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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 ).

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submandibular salivary gland

SUBMANDIBULAR SALIVARY GLAND

PROF PALANI MS FICS

slide3

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

  • larger superficial and a smaller deep lobe.
  • Drained by a single submandibularduct (Wharton’s duct).
  • It drains into the anterior floor of the mouth at the sublingual papilla.
important anatomical relationships of the submandibular glands
Important anatomical relationships of thesubmandibular glands

3 NERVES—Marginal mandibular branch of facial nerve

__hypoglossal nerve

__lingual nerve

2 MUSCLES__mylohyoid

__hyoglossus

1 ARTERY __facial artery.

ectopic aberrant salivary gland tissue
Ectopic/aberrant salivary gland tissue
  • most common ectopic salivary tissue is the Stafne bone cyst.
  • asymptomatic, clearly demarcated radiolucencyof 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 submandibulargland.
  • No treatment required.
inflammatory disorders
INFLAMMATORY DISORDERS

Acute, Chronic or Acute on Chronic.

Acute submandibularsialadenitis:

- Viral : The paramyxovirus (mumps).

- bacterial : secondary to obstruction.

obstruction and trauma
OBSTRUCTION AND TRAUMA
  • 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 submandibularstones are radio-opaque and can be identified on plain radiography.
slide18

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.
slide19

SIGNS:

  • enlarged firm submandibular gland, tender on bimanual examination.
  • Pus may be visible, draining from the sublingual papilla.
slide21

TREATMENT:

  • DISTAL TO LINGUAL NERVE:

-- INTRAORAL APPROACH.

  • PROXIMAL TO LINGUAL NERVE:

-- gland excision, stone removal and duct ligation.

excision
EXCISION
  • Incision and exposure of gland
  • Gland mobilisation.
  • Dissection of the deep lobe and identification of the lingual nerve.
  • Wound closure.
incision and exposure of gland
Incision and exposure of gland
  • Incision 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.
gland mobilisation
Gland mobilisation

intracapsulardissection

- inflammatory conditions

extracapsulardissection

-tumours.

dissection of the deep lobe and identification of the lingual nerve
Dissection of the deep lobe and identification of the lingualnerve
  • 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.
slide29

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.

complications of submandibular gland excision
Complications of submandibular gland excision

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 submentalskin anaesthesia.

submandibular gland tumors
SUBMANDIBULAR GLAND TUMORS
  • 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 submandibularlymphadenopathy.
  • Most salivary neoplasms, even malignant tumours, are often slow-growing, painless swellings.
etiology
ETIOLOGY
  • ENVIRONMENTAL : Radiation (ionising & UV radiation).

EBV.

Silica dust.

Early menarche & nulliparity.

Smoking (Warthin’s tumor).

Diet rich in PUFA (protective)

  • GENETIC.
pleomorphic adenoma
PLEOMORPHIC ADENOMA
  • most common benign tumor of both major & minor salivary glands.
  • Peak incidence 4th & 5th decade with slight female preponderance.
microscopy
MICROSCOPY

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

  • Areas of oncocyticmetaplasiaare 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.
slide42

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.

mucoepidermoid carcinoma
MUCOEPIDERMOIDCARCINOMA
  • 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.
adenoid cystic carcinoma
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%)

acinic cell carcinoma
ACINIC CELLCARCINOMA
  • 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
malignant mixed tumor
MALIGNANT MIXED TUMOR
  • Represents malignancy with both epithelial & mesenchymal elements.
  • 3 – 12 % of salivary gland tumors.
  • Carcinoma ex pleomorphic adenoma - arising from pre exsistingpleomorphic adenoma. Malignant & metastatic components are epithelial in origin.
  • De novo malignant mixed tumor (CARCINOSARCOMA) :

with malignant features of both epithelial and mesenchymal components

slide48

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.

slide49

Clinical features of malignant submandibulartumours

1. Rapid enlargement of the swelling.

2. Indurationand/or ulceration of the overlying skin.

3. Cervical node enlargement.

4. Ipsilateral weakness / numbness of tongue.

5. Fixity to mandible.

investigations
INVESTIGATIONS
  • FNAC [ sensitivity : 85 – 99 % specificity : 96 – 100% ]
  • Open surgical biopsy is contraindicated.
  • Trucut biopsy-inoperable tumor

-lymphoma.

slide51

CTbetter for identifying bone destruction of mandible .

  • MRI is better to detect - bone marrow involvement.

- perineural spread. - parapharyngeal space involv.

  • OTHERS : PET scan, color dopplersonography.
staging
STAGING
  • PRIMARY TUMOR (T) :

Tx primary tumor cannot be assessed

T0 no evidence of primary tumor

T1 tumor <2cms without extraparenchymal extension

T2 tumor >2cms but not >4cms without extraparenchymalexten.

T3 tumor >4cms and / or extraparenchymal extension.

T4 tumor invades skin, mandible.

slide54

REGIONAL LYMPH NODES (N)

Nx nodes cannot be assessed

N0 no nodal metastasis

N1 single ipsilateral LN <3cms

N2a single ipsilateral LN >3cms but <6cms

N2b multiple ipsilateral LN <6cms

N2c bilateral / contralateralLN < 6cms.

N3 LN >6cms

slide55

METASTASIS :

Mx distant metastasis cannot be assessed

M0 no distant metastasis

M1 distant metastasis

stage grouping
STAGE GROUPING

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

treatment
TREATMENT
  • SURGERY
  • RADIOTHERAPY
  • CHEMOTHERAPY
surgery for tumors
SURGERY FOR TUMORS
  • 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.
radiation therapy
RADIATION THERAPY
  • R

ECURRENT

ESIDUAL

ERFACTORY

slide65

NO RT

GIVE RT

ADENOMA

T1 – T2 MALIG

LOW GRADE

T3 – T4 TUM.

HIGH GRADE

CLOSE MARGIN

DEEP LOBE

PERINEURAL SPREAD

INTRAVASCULAR INV

N+

slide66

RADIOTHERAPY

TELE THERAPY + / - BRACHYTHERAPY

DOSE 50-70 Gy

NERVE GRAFT IS NOT C/I FOR RT

RT TO IPSILATERAL NECK

radiation therapy1
RADIATION THERAPY

COMPLICATIONS :

Severe xerostomia

Sensory neural hearing loss

Osteo necrosis of mandible.

chemotherapy
CHEMOTHERAPY

NO ROLE IN ADJV. SET.

USED SPARINGLY IN  METS

UNRESECTABLE

DRUGS  ADR

PLAT

5-FU

factor influencing survival
FACTOR INFLUENCING SURVIVAL

Stage.

Histology & grade.

Site.

Lymph node metastasis.

Surgical margins

Perineural spread.

Dedifferentiation. (detrimental outcome)

biological markers
BIOLOGICAL MARKERS

TUMOR SUPPRESSOR GENES & ONCOGENES

POOR 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 b2

amplification of Her-2 / Neu expression

DNA PLOIDY

aneuploidy poor prognostic indicator

tumor markers
TUMOR MARKERS

MEC – MUC 1, MUC 4, MUC 5AC, MUC 5B

SAG (salivary agglutinin)

MASPIN

CEA – glandular & highly diff. squamous cell ca.

LACTOFERRIN – glandular tumors

AMYLASE – ACC

PREKERATIN & VIMENTIN – pleomorphic

adenoma