Ameloblastoma

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Ameloblastoma
Ameloblastoma3.JPG
Ameloblastoma of the mandible
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Micrograph of an ameloblastoma showing the characteristic palisading and stellate reticulum. H&E stain.
Specialty Oncology, oral and maxillofacial surgery   OOjs UI icon edit-ltr-progressive.svg

Ameloblastoma is a rare, benign or cancerous tumor of odontogenic epithelium (ameloblasts, or outside portion, of the teeth during development) much more commonly appearing in the lower jaw than the upper jaw. [1] It was recognized in 1827 by Cusack. [2] This type of odontogenic neoplasm was designated as an adamantinoma in 1885 by the French physician Louis-Charles Malassez. [3] It was finally renamed to the modern name ameloblastoma in 1930 by Ivey and Churchill. [4] [5]

Contents

While these tumors are rarely malignant or metastatic (that is, they rarely spread to other parts of the body), and progress slowly, the resulting lesions can cause severe abnormalities of the face and jaw leading to severe disfiguration. Additionally, as abnormal cell growth easily infiltrates and destroys surrounding bony tissues, wide surgical excision is required to treat this disorder. If an aggressive tumor is left untreated, it can obstruct the nasal and oral airways making it impossible to breathe without oropharyngeal intervention. The term "ameloblastoma" is from Old English amel 'enamel'and Greek blastos 'germ'. [6]

Types

Four types of ameloblastoma have been described by the WHO 2017 classification: [7]

Conventional ameloblastoma

Previously known as solid/multicystic ameloblastoma. Usually presents with multiple large cystic areas.

Unicystic ameloblastoma

Ameloblastoma with a single cyst cavity account for around 10% of ameloblastomas. Present in younger patients in their second and third decades of life, often in relation to unerupted third molar. [8]

Metastasising ameloblastoma

Histologically atypical ameloblastoma can, rarely, lead to metastasis, usually in the lung. 'Metastasis' look histologically identical to the primary tumour and are benign in nature. [8]

Peripheral ameloblastoma

The peripheral subtype composes 2% of all ameloblastomas. [1]

Presentation

Ameloblastomas can be found both in the maxilla and mandible. Although, 80% are situated in the mandible with the posterior ramus area being the most frequent site. [9] The neoplasms are often associated with the presence of unerupted teeth, displacement of adjacent teeth and resorption of roots. [10]

Symptoms include a slow-growing, painless swelling leading to facial deformity. As the swelling gets progressively larger it can impinge on other structures resulting in loose teeth and malocclusion. Bone can also be perforated leading to soft tissue involvement. [9]

The lesion has a tendency to expand the bony cortices because the slow growth rate of the lesion allows time for the periosteum to develop a thin shell of bone ahead of the expanding lesion. This shell of bone cracks when palpated. This phenomenon is referred to as "Egg Shell Cracking" or crepitus, an important diagnostic feature.

Maxillary ameloblastomas can be dangerous and even lethal. Due to thin bone and weak barriers, the neoplasm can extend into the sinonasal passages, pterygomaxillary fossa and eventually into the cranium and brain. [8] Rare orbital invasion of the neoplasm has also been reported. [11]

Histopathology

A CT scan of a patient with an ameloblastoma. CT Scan of ameloblastoma.jpg
A CT scan of a patient with an ameloblastoma.


The resected left half of a mandible containing an ameloblastoma, initiated at the third molar Ameloblastoma.jpg
The resected left half of a mandible containing an ameloblastoma, initiated at the third molar

Conventional ameloblastomas have both cystic and solid neoplastic structures.

Solid structure

Solid areas contain fibrous tissue islands or epithelium that interconnect through strands and sheets. The epithelial cells tend to move the nucleus away from the basement membrane to the opposite pole of the cell. This process is called reverse polarization. Two main histological patterns most often occur: follicular and plexiform. Other less common histological variants include acanthomatous, basal cell, and granular cell patterns. [8]

Follicular

The most common follicular type has an outer arrangement of columnar or palisaded ameloblasts-like cells and inner zone of triangular shaped cells resembling stellate reticulum from the bell stage of tooth development. [8]

Plexiform

The plexiform type has epithelium that proliferates in a "Fish Net Pattern". The plexiform ameloblastoma shows epithelium proliferating in a 'cord like fashion', hence the name 'plexiform'. There are layers of cells in between the proliferating epithelium with well-formed desmosomal junctions, simulating spindle cell layers. The ameloblasts cells can be less prominent. [8]

Cystic structure

Large cysts up to a few centimetres in diameter can be found. In follicular type, cysts develop in the stellate reticulum and in the plexiform type, cysts are caused by degeneration of connective tissue stroma. [8]

Desmoplastic ameloblastoma

A distinctive histological variant of conventional ameloblastoma. Found in near equal frequencies in both maxilla and mandible. Resemble a fibro-osseous lesion with no obvious ameloblasts whilst dominated by dense collagenous tissue (desmoplastic). [8] In one center, desmoplastic ameloblastomas represented about 9% of all ameloblastomas encountered. [12] A systematic review showed a predilection for males and predominance in fourth and fifth decades in life. 52% desmoplastic ameloblastomas showed mandibular involvement, with a tendency to anterior region. Majority of tumours were found to have ill-defined margins radiographically. [13]

Diagnosis

Ameloblastoma is tentatively diagnosed through radiographic examination and must be confirmed by histological examination through biopsy. [8]

Radiographically, the tumour area appears as a rounded and well-defined lucency in the bone with varying size and features. Numerous cyst-like radiolucent areas can be seen in larger tumours (multi-locular) giving a characteristic "soap bubble" appearance. A single radiolucent area can be seen in smaller tumours (unilocular). [8] The radiodensity of an ameloblastoma is about 30 Hounsfield units, which is about the same as keratocystic odontogenic tumours. However, ameloblastomas show more bone expansion and seldom show high density areas. [14]

Lingual plate expansion is helpful in diagnosing ameloblastoma as cysts rarely do this. Resorption of roots of involved teeth can be seen in some cases, but is not unique to ameloblastoma. [10]

Differential diagnosis

Treatment

Tracheal intubation is difficult in this child with a large ameloblastoma. Ameloblastoma2.jpg
Tracheal intubation is difficult in this child with a large ameloblastoma.

While chemotherapy, radiation therapy, curettage and liquid nitrogen have been rarely effective in cases of ameloblastoma, surgical resection or enucleation remains the most definitive treatment for this condition. However, in a detailed study of 345 patients, chemotherapy and radiation therapy was contraindicated for the treatment of ameloblastomas. [1] Thus, surgery is the most common treatment of this neoplasm. A case of giant ameloblastoma was recently reported and managed with total mandibulectomy and pectoralis major myocutaneous flap reconstruction. [15] A systematic review found that 79% of desmoplastic ameloblastoma cases were treated by resection. Conservative treatment requires very careful case selection. [8]

Surgical resection

The aim of treatment and surgery is to remove the entire tumour with a margin of surrounding tissue (block resection) for a good prognosis. [10] Preferable removal includes 10mm of normal bone around the neoplasm. Larger ameloblastomas can require partial resection of the jaw bone followed by bone grafting. [8] There is evidence that the treatment of conventional ameloblastoma is best done by bone resection. [16] A systematic review found that 79% of desmoplastic ameloblastoma cases were treated by resection. [13]

Enucleation

Smaller mandibular neoplasms have been enucleated where the cavity of the tumour is curetted, allowing preservation of the bone cortex and the lower border of the mandible. Although, recurrence rate for this type of treatment is higher. Unicystic ameloblastomas—called intraluminal unicystic or plexiform unicystic ameloblastomas can be enucleated, as the epithelium is only limited to the inner cyst wall and lumen. [8]

Radiation and chemotherapy

Radiation is ineffective in many cases of ameloblastoma. [1] There have also been reports of sarcoma being induced as the result of using radiation to treat ameloblastoma. [17] Chemotherapy is also often ineffective. [17] However, there is some controversy regarding this [18] and some indication that some ameloblastomas might be more responsive to radiation that previously thought. [19] [5]

Follow-up and recurrence

Persistent follow-up examination including radiographs is essential for managing ameloblastoma. [20] [8] Follow-up should occur at regular intervals for at least 10 years. [21] Follow up is important, because 50% of all recurrences occur within 5 years postoperatively. [1]

Recurrence is common, although the recurrence rates for block resection followed by bone graft are lower than those of enucleation and curettage. [22] Follicular variants appear to recur more than plexiform variants. [1] Unicystic lesions recur less frequently than "non-unicystic" lesions. [1] A low recurrence rate of around 10% can be seen in unicystic ameloblastomas. [8] Recurrence within a bone graft (following resection of the original tumor) does occur, but is less common. [23] Seeding to the bone graft is suspected as a cause of recurrence. [20] The recurrences in these cases seem to stem from the soft tissues, especially the adjacent periosteum. [24] Recurrence has been reported to occur as many as 36 years after treatment. [25] To reduce the likelihood of recurrence within grafted bone, meticulous surgery [23] with attention to the adjacent soft tissues is required. [24] [20]

Molecular biology

BRAF V600E gene and SMO gene mutations have been found in ameloblastomas. V600E mutation is also seen in other malignant and benign neoplasms, which activate the MAP kinase pathway required for cell division and differentiation but is the most commonly seen mutation in ameloblastoma. [8] [7] 72% of BRAF mutations are found in the mandible. [7] A recent study discovered a high frequency of BRAF V600E mutations (15 of 24 samples, 63%) in conventional ameloblastoma. These data suggests drugs targeting mutant BRAF as potential novel therapies for ameloblastoma. [26]

SMO mutations lead to the activation of the hedgehog pathway giving similar results as V600E but is less frequently seen. [8] 55% of SMO mutations are found in the maxilla. [7]

Evidence shows that suppression of matrix metalloproteinase-2 may inhibit the local invasiveness of ameloblastoma, however, this was only demonstrated in vitro . [27] There is also some research suggesting that α5β1 integrin may participate in the local invasiveness of ameloblastomas. [28]

Epidemiology

People with African heritage have been shown to have a higher incidence compared to Caucasians, with the site often being in the midline of the mandible. [10] The annual incidence rates per million for ameloblastomas are 1.96, 1.20, 0.18 and 0.44 for black males, black females, white males and white females respectively. [29] Ameloblastomas account for about one percent of all oral tumors [17] and about 18% of odontogenic tumors. [30] Men and women are equally affected, though women average four years younger than men when tumors first occur, and tumors run larger in females. [1]

See also

Related Research Articles

<span class="mw-page-title-main">Cyst</span> Closed sac growth on the body

A cyst is a closed sac, having a distinct envelope and division compared with the nearby tissue. Hence, it is a cluster of cells that have grouped together to form a sac ; however, the distinguishing aspect of a cyst is that the cells forming the "shell" of such a sac are distinctly abnormal when compared with all surrounding cells for that given location. A cyst may contain air, fluids, or semi-solid material. A collection of pus is called an abscess, not a cyst. Once formed, a cyst may resolve on its own. When a cyst fails to resolve, it may need to be removed surgically, but that would depend upon its type and location.

<span class="mw-page-title-main">Gastrointestinal stromal tumor</span> Human disease (cancer)

Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal neoplasms of the gastrointestinal tract. GISTs arise in the smooth muscle pacemaker interstitial cell of Cajal, or similar cells. They are defined as tumors whose behavior is driven by mutations in the KIT gene (85%), PDGFRA gene (10%), or BRAF kinase (rare). 95% of GISTs stain positively for KIT (CD117). Most (66%) occur in the stomach and gastric GISTs have a lower malignant potential than tumors found elsewhere in the GI tract.

<span class="mw-page-title-main">Craniopharyngioma</span> Brain tumor of pituitary gland embryonic tissue

A craniopharyngioma is a rare type of brain tumor derived from pituitary gland embryonic tissue that occurs most commonly in children, but also affects adults. It may present at any age, even in the prenatal and neonatal periods, but peak incidence rates are childhood-onset at 5–14 years and adult-onset at 50–74 years. People may present with bitemporal inferior quadrantanopia leading to bitemporal hemianopsia, as the tumor may compress the optic chiasm. It has a point prevalence around two per 1,000,000. Craniopharyngiomas are distinct from Rathke's cleft tumours and intrasellar arachnoid cysts.

<span class="mw-page-title-main">Dentigerous cyst</span> Medical condition

A dentigerous cyst, also known as a follicular cyst, is an epithelial-lined developmental cyst formed by accumulation of fluid between the reduced enamel epithelium and the crown of an unerupted tooth. It is formed when there is an alteration in the reduced enamel epithelium and encloses the crown of an unerupted tooth at the cemento-enamel junction. Fluid is accumulated between reduced enamel epithelium and the crown of an unerupted tooth.

<span class="mw-page-title-main">Central giant-cell granuloma</span> Medical condition

Central giant-cell granuloma (CGCG) is a localised benign condition of the jaws. It is twice as common in females and is more likely to occur before age 30. Central giant-cell granulomas are more common in the anterior mandible, often crossing the midline and causing painless swellings.

<span class="mw-page-title-main">Odontogenic keratocyst</span> Medical condition

An odontogenic keratocyst is a rare and benign but locally aggressive developmental cyst. It most often affects the posterior mandible and most commonly presents in the third decade of life. Odontogenic keratocysts make up around 19% of jaw cysts. Despite its more common appearance in the bone region, it can affect soft tissue.

“Lateral periodontal cysts (LPCs) are defined as non-keratinised and non-inflammatory developmental cysts located adjacent or lateral to the root of a vital tooth.” LPCs are a rare form of jaw cysts, with the same histopathological characteristics as gingival cysts of adults (GCA). Hence LPCs are regarded as the intraosseous form of the extraosseous GCA. They are commonly found along the lateral periodontium or within the bone between the roots of vital teeth, around mandibular canines and premolars. Standish and Shafer reported the first well-documented case of LPCs in 1958, followed by Holder and Kunkel in the same year although it was called a periodontal cyst. Since then, there has been more than 270 well-documented cases of LPCs in literature.

<span class="mw-page-title-main">Calcifying odontogenic cyst</span> Medical condition

Calcifying odontogenic cyst (COC) is a rare developmental lesion that comes from odontogenic epithelium. It is also known as a calcifying cystic odontogenic tumor, which is a proliferation of odontogenic epithelium and scattered nest of ghost cells and calcifications that may form the lining of a cyst, or present as a solid mass.

<span class="mw-page-title-main">Glandular odontogenic cyst</span> Human jaw cyst

A glandular odontogenic cyst (GOC) is a rare and usually benign odontogenic cyst developed at the odontogenic epithelium of the mandible or maxilla. Originally, the cyst was labeled as "sialo-odontogenic cyst" in 1987. However, the World Health Organization (WHO) decided to adopt the medical expression "glandular odontogenic cyst". Following the initial classification, only 60 medically documented cases were present in the population by 2003. GOC was established as its own biological growth after differentiation from other jaw cysts such as the "central mucoepidermoid carcinoma (MEC)", a popular type of neoplasm at the salivary glands. GOC is usually misdiagnosed with other lesions developed at the glandular and salivary gland due to the shared clinical signs. The presence of osteodentin supports the concept of an odontogenic pathway. This odontogenic cyst is commonly described to be a slow and aggressive development. The inclination of GOC to be large and multilocular is associated with a greater chance of remission. GOC is an infrequent manifestation with a 0.2% diagnosis in jaw lesion cases. Reported cases show that GOC mainly impacts the mandible and male individuals. The presentation of GOC at the maxilla has a very low rate of incidence. The GOC development is more common in adults in their fifth and sixth decades.

<span class="mw-page-title-main">Ameloblastic fibroma</span> Medical condition

An ameloblastic fibroma is a fibroma of the ameloblastic tissue, that is, an odontogenic tumor arising from the enamel organ or dental lamina. It may be either truly neoplastic or merely hamartomatous. In neoplastic cases, it may be labeled an ameloblastic fibrosarcoma in accord with the terminological distinction that reserves the word fibroma for benign tumors and assigns the word fibrosarcoma to malignant ones. It is more common in the first and second decades of life, when odontogenesis is ongoing, than in later decades. In 50% of cases an unerupted tooth is involved.

<span class="mw-page-title-main">Odontoma</span> Benign tumour of dental tissue

An odontoma, also known as an odontome, is a benign tumour linked to tooth development. Specifically, it is a dental hamartoma, meaning that it is composed of normal dental tissue that has grown in an irregular way. It includes both odontogenic hard and soft tissues. As with normal tooth development, odontomas stop growing once mature which makes them benign.

Peripheral odontogenic fibroma(PFO) is a fibrous connective tissue mass that is exophytic and covered in surface epithelium that contains odontogenic epithelium. The World Health Organization (WHO) classifies peripheral odontogenic fibroma as a fibroblastic neoplasm with variable amounts of odontogenic epithelium that appears to be dormant. Dentine and/or cementum-like material may be present.

The calcifying epithelial odontogenic tumor (CEOT), also known as a Pindborg tumor, is an odontogenic tumor first recognized by the Danish pathologist Jens Jørgen Pindborg in 1955. It was previously described as an adenoid adamantoblastoma, unusual ameloblastoma and a cystic odontoma. Like other odontogenic neoplasms, it is thought to arise from the epithelial element of the enamel origin. It is a typically benign and slow growing, but invasive neoplasm.

<span class="mw-page-title-main">Adamantinoma</span> Rare bone tumor in the lower leg

Adamantinoma is a rare bone cancer, making up less than 1% of all bone cancers. It almost always occurs in the bones of the lower leg and involves both epithelial and osteofibrous tissue.

<span class="mw-page-title-main">Spiradenoma</span> Medical condition

Spiradenomas (SA) are rare, benign cutaneous adnexal tumors that may progress to become their malignant counterparts, i.e. spiradenocarcinomas (SAC). Cutaneous adnexal tumors are a group of skin tumors consisting of tissues that have differentiated towards one of the four primary adnexal structures found in normal skin: hair follicles, sebaceous sweat glands, apocrine sweat glands, and eccrine sweat glands. SA and SAC tumors were regarded as eccrine gland tumors and termed eccrine spiradenomas and eccrine spiradenocarcinomas, respectively. However, more recent studies have found them to be hair follicle tumors and commonly term them spiradenomas and spiradenocarcinomas, respectively. Further confusing the situation, SA-like and SAC-like tumors are also 1) manifestations of the inherited disorder, CYLD cutaneous syndrome (CCS), and 2) have repeatedly been confused with an entirely different tumor, adenoid cystic carcinomas of the salivary gland. Here, SA and SAC are strictly defined as sporadic hair follicle tumors that do not include the hereditary CCS spiradenomas and heridtary spiradenocarcinoms of CCS or the adenoid cystic carcinomas.

A borderline tumor, sometimes called low malignant potential (LMP) tumor, is a distinct but yet heterogeneous group of tumors defined by their histopathology as atypical epithelial proliferation without stromal invasion. It generally refers to such tumors in the ovary but borderline tumors may rarely occur at other locations as well.

Odontogenic cysts are a group of jaw cysts that are formed from tissues involved in odontogenesis. Odontogenic cysts are closed sacs, and have a distinct membrane derived from the rest of odontogenic epithelium. It may contain air, fluids, or semi-solid material. Intra-bony cysts are most common in the jaws, because the mandible and maxilla are the only bones with epithelial components. That odontogenic epithelium is critical in normal tooth development. However, epithelial rests may be the origin for the cyst lining later. Not all oral cysts are odontogenic cysts. For example, mucous cyst of the oral mucosa and nasolabial duct cyst are not of odontogenic origin.

Cysts of the jaws are cysts—pathological epithelial-lined cavities filled with fluid or soft material—occurring on the bones of the jaws, the mandible and maxilla. Those are the bones with the highest prevalence of cysts in the human body, due to the abundant amount of epithelial remnants that can be left in the bones of the jaws. The enamel of teeth is formed from ectoderm, and so remnants of epithelium can be left in the bone during odontogenesis. The bones of the jaws develop from embryologic processes which fuse, and ectodermal tissue may be trapped along the lines of this fusion. This "resting" epithelium is usually dormant or undergoes atrophy, but, when stimulated, may form a cyst. The reasons why resting epithelium may proliferate and undergo cystic transformation are generally unknown, but inflammation is thought to be a major factor. The high prevalence of tooth impactions and dental infections that occur in the bones of the jaws is also significant to explain why cysts are more common at these sites.

Ameloblastic carcinoma is a rare form of malignant odontogenic tumor, that develops in the jawbones from the epithelial cells that generate the tooth enamel. It is usually treated with surgery; chemotherapy has not been proven to be effective.

The ameloblastic fibro-odontoma (AFO) is essentially a benign tumor with the features characteristic of ameloblastic fibroma along with enamel and dentin. Though it is generally regarded as benign, there have been cases of its malignant transformation into ameloblastic fibrosarcoma and odontogenic sarcoma. Cahn LR and Blum T, believed in "maturation theory", which suggested that AFO was an intermediate stage and eventually developed during the period of tooth formation to a complex odontoma thus, being a hamartoma.

References

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  15. ↑ Ramesh M, Gurumoorthy AN, Sanjive JG (February 2022). "Giant ameloblastoma". Formosan Journal of Surgery. 55 (1): 27–30. doi: 10.4103/fjs.fjs_107_21 .
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  19. ↑ Miyamoto CT, Brady LW, Markoe A, Salinger D (June 1991). "Ameloblastoma of the jaw. Treatment with radiation therapy and a case report". American Journal of Clinical Oncology. 14 (3): 225–30. doi:10.1097/00000421-199106000-00009. PMID   2031509. S2CID   33468547.
  20. 1 2 3 Choi YS, Asaumi J, Yanagi Y, Hisatomi M, Konouchi H, Kishi K (January 2006). "A case of recurrent ameloblastoma developing in an autogenous iliac bone graft 20 years after the initial treatment". Dento Maxillo Facial Radiology. 35 (1): 43–6. doi:10.1259/dmfr/13828255. PMID   16421264.
  21. ↑ Su T, Liu B, Zhao JH, Zhang WF, Zhao YF (February 2006). "[Ameloblastoma recurrence in the grafted iliac bone: report of three cases]". Shanghai Kou Qiang Yi Xue = Shanghai Journal of Stomatology. 15 (1): 109–11. PMID   16525625.
  22. ↑ Vasan NT (March 1995). "Recurrent ameloblastoma in an autogenous bone graft after 28 years: a case report". The New Zealand Dental Journal. 91 (403): 12–3. PMID   7746553.
  23. 1 2 Dolan EA, Angelillo JC, Georgiade NG (April 1981). "Recurrent ameloblastoma in autogenous rib graft. Report of a case". Oral Surgery, Oral Medicine, and Oral Pathology. 51 (4): 357–60. doi:10.1016/0030-4220(81)90143-2. PMID   7015222.
  24. 1 2 Martins WD, Fávaro DM (December 2004). "Recurrence of an ameloblastoma in an autogenous iliac bone graft". Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontics. 98 (6): 657–9. doi:10.1016/j.tripleo.2004.04.020. PMID   15583536.
  25. ↑ Zachariades N (October 1988). "Recurrences of ameloblastoma in bone grafts. Report of 4 cases". International Journal of Oral and Maxillofacial Surgery. 17 (5): 316–8. doi:10.1016/S0901-5027(88)80011-0. PMID   3143780.
  26. ↑ Kurppa KJ, Catón J, Morgan PR, Ristimäki A, Ruhin B, Kellokoski J, Elenius K, Heikinheimo K (April 2014). "High frequency of BRAF V600E mutations in ameloblastoma". The Journal of Pathology. 232 (5): 492–8. doi:10.1002/path.4317. PMC   4255689 . PMID   24374844.
  27. ↑ Wang A, Zhang B, Huang H, Zhang L, Zeng D, Tao Q, Wang J, Pan C (June 2008). "Suppression of local invasion of ameloblastoma by inhibition of matrix metalloproteinase-2 in vitro". BMC Cancer. 8 (182): 182. doi: 10.1186/1471-2407-8-182 . PMC   2443806 . PMID   18588710.
  28. ↑ Souza Andrade ES, da Costa Miguel MC, Pinto LP, de Souza LB (June 2007). "Ameloblastoma and adenomatoid odontogenic tumor: the role of alpha2beta1, alpha3beta1, and alpha5beta1 integrins in local invasiveness and architectural characteristics". Annals of Diagnostic Pathology. 11 (3): 199–205. doi:10.1016/j.anndiagpath.2006.04.005. PMID   17498594.
  29. ↑ Shear M, Singh S (July 1978). "Age-standardized incidence rates of ameloblastoma and dentigerous cyst on the Witwatersrand, South Africa". Community Dentistry and Oral Epidemiology. 6 (4): 195–9. doi:10.1111/j.1600-0528.1978.tb01149.x. PMID   278703.
  30. ↑ Gordon J (2004). "Clinical Quiz: Painless Mass". Medscape . 3 (8).


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