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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


  • 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.


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.


SIGNS:

  • enlarged firm submandibular gland, tender on bimanual examination.

  • Pus may be visible, draining from the sublingual papilla.


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.


Three cranial nerves are at risk during removal of the lingualsubmandibular 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 lingualsubmandibular 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 lingual

  • 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 ORIGIN

  • 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 ORIGIN

  • most common benign tumor of both major & minor salivary glands.

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


Microscopy
MICROSCOPY ORIGIN

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.



Malignant submandibular gland tumor
MALIGNANT SUBMANDIBULAR GLAND TUMOR – 6.8 % in 10 yrs) and malignant progression.


Mucoepidermoid carcinoma
MUCOEPIDERMOID – 6.8 % in 10 yrs) and malignant progression.CARCINOMA

  • 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 – 6.8 % in 10 yrs) and malignant progression.

  • 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 CELL – 6.8 % in 10 yrs) and malignant progression.CARCINOMA

  • 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 – 6.8 % in 10 yrs) and malignant progression.

  • 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


Con………………. – 6.8 % in 10 yrs) and malignant progression.

  • 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.


Clinical features of malignant – 6.8 % in 10 yrs) and malignant progression.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 – 6.8 % in 10 yrs) and malignant progression.

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

  • Open surgical biopsy is contraindicated.

  • Trucut biopsy-inoperable tumor

    -lymphoma.


  • CT – 6.8 % in 10 yrs) and malignant progression.better 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 – 6.8 % in 10 yrs) and malignant progression.

  • 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.


  • REGIONAL LYMPH NODES (N) – 6.8 % in 10 yrs) and malignant progression.

    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


  • METASTASIS : – 6.8 % in 10 yrs) and malignant progression.

    Mx distant metastasis cannot be assessed

    M0 no distant metastasis

    M1 distant metastasis


Stage grouping
STAGE GROUPING – 6.8 % in 10 yrs) and malignant progression.

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 – 6.8 % in 10 yrs) and malignant progression.

  • SURGERY

  • RADIOTHERAPY

  • CHEMOTHERAPY


Surgery for tumors
SURGERY FOR TUMORS – 6.8 % in 10 yrs) and malignant progression.

  • 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.


Suprahyoid neck dissection
suprahyoid – 6.8 % in 10 yrs) and malignant progression. neck dissection


Radiation therapy
RADIATION THERAPY – 6.8 % in 10 yrs) and malignant progression.

  • R

ECURRENT

ESIDUAL

ERFACTORY


NO RT – 6.8 % in 10 yrs) and malignant progression.

GIVE RT

ADENOMA

T1 – T2 MALIG

LOW GRADE

T3 – T4 TUM.

HIGH GRADE

CLOSE MARGIN

DEEP LOBE

PERINEURAL SPREAD

INTRAVASCULAR INV

N+


RADIOTHERAPY – 6.8 % in 10 yrs) and malignant progression.

TELE THERAPY + / - BRACHYTHERAPY

DOSE 50-70 Gy

NERVE GRAFT IS NOT C/I FOR RT

RT TO IPSILATERAL NECK


Radiation therapy1
RADIATION THERAPY – 6.8 % in 10 yrs) and malignant progression.

COMPLICATIONS :

Severe xerostomia

Sensory neural hearing loss

Osteo necrosis of mandible.


Chemotherapy
CHEMOTHERAPY – 6.8 % in 10 yrs) and malignant progression.

NO ROLE IN ADJV. SET.

USED SPARINGLY IN  METS

UNRESECTABLE

DRUGS  ADR

PLAT

5-FU


Factor influencing survival
FACTOR INFLUENCING SURVIVAL – 6.8 % in 10 yrs) and malignant progression.

Stage.

Histology & grade.

Site.

Lymph node metastasis.

Surgical margins

Perineural spread.

Dedifferentiation. (detrimental outcome)


Biological markers
BIOLOGICAL MARKERS – 6.8 % in 10 yrs) and malignant progression.

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 – 6.8 % in 10 yrs) and malignant progression.

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


Thank you

THANK YOU – 6.8 % in 10 yrs) and malignant progression.


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