HAND WRITTEN STUDY NOTES FOR ORAL MEDICINE AND ORAL PATHOLOGY, Study notes of Oral Medicine

Download HAND WRITTEN STUDY NOTES FOR ORAL MEDICINE AND ORAL PATHOLOGY and more Study notes Oral Medicine in PDF only on Docsity! Salivary glands, whether major or minor, arise embryologically u_from the primitive ectoderm of the stomatodeum. u_ The gland primordia penetrate the submucosa u_as tubular invaginations that ultimately differentiate u_ into end bulbs with secretory capabilities. u Amature gland may contain three types of acinar (secretory) cells: u (1) mucous, u (2) seromucous, u_ (3) serous. u_ In some glands, mucous acini are capped by serous or seromucous demilunes. u Contractile myoepithelial cells that are surrounded by a basement membrane envelop the acinar cells. e = Intercalated ducts: small cuboidal lined e Striated ducts: mitochondrial rich e Extralobular ducts: much larger ducts composed of basilar reserve cells, stratified epithelium, and luminally oriented cuboidal or columnar cells. As these ducts reach the surface, they are lined by stratified squamous epithelium REACTIVE LESIONS e Salivary gland >>> Injury or obstruction >>> atrophic degeneration and necrosis, replacement of parenchyma with inflammatory cells >>> fibrous scarring. e Non-infectious. Obstruction to flow may occur as a consequence of duct blockage by e an object in the ductal lumen. e stricture of a duct with narrowing of the lumen. e severance of a duct with pooling of mucin within the tissue. e Once acini are no longer evident, the parenchyma undergoes a progressive fibrosis (sclerosis), a process common to all reactive lesions. In the salivary glands it is referred to as chronic Sclerosing sialadenitis. Common Causes of Chronic Sclerosing Sialadenitis Excretory obstructions Infections Radiation Autoimmune diseases Systemic and metabolic conditions Medications and drugs MUCOCELE A tissue swelling composed of pooled mucus that escaped into CT from a severed excretory duct. When the salivary duct is severed, the acinar cells will continue to secrete saliva into the severed duct. At site of severance the secretory products escape into the connective tissue forming a pool of mucus that distends the surrounding tissue. Mucocele - Minor salivary glands of the lower lip most prone, asa consequence of injury or lip biting. May occur in the floor of the mouth due to minor sublingual gland duct severance. Ranulas - mucoceles that are finely vascularized, distended with appearance of frog’s belly. MUCUS RETENTION CYST Swelling caused by an obstruction of a salivary gland secretory duct resulting in an epithelial-lined cavity containing mucus. Itis lined by epithelium. True mucoceles/Sialocysts - aneurysm-like dilatations of salivary ducts containing mucus. Blind cysts. These rarely involve major salivary glands, when they do, they can be multiple (dysgenic or polycystic disease of the parotid gland). Unilocular or multilocular in minor salivary glands. DD - mucocele, mucoepidermoid carcinoma. CLINICAL FEATURES Age adults throughout the third to eighth decades, although they may occur at any age. In major salivary glands, marked predilection for parotid gland, age is 45 yrs, located In superficial lobe. Appearance : Parotid cysts present as fluctuant, well-defined masses anterior to the ear or overlying the angle of the mandible. Within Oral cavity : The lesions are painless, cystic, fluctuant, and generally superficial. In these instances they have a translucent, bluish appearance. Site: Within the oral cavity, the floor of the mouth is the most common site, followed by the buccal mucosa and the lower lip. Oncocytic cyst - A specific histologic type of cyst that involves the minor salivary glands. It is most frequently seen in the buccal mucosa and lips in older patients (mean age: 60 years). e cysts are usually identified as painless, sessile, dome shaped masses of normal coloration that are located just below the surface in buccal mucosa, vestibule and lips. HISTOPATHOLOGY e The surface stratified squamous mucosal epithelium of the oral cavity is distended by a cystic cavity that is lined by cuboidal or, occasionally, columnar ductlike epithelium. e Thecytoplasm of these ductal lining cells is either eosinophilic or clear, 70% unilocular, 30% multilocular, sometimes with small papillary projections into the cystic lumens. The surrounding fibrous tissue may be compressed yet is rarely inflamed. The underlying gland lobules sometimes show evidence of chronic sclerosing sialadenitis. Those cysts arising in the parotid gland usually have a well defined fibrous capsule that separates the cyst from the parotid parenchyma. Although the cyst cavity may contain congealed mucin, there may not be evidence of a stone or another readily identifiable source of obstruction that might result in a focal, aneurysmal, ductal dilatation. e Theoncocytic cyst -The lining cells are columnar and often pseudostratified, and their cytoplasm is strikingly eosinophilic, typical of oncocytes. e Thelumen is filled with eosinophilic, proteinaceous material. e The adjacent gland lobules show evidence of obstructive chronic sclerosing sialadenitis. e Oncocytic changes are often seen in the ducts of the adjacent glands. e Treatment - simple excision. SIALOLITHIASIS The presence of one or more oval or round calcified structures (salivary stones) in a duct of a major or minor salivary gland. Salivary stones can form within the lumens of major and minor salivary glands. The submandibular gland is most commonly involved. the consequences of duct blockage in the major salivary glands are more significant than when stones form in oral mucosal minor salivary gland ducts. In the major salivary glands prolonged blockage can lead to complete degeneration of parenchyma with secretory shutdown. During the process of obstruction, salivary retention with ductal dilatation results in pain and swelling. Glands that are no longer functional become subject to retrograde bacterial infections that can cause severe pain. PATHOGENESIS Salivary stones are not associated with hypercalcemia; no specific secretory predisposing condition has been identified in sialolithiasis. For unknown reasons it is assumed that congealed mucin, protein, and desquamated ductal epithelial cells form a small nidus on which calcium salts precipitate. The small nidus then allows concentric, lamellar crystallizations to occur; the sialolith increases in diameter as layer after layer of salts becomes deposited, much like growth rings in a tree. Microliths would probably be expelled easily into the saliva. Those that are not expelled usually continue to enlarge until a duct branch or even the major duct becomes occluded. CLINICAL FEATURES The lobules become intensely infiltrated with mononuclear cells, and the ducts remain intact yet dilated. Eventually the infiltrate wanes and the lobules become progressively collagenized. Obstructed glands that become complicated by retrograde acute bacterial sialadenitis show tissue infiltration by neutrophils with purulent material in the ductal lumens. TREATMENT -Removed by manual manipulation of the stone through the major duct orifice. Surgery When signs and symptoms of an acute pyogenic infection exist, incision and drainage with antibiotic therapy should precede or accompany sialoadenectomy. CHRONIC SCLEROSING SIALADENITIS SIALADENITIS -An inflammatory response of salivary gland tissue to a wide spectrum of causative factors. CSS - Chronic inflammation of salivary gland tissue resulting in replacement of acini by lymphocytes,plasma cells and fibrous tissue but sparing much of ductal architecture. Most are chronic, result in the formation of a substantial amount of fibrous replacement of parenchyma, and occur as a consequence of mucous extravasation or duct blockage from salivary stones. In addition, direct trauma or compression of the glands, ducts, or both can cause sialadenitis. In addition to injuries, hyperplasias and neoplasms can lead to a secondary glandular inflammation. Regardless of the source or cause, when degeneration with fibrous replacement and chronic inflammation occurs, the process is referred to as chronic sclerosing sialadenitis. CLINICAL FEATURES Chronic sclerosing sialadenitis is most often the consequence of direct compression or ductal obstruction. The obstructed major salivary gland becomes enlarged because of the accumulation of secretions within the duct system and later as a consequence of inflammatory cell infiltration. The enlarged gland is generally firm yet freely movable. The firmness may increase with time as fibrotic replacement of acini increasingly occurs. In the minor salivary glands, various surface epithelial proliferations such as papilloma or squamous cell carcinoma and submucosal fibrous enlargements such as fibrous hyperplasia may obstruct the minor duct lumen or compress the extralobular ducts that exit from the gland proper. The flanges of dental prostheses, if overextended, can compress minor salivary glands in the vestibule, resulting in a sialadenitis. In addition, salivary gland neoplasms can compress adjacent normal glands, resulting in obstruction. As a consequence, minor gland chronic sclerosing sialadenitis will evolve, although it may not be clinically obvious. One of the major causes of sialadenitis is radiation therapy used to treat head and neck cancer. Complications-Xerostomia, Cervical caries, Oral mucositis Candidiasis HISTOPATHOLOGY The acinar units degenerate as mononuclear leukocytes, chiefly plasma cells and lymphocytes, infiltrate the lobules. In radiation sialadenitis the earliest changes include loss of secretory granules and cloudy swelling with edema of the acinar cells; neutrophilic infiltration, soon followed by mononuclear infiltration, also takes place. With time all acini are lost and the gland is no longer functional. The ductal elements remain intact, showing ectasia and sialodochitis, whereas the parenchyma becomes progressively fibrotic. These glands, particularly the major salivary glands, may then be subject to retrograde bacterial acute sialadenitis. e TREATMENT -Sources of irritation and obstruction must be removed, Sialoadenectomy. e For xerostomia: 1.Pilocarpine 2.Electrostimulatory devices 3.Daily fluoride gels 4.Meticulous oral hygiene NECROTIZING SIALOMETAPLASIA A spontaneous condition of unknown cause, usually of palate, in which a large area of surface epithelium, underlying CT and associated minor salivary glands become necrotic while ducts undergo squamous metaplasia. e Necrosis is the result of obstructive disease of the salivary glands generally occurs slowly. In necrotizing sialometaplasia, acute necrosis of entire lobules of minor salivary tissue occurs in a short period, this process is due to infarction. Reasons for Infarction 1. microvascular occlusion 2. thromboembolic disease 3. preservation of cellular outlines CLINICAL FEATURES e Hard and soft palate junction, tongue, retromolar pad, nasal cavity, antrum, and mojor salivary glands. In these non palatal sites the disease is often traced to a cause such as surgery, trauma, or radiation. Patients will show keratoconjunctivitis sicca, characterized by corneal keratotic lesions that stain pink when rose bengal dye is used. Tear meniscus and breakup time are reduced. The Schirmer test is used to assess lacrimal flow and is positive when the flow is reduced to less than 5 mm during a 5-minute sample period. This test uses a strip of filter paper that is placed between the eye and the eyelid to determine the degree of tearing, which is measured in millimeters. SECONDARY SS Secondary SS occurs when other signs or symptoms of autoimmune disease are present, the most common being rheumatoid arthritis. Other collagen-vascular diseases may occur in secondary SS, including lupus erythematosus, systemic sclerosis, dermatomyositis,and mixed connective tissue disease. Other extra salivary and lacrimal diseases: Raynaud disease, interstitial nephritis, interstitial pneumonitis, PUrPUra, and Polymyopathy. The risk for the development of extra salivary malignant lymphoma is increased. Specific laboratory findings are most often encountered in secondary SS and include an elevated erythrocyte sedimentation rate, hypergammaglobulinemia, and positive serologic tests for rheumatoid factors, antinuclear antibodies (ANAs), and anti-Ro (anti-SS-A) and anti-La (anti-SS-B). PATHOGENESIS The basic cause of SS is unknown. The antigens that stimulate this immune mechanism are not well defined. A viral origin has been suggested whereby immunologic responses to viral proteins cross-react with host cell proteins in salivary epithelia molecular mimicry). The signs and symptoms of dryness and swelling are the result of the immunologic reaction that occurs in the parenchymal tissue with consequential acinar loss and lymphocytic infiltration. Parotid gland enlargement is observed in approximately 45% of SS patients, and the glands feel firm yet doughy. e When enlargement is seen, it is usually bilateral. e The parotids are the primary major salivary glands to be involved; some patients also have submandibular gland involvement. e Imaging with contrast sialography, pertechnetate scintigraphy,CT, or MRI will often assist with the diagnosis, because these techniques will usually demonstrate inflammatory rather than neoplastic imaging features. A sialogram reveals a characteristic appearance of pooling of the opaque dye that resembles shotgun pellets throughout the gland. MANIFESTATIONS Dry mouth (xerostomia) Dry eyes (xerophthalmia) Mucosa in both eyes and mouth becomes thinned, inflamed, and painful with a burning sensation Candidiasis in dry mouth Predilection for root caries HISTOPATHOLOGY e With increasing numbers of infiltrating lymphocytes, progressive destruction and loss of acinar units takes place. e The ductal and periductal myoepithelial cells undergo hyperplasia, resulting in islands of epithelial cells. The histopathologic changes seen in the minor salivary glands in SS consist of aggregates of lymphocytes oriented around intralobular ducts. These lymphoid foci are primarily composed of T lymphocytes. TREATMENT No effective therapy exists for SS. The development and progression of root caries can be minimized by daily application of topical fluoride gels and meticulous dental hygiene. Candidiasis can be managed with the use of antifungal medications. Salivary substitutes or lemon-flavored glycerin and water can be carried and constantly sipped to offer some relief for the sensation of dryness. Pilocarpine and transmucosal neurostimulatory devices may stimulate secretions in those patients who retain some degree of secretory function. Immunosuppressive agents for Secondary SS. SALIVARY GLAND TUMORS Table 10-3: Distinguishing Features of Benign and Malignant Salivary Gland Tumors Benign Malignant ‘CLINICAL FEATURES MICROSCOPIC FEATURES Smooth, uniform surlace; normal surface col- oration; round, dome shaped; intact overlying mucosa/skin; movable; asymptomatic Distinct and intact capsule; uniformity of cells; tissue structures resemble normal; neoplastic cells displace nerves; normal stroma; no necrotic areas Nodular surface; surface telangiectasia; irregularly shaped; ulcerated; fixed and indurated; occasional nerve deficits Lacks encapsulation; cells irregular in size and shape; altered tissue patterns; neo- plastic cells invade nerves; lacks sufficient stroma; occasional areas of necrosis DEMARCATED Capsule component B Cystic component FIGURE 10-21 Growth patterns of salivary tumors. A, Adenoma (well-demarcated, encapsulated submucosal tumor). B, Low-grade adenocarcinoma (multicystic and well demarcated without encapsulation). , Adenocarcinoma showing ulceration and lack of encapsulation and focal invasion. CLINICAL FEATURES BASAL CELL ADENOMA Age: Adults, 7h decade Location: Parotid gland, upper lip and buccal mucosa Females more often In parotid, arise in the superficial lobe, are well encapsulated, and movable. On palpation, firmer than mixed tumors. Size: small, less than 3 cm in diameter. CANALICULAR ADENOMA Age: Older patients, 7th decade Rarely in children, more in Females Site: 75% in upper lip, Buccal mucosa less than 2cm in diameter. Freely moveable and encapsulated. Normal or slight bluish tinge. HISTOPATHOLOGY BASAL CELL ADENOMA Fibrous capsule, Cell clusters in oval nests. The outermost layer of cells that surround each cell nest are usually cuboidal. Centrally located cells: uniform, basilar in stratified squamous epithelium. Three patterns are seen: 1. Individual nests : small and well defined 2. Diffuse sheets of basaloid cells (some with keratin pearl formation) 3. Trabecular pattern with elongated anastomosing cords of basal cells. e Trabecular pattern 0 Ducts with cuboidal epithelium Filled with eosinophilic secretion product And surrounding basaloid nests. 0) Basal cell adenomas show membranous or dermal analogue adenoma: islands of tumor cells that are enveloped by a prominent hyalinized basal lamina. CANALICULAR ADENOMA Presence of capsule Single layered cuboidal or columnar ductal cells arranged in elongated anastomosing cords. The nuclei are oval or elongated and monomorphic. Ductal Lumen has nuclei polarized towards the basement membrane. Stroma: Myxomatous eosinophilic-staining hypocellular mucoid matrix. Dilated capillaries, extensive ductal and anastomosing network of cuboidal and columnar cells. Papillary fronds present in cystic areas. TREATMENT Simple excision, Recurrence uncommon. PAPILLARY CYSTADENOMA LYMPHOMATOSUM/WARTHIN'S TUMOR ABSGL with limited growth potential primarily occurring in the tail of the parotid gland; it is composed of cystic spaces with intraluminal projections lined by adouble cell layer of eosinophilic columnar cells and contains abundant lymphoid tissue in the underlying CT. e Self Limited growth potential, Mixture of cystic salivary ductal elements and normal lymphoid tissue. PATHOGENESIS 1. Lesion arises from ductal cells that have permeated and proliferated within parotid gland lymph nodes or lymphoid aggregates. 2. Presence of the cystic adenomatous proliferation initiates a secondary lymphoid reactive response in the stroma. CLINICAL FEATURES Primarily occurs in Parotid glands, Rare in other glands. Slight predilection for males. . bth and 7th decades of life, 10% bilateral cases. e Site: overlies the angle of the mandible in the superficial lobe, well encapsulated and movable. e When compressed with the fingers, the tumor usually feels doughy. e Diagnosis 0 Technetium 99m pertechnetate radioisotope scanning is often helpful, because the tumor readily takes up the isotope and appears as a hot nodule. HISTOPATHOLOGY Dense fibrous capsule. Clear, yellow, or brown viscous material in cysts. Cysts are lined by pseudostratified columnar cells with a very distinct eosinophilic cytoplasm (columnar oncocytes) and are in a double row, with the nuclei oriented in the basilar area of the bottom row and in the superior aspect of the upper row. Papillary fronds extend into the cystic spaces. Lymphoid tissue with scattered germinal centers are also in the lumen. Mucus goblet cells rarely present. Malignancy into adenocarcinoma may occur. Germinal centers Papillary fronds, columnar ductal cells e TREATMENT- Simple enucleation Superficial lobectomy CLINICAL FEATURES e Age: Adults, third to the seventh decades. Occasionally teenagers. e Gender: Females, for tongue and retromolar minor glands. e Sites: 50% in parotid, 20% in palate, Buccal mucosa,Lips, Tongue, Mandible and Retromoloar areas. e Inthe parotid gland 1. Arise in superficial lobe 2. Appear as well defined focal nodules 3. May be movable, which is an uncommon feature for a malignant lesion. 4. The low-grade lesions are often fluctuant 5. High-grade tumors are usually indurated and fixed to adjacent tissue. Range from 1 to 4 cm in diameter. High grade tumor may be involved with Facial nerve involvement, manifested as facial weakness or paralysis. NO e Within the oral cavity most low-grade tumors are submucosal masses that have an intact, nonulcerated surface. e Low-grade lesions, which are often composed of Multiple cystic structures containing mucin, may yield a bluish tinge to the overlying mucosa and are easily mistaken for Mucoceles. e Diagnosis - MRI. e Central (intraosseous) mucoepidermoid carcinoma of the jaws is most often located in the mandible. Bony enlargement can occur, seen on radiographs. Unilocular or multilocular radiolucencies occurring mostly in the mandibular 3rd molar region. HISTOPATHOLOGY Three dominant cell types: 1. Mucous 2. Epidermoid 3. Intermediate Arranged in Nests or Diffuse sheets and surround the cystic spaces. Lacks true capsule, sometimes, leading edge is well demarcated. Infiltration into normal salivary tissue, connective tissue, or muscle can occur. e The individual cells show neither significant cytologic features of malignancy nor evidence of increased mitotic activity. Low Grade Tumors-Mucus cells and multiple cystic spaces High grade tumors: 1.More solid islands 2.Fewer mucus secreting cells 3.High proportion of stratified squamous epithelial (epidermoid) cells e Intermediate-grade tumors fall between these two extremes. LOW-GRADE MUCOEPIDERMOID CARCINOMA 1. Goblet mucus-secreting cells and columnar ductal cells line the multiple cystic spaces. 2.Papillary fronds surfaced by both mucous and columnar cells are commonly encountered. 3.Focal nests of squamous cells. 4.Mature fibrous stroma between tumor islands and cystic structures. 5.Marginal tissue is infiltrated by lymphocytes with occasional germinal center formation. HIGH-GRADE MUCOEPIDERMOID CARCINOMA 1The proliferating squamous cells predominate. 2.Few cystic spaces are encountered. 3.Only occasional nests of mucus-secreting cells are noted. The High-grade tumors resemble squamous cell carcinoma to some extent but usually do not show the keratin pearl formation. 4.Some degrees of pleomorphism and hyperchromatism are usually seen in high-grade tumors. e Aclear cell variant exists and is characterized by sheets of vacuolated cells that fail to stain for mucin. These clear cells merge with the squamous cells. The clear cell variant is classified as intermediate to high grade. Intermediate-grade tumors also show cystic spaces; however, they are neither numerous nor large. The so-called intermediate cells, which are polygonal but lack true squamous differentiation, are often arranged in diffuse sheets that intervene between the ductal, mucous, and squamous cells. e Central mucoepidermoid carcinoma of the jaws - An odontogenic cyst with extensive mucous cell metaplasia and the glandular or sialo-odontogenic cyst. TREATMENT 1.lobectomy with cervical node dissection 2.elective neck dissection. 3.Postoperative radiotherapy A.wide local excision 5.palatectomy or partial maxillectomy 6.Hemiglossectomy 7en bloc resection ADENOID CYSTIC CARCINOMA AMSGT composed of cuboidal cells in a solid, cribriform (swiss cheese) or tubular pattern with a predilection for invading perineural lymphatic spaces. Also called cylindroma. The individual tumor cells resemble the intercalated ducts of normal glands. This tumor is prone to recur after surgery. CLINICAL FEATURES e The peak incidence is in the sixth decade of life, Female predilection. e Common in parotid and submandibular gland. e rarely exhibit facial nerve compression and paralysis. e Inthe lio and buccal mucosa, a firm and well-defined submucosal mass is detected, either visually or by palpation. HISTOPATHOLOGY e Thecells of acinic cell carcinoma may be serous, mucus, or seromucous. e Microscopy shows that the individual cells are usually rich in cytoplasm and the contents stain lightly basophilic or amphophilic. e Zymogen granules are rare. In the unusual zymogen-secreting tumors, the acinar cell components are stippled with richly basophilic granules. e The mucosubstances stain with periodic acid-Schiff (PAS) and are diastase resistant, indicating that they do not contain large amounts of glycogen. e Acinar cells arranged in growth patterns 1. Solid - fine capillary septa divide sheets of acinar cells into indistinct lobules 2. Microcystic - same pattern is encountered in the microcystic variant, except that varying sizes of microcysts are scattered 3. Papillary cystic - large cystic spaces are seen and large papillary fronds of solid and microcystic acinar configurations protrude into the cystic spaces 4. Follicular. e Acharacteristic finding in microcystic and papillary cystic foci are acinar cells that appear to be beaded or yield a hobnail pattern when they linea cystic space. e The outer margin is Lobulated, Well demarcated and sometimes partially encapsulated, lymphoid tissue with germinal centers is commonly encountered around the periphery. TREATMENT 1.Surgical excision 2.Lobectomy 3.Total parotidectomy 4.Neck dissection POLYMORPHOUS LOW-GRADE ADENOCARCINOMA AMSGT with a predilection for minor glands that is composed of a wide variety of lobular and cribriform patterns in the central areas, laminated single file tubular patterns in the periphery, and has a low potential for metastasis. e Generally occurs in the minor salivary glands of the oral cavity. Some will show growth patterns strikingly similar or identical to polymorphous low-grade adenocarcinoma. e The population of tumor cells is quite varied, with many growth patterns encountered; hence the term polymorphous. Most of the cells resemble the intercalated or terminal salivary ducts. CLINICAL FEATURES e Female, sixth to eighth decades. e Site: palate 60%, 35% are found in the ligs and buccal mucosa ,only a few tumors are found in other oral mucosal sites. painless masses, firm on palpation, fixed when in the palate. e Surface ulceration is rarely seen. Slow growth. e Size: smaller than 3cm in diameter. HISTOPATHOLOGY e DD: Adenoid cystic carcinoma, well demarcated but is not encapsulated. e Invasive tumor nests are generally seen around the periphery with extension into adjacent minor salivary gland lobules or muscle fibers, depending on the location. e Two basic growth patterns; lobular and cribriform. e The lobular pattern is composed of ovoid or round nests of basaloid cells with monomorphic nuclei; the connective tissue stroma is scant and mature. e The cribriform pattern is similar to that of adenoid cystic carcinoma; it has a “Swiss cheese” appearance, because the tumor lobules are riddled with multiple microcysts. e Inthe periphery, tumor cells are arranged in parallel arrays of elongated, single-file tubular formations. These single-file tubular structures appear to be stacked upon one another, producing an “onionskin” or laminated appearance. e The nuclei are large, yet uniform, Nucleoplasm is granular or stippled. Perineural invasion may also be seen and therefore not a reliable feature in differentiating this tumor from adenoid cystic carcinoma. TREATMENT 1.Surgical excision including wide margins is the treatment of choice. 2.1n the palate a partial maxillectomy is recommended.