Salivary gland disease l Oral medicine MCQs for dental students

Salivary gland disease : Inflammatory latrogenic disease , Disturbances in salivary flow (Xerostomia and Sialorrheaa) and Systemic diseases affecting saliva as Sjogren’s syndrome l Oral medicine MCQs (multiple choice question) for dental students

Salivary gland disorders

• All salivary glands are exocrine glands
• Saliva collection to determine quantity is done over 5 minutes
• Un stimulated saliva is more accurate because it represents the resting state. Stimulated saliva is only temporary during eating
• Total daily salivary flow is 500-600ml/day

1. Unstimulated salivary flow rate = 300 ml [mostly from sub mandibular gland ( serous and mucous) + parotid gland ( serous) ] → unstimulated saliva is relatively mucous
2. Stimulated salivary flow rate = 200 ml [mostly from parotid → saliva is relatively serous]

 

Inflammatory latrogenic

Viral sialadenitis - Mumps

• Affects mainly parotid gland or submandibular glands
• Caused by paramyxovirus
• Route = direct contact with saliva droplets
• Pain is exacerbated during eating due to partial blockage of stensen’s duct
• Prodromal symptoms of fever, malaise, pain because it is a viral infection
• Treatment : symptomatic care – corticosteroids in severe cases to prevent complications [ orchitis, oophoritis, encephalitis, myocarditis, nephritis]

 

Q: why should corticosteroids be used with great caution when dealing with mumps?

• Because they cause immune suppression , if given at the wrong time [ while the virus is still replicating ] they will help the virus spread even more. They should only be given after the virus replication has stopped to prevent complications like oophiritis and orchitis

 

Acute bacterial sialadenitis

• Mostly parotid gland is infected
• Ascending duct infection [ bacteria goes against the salivary current to infect the gland - xerostomia, sialolith, post surgery scar will allow bacteria to infect the gland because there is no flushing effect of saliva]
• You need to milk the gland to confirm the presence of puss
• Pain during meal time , swelling , foul taste
• Strep pyogenes or staph aures mostly involved
• Treatment : copious water intake + avoid having the mouth dry + ABX

Acute radiation sialadenitis

• Starts 24- 36 hours after radiation → inflammation and early necrosis of the acini

 Chronic radiation sialadenitis

• Fibrosis + acinar atrophy - monitor for stomatitis and caries

Iodine – induced sialadenitis

• Mainly parotid is affected

N.B:

• Radioactive iodine is only picked up by the thyroid gland to treat thyroid cancer and will not affect other organs but it is somehow picked by the salivary glands causing sialadenitis.

Treatment: 

• copious water + massaging the glands [ ABX if there is bacterial infection] + monitor stomatitis and caries

 

Disturbances in salivary flow

• Hyposalivation : reduction in salivary flow [ reversible , mostly caused by drugs]
• Xerostomia : no saliva  

 

Xerostomia

• Most common salivary problem

Causes :

1. Drugs [ antihistamines, anti depressants, anti psychotics]
2. Systemic diseases [ sjogren’s , cystic fibrosis, sarcoidosis ]
3. Psychogenic [ anxiety and depression , normal salivary flow but the pt feels like their mouth is dry]

Diagnosis:

• Sialometry [done in the morning]

1. N → 3.5ml in 5 minutes (stimulated)
2. N → 0.5ml in 5 minutes (unstimulated)

• Sialography [ in cases of obstruction]
• Scintigraphy [investigates all glands at once]

Treatment:

1. Identify the cause [ if medication → change medication ]
2. Saliva substitutes and oral lubricants
3. If there are still functional acini → encourage salivation by sugar free gums and sialo gauge
4. Prevent complications of reduced salivary flow [ candida, caries etc]
5. Sialogauge : a drug that will stimulate salivary glands + other glands in the body [ sweat glands, GIT etc ..] → increase in saliva, sweat and GIT secretions [ GIT disturbance]

Consequences of xerostomia:

• Lack of lubrication

1. Difficulty swallowing / speaking and denture retention
2. Disturbed taste

• Infections

1. Caries, angular chelitis, candida ascending sialadenitis

 

Sialorrhea

• Usually rpresented as a laceration on the corner of the mouth
• Transient → wearing of a new denture, oral infections (e.g. HSV), RAS
• Episodic → GORD (GERD) to buffer stomach acidity (in this case called “water brash”)
• Constant → rabies, heavy metal poisoning and some drugs (lithium and cholinergic agonists)
• Permanent → poor neurological control [ strokes – called false sialorrhea] , such as in CP, mandibular or tongue resection

Treatment :

1. Transient → no treatment
2. Due to GERD , poisoning , rabies → identify the cause and treat it
3. Anticholinergic drugs [ have side effects]
4. Severe cases → gland excision, gland relocation or duct litigation

 

Systemic diseases affecting saliva

Sjogren’s syndrome [ SS] :

• Autoimmune disease – polyclonal B cell hyperactivity due to the loss of T cell regulation
• Dry eyes [ xeropthalmia or keratoconjunctivitis sicca] + dry mouth [ xerostomia]
• Affects lacrimal glands + Bartholin’s glands in the vagina + salivary glands + sweat glands
• Mainly women **
• Such patients will tell you “ I feel I constantly have sand in my eyes”

1. Primary SS → only exocrine glands are affected
2. Secondary SS → exocrine glands + other CT disease [ Rhuematoid arthritis, systemic lupus etc]

 

Diagnosis: Two of the following three:

• Positive serum antibodies  
• anti-SSA/Ro and/or anti-SSB/La
• positive rheumatoid factor and ANA titre
• Labial salivary gland biopsy exhibiting focal lymphocytic sialadenitis with a focus score 1 focus/4mm2 [ salivary gland parenchyma are replaced by lymphocytic infiltrate]
• Keratoconjunctivitis sicca with ocular staining score 3

 

N.B :

• Schimmer’s test is used to see tear production [ paper is place on the lower eye lid to test lacrimal gland production]

CAUTION:

• Patient’s with SS are at risk of developing mucosa associated lymphoid tissue malignancy [MALT] – you need to monitor for lymph node lumps and masses

Complications of  Sjogren’s syndrome : 

1. Candida infections / bacterial infections
2. Parotid gland enlargement
3. Increased risk of lymphoma 

Management :

1. Refer to an ophthalmologist + assessment by physician
2. Regular follow ups for lymphomas
3. Treat candida infections / bacterial infections
4. Fluoride applications
5. Saliva substitues

 

sarcoidosis

• Granulomatous disease
• Most affected organ = lymphoid tissue
• Causes bilateral hilar lymphadenopathy → respiratory failure and death
• Chest x-ray = bilateral radio opacity

• Blood test =

1. ↑ calcium
2. ↑ ACE
3. ↑lysozome
4. ↑ adenosine deaminase

• Histologically :

1. non caseating granulomas [ clean granulomas]

N.B :

• TB and deep fungal infections the granulomas that form are contaminated since they contain the micro organism
• But in chron’s and sarcoidosis granulomas are clean without a microorganism
• Chron’s disease → granulomas only in the GIT
• Sarcoidosis → granulomas in any organ
• Wegner’s granulomatosis → necrotizing granulomas

 

Sialosis

• Non-inflammatory, non-neoplastic , Painless recurrent bilateral swelling of the salivary glands
• Serous gland hypertrophy and decrease in granularity  in association with:

1. hormonal disturbances
2. diabetes
3. malnutrition
4. liver cirrhosis
5. medications eg. phenylbutazone (anti-inflammatory)
6. Iodine containing drugs
7. Alcohol
8. GERD 

Reactive salivary gland lesions

• Mucocele: Can be mucus extravasation phenomenon or mucus retention cyst
• Ranula : mucus extravasation phenomenon and mucus retention cyst that occurs specifically in the floor of the mouth

 

MUCOUS EXTRAVASATION PHENOMENONA:

• Trauma will cause severance of the salivary duct but the acinar cells will continue to secrete saliva into the severed duct → mucous pools into the CT forming a mucocele
• Most common site for mucous extravasation cyst = the lower lip
• Initially the mucoceles are well circumscribed but with repeated trauma they become nodular and firm

• MS =

1. Free mucin in connective tissue with no epithelial lining
2. The base of the mucocele will reveal feeder duct.
3. Salivary gland changes (in long standing case) shows:

• Ductal dilation
• Chronic inflammation
• Acinar degeneration
• Increased fibrosis

 

Differential diagnosis of mucous retention cyst:

1. Mucoepidermoid carcinoma
2. Cavernous hemangeoma
3. Blisters seen in some bullous and desqumative disease.
4. Soft tissue neoplasms (neurofibroma & lipoma)

Treatment:

• Surgical excision with the feeder gland.
• Post surgical parasthesia might occur

 

Mucous retention cyst [ obstructive sialadenitis]

• obstruction of a salivary duct resulting in an epithelial lining cavity containing mucus
• The mucus retention cyst could occur in the major salivary gland, when they do occur they are multiple [ poly cystic disease of the parotid gland]
• Most common site for mucous retention cyst → floor of the mouth

• MS =

1. The cyst has compressed ductal epithelial linning
2. Cyst lumen contains mucin or occasionally a sialolith

 

Differential diagnosis of mucous retention cyst:

1. Salivary gland neoplasm
2. Mucus extravasation phenomenon
3. Benign CT neoplasm
4. Dermoid cyst

Treatment :

• excision with caution of rupturing the cystic sac [ damage to the adjacent gland may result in
• a mucocele formation]

 

MAXILLARY RETENTION CYST :

• Due to blockage of antral sero-mucus gland → ductal epithelium lined cystic structure filled with mucin.
• Asymptomatic, appear as hemispheric, homogenous well- defined radiopacity
• No treatment just observation

 

SALIVARY GLAND OBSTRUCTION – SIALOLITH:

• Usually associated with the submandibular gland – Wharton’s duct
• causes intermittent swelling and pain often at meal times [ when there is increased demand for saliva]
• Treatment: surgical removal of the stone with or without the gland
• Gout is the only systemic disease known to cause salivary calculi and these are composed of uric acid

Predisposing factors for sialolith formation:

1. increase in water hardness
2. smoking
3. xerostomia

Q: why is it more common to get sialoliths in the sub mandibular gland?

1. Saliva more alkaline
2. Higher concentration of calcium and phosphate in the saliva
3. Higher mucus content
4. Longer duct
5. Anti-gravity flow

 

Q: how can calculi/ sialolith be detected?

• Plain occlusal films [ for intra ductal stones]
• Ct scan
• Ultrasound
• Sialography [ descriptions]:

1. Tree in winter → normal parotid gland
2. Bush in winter → normal sub mandibular gland
3. Snowstorm / cherry blossom → sjogren’s syndrome
4. Sausage link appearance [ dots , blobs] → sialodochitis

• Radio isotope imaging
• MRI [ gold standard]
• Diagnostic Sialendoscopy: Allows complete exploration of the ductal system, direct visualization of duct pathology- but has risk of perforating the duct and can lead to duct stenosis

 

Q: how can sialolith be treated ?

• No treatment → just give ABX and anti inflammatory and hope for the stone to pass
• Stone excision → [ lithotripsy, interventional sialondoscopy , simple excision]
• Gland excision .

 

Q: when can you remove a sialolith transorally? 

• If you can palpate it through the mouth, if you can visualize it on an occlusal radiograph , if it is no more than 2 cm from the punctum

Q: when do you need to remove the gland? 

• If transoral approach fails, intraglandular stones , very posterior stones

Q: how does the epithelium in the gland react to the sialolith? 

• The epithelium shows squamous and mucus cell metaplasia + changes to stratified squamous epithelium with goblet cells

NECROTIZING SIALOMETAPLASIA:

• Caused by ischemia due to LA vasoconstriction - mostly in the palate
• large area of epithelium + underlying connective tissue and minor salivary glands become necrotic while the ducts undergo squamous metaplasia [ within the ulcer you’ll see gray granular lobules which represents the necrotic minor salivary glands]
• MS = pseudo epitheliamatous hyperplasia
• self limiting [ no treatment needed ] – heals in 6-8 weeks