idiopathic non neoplastic salivary gland diseases

8/8/2019 Idiopathic Non Neoplastic Salivary Gland Diseases

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IDIOPATHIC NON NEOPLASTIC

SALIVARY GLAND DISEASES

SUBMITTED BY

RANJAN KUMAR DAHIYA


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NECROTIZING SIALOMETAPLASIA

(SALIVARY GLAND INFARCTION)

Necrotizing sialometaplasia is a non

neoplastic inflammatory condition of the

salivary gland.

The clinical & histopathological features of

NS often simulate those of malignancies

such as squamous cell carcinoma ormucoepidermoid carcinoma.


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ETIOLOGY

NS arise spontaneously.

associated with history of trauma, radiation

therapy, surgery. It believed to be related to vascular

ischemia.

Tobacco use is suggested as a etiologicrisk factor for NS.


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PATHOGENESIS

Traumatic injuries, dental infections, upper respiratoryinfections, tumuor, denture.

Compromised blood supply

ischemia

infarctions

necrosis of acinar cells


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CLINICAL FEATURES

AGE : range of 17 80 yrs

SEX : M > F 2:1

SITE : Minor salivary glands of the oral

cavity, particularly those of palate.

Minor salivary glands of the retromolar padarea, buccal mucosa, tongue, incisive

canal & labial mucosa.


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Painless

Swelling with or without ulceration

Crateriform ulcer of the palate

Usually unilateral

But bilateral synchronous lesions &

metachronous lesions can occur

Some lesions of necrotizing sialometaplasia maypresent as a submucosal swelling, without

ulceration of the overlying mucosa.


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HISTOLOGICAL FEATURES

Microscopic features of necrotizing metaplasia includecoagulative necrosis of glandular acini & squamousmetaplasia of its ducts.

Mucin pooling present.

Associated with inflammatory infiltrate consists ofmacrophages, neutrophils & less commonly, lyphocytes,plasma cells & eosinophils.

Pseudoepitheliomatous hyperplasia can also be present.

But the cytologic features the epithelial atypia are usuallyabsent.

The microscopic differential diagnosis for NS includesmucoepidermoid carcinoma & Sq cell carcinoma.


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TREATMENT & PROGNOSIS

Treatment is not necessary.

The prognosis for NS is excellent.

The average healing is approximately 5weeks.


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LYMPHOEPITHELIAL CYST

Lymphoepithelial cyst is an uncommon

lesion of the mouth, major salivary glands

or neck.


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PATHOGENESIS

It is thought to be arise from an

entrapment of epithelium within lymph

nodes or lymphoid tissue during

development.


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CLINICAL FEATURES

AGE : May develop in people of almost

any age.

SEX : M = FSITE :

Most common - floor of the mouth.

Less common ventral surface & posterior

lateral border of tongue.

Palatal tonsil & soft palate.


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Small submucosal mass.

Firm & soft to palpation.

Overlying mucosa is smooth & ulcerated.

The lesion is typically white or yellow &often contains creamy or cheesykeratinous material in the lumen.

The cyst is usually asymptomatic.Pain is rare but may occur secondary to

trauma.


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HISTOPATHOLOGIC FEATURES

It is lined by stratified squamous epithiliumwithout rete ridges.

This epithelium is typically parkeratinized, withdesquamated epithelial cells seen filling the cystlumen.

Most striking feature is the presence of lymphoidtissue in the cyst wall.

In most instances lymphoid tissue encircles the

cyst, but sometimes it involves only a portion ofthe cyst wall.

Germinal centres, usually, but not alwayspresent.


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TREATMENT

No treatment is usually necessary

Most lesions are removed by conservative

surgical excision.


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CHEILITIS GLANDULARIS

(Actinic cheilitis, Sq cell carcinoma)

Uncommon & poorly defined understood

inflammatory disorder of the lip.

Characterized by progressive enlargement& eversion of the lower labial mucosa that

results in obliteration of the mucosal

vermilion interface.


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TYPES

1. SIMPLE TYPE multiple, painless, papular surface lesion with central

depression & dilated canals are seen.

2. SUPERFICIAL TYPE (SUPPURATIVE) Also known as BAELZ DISEASE

Consists of painless, indurated swelling of the lips withswallow ulcerations & crusting.

3. DEEP SUPPURATIVE TYPE ( CG Apostematosa, CG suppurativa profunda,

myxadenitis labialis )

Deep seated infections & fistula that eventually formsa scar.


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ETIOLOGY

1. Occurs because of chronic exposure of

sun, wind & dust as well as use of

tobacco.

2. In several cases, emotional disturbances

as well as familial occurrence.

3. Inflammation of enlarged heterotrophic

salivary glands may also leads to

glandularis cheilitis.


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CLINICAL FEATURES

AGE : between 4th & 7th decade of life.

SEX : M > F

Characteristically occurs on the lower lips.

Swelling & eversion of the lower lip as a result

of hypertrophy & inflammation of the gland.

Opening of the minor salivary are inflammed

dilated & pressure on the gland may producemucopuralent secretions.


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4. It is a chronic progressive condition.

5. Patients complaints vary according to the nature & thedegree of pain, the enlargement & the loss of elasticityof the lips.

6. A burning discomfort or a sensation of rawness referableto the vermilion border may be reported.

7. It is associated with atrophy, speckled leukoplakicchange, erosion, or frank ulceration with crusting.

8. It has been associated with heightened risk for the

development of squamous cell carcinoma.9. The risk of dysplasia & carcinoma increases with age,especially in fair skined individuals with sun damagedskin.


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HISTOPATHOLOGIC FEATURES

Presence of stratified squamous epitheliumwhich covers inflammatory connective tissue.

In a milder form, there is some fibrosis

surrounding the salivary glands & in the moresevere forms, there may be a dense,inflammatory infiltrate.

The underlying salivary gland tissue shows

hypertrophy & inflammation. In some cases there is dysplastic changes can

be seen in the epithelium.


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DIFFERENTIAL DIAGNOSIS

Actinic keratosis

Atopic dermatitis

Cheilitis granulomatosa( miescher-melkersson-rosenthal

syndrome )

SarcoidosisSquamous cell carcinoma


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TREATMENT

Vermilionectomy

If the lips are grossly enlarged, excision of

an elongated ellipse of tissue may berequired.


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SJOGRENS SYNDROME(SICCA

SYNDROME)

Sjogrens syndrome is a condition originallydescribed by HENRIK SJOGREN in 1933,as atriad consisting of keratoconjunctivitis sicca,xerostomia and rheumatoid arthritis.

It has been found that some pts. Present onlywith dry eyes and dry mouth(sicca complex orprimary sjogrens syndrome)

While others also develop systemic lupus

erythematosus, polyarteritis nodosa,polymyositis or scleroderma, as well asrheumatoid artheritis ( secondary sjogrenssyndrome )


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ETIOLOGY

various causes of these disease have

been suggested : genetic, hormonal,infectious & immunologic.

Unknown cause :EBV virus or Human T

lymphotrophic virus


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CLINICAL FEATURES

AGE : approx 40 Yrs

SEX : F > M Ratio 10:1

Dryness of mouth and eyes as a result ofhypofunction of the salivary and lacrimalglands.

Painful and burning sensations of oralmucosa.

In addition various secretory glands of thenose, larynx, pharynx and tracheobronchialtree as well as of the vagina are involved withthis dryness.

Reduced salivary flow was noted in bothgroups.

80% of pts. With primary sjogrens syndromehave parotid enlargement in contrast to only14% with secondary sjogrens syndrome.

Lymphadenopathy is more than twice ascommon in the primary form of the disease.


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Rheumatoid arthritis is an integral part of

secondary sjogrens syndrome.

Sicca complex or primary sjogrenssyndrome, more frequently manifest

parotid gland enlargement,

lymphadenopathy, purpura, raynauds

phenomenon, kidney involvement andmyositis.


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HISTOLOGICAL FEATURES

Three types of histologic alterations in the majorsalivary glands are

In one case there may be intense lymphocyticinfiltration of the gland replacing all acinarstructures.

In another there may be proliferation of ductalepithelium and myoepithelium to formepimyoepithilial island.

The third alteration may be simply an atrophy ofthe glands sequential to the lymphocyticinfiltration.


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LABORATORY FINDINGS

Over 75% of pts with primary sjogrenssyndrome have a polyclonal hyperglobulinemia& many develoved cryoglobulins.

Multiple organs or tissue specific antibodies arefound, including antisalivary duct antibodies,rheumatoid factor & antinuclearantibodies,rheumatoid factor and antinuclearantibodies.

The presence of antisalivary duct antibody isthree times more common in those withsecondary sjogrens sydromes with the siccacomplex.


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RADIOGRAPHIC FEATURES

Sialographic may be of dianostic value in

sjorgens syndrome.

Sialograph demonstrates the formation ofpunctate, cavitary defect which are filled

with radioopaque contrast media.

This filling defects have been said to

produce a cherry blossom or branchless

fruit laden tree effect radiographically.


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TREATMENT

There is no satisfactory treatment for sjogrenssyndrome.

Most patient are treated symptomatically.

Keratoconjuctivitis is treated by instillation of ocular

lubricants such as artificial tears containing methylcellulose.

Xerostomia is treated by saliva substitute.

Extensive dental caries is a complication which is quitecommon & frequent flouride applications is indicated to

reduce this problem. There is no specific treament for enlargement of salivarygland.

Surgery has been employed but is generallyrecommended only in patients with discomfort


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idiopathic non neoplastic salivary gland diseases

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