9 Mucocele Etiology Extravasation type Physical-traumatic injury to minor gland excretory ductMucus extravasation into periductal soft tissue produces a local inflammatory response and granulation tissue “encapsulation.”
10 Clinical Presentation Lower lip most common site; also buccal mucosa, anterior ventral tonguePainless bluish hue when mucin is near surfaceOften waxes and wanes in sizeMicroscopic FindingsMucus pool surrounded by granulation tissueMacrophage and neutrophil response to free mucinFocal chronic sialadenitis
18 Differential Diagnosis Microscopic FindingsThin, dilated, epithelial-lined salivary excretory ductLining is cuboidal to columnar with occasional mucus-producing cells presentAdjacent salivary gland lobules minimally altered but may show obstructive inflammatory changesDiagnosisMicroscopic findingsDifferential DiagnosisExtravasational mucoceleSalivary gland neoplasm, especially mucoepidermoid carcinoma
19 Treatment Prognosis Excision of cyst with adjacent gland(s) Recurrence is rare.
20 Necrotizing Sialometaplasia EtiologyLocal ischemic injury of salivary gland lobulesMay be preceded by trauma or local anesthetic injury, or it may appear spontaneously
21 Clinical Presentation Both major and minor salivary glands can be affected.Hard palate most common site, usually unilateralInitially a painful to dysesthetic submucosal swellingUltimately, a central necrotic crater develops.May extend to and involve deep soft tissue and palatal bone
23 Microscopic FindingsSalivary gland inflammation and lobular necrosis (necrosis is not always demonstrable on biopsy)Ductal squamous metaplasia (bland cytology)Lobular architecture of salivary glands persists
26 RanulaEtiologyObstruction of the sublingual (usually) or submandibular salivary gland by a sialolith or by traumaSecondary to obstruction, extravasation of saliva into the soft tissue of the floor of the mouth
27 Clinical Presentation Unilateral, fluctuant, soft tissue mass on the floor of the mouthUsually has a bluish, slightly translucent qualityWhen above the mylohyoid muscle, presentation is intraoral.If extravasation extends below the mylohyoid muscle, a plunging ranula forms.Occlusal radiographs may demonstrate a suspected sialolith.
33 Treatment Prognosis Marsupialization as an initial procedure Excision of the involved gland (extravasation type)Sialolithectomy (in obstructive type)PrognosisNo recurrence with sialadenectomyRecurrence risk with sialolithectomy secondary to duct scarring or reformation of stone
34 Sialolithiasis Etiology Sialoliths are calcified structures that develop within the salivary ductal system. They are believed to arise from deposition of calcium salts around a nidus of debris within the duct lumen. This debris may include inspissated mucus, bacteria, ductal epithelial cells, or foreign bodies.The cause of sialoliths is unclear, but their formation can be promoted by chronic sialadenitis and partial obstruction. Their development is not related to any systemic derangement in calcium and phosphorus metabolism.
35 Salivary obstruction from stones, mucous plugs, and mucous extravasation phenomenon.
36 Clinical Presentation Sialolithiasis can form in all of the salivary glands, including minor salivary glands, but the gland that most commonly produces such stones is the submandibular gland.The so‐called stones that form in the parotid duct system are rarely calcified and are actually mucous plugs that do not appear on radiographs.Stones that form in the submandibular duct system are almost always radiopaque because they are composed of calcium carbonate and calcium phosphate.
37 They can occur along any part of the duct and are most frequent at anatomic bends. In the submandibular duct, stones are often found at the duct's bend around the posterior edge of the mylohyoid muscle.When sialoliths form, they will obstruct the duct either partially or completely. Therefore, individuals present with a painful swelling of the gland and usually with signs of secondary infection, including a suppurative exudate from the duct, fever, and mild to moderate leukocytosis .Individuals will report an increase in pain and swelling upon eating. The gland will be palpably firm and anywhere from mildly tender to very painful.
40 DiagnosisCT scan with 2‐ to 3‐mm cuts to identify the location of the stone.Most obstructed submandibular glands will have both inflammation and fibrosis in a homogeneous pattern throughout the gland.
41 Differential Diagnosis Calcified lymph nodes from previously resolved tuberculosisPhleboliths (particularly if an old cavernous hemangioma were present)TonsolithsCalcifications of the carotid bifurcation.
42 TreatmentStones that are accessible in the floor of the mouth are removed via a direct approach, and the damaged duct is sutured to the mucosa of the floor of the mouth (sialodochoplasty).Parotid stones usually do not produce a long‐term clinical problem. Most are passed with parotid flow, and a few require removal from the duct with either a repair or duct transposition.
43 PrognosisIf the sialolith has been present for a short time, the gland may recover after sialolith removal.If the sialolith is of long standing, the gland may harbor irreversible inflammation and fibrosis, so that it cannot recover even if the sialolith is removed.
44 Sialorrhea (Sialosis) EtiologyVaried; may include idiopathic paroxysmal sialorrhea, parkinsonism, stomatitis (acute), newly inserted oral appliances, expectorants, neostigmine, and others
47 Diagnosis Direct observation and analysis of history Flow-rate measurement
48 TreatmentScopolamineIf related to medication use, an alternate medication should be chosen, if possible.PrognosisGuarded/indeterminate
49 Adenomatoid hyperplasia EtiologyIt is a nonneoplastic enlargement of the minor salivary glands of the hard palate.The cause is unknown, although there is some evidence to suggest that trauma plays a role.
50 Clinical Presentation The palate is the chief site of involvement of this salivary gland hyperplasia.There is a male predominance, and age ranges from 24 to 63 years.The clinical presentation is a unilateral swelling of the hard and/or soft palate.This lesion is asymptomatic, broad based, and covered with intact mucosa of normal color and quality.
51 Differential Diagnosis Salivary neoplasmsLymphomaExtension of nasopharyngeal or sinonasal disease into the oral cavity.
52 TreatmentSubsequent to identification by means of an incisional biopsy, no treatment is necessary, given the purely benign nature of this process.PrognosisThere is no neoplastic potential.
53 Sjögren’s Syndrome Etiology An autoimmune disease resulting in exocrine gland dysfunction secondary to mononuclear cell infiltrationIncreased prevalence of human leukocyte antigen DR/DQ allelesAutoantibody production against nuclear antigens SS-A and SS-BNo specific agent identified; postulations include the following:Potential role for viruses/retroviruses as cofactorsPossible role of cytokine and hormonal influence on signal transduction and secretion
54 Clinical Presentation Decrease in exocrine gland functionXerostomiaXerophthalmia/keratoconjunctivitis siccaSalivary and lacrimal gland enlargement (one-third of cases)Secondary effects of exocrine dysfunction are as follows:Dental cariesOral candidiasisOcular/corneal discomfortPrimary form: exocrine dysfunction dominatesSecondary form: exocrine dysfunction; other associated autoimmune conditions—usually rheumatoid arthritis, less often lupus erythematosus
58 Diagnosis Demonstration of objective xerostomia and xerophthalmia Serologic demonstration of associated SS-A or SS- B antibodiesCorrelation of clinical and serologic findings with labial salivary gland biopsy; demonstration of presence of periductal lymphocytic sialadenitis