Lymphangioma of the Palatine Tonsil.
Three morphologic types of lymphangiomas are distinguished. Capillary, or simple, lymphangiomas are usually found in the superficial skin and composed of capillary-sized, thin-walled lymphatic vessels. Cavernous lymphangiomas are subcutaneous lesions composed of mildly dilated, large spaces that are larger than those seen in capillary lymphangiomas. Cystic hygromas, the third type, are most common in the neck and composed of large, dilated, cystic lymphatic spaces. (3) Thus, these 3 types of lymphangiomas can be differentiated from one another based purely on the characteristics of the component lymphatic spaces. In addition, combinations of the 3 types can sometimes be found in a single lesion. Therefore, the 3 types of lymphangiomas represent the same pathologic process along a spectrum and should be considered as a unified concept. (1) Moreover, differentiating lymphangiomas on the basis of histologic type appears without clinical implications.
Lymphangiomas tend to occur in places where lymphatics are abundant, with more than 90% of all lymphangiomas arising in the head and neck region. Most are found in the skin and subcutaneous tissues, but they have also been described in the larynx, parotid gland, mouth, and tongue. (4) The palatine tonsil is a far less common site for the development of lymphangioma and has rarely been reported in the literature. A recent case of tonsillar lymphangioma at our institution inspired our review of this unusual entity. Our search of the English literature found 31 other reported cases of this lesion, dating back to the 1930s, as shown in the Table. Although the various authors assign different terminology to describe these lesions, upon review of the reported microscopic features, all of the listed cases are histologically consistent with lymphangioma.
The Table lists the 32 cases of lymphangioma of the palatine tonsil (31 previously reported cases and our case) reported in the English literature, including patient age and sex, presenting symptoms, lesion laterality, and size (greatest dimension). The 18 males and 14 females range in age from 3 to 80 years, with a mean age at presentation of 25.9 years (median, 22.5 years).
A tonsillar lymphangioma may be asymptomatic, especially when small in size, and may, therefore, be discovered incidentally on physical examination or posttonsillectomy. When symptomatic, common presenting symptoms include dysphagia, recurrent sore throat, and foreign body sensation in the throat, which may cause a nonproductive cough. (5) A change in the quality of the patient's voice has also been reported as a result of this lesion. (6) A remarkably large mass may compress surrounding structures to produce respiratory difficulty, stridor, or nausea. Difficulty with swallowing may progress, causing excessive saliva in the oral cavity. (5)
On examination of the oral cavity, a lymphangioma is typically found to be an oval, pediculate mass protruding from the surface of the palatine tonsil. There is 1 report of a patient with a lymphangioma arising from the adenoids, presenting as a mass in the nasopharynx. (7) Lymphangiomas are almost always unilateral, with no apparent side predilection. Of the cases in our review that reported lesion laterality, 12 were on the right, 13 were on the left, and there was 1 case of bilateral lymphangiomas of the palatine tonsils. (8) On palpation, a lymphangioma is smooth and firm with intact mucosa, and a crepitant sound may be produced as lymphatic fluid is pushed from one area to another. (2) Cervical lymphadenopathy is not typically present. (7) However, Evans and Odom (9) reported a case of a 13-year-old girl with lymphangioma of the right palatine tonsil who had palpable lymph nodes in the right cervical region.
Grossly, a tonsillar lymphangioma appears as an exophytic polypoid nodule arising from the palatine tonsil. The lesion is generally pedunculated, but it may instead be sessile. (7) The lesions in our review range in size from 0.5 to 5 cm (mean, 2.49 cm) in largest diameter. The outer surface of the lesion is typically smooth, but 1 reported case is remarkable for a villous appearance of the external surface, with multiple fronds of varying sizes. (10) The consistency of the lesions varies from spongy to firm, and the cut surface is uniformly smooth, appearing white, tan, or yellow in color. (7)
The microscopic findings associated with tonsillar lymphangiomas are well described. Of note, the Figure referenced below is from our recent case.
Microscopically, the surface of the lymphangioma is remarkable for stratified squamous epithelium (Figure 1A).
Variable hyperplasia and dyskeratosis may be present, but dysplasia is not seen. Rarely, tonsillar lymphangiomas may have papillary architecture; this feature has been reported exclusively in tonsillar lymphangiomas affecting children. (7)
Diffusely distributed within the submucosa are numerous dilated lymphatic spaces lined by endothelial cells, with the walls of larger spaces sometimes containing a few disorganized smooth muscle bundles. This lymphatic proliferation is characteristically present underneath the overlying epithelium, with little or no intervening connective tissue. Valves can often be appreciated within the lymphatic spaces (Figure 1B). The lymphatic spaces can also contain proteinaceous material, as well as occasional lymphocytes and erythrocytes (Figure 1C). (2)
The stroma of the lymphangioma is comprised of adipose tissue, fibrous tissue, and lymphocytes (Figure 1D). Adipose tissue is present in varying amounts; some reports note absence of this component entirely, and in our case only a small amount was present. The collagenous component is much more abundant. Collections of lymphocytes are found not only in the submucosa but also within the squamous epithelium of the lesion. (4) Some cases display a nested epitheliotropism of lymphocytes, which refers to small lymphocytes clustered into rounded intramucosal spaces. (7) In the submucosa, foci of well-organized lymphoid tissue may sometimes be found as well (Figure 1E). (5) Regardless of the location of these lymphocytes, they display the morphology of normal mature lymphocytes, with small round nuclei and a small rim of cytoplasm. Cytologic atypia is notably absent from tonsillar lymphangiomas, as is infiltration of the underlying stroma of the normal tonsil. (7)
Routine hematoxylin-eosin sections are sufficient for making the diagnosis of tonsillar lymphangioma, but Kardon et al (7) used immunohistochemical staining to determine the immunoprofile of these lesions. In the 15 cases examined, the endothelium and subendothelium of the lymphatic channels stained positive for factor VIII-related antigen, and the majority of channels stained positive for either anti-CD31 or anti-CD34. Additionally, the walls of the dilated lymphatic vessels expressed smooth muscle actin. As far as the lymphoid population of cells, the leukocyte markers CD3, CD20, and CD45 (leukocyte common antigen) revealed a distribution of lymphocyte expression consistent with tonsillar tissue. Intraluminal and intraepithelial lymphocytes were predominantly CD3 immunoreactive. Thus, Kardon et al (7) confirmed the endothelial origin of the vascular proliferation and a mixed lymphoid population.
Our recent case was stained with D2-40 (podoplanin), a sialoglycoprotein found on lymphatic endothelial cells, which highlighted the lymphatic spaces within the lesion (Figure 1F). The small, endothelium-lined vessels that were negative for D2-40 were presumably capillaries. Positive staining with MECA-79 has also been documented in tonsillar lymphangiomas. This antibody recognizes a carbohydrate epitope expressed in high endothelial venules, specialized structures involved in lymphocyte homing into lymphoid tissues. (11) Lastly, immunohistochemical staining for fibronectin and collagens I and III revealed a decreased and disorganized distribution of these extracellular matrix proteins in lymphangiomas compared with normal tonsils. (11)
Unilateral tonsillar enlargement may be caused by a malignant neoplasm, benign lesion, or acute or chronic inflammation. Alternatively, a parapharyngeal mass may result in apparent tonsillar enlargement because of medial displacement of the tonsil. (7) In a study of approximately 2000 tonsillar neoplasms during a 30-year period from the Otolaryngic Pathology Registry of the Armed Forces Institute of Pathology, the most common malignant neoplasms of the palatine tonsils included squamous cell carcinoma and lymphoma. Benign neoplasms represented 25% of total cases, with tonsillar lymphangiomas representing 8% of the benign entities. (12) Because these statistics are likely influenced by referral bias, the lesion may be encountered even more infrequently, especially in the community hospital setting.
The differential diagnosis of a benign polypoid tonsillar lesion includes squamous papilloma, lymphangioma, epidermal inclusion cyst, juvenile angiofibroma, hemangioma, fibroepithelial polyp, fibroma, fibroxanthoma, lipoma, adenoma, and chondroma. (12) Of these benign entities, the most common is squamous papilloma, which is a proliferation of the surface epithelium without involvement of the underlying stroma and with absence of lymphatic and lymphocytic components. (7) An epidermal inclusion cyst appears as a small, tense, yellow mass just beneath the mucosa, and it represents a true cyst with a squamous lining. A fibroepithelial polyp arises from the mesodermal tissue and is composed of varying amounts of stroma covered by squamous epithelium. Hemangioma, fibroma, lipoma, adenoma, and chondroma refer to benign proliferations of blood vessels, fibrous tissue, mature fat cells, glandular elements, and hyaline cartilage, respectively. (12)
Differentiating a lymphangioma from a juvenile angiofibroma is especially important because the latter diagnosis warrants a more aggressive surgical resection and carries an increased risk of recurrence. (13) Histologically, the stroma of an angiofibroma is more cellular, consisting of cells with plump nuclei arranged radially around staghornlike thin walled vascular channels; lymphocytes are not a prominent cell type. (7) Therefore, the characteristic histologic features of a tonsillar lymphangioma allow pathologists to differentiate it from tonsillar lesions that may appear similar clinically.
CURRENT TREATMENT AND PROGNOSIS
The prognosis of a tonsillar lymphangioma is excellent. Tonsillar lymphangiomas are treated by wide surgical excision, with tonsillectomy as the preferred procedure to ensure complete removal. Because of their lack of encapsulation, recurrences of lymphangiomas, in general, are common if they are not completely removed. (1) Recurrence of tonsillar lymphangiomas after complete removal has not been reported in the literature. However, the length of patient follow-up is not always reported, and the longest reported follow-up period is 5 years. Thus, total absence of recurrence cannot be proven. These lesions are radio-resistant, so radiotherapy is ineffective and increases the risk for maldevelopment and malignancies of the head and neck. (14)
The pathogenesis of tonsillar lymphangioma is controversial. Chronic inflammation and associated obstruction of lymphatic channels have previously been suggested as a possible mechanism, with congestion eventually leading to mucosal prolapse and the appearance of a polypoidal swelling. (15) However, evidence against this explanation is that chronic tonsillitis occurs much more commonly than tonsillar lymphangiomas, and many patients presenting with tonsillar lymphangioma lack a history of tonsillitis. The recurrent sore throats some patients experience could be a consequence, rather than a cause, of a tonsillar lymphangioma. (16) Furthermore, a study of 14 cases of tonsillar lymphangioma found no gross evidence of lymphatic obstruction in the lesions or associated resected normal tonsils, even after serial sectioning of the tissue specimens. (11) This suggests that another mechanism is likely responsible for the pathogenesis of these tumors.
Wiegand et al (17) proposed several theories for the pathogenesis of tonsillar lymphangioma. One hypothesis is that the failure of primordial lymphatic sacs to drain into veins produces dilation of the isolated lymphatic channels. Alternatively, abnormal sequestration of lymphatic tissue early in embryogenesis with subsequent failure to join the normal, more central, lymphatic channels may explain the morphology of the more peripheral lesions, such as capillary and cavernous lymphangiomas. Another theory involves abnormal budding of the lymphatic structures, with the aberrant buds losing their connections with the primordial lymphatics and eventually canalizing to form lymph-filled cysts. These cysts maintain their ability to branch and grow, and do so in an uncontrolled, disorderly manner, with a tendency to penetrate and destroy normal anatomic structures.
Many argue that lymphangiomas represent hamartomatous lesions. Reported tonsillar lymphangiomas contain an admixture of fibrous and adipose elements, lymphatic spaces, and lymphocytes. These components are normal constituents of the tonsil, but are arranged in a disordered manner, consistent with the haphazard arrangement of elements in a hamartoma. (16) Reinforcing this notion is the finding of a disorganized pattern of distribution of fibronectin and collagens I and III within the stroma of lymphangiomas, revealed using immunohistochemical staining. (11)
Another possibility is that the pathogenesis of tonsillar lymphangiomas may be multifactorial, due to a combination of the proposed factors, occurring sequentially or synchronously. First, aberrations during development may produce a hamartomatous focus with its own growth potential. Second, chronic inflammation, secondary to stimuli such as trauma or infections, may trigger a growth phase responsible for the eventual polypoid mass. (18) A delay in this second event would help explain the occurrence of lymphangiomas in older patients.
More recent studies have proposed that lymphangiomas develop as a result of a neoplastic proliferation of lymphatic vessels, leading to a network of lymphatics that never achieve sufficient anastomosis with larger lymphatic vessels. The uncontrolled proliferation of lymphatic vessels is thought to be caused by a dysregulation of growth factors involved in lymphangiogenesis, such as Prox-1 and vascular endothelial growth factor C (VEGF-C). The transcription factor Prox-1 is expressed in lymphatic endothelial cells and lymphangioblasts, and its expression has been detected in the endothelium of lymphangiomas. Additionally, the growth factor VEGF-C and its receptor VEGFR-3 have been shown to have increased expression in the lymphatic endothelium of lymphangiomas versus normal lymphatic vessels. Lastly, 2 inhibitors of angiogenesis, pigment epithelium-derived factor and thrombospondin-1, have been found to have reduced expression in lymphangiomas. (17) Therefore, the development of lymphangiomas may depend on active lymphangiogenesis as well as increased angiogenesis.
Regardless of the uncertain pathogenesis of tonsillar lymphangiomas, these lesions have histologic features that differ from their counterparts in other anatomic locations. Although the lymphatic spaces of tonsillar lymphangiomas are frequently dilated, they are generally not as large or as prominent as in the lymphangiomas found elsewhere. Furthermore, the lymphoid and fibrous stromal components in tonsillar lymphangiomas are frequently more abundant than the lymphatic vessels. (19) Although some lymphangiomas involute over time, the involution of tonsillar lymphangiomas has not been described in the literature to date. (7) Thus, tonsillar lymphangiomas may represent a somewhat unique lesion.
In part because of the controversy over its pathogenesis, the classification of tonsillar lymphangiomas has been inconsistent, adding to the difficulty in assessing the lesion's true incidence. Reports in the literature use different nomenclature when referring to these lesions, such as tonsillar lymphangiomatous polyp, angioma, angiofibroma, fibrolipoma, polypoid tumor containing fibroadipose tissue, hamartomatous tonsillar polyp, and lymphangiectatic fibrous polyp. (4) The more recent reports have addressed this issue, and hopefully, with increased awareness of this lesion, a more uniform classification system will emerge. The reported incidence will likely increase as more clinicians and pathologists recognize this lesion.
In summary, lymphangioma of the palatine tonsil presents as a mass lesion constituting a benign proliferation of dilated lymphatic spaces amid stroma with fibrous, lymphoid, and adipose components, covered by stratified squamous epithelium. The histologic features, which suggest that the lesion represents a hamartomatous proliferation, allow differentiation from other possible entities included in the differential diagnosis of a tonsillar mass. The true incidence of tonsillar lymphangiomas may be higher than reported, because of historical underrecognition in the literature and inconsistencies in the terminology used to classify the lesion.
(1.) Zadvinskis DP, Benson MT, Kerr HH, et al. Congenital malformations of the cervicothoracic lymphatic system: embryology and pathogenesis. Radiographics. 1992; 12(6):1175-1189.
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Stacey Mardekian, MD; Julie Katz Karp, MD
Accepted for publication February 07, 2013.
From the Department of Pathology, Thomas Jefferson University Hospital, Methodist Division, Philadelphia, Pennsylvania.
The authors have no relevant financial interest in the products or companies described in this article.
Reprints: Julie Katz Karp, MD, Department of Pathology, Thomas Jefferson University Hospital, Methodist Division, 2301 S Broad St, Philadelphia, PA 19148 (e-mail: firstname.lastname@example.org).
Caption: Lymphangioma of the palatine tonsil. A, Polypoid structure with a pedicle seen at the upper left. Abundant dilated lymphatic spaces with overlying stratified squamous epithelium. B, Lymphatic space with valve leaflets visible beneath the nonkeratinized stratified squamous epithelium. C, Lymphatic spaces with clusters of lymphocytes and red blood cells. D, Stroma composed of adipose tissue, fibrous tissue, and lymphocytes. E, Focus of well-organized lymphoid tissue and lymphocytic epitheliotropism. F, D2-40 immunohistochemical stain highlights the lymphatic endothelium (hematoxylin-eosin, original magnifications X10 [A], X100 [B,C], X40 [D], X100 [E]; original magnification X100 [F]).
Caption: Please Note Illustration(s) are not available due to copyright restrictions.
Reported Cases of Lymphangioma of the Palatine Tonsil in the English Literature Case Source, y Presenting Symptoms Age, No. (Duration) y/Sex 1 Evans and Odom, Mass (2 wk) 13/F (9) 1939 2 Harrison and Sore throat, 27/F Johnson, (20) 1960 "spitting up blood" (2 wk) 3 Lake et al, (21) Mass (1 y) 30/F 1962 4 Visvanathan, (15) Dysphagia for 31/M 1971 solids, sore throat (5-6 mo) 5 Purghit and Mass (5 mo) 18/F Chhangani, (6) 1980 6 Purghit and Mass (6 mo), change 22/M Chhangani, (6) in voice, sore 1980 throat 7 Al Samarrae et al, Mass (6 y), 32/M (16 1985 recurrent sore throat 8 Al Samarrae et al, Slowing 35/F (16) 1985 deglutition, bilateral tinnitus 9 Hiraide et al, Mass (10 y), 13/F (22) 1985 recurrent tonsillitis 10 Hiraide et al, Asymptomatic, 44/M (22) 1985 incidental finding 11 Hiraide et al, Mass (20 y), FBS, 60/M (22) 1985 recurrent tonsillitis 12 Pyun and Friedman, Difficulty speaking 13/F (10) 1985 (9 mo), recurrent tonsillitis 13 Kasznica and Recurrent bilateral 3/M Kasznica, (18) serous otitis media 1991 14 Lupovitch et al, Asymptomatic, 80/F (23) 1993 incidental finding 15 Hazra et al, (14) FBS (8 mo), sore 38/F 1996 throat 16 Roth, (19) 1996 Mass, FBS 14/M 17 Sah et al, (24) Mass (6 mo), 23/M 2000 excessive salivation, FBS (1 mo) 18 Shetty et al, (25) Mass, FBS 36/M 2000 19 Raha et al, (26) Mass (3 y), 8/M 2005 tonsillitis, sleep apnea 20 Ohtsuki et al, Tonsillar swelling 41/F (27) 2006 (6 y), sneezing, sleep apnea 21 Barreto et al, Recurrent 14/F (28) 2007 tonsillitis 22 Barreto et al, Recurrent 17/M (28) 2007 tonsillitis 23 Barreto et al, Dysphagia, sore 20/F (28) 2007 throat (40 d) 24 Barreto et al, Dysphagia, mass (7 27/M (28) 2007 mo) 25 Barreto et al, Mass 28/M (28) 2007 26 Barreto et al, Dysphagia, mass (4 56/M (28) 2007 mo) 27 Duggal et al, (29) Nonproductive cough 13/M 2008 (2 y), recurrent vomiting (15 d) 28 Chen et al, (8) Obstructive 4/F 2010 breathing 29 Balatsouras et al, FBS, cough (2-3 17/M (5) 2011 wk), dysphagia (3 d) (3 d) 30 Park et al, (13) Dysphagia for 3/F 2011 solids 31 Lyngdoh et al, Tonsillar swelling 32/M (30) 2013 (3 y), sneezing, dysphagia 32 This study, 2013 Mass (8-10 wk), FBS 17/M Case Laterality Size, Diagnosis No. cm 1 R 4 Polyp 2 R 1.4 Lymphangioma 3 R 5 Polypoid tumor containing fibroadipose tissue 4 L 2.5 Lymphangioma 5 R 2 Lymphangioma 6 R NR Lymphangioma 7 L 2.5 Polypoid lymphangioma 8 L 2.8 Polypoid lymphangioma 9 R 2.1 Lymphangiectatic fibrous polyp 10 L 2.1 Lymphangiectatic fibrous polyp 11 L 1.8 Lymphangiectatic fibrous polyp 12 R 3.5 Papillary lymphoid polyp 13 R 1.2 Polypoid lymphangioma 14 L 1.1 Benign hamartomatous polyp 15 L 4.5 Lymphangioma 16 L NR Lymphangiomatous polyp 17 R 2 Lymphangiectatic fibrolipomatous polyp 18 L 3 Lymphangiomatous polyp 19 L 5 Lymphangioma 20 R 3.8 Pedunculated hamartomatous polyp 21 NR 1 Lymphoid polyp 22 NR 1.2 Lymphoid polyp 23 NR 2 Lymphoid polyp 24 NR 1.5 Lymphoid polyp 25 NR 0.8 Lymphoid polyp 26 NR 4 Lymphoid polyp 27 L 3.5 Pedunculated hamartomatous polyp 28 B 0.5 Lymphangiomatous polyp 29 R 2.6 Lymphangioma 30 R NR Lymphangiomatous polyp 31 L 1.5 Pedunculated hamartomatous polyp 32 L 3.2 Lymphangioma Abbreviations: B, bilateral; FBS, foreign body sensation; NR, not reported.
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|Author:||Mardekian, Stacey; Karp, Julie Katz|
|Publication:||Archives of Pathology & Laboratory Medicine|
|Date:||Dec 1, 2013|
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