructural studies of the parotid glands in sialadenosis. Virchows Arch A Pathol Anat Histol 1975; 365(2):119-135. 11. Ascoli V, Albedi FM, De Blasiis R, Nardi F. Sialadenosis of the parotid gland: report of four cases diagnosed by fine-needle aspiration cytology. Diagn Cytopathol 1993;9(2):151-155. 12. Coleman H, Altini M, Nayler S, Richards A. Sialadenosis: a presenting sign in bulimia. Head Neck 1998;20(8):758-762.
1208 JADA 143(11)
http://jada.ada.org
13. Vitali C, Bombardieri S, Jonsson R, et al; European Study Group on Classification Criteria for Sjögren’s Syndrome. Classification criteria for Sjögren’s syndrome: a revised version of the European criteria proposed by the American-European Consensus Group. Ann Rheum Dis 2002;61(6):554-558. 14. Harris NL. Lymphoid proliferations of the salivary glands. Am J Clin Pathol 1999;111(1 suppl 1):S94-S103. 15. Batsakis JG. Tumors of the Head and Neck: Clinical and Pathological Considerations. 2nd ed. Baltimore: Williams and Wilkins; 1979:101-103.
November 2012
Copyright © 2012 American Dental Association. All rights reserved.