Ministry of Health of Ukraine Ukrainian Medical Stomatolgical Academy

Methodical Instructions for independent work of students during the training for the practical studies

Academic discipline Surgical stomatology Моdule № 6 The topic of the stadies Benign tumors and cysts of the salivary glands. № 10 Management of salivary fistulas. Benign tumors of the soft tissues. Vascular tumors and birthmarks. Immunological concept of tumor development. Course V Faculty Foreign Students Training, Stomatological

Poltava -2020 1. Relevance of the topic:

Problems of the salivary glands are uncommon; however, the spectrum is quite varied and challenging. The salivary glands consists of the major and minor salivary glands; the parotid, submandibular, and sublingual glands constitute the major salivary glands and the minor salivary glands are found essentially anywhere in the upper aerodigestive tract, including the trachea and paranasal sinuses. When functioning properly, the salivary glands are rarely noticed, but when affected by neoplastic disease, they can be a challenge in diagnosis and treatment. enlargement is less often caused by neoplasia than by inflammatory or other nonneoplastic conditions. Less than 3% of all tumors of the head and neck are salivary gland neoplasms. Of all neoplasms of salivary gland origin, about 85% occur in the . Of these, 80% are benign, whereas only about 50% of the submandibular tumors and approximately 25% of the minor salivary gland neoplasms are benign. Although extremely rare, tumors of the sublingual gland are almost always malignant. The salivary glands neoplasms are rare and represent a variable group of benign and malign tumors with different behavioral characteristics . The pathologic diagnosis is critical for the correct management of these lesions since the aggressivity grade depends on their histological types. Vascular anomalies are a heterogeneous group of congenital blood vessel disorders more typically referred to as birthmarks. Subcategorized into vascular tumors and malformations, each anomaly is characterized by specific morphology, pathophysiology, clinical behavior, and management approach. Hemangiomas are the most common vascular tumor. Lymphatic, capillary, venous, and arteriovenous malformations make up the majority of vascular malformations.

2. THE SPECIFIC AIMS:

2.1. To analyze the causes of tumors of the salivary glands. 2.2. To explain topographic anatomical features of large and small salivary glands. 2.3. To propose a plan for examination of the patient with tumors of the salivary glands. 2.4. To classify tumors of the salivary glands. 2.5. To propose various surgical options to treatment of tumors of the salivary glands. 2.6. To draw topography of the facial in the parotid gland. 2.7. To analyze long-term results of surgical treatment of mixed tumors. 2.8. To make a plan of treatment of a patient with a benign tumors of the salivary glands.

3. BASIC KNOWLEDGE, ABILITIES, SKILLS, WHICH ARE NECESSARY FOR STUDY THEMES (intradisciplinary integration) Names of the previous The received skills disciplines 1. Human anatomy. To be guided in the main questions of a structure of salivary glands. 2. Histology. To prepare a material for histological or cytological research of tumors of salivary glands. 3. Pathoanatomy. To make the exact diagnosis. 4. Pathophysiology. Etiology and pathogenesis of developments of benign tumors of salivary glands. 5. Topographical anatomy and To be guided in a choice of operative accesses at operative surgery. treatment of benign tumors of salivary glands. 6. General oncology. To make a prognosis at treatment of patients with epithelial and non-epithelial tumors of salivary glands. 7. Surgical stomatology and Treatment of benign tumors of salivary glands. maxillo-facial surgery.

4. Tasks for independent work in preparation for the lesson 4.1. The list of the basic terms, parameters, characteristics which the student should master at preparation for employment:

Term Definition 1. Biopsy. Lifetime receiving a material for histological research. 2. Sclerotherapy Introduction to the cavity of vessel tumor of aggressive chemical substance (ethyl spirit, formalin and other). 3. Neavus New formation from pigmented cells.

4.2. Theoretical questions to lesson: 1. Anatomy and physiology of salivary glands of the human. 2. Embriogenesis and histologic structure of major and minor salivary glands. 3. Theories of an origin of benign tumors of salivary glands. 4. Histological and clinical classifications of benign tumors of salivary glands. 5. Diagnostics and differential diagnostics of benign tumors of salivary glands. 6. Methods of treatment of benign tumors of salivary glands. 7. Complication at and after treatment of benign tumors of salivary glands. 8. Main and additional methods of diagnostics of benign tumors. 9. Classification of tumors of vessels. 10. Clinic and diagnostics of tumors of vessels. 11. Methods of treatment of tumors of vessels.

4.3. Practical works (task) which are executed on lesson: 1. To be able to collect anamnesis from a maxillofacial patient. 2. To be able to examine the patient. 3. To be able to prescribe additional examination methods. 4. To be able to read laboratory data. 5. To be able to read contrast x-rays foto of the head and neck. 6. To be able to carry out a differential diagnosis for patients with vascular tumors. 7. To know how to write a medical card for dental patient. 8. To spend curation of patients with benign tumors of salivary glands. THE CONTENT OF THE TOPIC:

The salivary glands may be divided into major salivary glands that include the parotid glands, submandibular and sublingual and the minor salivary glands.

The main and largest of them is the parotid gland. It's located close to the external ear (par, close + otid, ear), between the jaw branch and the mastoid process. Above it, the parotid bed is limited by the floor of the external auditory meatus and the zygomatic process of the temporal bone. In the middle, there is the temporal bone stiloid process and its associated muscles. It's laterally limited by the parotid fascia superficial blade and the skin. The rear wall extends between the mastoid and stiloid processes. The front wall is formed by the jaw branch and its fixed muscles (masseter and medial pterygoid). From the surface to the depth, the structures crossing the gland are: the , the retromadibular vein and the external carotid . Vascularization by the and its terminal branches (superficial, temporal and maxillary) and parasympathetic innervation by the glossopharyngeal.

The is along the jaw's structure and is partially superficial and partially deep in the mieloid muscle. It has a U format and approximately half of the parotid size. It takes almost all the submandibular fornix and has a relationship with the facial vein (superficial to the gland), facial artery (deep in the gland) and the marginal mandibular nerve (flows up along the lower edge of the jaw, superficial to the facial vein). The sublingual glands are located in the floor of the oral cavity between the jaw and the genioglossal muscle. The minor salivary glands consist of 600 to 1.000 small independent glands found across the oral cavity, palatine tonsils, and larynx. Epidemiology. These correspond to approximately 1% of the head and neck tumors, with an approximate incidence of 1.5 cases/100.00. Despite the incidences vary according to the literature, 67.7% to 84% of the neoplasms start in the parotid, 10% to 23% in the submandibular gland and the other cases in the sublingual gland and in the minor salivary glands (2,4,5,6). 95% of the cases occur in adults and are rare in children.

About 75% of the neoplasms are benign and the pleomorphic adenoma is the most common histological type. The smaller the gland, the greater the probability for the neoplasm to be malign: 25% of the parotid tumors are malign, while in the submandibular gland this number goes up to 43% and hits 82% in the minor salivary glands.

In the parotids, the most common histological subtype is the pleomorphic adenoma (53.3%), followed by the Warthin's tumor (28.3%) and by the mucoepidermoid carcinoma (9%). In the other glands the pleomorphic adenoma is also the most common (36% in the submandibular and 43% in the sublingual and minor glands), followed by the cystic adenoid carcinoma (25% in the submandibular and 34% in the sublingual and minor glands) and by the mucoepidermoid carcinoma (12% in the submandibular and 11% in the sublingual and minor glands). Risk Factors The etiologic factor for the general salivary glands neoplasms isn't well defined, but some research's statements suggest associations with:

 Radiation: radiotherapy in low dosages has been implied in the pleomorphic adenoma pathogenesis, squamous cell carcinoma and mucoepidermoid carcinoma after 15 to 20 years of exposure. The greater evidence of such association is in the increased incidence of these tumors in survivors from areas exposed to atomic bomb.  Smoking: in spite it's not bound to the development of salivary glands carcinoma, smoking has been associated to the Warthin's tumor.  Epstein-Barr's Virus: except for the undifferentiated carcinoma, the viral etiologic role was not present in the salivary glands neoplasms .  Genetic Factors.

FIGURE. Parotid mixed tumor.

Clinical History. They appear as slow growth asymptomatic masses. Pain is not common, but in the benign neoplasms there may occur infection, hemorrhage or cystic increase. In the malign neoplasms the pain may indicate neural invasion, but the pain should not be used as a parameter for differentiation among the neoplasms. The facial nerve paralysis strongly suggests a malign tumor, although it's not patognomonic, once it may occur through the nerve compression or stretching by lengthy benign tumors. Other suggestive signals of malignity are the mass fixing and the lack of definition of adjacent structures. The minor salivary glands have a variable shape depending upon their location. in the oral cavity as non-ulcerated and painless masses generally in and the floor of the ; in paranasal sinuses they include sinusitis and rhinitis symptoms; in the laryngotracheal region with raucousness, dysphagia, cough and sensation of foreign body; in the parapharyngeal space they are asymptomatic until reaching a large size, and repel several peripheral structures leading to dysphagia and "hot potato" voice. Because of its low relative frequency, the immediate recognition of the neoplasm demands attention by the specialist doctor. However there are no reliable clinical criteria to differentiate them and it's necessary to request complimentary exams for the adequate diagnosis of the tumors. Conventional radiography and sialography are rarely used because they provide little useful information. Nuclear imaging using technetium 99m pertechnetate is helpful only with oncocytic and Warthin's tumors (Higashi et al, 1989). Because a needle biopsy can provide better information, nuclear imaging is rarely obtained. The CT scan and MRI are very helpful in determining the extent of disease but do not differentiated between benign and malignant tumors. High-resolution ultrasound or sonography is useful in the hands of experienced radiologists and may detect calculi, abscesses, and cysts, and can even correctly assess up to 90% of benign versus malignant tumors (Gritzman, 1989). A biopsy is always required to make a diagnosis of salivary gland disorders. Various types of biopsies are used and include fine- needle aspiration (FNA), core-needle biopsy, and incisional and excisional biopsies. Dr. John Conley refers to a superficial parotidectomy as a "grand biopsy". FNA biopsies are now an acceptable and commonly used method to evaluate salivary gland neoplasms. Of importance is obtaining a good sample of the tumor and having an experienced cytologist. One must correlate the FNA report with the clinical findings. The accuracy of the FNA for differentiating benign from malignant tumors should approach 90% (Sismanis et al, 1981). CT and MRI locate the tumor and describe its extent. Fine-needle aspiration biopsy of the mass confirms the cell type. A search for spread to regional nodes or distant metastases in the lung, liver, bone, or brain may be indicated before treatment is selected.

Benign epithelial tumors Benign Tumors. Adenomas. Pleomorphic adenomas (benign mixed tumors) are the most common tumors of the salivary gland. The great majority arise in the parotid gland. The term pleomorphic describes the embryologic basis for these tumors with their origin of epithelial and connective tissue. Although the histogenesis o this tumor has been debated, the current theory is that pleomorphic adenomas arise from intercalated and myoepithelial cells. This tumor usually presents in the fourth or fifth decades. It is painless, slow growing, and usually found as an incidental mass in the or near the angle of the . About 90% of these tumors arise superficial to the plane of the facial nerve. The 10% that arise in the deep lobe may extend through the space between the angle of the mandible and the styloid process and present as a parapharyngeal space mass. They may also present with intraoral swelling and medial displacement of the tonsil and lateral pharyngeal wall. In most cases, the masses are firm and mobile. Pleomorphic adenomas of the submandibular and minor salivary glands present as swellings in those glands. When present in the minor salivary glands, most occur in the hard and . The second most common place is the upper . Unlike most mixed tumors, those in the palate and lip frequently lack a capsule. Commonly pleomorphic adenomas of the parapharyngeal space present as asymptomatic masses. Although the parapharyngeal space contains the great vessels and cranial nerve IX to XII, involvement of these structures is rare. Many of the tumors arise from the deep lobe of the parotid, but they can also arise from separate islands of parotid and minor salivary gland tissue that naturally occur in the parapharyngeal space. The treatment is surgical excision. On gross pathologic examination a pleomorphic adenoma is a solitary, firm, round tumor with a thin, delicate, incomplete capsule. Commonly pseudopods of tumor extend through the capsule. Recurrent tumors are frequently multinodular. The cut surface is characteristically solid and is hard or rubbery to soft in consistency. The color varies from white to gray to pale yellow. Microscopically the tumors have islands of stellate and spindle cells that are interspersed with a mixoid background. Glandular areas of tubular have also been reported. Variations on this tumor are common and may include squamous metaplasia, calcification, cartilage-like tissue, oxyphilic cells, and a palisading appearance of the underlying stroma. Malignant transformation may occur in these tumors, more often in longstanding tumors. Case reports of clinically metastatic disease with histologically benign tumors have also been reported. These tumors should not recur after adequate surgical excision. Most recurrences can be traced to enucleation of the mass with no appreciation of the pseudopod extensions of tumor. Although encapsulated, if a cuff of normal tissue is not removed along with the tumor, recurrence may be an expected complication. Consequently, the treatment of choice for a pleomorphic adenoma of the parotid, submandibular gland, or minor salivary gland is excision of tumor with a surrounding cuff of normal tissue. In the parotid gland the treatment is usually a superficial or total parotidectomy with facial nerve preservation. A recurrent pleomorphic adenoma changes the treatment plan. If a supericial parotidectomy has been previously performed, the deep lobe of the parotid must be removed. Obviously, great care must be taken to protect the facial nerve, which may be vulnerable because of the altered anatomy and scarring. With submandibular or minor salivary gland involvement the recurrent tumor and an extra cuff of normal tissue should be removed. Radiotherapy plays a questionable role in the recurrent pleomorphic adenoma when surgery is no longer a feasible option. Chemotherapy plays no role in the management of these tumors. Monomorphic adenomas are benign tumors of the salivary glands that also arise from ductal epithelium. These tumors usually occur in the parotid gland and the minor salivary glands of the upper lip. They have also been described in other areas where minor salivary glands are found, like the hard and soft palate and buccal mucosa; these tumors only represent 1% to 3% of all salivary gland neoplasms (Batsakis, 1991). There is no sex predilection and the average patient is over 60 years of age. As with most benign tumors, monomorphic adenomas classically appear as asymptomatic, slow-growing masses. Facial nerve involvement is very rare. Histologically these tumors are distinguished from pleomorphic adenomas by the absence of chondromyxoid stroma and the presence of a uniform epithelial pattern. Basal cell adenomas. Basal cell adenomas are the predominant tissue type of monomorphic adenoams. The average patient is 60 years of age. Most of these tumors also occur in the parotid gland or in the minor salivary glands of the upper lip. The tumors are solid and well circumscribed. The cut surface is gray-white, gray-red, or pink-brown. Tumors arising in the parotid gland usually have a capsule, whereas those arising in the lip do not. Histologically, a solid growth pattern is more common in the parotid tumors, consisting of isomorphic cells with dark nuclei and rare mitoses. The epithelium is demarcated from surrounding stroma by a row of peripheral cells that demonstrate prominent nuclear palisading. This efect is due to the presence of an intact basement membrane and helps to differentiate this tumor from a pleomorphic adenoma. Adenomas arising in the upper lip usually have a tubular or canalicular pattern. Clinically, basal cell adenomas may be confused with enlarged nodes, sebaceous cysts, mucoceles, lipomas, nasolabial cysts, or pleomorphic adenomas. Histologically, these tumors must be differentiated from adenoid cystic carcinomas. Basal cell adenomas are not always encapsulated; instead of invading surrounding tissue, they usually show a pattern of circumscription. The stroma is also more vascular. Because basal cell adenomas are benign, treatment is excision with a cuff of normal surrounding tissue.

Warthin's tumor is also known as papillary cystadenoma lymphomatosum or adenolymphoma. This tumor occurs almost exclusively in the parotid gland and accounts for 2% to 10% of all parotid tumors. The only salivary gland tumor that is more common is the benign mixed tumor. Warthin's tumor is unique in several ways. It contains lymphoid tissue, has a striking male predominance, is bilateral in 10% of cases, commonly has unilateral focal involvement, and is rare in blacks. Presentation is usually during the sixth decade. Although the masses are classically asymptomatic, a small minority of patients complain of pain. A Warthin's tumor commonly is found in the superficial lobe of the parotid gland near the angle of the mandible. This tumor has also been reported in the parapharyngeal space and less commonly in the submandibular gland and the minor salivary glands of the lower lip and palate. Embryologically the parotid gland is the first salivary gland to develop and the last to become encapsulated. During this late encapsulation, salivary ducts are trapped in lymph nodes and become the genesis for a Warthin's tumor. The identification of normal nodal structures such as subcapsular sinuses and the occurrence of these tumors in lymph nodes outside the parotid support this hypothesis. Further support lies with T- and B-cell markers that represent normal lymph nodes that have also been identified in Warthin's tumors. Also, the almost total confinement of this tumor to the parotid region may be explained by the fact that ductal elements are found only in parotid tissue. Oncocytes are found in Warthin's tumors and oncocytomas, the only other tumor with frequent bilateral presentation. Oncocytes selectively incorporate technetium 99m and appear as hot spots on a scan. Most other neoplasms show either normal uptake or appear as cold nodules. The technetium is accumulated because of a functional abnormality in the oncocyte and its altered mitochondria. Grossly, Warthin's tumors are encapsulated with a smooth or lobulated surface. Papillary cysts are commonly found on sectioning and may contain mucoid brown fluid (Fig. 61-5). Solid gray tissue encapsulates white nodules of lymphoid tissue. Lymph node architecture may be distorted by epithelial components compressing the sinuses. Electron microscopy shows a tremendous number of mitochondria in the epithelial cells. This in turn causes a granular-appearing eosinophilia. Treatment is a superficial parotidectomy with preservation of the facial nerve. Inadequate excision or tumor multicentricity may explain tumor recurrence.

Benign nonepithelial tumors Hemangiomas are the most common SGTs in children and usually involve the parotid gland. Less often, they may involve the submandibular gland. These vascular tumors may be distinguished from vascular malformations by their presence early in life, rapid growth phase in children aged approximately 1-6 months, and gradual involution over 1-12 years. The typical presentation is an asymptomatic, unilateral, compressible mass. Gross examination reveals a dark red, lobulated, unencapsulated mass. Microscopically, hemangiomas are composed of solid masses of cells and multiple anastomosing capillaries that replace the acinar structure of the gland. Because they lack a capsule, they tend to infiltrate neighboring structures. Treatment should initially consist of steroids administered 2-4 mg/kg/d. Although the response may be immediate, only 40-60% of hemangiomas exhibit a response to steroids. Despite the tendency toward spontaneous involution, specific conditions may warrant surgical excision.

Lymphangioma (cystic hygroma) are most commonly located in the head and neck region of infants and children. They are believed to be due to lymphatic sequestration of primitive embryonic lymph ducts that undergo irregular growth and canalization. They are spongy, multiloculated masses with a yellowish or bluish surface and are formed by endothelial-lined spaces. More than 50% manifest at birth, and 80% manifest by age 2 years. Usually, they manifest as painless masses that may involve parotid glands, submandibular glands, or both. Diagnosis is made based on clinical findings. Surgical excision with preservation of the vital structures is the treatment of choice. Lymphangiomas rarely cause symptoms of airway obstruction, and excision is usually for cosmetic reasons.

Lipoma tumors are relatively uncommon in a major salivary gland. They derive from fat cells and appear grossly as smooth, well-demarcated, bright-yellow masses. Histologically, the tumor consists of mature adipose cells with uniform nuclei. These tumors manifest as soft, mobile, painful masses and peak in the fifth and sixth decades of life, with a male-to-female ratio of 10:1. They are slow-growing tumors with an average diameter of 3 cm. Treatment is surgical excision.

Tumor-like lesions of the salivary glands Tumor-like lesions of the salivary glands include sialadenosis, oncocy-tosis (diffuse oncocytosis and focal adenomatous oncocytic hyperplasia), necrotizing sialometaplasia (salivary gland infarction), benign lymphoepi-thelial lesion (chronic myoepithelial ), salivary cysts (mucoceles of the minor salivary glands of extravasation or retention type, cysts of the major salivary glands, and dysgenetic polycystic disease of the parotid gland), chronic sclerosing sialadenitis of the submandibular gland (Kuttner tumour), and cystic lymphoid hyperplasia in AIDS. All these diseases in some cases can mimic the true neoplasm and are usually associated with higher risk for the tumor development.

Mucocele Mucocele is a tumor-like lesion of the salivary glands, which is a result of obstruction of the salivary outflow tracts and extravasation of mucus into the surrounding tissues. Salivary ducts, especially those of the minor salivary glands, are occasionally traumatized, commonly by lip biting. Subsequent saliva production may then extravasate beneath the surface mucosa into the soft tissues. Saliva leaking from a damaged duct into the superficial surrounding tissues excites an inflammatory reaction. Over time, the pools of saliva form a rounded collection of viscous fluid, surrounded by compressed connective tissue without an epithelial lining. As it has no epithelial lining, mucocele is not a true cyst. Mucoceles mainly affect the minor salivary glands, particularly of the lip. Other typical sites are buccal mucosa and sublingual gland (ranula). Retention cysts of the minor salivary glands are usually superficial and rarely larger than 1 cm in diameter. They manifests as rounded, soft, compressible mass. Later, they become hemispherical, fluctuant and bluish due to the thin wall. Cyst is filled with viscous clear yelowish or blue-gray mucus. Patients may relate a hystory of cyst rupture followed by lession reccurence.

Ranula are large retention cysts occurring in the sublingual gland. Their pathogenesis and histological structure is usually the same as in other salivary retention cysts. The term "ranula" has its derivation traced to the oral anatomy of the frog. The origin of a ranula is due to obliteration of one of the minor ducts of the sublingual gland, while the main excretory duct remains patent. Extravasation of saliva moves throughout the sublingual gland and into the submucosal space via hydrostatic pressure as the sublingual gland continues to produce saliva. The extravasated mucus can gradually spread around or through the into the submental or submandibular spaces. Simple ranulas are located above the mylohyoid muscle in the . Complex or plunging ranulas develop when the lesion extends beyond the level of the mylohyoid muscle into the submandibular or . Plunging ranula may be quite large and extend to the inferior aspect of the neck or the chest wall. The ranula clinically manifests as a painless mucus pseudocyst on the floor of the mouth. Usually they have 2 or 3 cm in diameter, but occasionall extend across the whole of the floor of the mouth. They are soft, fluctuant on bimanual palpation, painless and bluish in color. They usually enlarge slowly but may become large enough to elevate the and interfere with speech or mastication. The usual presentation of a plunging ranula is a soft, compressible mass in the submandibular or submental region. These may be initially misdiagnosed as sialadenitis or a salivary tumor. Transillumination of the mass may be feasible in the larger ranula. Intraoral examination should demonstrate an intraoral component combined with the cervical component. Magnetic resonance imaging (MRI) in this cases can show herniation of the sublingual tissue and cystic material through the mylohyoid muscle. Tl- weighted images are usually low enhancing while T2-weighted images are bright. The use of ultrasound of the neck in the evaluation of a plunging ranula may also reveal deficiencies in the mylohyoid muscle with herniation of the sublingual gland. With computed tomography (CT), a plunging ranula can be readily identified preoperatively as a cystic unilocular mass in the suprahyoid anterior neck.

Cysts of the parotid gland. Retention cists that occur in the parotid gland are more common in men often in their seventh or eighth decades. They present as a slow growing swelling in the affected gland, which on aspiration reveals a clear colored fluid. They also often completely disappear on aspiration. In the majority of cases the diagnosis is only made when the cyst is removed. It is not always easy to distinguish it from cystic form of adenolymphoma preoperatively. Treatment of the salivary glands cysts Treatment of a small superficial mucocele consists of excision of the mucocele and the associated minor salivary glands that contributed to its formation. If the damaged minor salivary gland has not beer removed recurrence of the disease is very likely. An operation is usually performed under the local anesthesia. Infiltration or mental nerve-block can be used. It is advised to delineate the boundaries of the mucocele first because the local infiltration of anesthetic may distort the anatomy. An elliptical superficial incision through the mucosa is made around the mucocele. Careful dissection around the cyst may permit its complete removal. The regional associated minor salivary glands are also removed and sent for pathohistologic evaluation. Hemostasis is achieved with an electrocautery device and the wound is closed with absorbable suture. The recurrence rates of mucoceles after surgical removal are not very high and usually they are caused by incomplete removal or repeat trauma to the minor salivary glands. In cases of ranula different treatment modalities can be used. The usual treatment is marsupialization, in which a portion of the of the floor of the mouth is excised, along with the superior wall of the ranula. Subsequently, the ranula wall is sutured to the oral mucosa of the floor of the mouth and allowed to heal by secondary intention. The preferred treatment for recurrent or plunging ranulas is excision of the ranula and sublingual gland via an intraoral or extraoral approach. In this cases the general anesthesia with nasal intubation is often required. An intraoral approach is made with an incision along the axis of the gland. The is identified, either by dissection or following can-nulation with a probe to prevent its injury during the resection. The sublingual gland and the cyst are dissected in a subcapsular space. At the posterior pole of the gland the is identified as it crosses the Wharton's duct and is preserved. The sublingual gland is dissected from anteriorly, and the final excision is the posterior pole after visualizing the lingual nerve. After completion of the dissection and removal of the gland, careful hemostasis is achieved. Closure of the wound is performed with absorbable sutures in a single layer. Some patients plunging ranulas with may require an incision on the neck for exposure and excision of the ranula. This incision is performed 2,5 cm below the inferior margin of the mandible. The submandibular gland is identified and carefully mobilized away from the ranula. In addition to identifying the submandibular duct and lingual nerve during the dissection, in this cases care must be taken not to rupture the pseudocyst as the ranula is followed through the mylohyoid muscle. Completion of the posterior and inferior extent of the plunging ranula is performed after careful identification of the facial artery and veins to prevent bleeding in the operative site. After the cyst removal incision is closed by layered suture. In cases when adenocystectomy is performed the recurrences are rather uncommon. Complications of the surgical treatment for retention cysts of the salivary glands include recurrence, injury of the lingual or hypoglossal , Wharton's duct injury, bleeding and development of infection.

Operations used to remove parotid tumors include:  Removing part of the parotid gland. For most parotid tumors, surgeons may cut away the tumor and some of the healthy parotid gland tissue around it (superficial parotidectomy).  Removing all of the parotid gland. Surgery to remove all of the parotid gland (total parotidectomy) might be recommended for larger tumors and those that affect the deeper parts of the parotid gland.  More extensive surgery for larger cancers. If parotid cancer has grown into nearby bone and muscles, a more extensive operation may be necessary. Surgeons try to remove all of the cancer and a small amount of the healthy tissue that surrounds it. Then they work to repair the area so you can continue to chew, swallow, speak, breathe and move your face. This may involve transferring skin, tissue, bone or nerves from other parts of your body to make repairs. To access the parotid gland, surgeons make an incision near the ear. During the operation, special care is taken to avoid damage to nearby structures, such as the facial nerve that runs through the parotid gland. The facial nerve controls facial movement, so stretching or cutting the nerve can cause partial or complete paralysis of the face that can be temporary or permanent. If the facial nerve must be cut in order to remove all of the tumor, surgeons can repair it using nerves from other areas of your body or processed nerve grafts from donors. Radiation therapy uses powerful beams of energy, such as X-rays, protons or neutrons, to kill cancer cells. If your parotid tumor is cancerous, radiation therapy might be recommended after surgery to kill any cancer cells that remain. Radiation therapy is sometimes used as an initial treatment when surgery isn't an option. Chemotherapy is a drug treatment that uses medications to kill cancer cells. It's not routinely used to treat parotid tumors. But sometimes it's combined with radiation therapy to treat parotid cancers that have a high risk of spreading or cancers that can't be removed completely with surgery. Chemotherapy might also be an option for people with advanced parotid cancers that have spread to other parts of the body. Malignant tumors are less common and can be characterized by rapid growth or a sudden growth spurt. They are firm, nodular, and can be fixed to adjacent tissue, often with a poorly defined periphery. Eventually, the overlying skin or mucosa may become ulcerated or the adjacent tissues may become invaded. Mucoepidermoid carcinoma is the most common salivary gland cancer, typically occurring in people in their 20s to 50s. It can manifest in any salivary gland, most commonly in the parotid gland but also in the submandibular gland or a minor salivary gland of the palate. Intermediate and high-grade mucoepidermoid carcinomas may metastasize to the regional lymphatics. Adenoid cystic carcinoma is the most common malignant tumor of minor salivary glands (and of the trachea). It is a slowly growing malignant transformation of a much more common benign cylindroma. Its peak incidence is between ages 40 and 60, and symptoms include severe pain and, often, facial nerve paralysis. It has a propensity for perineural invasion and spread, with disease potentially extending many centimeters from the main tumor mass. Lymphatic spread is not a common feature of this tumor. Pulmonary metastases are common, although patients can live quite long with them. Acinic cell carcinoma, a common parotid tumor, occurs in people in their 40s and 50s. This carcinoma has a more indolent course, as well as an incidence of multifocality. Carcinoma ex mixed tumor is adenocarcinoma arising in a preexisting benign mixed tumor. Only the carcinomatous element metastasizes. Infantile hemangiomas are the most common tumor in infancy and occur in approximately 10% of the population. Identifiable risk factors include female sex, prematurity, low birth weight, and fair skin. They consist of rapidly dividing endothelial cells. Because their growth is attributed to hyperplasia of endothelial cells, they are classified as, and are the most common, vascular tumors. Hemangiomas are further categorized into two types: “infantile” or “congenital.” The rare “congenital” hemangioma is less understood and present at birth. Congenital hemangiomas either rapidly involute (rapidly involuting congenital hemangioma (RICH)) over a very brief period in infancy or never involute (noninvoluting congenital hemangioma; (NICH)). The remaining sections will focus on the more common “infantile” hemangiomas. The pathogenesis of infantile hemangiomas remains unclear, although two theories dominate current thought. The first theory suggests that hemangioma endothelial cells arise from disrupted placental tissue imbedded in fetal soft tissues during gestation or birth. Markers of hemangiomas have been shown to coincide with those found in placental tissue. This is further supported by the fact that they are found more commonly in infants following chorionic villus sampling, placenta previa, and preeclampsia. A second theory arose from the discovery of endothelial progenitor and stem cells in the circulation of patients with hemangiomas. The development of hemangiomas in animals from stem cells isolated from human specimens supports this theory. However, infantile hemangiomas most likely arise from hematopoietic progenitor cells (from placenta or stem cell) in the appropriate milieu of genetic alterations and cytokines. Abnormal levels of matrix metalloproteinases (MMP-9) and proangiogenic factors (VEGF, b-FGF, and TGF-beta 1) play a role in hemangioma pathogenesis. Genetic errors in growth factor receptors have also been shown to affect development of hemangiomas. Diagnosis. Infantile hemangiomas present shortly after birth most often as well- demarcated, flat, and erythematous red patches. At this stage, hemangiomas may be confused with other red lesions of birth, but rapid proliferation and vertical growth will trigger the diagnosis. Generally speaking, hemangiomas do not spread outside their original anatomical boundaries. Hemangiomas follow a predictable course with three distinct developmental phases: proliferation, quiescence, and involution. In most hemangiomas, eighty percent of proliferation occurs by three months of life but may last longer. During proliferation, rapid growth can lead to exhaustion of blood supply with resulting ischemia, necrosis, ulceration, and bleeding. Hemangiomas can be superficial, deep, or compound. The superficial hemangioma is red and nodular with no subcutaneous component. A deep hemangioma presents as a protrusion with an overlying bluish tint or telangectasia. Compound hemangiomas have both deep and superficial components.

Figure. (a) Proliferating hemangioma at 3 months of age. (b) Same hemangioma at involution at 4 years of age.

Nomenclature for describing hemangioma types. Old nomenclature New nomenclature Strawberry or capillary hemangioma Superficial hemangioma Cavernous hemangioma Deep hemangioma Capillary cavernous hemangioma Compound hemangioma Following proliferation, hemangiomas enter a slower or no growth phase, known as quiescence. This phase typically lasts from 9 to 12 months of age. The final and unique phase of the hemangioma lifecycle is involution. This phase is marked by graying of the overlying skin and shrinking of the deeper components. Historical reports suggest that involution of 50%, 70%, and 90% of the hemangioma occurs by 5, 7, and 9 years of age with some variability. At the final stages of involution, a fibrofatty protuberance may remain. Another subclassification for hemangiomas is focal versus segmental disease. Focal hemangiomas are localized, unilocular lesions which adhere to the phases of growth and involution. Multifocal hemangiomatosis also exists, and infants with greater than 5 lesions should undergo workup to rule out visceral involvement. Segmental hemangiomas are more diffuse plaquelike and can lead to untoward functional and aesthetic outcomes. The limb and face are common locations for disease. Head and neck lesions frequently coincide with the distribution of the trigeminal nerve. A beard-like distribution is associated with a subglottic hemangioma 60% of the time. Regardless, a stridulous child with either a focal or segmental hemangioma should be presumed to have subglottic disease until proven otherwise.

Figure. (a) Segmental hemangioma in trigeminal (V3) distribution. (b) Same hemangioma after 2 months of therapy with propranolol (2 mg/kg divided tid). Vascular malformations are rare vascular anomalies composed of inappropriately connected vasculature. Any blood vessel type, or a combination thereof, can be affected in a vascular malformation. These lesions infiltrate normal tissue which makes them very difficult to manage. The most common vascular malformations include lymphatic malformations (LMs), capillary-venular malformations (CM), venous malformations (VMs) and arteriovenous malformations (AVMs) which have been selected to be covered in this paper. While different in their biologic and clinical profile, as a whole, vascular malformations do not regress and continue to expand with time. Periods of rapid growth, infiltration, and soft tissue destruction will spur therapeutic approaches that depend upon the malformation involved. Lymphatic malformations (LMs) are composed of dilated lymphatic vessels with inappropriate communication, lined by endothelial cells and filled with lymphatic fluid. Their incidence is approximated to be 1 in 2000 to 4000 live births. Lesions are classified as macrocystic (single or multiple cysts >2 cm3), microcystic (<2 cm3), or mixed. Previous terminology, that is no longer used, has included “cystic hygroma” and “lymphangioma” to describe these entities. The etiology of LM is unclear. Although most are congenital, there have been reports of LM occurring after trauma or infection. Receptors involved in the formation of lymphatic vascular channels, such as VEGFR3 and Prox-1, may play a role in the development of this disease. Diagnosis. Lymphatic malformations may be macrocystic, microcystic, or mixed. Gradual growth and expansion is typical. Approximately half of the lesions are present at birth and 80–90% by 2 years of age. Local infections approximating the course of lymphatic drainage will cause LM to swell, protrude, and sometimes become painful. This is a hallmark of a LM versus other vascular anomalies that do not present in this fashion. Clinically, the appearance of macrocystic disease differs from that of microcystic. Macrocystic LMs present as a soft, fluid-filled swelling beneath normal or slightly discolored skin. Intracystic bleeding or a mixed lymphatic venous malformation may result in blue discoloration of the overlying skin. Microcystic LMs are soft and noncompressible masses with an overlying area of small vesicles involving the skin or mucosa. These vesicles can weep and at times cause pain or minor bleeding.

Figure. (a) Macrocystic lymphatic malformation (LM) of right neck in toddler. (b) Microcystic lip LM displaying mucosal vesicles. (c) Microcystic LM in older patient with bone involvement and mandibular hypertrophy. LM can occur anywhere on the body, and symptoms are determined by the extent of disease. Most LMs are found in the cervicofacial region and extend to involve the oral cavity or airway, especially when mixed or microcystic. Symptoms secondary to bulky disease often include pain, dysphagia, odynophagia, impaired speech, or in severe cases, airway obstruction. When involving the skeletal framework in this area, LMs often cause osseous hypertrophy leading to dental or extremity abnormalities. Although these malformations can usually be diagnosed by physical examination, MRI is used to confirm diagnosis, identify cystic architecture, and determine extent of disease. Management. An ideal option for treatment of LM does not exist. Several interventions may be required. There have been rare cases of sporadic resolution of a lesion although the majority of these malformations continue to enlarge with age. Macrocystic lesions are more amenable to treatment and have a better prognosis. Swelling from acute infection is best controlled with a short course of systemic steroids and antibiotics. Definitive treatment is delayed until resolution. LM may be detected on prenatal ultrasound and may require special interventions during delivery. The EXIT (ex utero intrapartum treatment) procedure provides good airway control of the infant if compromise is suspected to occur at birth. Sclerotherapy is frequently employed for lymphatic malformations, especially if deep seated and difficult to access surgically. It involves injection of a sclerosing agent directly into the lesion leading to fibrosis and ultimately regression of the cysts. Several treatments are usually required, and swelling is expected following therapy. Macrocystic lesions are more easily treated in this fashion, but there have been reports of success in microcystic lesions. Several agents have been utilized for lymphatic malformations including ethanol, bleomycin, OK-432, and doxycycline. Complications include skin breakdown, pain, and swelling. Severe swelling can at times occur and may lead to airway obstruction requiring intensive care. Risks to local nerves are also real but usually result in only transient loss of function. Carbon dioxide laser therapy may also be employed in limited disease of the airway and oral mucosa. Macrocystic disease is often cured with surgical extirpation. Surgical excision is also frequently employed for microcystic disease although it is more aggressive, invasive, and difficult to control. Infiltration of normal soft tissue and bone by extensive microcystic LM requires massive resections and local or free- flap reconstruction. Failure to completely excise microcystic LM often leads to recurrence. Surgery is also employed in the correction of secondary deformities caused by LM such as bony overgrowth of the facial skeleton. Overall, treatment for LM should be aimed at complete elimination of disease. When this is not feasible, multiple treatment modalities are combined to control disease and provide satisfactory functional outcomes. Capillary malformations (CMs) are sporadic lesions consisting of dilated capillary- like channels. They occur in approximately 0.3% of children. CMs can present on any part of the body, but are mostly found in the cervicofacial region. They are categorized as medial or lateral lesions depending on their locations. Medial CM gradually lighten with time and eventually disappear. Colloquially they are referred to as stork bites on the nape of the neck and angel kisses on the forehead. Lateral lesions, commonly referred to as port-wine stains, have a more protracted course.

Figure. Capillary malformation (port wine stain) of the left face in infant Pathogenesis of isolated capillary malformations is unknown. A genomewide linkage analysis has identified a locus on chromosome 5q associated with familial disease. A rare autosomal dominant inherited disease consisting of a combination of CM and arteriovenous malformations (AVM) is associated with a loss-of-function mutation in RASA1 gene. This has spurred further research into the cause of the more common sporadic form of CM. Diagnosis. CMs present at birth as flat, red or purple, cutaneous patches with irregular borders. They are painless and do not spontaneously bleed. Lateral CMs, or port-wine stains, usually involve the face and present along the distribution of the trigeminal nerve. CMs tend to progress with time as the vessel ectasia extends to involve deeper vessels to the level of the subcutaneous tissues. This causes the lesion to become darker in color, as well as more raised and nodular. Although they are mostly solitary lesions, CM may exist as a part of a syndrome. The most common of these is the Sturge-Weber syndrome (SWS) and is characterized by a CM in the region of the ophthalmic branch of the trigeminal nerve, leptomeningeal angiomatosis, and choroid angioma. Symptoms of SWS are variable among cases and include intractable seizures, mental retardation, and glaucoma. CM may also be present in Klippel-Trenaunay Syndrome (KTS). This syndrome consists of a combination of multiple lymphatic, venous, and capillary abnormalities. Diagnosis is usually made by physical examination alone. If here are findings inconsistent with CM exist, for example, pain or spontaneous bleeding, an MRI may be performed. An MRI of the brain as well as an annual ophthalmological exam is warranted when suspicion for SWS is present. Treatment. The mainstay of treatment for CM is laser therapy. The FPDL is efficacious in treating these lesions. The laser slowly causes the redness of the lesion to fade; therefore, many treatments are often necessary. Early treatment of these lesions appears to slow the progression of the disease. The argon, potassium-titanyl- phosphate (KTP) lasers, and 755 nm laser have also been utilized in more advanced lesions with good outcomes. Surgical excision is also an option in lesions not amenable to laser therapy. This is especially true in advanced lesions which have become nodular. Venous malformations (VMs) are slow-flow vascular anomalies composed of ectatic venous channels. These aberrant venous connections lead to venous congestion, thrombosis, and gradual expansion of these lesions. As a result, VMs persist and progress until therapeutic intervention. The incidence of VMs is approximately 1 in 10,000. VMs more commonly occur sporadically, but research into multifocal disease and familial patterns has helped discover suspected genetic loci involved in their development. There are inherited forms of VMs, the cause of which has been localized to chromosome 9p. Recently a loss-of-function mutation was discovered on the angiopoetin receptor gene TIE2/TEK in many solitary and multiple sporadic venous malformations. In addition, upregulation of several factors including tissue growth factor beta (TGF-beta) and basic fibroblast growth factor (beta-FGF) has been discovered in patients with venous malformations. Progesterone receptors have been discovered in venous malformations. This likely explains their tendency to grow rapidly during hormonal changes. Diagnosis. Venous malformations are often visible at birth but may present as a deep mass. Protrusion may be the only presenting symptom. They are known to grow proportionately with the child with sudden expansion in adulthood. Rapid growth may occur during puberty, pregnancy, or traumatic injury. VM can be either well localized or extensive. The overlying skin may appear normal or possess a bluish discoloration. With more cutaneous involvement, the lesions appear darker blue or purple. Upper aerodigestive involvement is common, and VM are particularly evident when mucosa is affected.

Figure. Cervicofacial venous malformation involving the right neck (a) and oropharyngeal mucosa (b). VMs are compressible and swell when the region is dependent or there is an increase in hydrostatic pressure such as during a valsalva maneuver. With time, pain and swelling will occur with the formation of phleboliths (calcified thrombi), or small clots, secondary to trauma or venous stasis. For very large lesions with significant thrombosis the risk of distal emboli remains low but real. D-dimers may be elevated and a marker of disease. When isolated, VM are generally benign with slow growth. They expand secondary to venous stasis and elastic vascular expansion. Airway obstruction, snoring, and sleep apnea may also be present with recumbence. VM can occur anywhere in the body but often are found in the head and neck where they involve the oral cavity, airway, or cervical musculature. MRI is the imaging modality of choice when diagnosing VM and offers superior delineation of disease for treatment planning. Treatment. No single treatment modality is favored in the treatment of VMs and often more than one modality is utilized. Surgery, Nd : YAG laser therapy, and sclerotherapy (directed vascular injury) are all options for treating VM. Conservative observation of small VM in children may be an option with the knowledge that growth is imminent. Elevating the involved area can decrease hydrostatic pressure and vascular expansion and may impede growth. In large lesions, elevation also decreases swelling and improves pain and airway obstruction. Similarly, compression garments are the initial treatment of choice for advanced limb lesions allowing risks from other treatment options to be avoided. Low-molecular- weight heparin can improve pain from thrombosis. Treatment of larger airway and multifocal disease is often warranted. Symptom- directed therapy is the goal for these lesions. Management techniques typically aim to relieve airway symptoms, pain, and/or disfigurement. Surgical resection and sclerotherapy alone can, at times, be curative for smaller lesions. Local recurrence may occur years after treatment. Laser therapy provides good control of VM. Use of the Nd : Yag and KTP lasers has been described. The Nd : Yag laser can be used via a fiber attached to an endoscope to treat intraoral and airway venous malformations. Direct injury to deep venous malformations may also be performed by passing the laser directly into the lesion (interstitial therapy). The laser causes shrinking of the lesion along with thrombosis. Serial treatment with these lasers offers reduction and control of disease. Nerve injury may occur with interstitial laser. Sclerotherapy, as described above, has been used extensively for treatment of VM. The sclerosants most commonly used include ethanol and sotradecol. Complications of sclerotherapy include skin and mucosal injury, swelling leading to airway compromise, infection, and nerve injury. In addition, each sclerosant has its own risk profile. Cardiovascular shock can occur with ethanol, shock-like symptoms with OK- 432, interstitial pneumonia or pulmonary fibrosis with bleomycin, and tooth discoloration or electrolyte abnormalities with doxycycline. Surgery remains one of the most superior treatment options and may offer a cure for localized VM. Excision of complex lesions remains difficult secondary to intraoperative bleeding. Preoperative sclerosant can be used prior to excision (24–48 hours) to decrease surgical risk. Patients with extensive disease will often require combined modality therapy. Cure is not common, but disease control for many years is often achieved. Arteriovenous malformations (AVMs) are congenital high-flow vascular malformations composed of anomalous capillary beds shunting blood from the arterial system to the venous system. They are often misdiagnosed at birth as other vascular lesions because of the delay in presentation of characteristic signs of the malformation. Puberty and trauma trigger the growth of the lesion and manifestation of its troublesome symptoms. They are infiltrative causing destruction of local tissue and often life-threatening secondary to massive bleeding. Extracranial AVMs are different from their intracranial counterpart and are found in several areas in the cervicofacial region. Little is known about the origin and pathogenesis of AVM. A defect in vascular stabilization is thought to cause AVM, but it remains unclear whether these lesions are primarily congenital in origin. Most AVM, are present at birth, but there are several case reports of these lesions presenting after trauma in adults. Defects in TGF-beta signaling and a genetic two-hit hypothesis are the prevailing theories to the pathogenesis. Progesterone receptors have been isolated in AVMs explaining their expansion during puberty. Diagnosis of AVM is based upon clinical examination and imaging. A growing hypervascular lesion may have been present as a slight blush at birth. AVMs are often quiescent for many years and grow commensurate with the child. Intermittent expansion will suggest the diagnosis. Hormonal changes are thought to influence growth. The distinguishing characteristics of an AVM will be palpable warmth, pulse, or thrill due to its high vascular flow. The overlying skin may have a well- demarcated blush with elevated temperature relative to adjacent skin.

Figure. Evidence of skin involvement in limb AVM. Patchy erythematous areas are palpably warmer and pulsatile relative to adjacent skin. The natural course of AVM is early quiescence, late expansion, and ultimately infiltration and destruction of local soft tissue and bone. Common sites for occurence are the midface, oral cavity, and limbs. Oral lesions can present early due to gingival involvement, disruption of deciduous teeth, and profuse periodontal bleeding. Although both focal (small vessel) and diffuse lesions exist, AVMs are by far the most difficult vascular anomaly to manage due to the replacement of normal tissue by disease vessels and very high recurrence rates. Imaging is essential in identifying the extent of AVM. MRI may be useful, but MRA and CTA can give a superior outline of these lesions. Numerous hypolucent arterial flow voids are the hallmark of AVM by MRI. CTA allows evaluation of surrounding tissues and bones. Individual arterial feeders can be visualized with this imaging as well. An arteriogram, the time-tested approach to diagnosing AVM, will provide good definition of central “nidus” of affected vessels and provide access for intravascular treatment when necessary. Treatment of AVM consists of embolization, surgical extirpation, or a combination of these modalities. Treatment and timing are often individualized to the patient and the extent of disease. For example, small-vessel AVMs are known to be localized and can be resected with good long-term outcomes. Historically, young children were closely observed until disease expansion with the concept that the treatment should not be worse than the disease. However, this approach is currently being challenged due to the high recurrence rates experienced with AVM. Diffuse lesions are a lifelong problem. Long-term followup with a dedicated multidisciplinary team is important for AVM management. Intravascular embolization of AVM can be used alone or in combination with surgical excision. Absolute ethanol, polyvinyl alcohol, and ONYX have been employed as AVM embolization materials. These agents selectively obstruct and destroy the treated. Complications of this approach include local skin ulceration, soft tissue necrosis, mucosal sloughing, or nerve injury. Embolization provides temporary control of disease, but recurrence is high. This is theoretically due to collateralization and recruitment of new vessels to support an undetected portion of the “nidus.” Frequent serial embolizations may improve patient outcomes. In general, surgical management of AVMs requires preoperative supraselective embolization, judicious removal of tissue, and complex reconstructive techniques. In focal lesions, surgical excision has been shown to cure AVM. However, diffuse AVMs have recurrence rates as high as 93%. Excision is preformed 24–48 hours after embolization. This helps control blood loss and define surgical margins of the lesion. Close postoperative observation with expected management of local recurrence is required. Recruitment of new vessels occurs after excision as well. In essence, AVMs are debilitating vascular malformations that are often misdiagnosed early in life. Despite successful initial therapy, these lesions may recur many years later making vigilant management necessary.

6. MATERIALS FOR SELF-CONTROL: A. Questions for self-control: 1. Scheme and algorithm of examination and surgical treatment of patients with benign tumors of salivary glands.

B. Tasks for self-control: 1. 4.1. The patient, 65 years, came to the surgeon-stomatologist with complaints to a swelling in the left half of the face. At the objective examination: in the left parotid region lesion in the size 3*4 sm. At a palpation the neoplasm has dense character, painless. After carrying out contrast radiological research on sialogrammes is revealed that normal drawing of excretory channel the passage sharply breaks on a limit with pathological process. To put previous diagnose in this case. (Answer: tumor of salivary gland) 4.2. The patient of 57 years came to the surgeon-stomatologist with the complaint to asymmetry of the face. Objectively: in a site of the right parotid salivary gland the tumor of densely elastic consistence is found painless, mobile, a roundish form with a hilly surface. The tumor tends to slow increase. To put previous diagnose in this case. (Answer: the mixed tumor) 4.3. At objective examination of the patient: there is bright red color stain with clear borders on skin of cheek. Tissues in the region of spot are soft and painless. Gently finger pressure on the surface of neoplasm leads to pale in color. To put primary diagnose in this case. (Answer: the capillary hemangioma of cheek)

C. Materials for test control. Test tasks with the single right answer (a=II): 1. Ranula is more often located: A. In submaxillary salivary gland B. In parotid salivary gland C. In hypoglossal salivary gland (Right answer: С) 2. Clinical picture of adenoma of salivary glands: A. Tumor painless, dense, with smooth surface, not soldered to surrounding tissues. B. Tumor painless, mobile, the round or extended form, a dense-elastic consistence. C. The tumor grows quickly, is soldered to surrounding tissues. D. Tumor painless, immobile, the correct form, dense-elastic consistence, grown together with skin. (Right answer: А) 3. What method of treatment is surgical treatment of tumors of salivary glands? A. across Lviv. B. on Kovtunovich-Muhin. C. according to Hitrov. D. according to Gorbushenina. E. according to Limberg. (Right answer: В)

D. Educational tasks of 3th levels (atypical tasks): 1. On the mucosa of the left cheek bluish-crimson rounded neoplasm 5x5 mm was revealed. New formation is elastic consistency, smooth, painless at palpation. At puncture of lesion pure blood was obtained. To put primary diagnose. (Answer: hemangioma) 2. Objective examination of the patient: under the on the inner surface of the lower lip spherical new formation was revealed. The surface is smooth, translucent, bluish color. Lesion has elastic consistency and clear borders, new formation is non-mobile. At puncture viscous, clear liquid was obtained. To put primary diagnose. (Answer: retention cyst of salivary glands of the lower lip).

LITERATURE

Basic literature: 1. Oral and maxillofacial surgery: textbook / Ed. by prof. V. Malanchuk / part one. – Vinnytsia: Nova Knyha Publishers, 2011. – 424 p. 2. Oral mucosa diseases: textbook / Ed.by A.V. Borysenko/ -Odesa-2015.-328p. 3. Avetikov D.S. Using of modern methods of diagnostics in the practice of oral surgery: Text-book / Avetikov D.S, Skikevych M.G., Lokes K.P., Bojchenko O.M.-Poltava-2018 -122p. 4. Avetikov D.S. Precancerous diseases of maxillofacial area: Text-book / Avetikov D.S, Aipert V.V., Lokes K.P.-Poltava-2017 - 125p. 5. Avetikov D.S. Modern methods of treatmentof cysts of jaws: Text-book/ Avetikov D.S, Lokes K.P., I.V. Yatsenko, S.o. Stavicij.-Poltava-2014-83p. 6. S.I. Danylchenko Operative surgery and topographical anatomy: Text-book/ S.I. Danylchenko, E.N. Pronina, D.S.Avetikov .- Poltava-2011-239p. 7. Skikevych M.G. Maxillofacial surgery. Benign tumours and precancer diseases: Text-book/ Avetikov D.S, Khalaf A.A.-Poltava-ASMI, 2014.-199p. 8. Skikevich M.G. The basics of stomatology / M.G. Skikevich, D.S. Avetikov. – Poltava. – ASMI, 2012. – 176 p.

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