submandibular salivary gland

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PROF PALANI MS FICS SUBMANDIBULAR SALIVARY GLAND

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SUBMANDIBULAR SALIVARY GLAND. PROF PALANI MS FICS. P aired salivary glands that lie below the mandible on either side. larger superficial and a smaller deep lobe. D rained by a single submandibular duct (Wharton’s duct ). - PowerPoint PPT Presentation

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Page 1: SUBMANDIBULAR SALIVARY GLAND

PROF PALANI MS FICS

SUBMANDIBULAR SALIVARY GLAND

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Paired salivary glands that lie below the mandible on either side.

larger superficial and a smaller deep lobe.

Drained by a single submandibular duct (Wharton’s duct).

It drains into the anterior floor of the mouth at the sublingual papilla.

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3 NERVES—Marginal mandibular branch of facial nerve

__hypoglossal nerve __lingual nerve2 MUSCLES__mylohyoid __hyoglossus1 ARTERY __facial artery.

Important anatomical relationships of the submandibular glands

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CLINICAL EXAMINATION

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most common ectopic salivary tissue is the Stafne bone cyst.

asymptomatic, clearly demarcated radiolucency of the angle of the mandible.

Formed by invagination into the bone on the lingual aspect of the mandible of an ectopic lobe of the juxtaposed submandibular gland.

No treatment required.

Ectopic/aberrant salivary gland tissue

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Acute, Chronic or Acute on Chronic.Acute submandibular sialadenitis: - Viral : The paramyxovirus (mumps). - bacterial : secondary to obstruction.

INFLAMMATORY DISORDERS

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most common cause is stone formation.Eighty per cent of all salivary stones occur in

the submandibular glands because their secretions are highly viscous.

Eighty per cent of submandibular stones are radio-opaque and can be identified on plain radiography.

OBSTRUCTION AND TRAUMA

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SYMPTOMS:Acute painful swelling in the region of the

submandibular gland, precipitated by eating.Swelling occurs rapidly and often resolves

spontaneously over 1–2 hours after the meal is completed—complete obstruction.

Minimal discomfort and swelling, not confined to mealtimes—partial obstruction.

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SIGNS:enlarged firm submandibular gland, tender

on bimanual examination.Pus may be visible, draining from the

sublingual papilla.

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TREATMENT:DISTAL TO LINGUAL NERVE: -- INTRAORAL APPROACH.PROXIMAL TO LINGUAL NERVE: -- gland excision, stone removal and

duct ligation.

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Incision and exposure of glandGland mobilisation.Dissection of the deep lobe and identification

of the lingual nerve.Wound closure.

EXCISION

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Incision and exposure of glandIncision should be

marked at least 3–4 cm below the lower border of the mandible to avoid damage to the marginal mandibular branch of the facial nerve.

Superficial veins, including the anterior facial vein, require ligation.

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Gland mobilisationintracapsular

dissection - inflammatory

conditionsextracapsular

dissection -tumours.

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Important landmark in submandibular gland dissection is the posterior border of the mylohyoid muscle.

The gland is retracted inferiorly, invariably attached to the lingual nerve through parasympathetic secretor motor fibres. Lingual nerve preserved.

Duct ligated and gland excised.

Dissection of the deep lobe and identification of the lingualnerve

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Three cranial nerves are at risk during removal of the submandibular gland:

1 The marginal mandibular branch of the facial nerve.

2 The lingual nerve. 3 The hypoglossal nerve.

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1. Haematoma;2. wound infection;3. marginal mandibular nerve injury;4. lingual nerve injury;5. hypoglossal nerve injury;6. transection of the nerve to the mylohyoid

muscle producing submental skin anaesthesia.

Complications of submandibular gland excision

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Only 50% of submandibular gland tumours are benign, in contrast to 80–90% of parotid gland tumors.

In many circumstances, the swelling cannot, on clinical examination, be differentiated from submandibular lymphadenopathy.

Most salivary neoplasms, even malignant tumours, are often slow-growing, painless swellings.

SUBMANDIBULAR GLAND TUMORS

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BENIGN & MALIGNANT NEOPLASMS ACCORDING TO SITE OF ORIGIN

parotid submandibular minor0

10

20

30

40

50

60

70

80

90

75

57

18

25

43

82

benign malignant

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MALIGNANT SALIVARY NEOPLASMS

18%

13%

7%

4%

3%

33%

22%

Adenocarcinoma

Malignant mixed

Acinic cell

SCC

Other

Mucoepidemoid

Adenoid cystic

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ENVIRONMENTAL : Radiation (ionising & UV radiation).

EBV. Silica dust. Early menarche &

nulliparity. Smoking (Warthin’s

tumor). Diet rich in PUFA

(protective)

GENETIC.

ETIOLOGY

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PLEOMORPHIC ADENOMA most common benign tumor of both

major & minor salivary glands.

Peak incidence 4th & 5th decade with slight female preponderance.

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Epithelial & modified myoepithelial cells intermingle with a stroma can be mucoid, myxoid, fibrous or chondroid.

Areas of oncocytic metaplasia are common & it can be misdiagnosed as oncocytoma.

Most characteristic appearance of stroma is the formation of mucoid or myxochondroid areas containing scattered epithelial cells with cartilaginous or osseous metaplasia.

MICROSCOPY

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Principal clinical problem is recurrence (3.4 % in 5 yrs – 6.8 % in 10 yrs) and malignant progression.

RISK FACTORS FOR RECURRENCE :Variable / Absent capsulation.Intracapsular invasion.Improper excision.

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MALIGNANT SUBMANDIBULAR GLAND TUMOR

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MC malignant tumor of salivary gland..

Low grade : predominance of mucous secreting cells with well differentiated epidermoid cells.

High grade : few or no mucous producing cells and poorly differentiated epidermoid cells.

MUCOEPIDERMOIDCARCINOMA

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ADENOID CYSTIC CARCINOMA 15 % of salivary neoplasms. 2nd most common malignant tumor of

salivary glands. MC malignant tumor in submandibular, sublingual & minor salivary glands.

Peak incidence 5th & 6ht decade.MC site : oral cavity (50%) sinonasal tract (18%)

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5 – 11 % of malignant tumors of salivary glands.

Presents at a younger age.Affects women > men.Arises MC in parotid.MICROSCOPY : cells with basophilic

cytoplasm associated with lymphoid infiltrate.Subtypes : solid, microcystic, papillary cystic

& follicular

ACINIC CELLCARCINOMA

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Represents malignancy with both epithelial & mesenchymal elements.

3 – 12 % of salivary gland tumors.Carcinoma ex pleomorphic adenoma -

arising from pre exsisting pleomorphic adenoma. Malignant & metastatic components are epithelial in origin.

De novo malignant mixed tumor (CARCINOSARCOMA) :

with malignant features of both epithelial and mesenchymal components

MALIGNANT MIXED TUMOR

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Con………………. malignant transformation occurs in 3 – 4 % of

all benign mixed tumors.Risk of malignant transformation of pleomorphic

adenoma increases with duration of disease. ( 1.5% within 5 yrs -

9.5% within 15 yrs).Features of malignancy in pleomorphic adenoma

Necrosis, calcification, hemorrhage and excessive hyalinization.

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Clinical features of malignant submandibular tumours

1. Rapid enlargement of the swelling.2. Induration and/or ulceration of the

overlying skin.3. Cervical node enlargement.4. Ipsilateral weakness / numbness of tongue.5. Fixity to mandible.

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FNAC [ sensitivity : 85 – 99 % specificity : 96 – 100% ]

Open surgical biopsy is contraindicated.Trucut biopsy-inoperable tumor -lymphoma.

INVESTIGATIONS

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CT better for identifying bone destruction of mandible .

MRI is better to detect - bone marrow involvement.

- perineural spread. - parapharyngeal

space involv.

OTHERS : PET scan, color doppler sonography.

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PRIMARY TUMOR (T) : Tx primary tumor cannot be assessed

T0 no evidence of primary tumorT1 tumor <2cms without extraparenchymal extensionT2 tumor >2cms but not >4cms without extraparenchymal exten.T3 tumor >4cms and / or extraparenchymal extension.T4 tumor invades skin, mandible.

STAGING

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REGIONAL LYMPH NODES (N)Nx nodes cannot be assessed N0 no nodal metastasisN1 single ipsilateral LN <3cmsN2a single ipsilateral LN >3cms but <6cmsN2b multiple ipsilateral LN <6cmsN2c bilateral / contralateral LN < 6cms.N3 LN >6cms

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METASTASIS :Mx distant metastasis cannot be assessedM0 no distant metastasisM1 distant metastasis

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STAGE I T1,2 N0 M0

STAGE II T3 N0 M0

STAGE III T1,2 N1 M0

STAGE IV T4 N0 M0 T3,4 N1 M0 ANY T N2 M0 ANY T N3 M0 ANY T ANY N M1

STAGE GROUPING

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SURGERY

RADIOTHERAPY

CHEMOTHERAPY

TREATMENT

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Tumours, surgical excision with a cuff of normal tissue is the goal.

suprahyoid neck dissection, preserving the marginal mandibular branch of the facial nerve, lingual nerve and hypoglossal nerves.

In cases of overt malignancy, modified neck dissection or radical neck dissection is appropriate.

SURGERY FOR TUMORS

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suprahyoid neck dissection

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RADIATION THERAPY

R ECURRENT ESIDUAL

ERFACTORY

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ADENOMA T1 – T2 MALIG LOW GRADE

T3 – T4 TUM. HIGH GRADE CLOSE MARGIN DEEP LOBE PERINEURAL SPREAD INTRAVASCULAR INV N+

NO RT

GIVE RT

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RADIOTHERAPY

TELE THERAPY + / - BRACHYTHERAPY

DOSE 50-70 Gy

NERVE GRAFT IS NOT C/I FOR RT

RT TO IPSILATERAL NECK

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RADIATION THERAPY COMPLICATIONS :

Severe xerostomia Sensory neural hearing loss Osteo necrosis of mandible.

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CHEMOTHERAPYNO ROLE IN ADJV. SET.USED SPARINGLY IN METS

UNRESECTABLE

DRUGS ADR PLAT 5-FU

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FACTOR INFLUENCING SURVIVAL

Stage. Histology & grade. Site. Lymph node metastasis. Surgical margins Perineural spread. Dedifferentiation. (detrimental outcome)

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BIOLOGICAL MARKERSTUMOR SUPPRESSOR GENES & ONCOGENESPOOR PROGNOSTIC INDICATORS :

point mutation of TP 53 tumor suppressor gene

activation of c-myc & ras p 21 proto oncogene

low p 27 tumor suppressor gene expression

over expression of c-erb b2amplification of Her-2 / Neu

expressionDNA PLOIDY

aneuploidy poor prognostic indicator

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TUMOR MARKERS MEC – MUC 1, MUC 4, MUC 5AC, MUC 5BSAG (salivary agglutinin)MASPIN CEA – glandular & highly diff. squamous cell ca.LACTOFERRIN – glandular tumorsAMYLASE – ACCPREKERATIN & VIMENTIN – pleomorphic adenoma

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EFFECT OF STAGE ON SURVIVAL

94

50

18

81

40

10

73

33

00

102030405060708090

100

10 yr 15 yr 20 yr

SUR

VIVA

L %

STAGE I

STAGE II

STAGE III & IV

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