Dieseases of salivary glands

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Oral patho lec.7 4/11/2013

Dr. faleh

Dieseases of salivary glands

Salivary glands consist of three paired major glands ( parotid , submandibular and sublingual ) ,and countless minor salivary glands found within the oral cavity .

Developmental anomalies of salivary glands are rare ..; such as :

1) aplasia > no major salivary gland at all

2) hypoplasia >salivary gland is smaller than its normal size ( could be seen with melkersson-rosenthal syndrome )

3) ectopic tissue > it has been reported from a variety of sites in the head and neck , the most frequent sites are in the mandible , in cervical lymph nodes and in the middle ear .

4) accessory salivary glands such as : accessory parotid tissue which is found around buccinator muscle .

5)atreisa > some of major/minor salivary glands ducts aren’t found .


Inflammatory disorders of major salivary glands are usually the result of bacterial or viral infection or due to systematic disease or to other local causes such as trauma , irradiation and allergic reaction .

Bacterial sialadenitis

May present as an acute or chronic condition depending on its duration and severity

1) acute bacterial sialadenitis

- uncommon to see nowadays due to the production of antibiotic .

- acute bacterial sialadenitis is an ascending infection , because the bacteria reach the gland from the oral cavity by ascending the ductal system

Why it affects parotid more than submandibular gland despite that the movement of bacteria is easier downward (to submandibular gland ) ????

-reduced salivary flow is the major predisposing factor which is seen in xersotomic patients ; this dryness can be seen in :

1)patients who expose to radiation .

2)after using drugs with xerostomic side effect such as tricyclic antidepressant and antipsychotic .

3)patients with sjorgren syndrome .

4)patients with obstructed salivary glands .

5)immunocompromised patients .

Microbiology : mixed ; aerobic and anaerobic bacteria ((as a group of bacteria such as streptococcus pyogens and staphylococcus aureus ))

Clinically :

-rapid onset of pain - swelling (especially in parotid and peri auricular area )

-trismus (inability to open his mouth easily ) - fever,pain and malaise

- lymphadenopathy -redness

How to know if it is bacterial infection ?? by seeking for a pus that is exposed from the opening of parotid gland (stenson`s duct ) >>that is seen as an elevation around the opening which shouldn’t be misdiagnosed with polyp .

-no biobsy , no sialography

Features could be seen in the affected salivary gland :

1)intense AICI in acini ,peri ductal and within ducts .

2) dilatation of the ducts

3) abscess is often formed in the duct

2 ) chronic bacterial sialadenitis

It is usually associated with duct obstruction and decrease of secretion .-

The submandibular gland is much more commonly involved than parotid ?? because the obstruction is mostly seen in submandibular gland

The chronic sialedanitis is usually unilateral ; because the obstruction is mostly unilateral

The symptoms is a tender swelling of the affected salivary gland especially after stimulation (while eating > the salivary gland is stimulated )

-redness or inflammation on the orifice of salivary gland .

-production of pus (especially if it is transformed from chronic to acute )

Histological examination :

Irreversible damage and destruction of acini due to the chronic inflammation –

-dilatation of ductal system and hyperplasia of duct epithelium .

-scattered CICI

-after period of time any destruction or atrophy of acini will be replaced by interstitial fibrosis .

* in the submandibular gland , progressive chronic inflammation may result eventually in almost complete replacement of parenchyma by fibrous tissue producing a hard firm mass with no production of saliva and it becomes better in infection resistance … this type of inflammatory reaction may be referred to as chronic sclerosing sialadenitis .

3) recurrent parotitis

It’s a rare disorder which can affect children , appears as enlargement of gland with pain ,redness and trismus .

- recurrent attacks .

- etiology : unknown

-this condition may be unilateral or bilateral and is associated with recurrent painful swelling of gland with redness and trismus + pus may be expressed from the duct orifice .

- during childhood the infection could be treated by antibiotic, and in most cases the condition resolves spontaneously by the time the patient reaches early adult life , but if the disease remained in adulthood this will cause irreversible damage to the gland .

MUMPS ( viral sialadenitis ) :

Most common especially before immunization period ; this disease is decreased nowadays due to production of triple immunization vaccine against mumps, measles and rubella which is generally administrated to children around the age of one year with second dose around the age of 3 years .

-highly infectious and can be transmitted from child to other child by airborne droplets and saliva .

- the parotid glands are almost always involved bilaterally .

-nonspecific predormal symptoms of fever and malaise are followed by painful swelling of sudden onset involving one or more salivary glands .

-duration = 7-10days

-no pus > because it’s a viral infection

-submandibular glands and sublingual gland may be affected too

-occasionally in adults other internal organs are involved , such as testes , ovaries central nervous system and pancreas . orchitis is the most common complication , occurring in adult males

The diagnosis of mumps :

1)it is usually on clinical ground

2)by increasing amylase in blood

3) AB to "s" and "v" ags

- after an attack immunity is long acting so recurrent infection is rare

Radiation induced sialadenitis

Serous acini are most sensitive to radiation damage than mucous acini >> so the most sensitive gland to radiation is parotid gland

-it causes xerostomia within 24 hours after exposure to radiation ,and if it is with high dose it will cause irreversible fibrous replacement & sq metaplasia

-complication :the same complications of dryness of the mouth ( will be discussed later on )

Sialadenitis of minor salivary glands

It is seen most frequently in association with mucous extravasation cysts and stomatitis nicotina of the palate , and is also seen in sacroidosis and sjogren syndrome

Obstructive and traumatic lesions :

Obstruction to the duct orifice is usually due to chronic trauma and stones formation

Causes :

*sialoliths :

This may form in ducts within the glands or in the distal 1/3 of the duct near the floor of the mouth .

-the submandibular gland is most frequently involved, the parotid gland is the 2nd most commonly involved , whereas sialolithiasis in sublingual and minor glands is uncommon (rare)


-in adults ; males > females

-unilateral stones

-multiple stones

-most cause symptoms : pain,swelling and retrograde infection (these symptoms are seen during stimulation while eating )

-its more susceptible to chronic sialadenitis due to the obstruction and reduction of salivary flow .

Diagnosis :

1) by palpation(manually) or by vision (at the orifice of the affected salivary gland )

2) radiograph >>- large stones in submandibular glands by using the occlusal film

-40% of parotid gland stones are radiolucent

-20% of submandibular glands stones are radiolucent

3)sialography : injection of radio opaque material to see the stones in the ducts

Pathogenesis : it is generally thought that they form by deposition of ca salts , PO4 and bicarbonate around an initial organic nidus which might consist of altered salivary mucins together with desquamated epithelial cells and microorganisms (bacteria ) .

Hist :

>>Stone :

*Grossly > - yellowish –white in color

-round/oval in shape

-rough or smooth surface

It consists of Ca , Po4 and bicarbonate

>>Gland changes (same as seen in chronic sialadenitis )

-duct dilatation with sq metaplasia

-periductal CICI and fibrosis

-acinar atrophy and replacement of fibrosis

- CICI of lobules

* The parotid papilla:

A very obvious structure in the oral cavity, due to that its susceptible to trauma that would be from an appliance , surgery in the area or a major aphthous ulcer affecting the area that might lead to fibrosis in the papilla that will lead to its destruction specially at its opening.

Other causes of obstruction of ducts rather than stones, trauma or major aphthous ulcer such as a tumor in the same gland or around it that will press on the opening ( duct) or a surgery in the area that lead to a trauma to the duct.

* Necrotizing Sialometaplasia:

- a rare disease affecting salivary glands

- of unknown etiology but it could be due to an ischemia to the minor salivary glands that will lead to necrosis in these glands so ulcer( chronic ulcer) in the area of ischemia would occur.

- the most common site is the junction between the hard and soft palate.

- its appearance will make the patient think that’s it’s a cancer (like squamous cell carcinoma)

-painless which make it a suspicious condition.

- the duration of its presence can last for 1 or 2 months ( long duration)

“So a person who has an ulcer that is painless and is present from 1 or 2 months and deep these findings will make us think about squamous cell carcinoma where its not.”

- occur in middle aged people.

- its size might be big up to 2cm

But what makes the situation worse is the histopathalogical findings that look like cancer:

  1. The surface epithelium around the ulcer shows hyperplasia(Pseudoepitheliomatous hyperplasia) that looks like invasive squamous cell carcinoma

  2. In the area of the ulcer we will see salivary gland tissue, their architecture and distribution looks like mucoepdermoid carcinoma that shows:

* mucoextravasation

* squamous metaplasia in the ducts and acini.

* necrosis in the salivary glands, nodules.

* chronic inflammatory cell infiltrates (CICI) in the area

All these findings look like the ones found in the mucoepidrmoid carcinoma.

So clinically and histopathalogically it looks like cancer that’s why in some cases it will be treated by major surgery where they make a cut in the maxilla (all of maxilla) by that they will treat the lesion although it’s a revesible lesion that can be treated by a less invasive methods.

After 3 months from its first presence it will heal and no need for any intervention . so a careful diagnosis and histopathology

It’s not mucoepidermoid carcinoma but looks like it.

The healing occur gradually after a time of 2 months or 10 weeks the healing starts . the size decreases with healing , but if its squamous cell carcinoma its size will not decrease with time.

* sailosis (sialadenosis):

- the patient will come with an enlarged parotid gland which is usually painless.

- inflammation isn’t the cause ( non-inflammatory) and also its not bacterial or viral infections , its not a tumor .

- it’s a cell enlargement ( hypertrophy of the acini and tissue of the glands)

- no reduction in the saliva flow so its mainly enlargement of the gland.

- definition:

Non-inflammatory , non-neoplastic , bilateral parotid gland enlargement.

- unknown etiology but might be due to a problem with the innervations of the gland ( sympathetic and parasympathetic systems)

- in these patients we should exclude certain systemic diseases that are associated with cyanosis such as alcoholism or liver cirrhosis, diabetes mellitus, hyperthyroidism, acromegally, pregnancy , bulimia nervosa, Antipsychotic drugs , malnutrition and chronic renal failure . all these should be excluded during medical history taking that might help in the diagnosis of these diseases.

- histopathalogically:

1. hypertrophy in the acini and edema of the connective tissue.

2. no inflammation or tumor like findings

* Sojegren’s Syndrome:

- the main complain in these patient is dry mouth for a long period of time and when the saliva flow decreases many features would occur and cause a lot of problems for the patient

- if the patient doesn’t take any drugs or exposed to radiation that might cause this dryness then we should think about sojegren’s syndrome.

- pathogenesis:

Occurs due to the destruction of the acini by cell-mediated immunity (the gland will be a mass of cell-mediated inflammatory cell like lymphocytes instead of acini and ducts)

- so its an immune mediated chronic inflammatory cells disease, non-organ specific autoimmune disease or cell mediated disease .

- tell now we don’t know what is the antigen that the antibodies are produced against it and causing the disease and also we don’t know whether its a strict cell-mediated or not because there is production of auto-antibodies. ( its not clear whether its an autoimmune disease or not because there is cell immunity and humeral immunity also)

- symptoms:

  1. xerostomia or mouth dryness but this isn’t restricted only in salivary glands it affect all the exocrine glands such as lacrimal glands but mainly salivary glands, dryness and irritation in the eye that will lead to conjunctivitis and keratotic lesion on the cornea and failure of tear secretion . So upon examination we check for eye dryness also ( dryness of mouth mainly with dry eyes)

* schirmer test:

  • its done to make sure whether we have eye dryness or not.

  • Its done by the ophthalmogest by putting a thing like a filter paper in the inner canthus of the eye and leave it for 5 min . in a normal person this paper will become wet but with a dry eye the wetting will be less ( less than 5mm wetting of the paper means dryness).

  1. discomfort in the oral cavity.

  2. soreness

  3. difficulty in eating, swallowing and speaking

  4. metallic taste.

  5. Atrophic mucosa because of decreased salivation.

  6. More susceptible to infection like Candida.

  7. Sialadenitis

  8. Increased carries presence ( rampant and root carries)

  9. Mucosa is red, dry and shinny. Mirror sticks on mucosa during examination.

  10. Tongue shrinkage ( scroutum tongue)

  11. Arathlgia( joints pain) and xeroderma ( dryness of the skin) because as we said it affect the secretion of the exocrine glands.

  12. Tiredness they can sleep up to 20 hrs.

  13. More prone for infections and inflammations in respiratory tract and sinuses.

  14. Atrophic gastritis and pancreatitis.

- clinically, it approximately affect 1% of the population

- affect mainly middle aged females or postmenopausal women ( 80%)

Because its autoimmune we it affect females more.

- of 2 types:

  1. primary type:

only xerostomia and xerophthalmia ( mouth and eye dryness)

  1. secondary type:

mouth and eye dryness accompanied with a connective tissue diseases (autoimmune disease) such as rheumatoid arthritis( 15% of rheumatoid arthritis patients has sojegren’s syndrome) , systemic lupus (30% of them has sojegren’s syndrome) , systemic sclerosis, primary biliary cirrhosis and dermatomyostits .

“The most common autoimmune disease to be associated with this syndrome is systemic lupus.”

- a CBC test shows: Anemia, thrombocytopenia

- 30% of the patients shows a salivary enlargement

So tell now we have 2 causes for the salivary gland enlargement in the sojegeren’s syndrome:

  1. the disease itself.

  2. Bacterial siadenitis due to the decreased saliva flow.

  3. Lymphoma which one of the syndrome’s complications.

- histologically : (easy to distinguish)

  1. It’s a cell-mediated disease so we will see lymphocytic infiltrates mainly T-lymphocytes . ( firstly these infiltrates start around the intralobular ducts then it will extend to affect other glandular tissue)

  2. Acini atrophy because the saliva production is reduced.

  3. due to inflammation the ducts will show proliferation and it will have the appearance of separate islands of epithelial cells and myoepethelial cells ( epimyoepethelial islands) .

about the myoepethelial cells:

  • they have a clear cytoplasm unlike regular epithelial cells .

  • helps in saliva secretion .

- the inflammation doesn’t penetrate the interlobular septum and the capsule of the gland will not separate. So if we see that the inflammation did penetrate the septum then we exclude sojegeren’s syndrome from the diagnosis and we will think about lymphoma.

* how to confirm the syndrome diagnosis?

  1. Mainly by sialometry ( measuring the amount of saliva for the patients) if the syndrome is present the measurement will be less than 0.1 ml or in 5 min it will be less than 0.5 ml)

  2. Schirmer test can be done also ( the wetting will be less than 5mm)

  3. how to detect whether we have changes in the salivary glands or not ?

taking a biopsy , but for example taking it from the parotid gland will produce many complications such as fibrosis, scaring, fistula, infections or damage to the facial nerve . that’s why biopsy is done mainly for minor salivary glands. The features that are seen in the major ones will be also seen in the minor ones too and its easer to take a biopsy from minor glands such as labial mucosa glands in the lower lip . then exam it under the microscope with a special stain .

we will see inflammatory cell-mediated immunity around the ducts ( the T-cells) the count of these cells should be more than 50.

The dr said:In the sojegren’s syndrome we need more than 1focus per 4mm square to say this is consistancde with sojegren’s syndrome because there is other causes that induce inflammation in the gland and make the T-cell count more than 50 other than the syndrome that’s why we do the focus

  1. sialography : because there is damage for the ducts and the acini when we inject a radio opaque material it will go out the ducts and it will accumulate around the ducts . major salivary glands in sailography will look like snow storm . an easy method and helps in the diagnosis of the syndrome.

  2. Salivary scintiscaning by pertechnelate uses an isotope that goes to the salivary gland then it will be secreted with saliva if the glands destructed this material will not be uptake

  3. Seriology or immunological tests such as SS-A (sojegren’s syndrome auto antibodies) , SS-B antibodies, rheumatoid factor (RF) it will be positive but if the patient was RF +ve this doesn’t confirm 100% that its secondary type of sojegren’s syndrome, a patient that has the primary type might be RFand ANA +ve . also antibodies for lupus to know if we have a systemic lupus or not.

“ diagnosis of secondary sojegren’s syndrome is done clinically not by immunological tests.

* patients will have problems in CBC tests, sedimentation test and increase in the Igs level ( hyperglubulanamia)

- etiology is unknown can be an autoimmune disease , they also suggest that it might be caused by a group of viruses such as CMV, EBV, HSV-6, Retrovirus but there is no 100% certainty that they cause the syndrome.

* Complications of the syndrome:

  1. due to the presence of cell-mediated immunity in the affected glands it might turn into B-cell malignant lymphoma ( up to 5% specially the primary type turn to lymphoma)

  2. dryness of mouth and eyes is more severe in primary type patients

Good luck

Done By:

Yasmine Abu Salem


Duaa Momani

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