ANATOMY OF SALIVARY GLANDS

The parotid gland

This is the largest of the salivary glands,

lying wedged between the mandible and sternocleidomastoid and overflowing both these bounding structures.

The parotid and its surrounds in a schematic horizontal section—the facial nerve is the most superficial of the structures traversing the gland.

Relations

Above—lie the external auditory meatus and temporomandibular joint.

Below—it overflows the posterior belly of digastric.

Anteriorly—it overflows the mandible with the overlying masseter.

Medially —lies the styloid process and its muscles separating the parotid from the internal jugular vein, internal carotid artery, last four cranial nerves and the lateral wall of the pharynx.

The gland itself is enclosed in a split in the investing fascia, lying both on and below which are the parotid lymph nodes.

Antero-inferiorly, this parotid fascia is thickened and is the only structure separating the parotid from the submandibular gland (the stylomandibular ligament).

Traversing the gland (from without in) are

1. the facial nerve;

2. the retromandibular (posterior facial) vein, formed by the junction of the superficial temporal and maxillary veins.

3. the external carotid artery, dividing at the neck of the mandible into its superficial temporal and maxillary terminal branches

The parotid duct (of Stensen)

The parotid duct (of Stensen) is 2in (5cm) long.

It arises from the anterior part of the gland,

runs over the masseters a finger’s breadth below the zygomatic arch to pierce the buccinator and

open opposite the second upper molar tooth.

The duct can easily be felt by a finger rolled over the masseter if this muscle is tensedby clenching the teeth.

THE RELATIONS OF THE FACIAL NERVE TO THE PAROTID

• The facial nerve is unique in traversing the substance of a gland, a fact of considerable importance .

• This coexistence is explained embryologically; the parotid gland develops in the crotch formed by the two major branches of the facial nerve.

• As the gland enlarges it overlaps these nerve trunks, the superficial and deep parts fuse and the nerve comes to lie buried within the gland.

• The facial nerve emerges from the stylomastoid foramen, winds laterally to the styloid process and can then be exposed in the inverted V between the bony part of the external auditory meatus and the mastoid process.

• This has a useful surface marking, the intertragic notch of the ear, which is situated directly over the facial nerve.

• Just beyond this point the nerve dives into the posterior aspect of the parotid gland and bifurcates  almost immediately into its two main divisions (occasionally it divides before entering the gland).

• The upper division divides into temporal and zygomatic branches;

• the lower division gives the buccal, mandibular and cervical branches.

• These two divisions may remain completely separate within the parotid, may form a plexus of intermingling connections,

• The branches of the nerve then emerge on the anterior aspect of the parotid to lie on the masseter, thence to pass to the muscles of the face.

• No branches emerge from the superficial aspect of the gland,

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Anatomy of the Bones of Cervical Spine

Anatomy of the Bones of Cervical Spine

Atlas

1^st Cervical Vertabrae

 

Lack of Body

 

Superior Articular Foveae

Inferior Articulating Foveae

      Fovea Dentis 

Axis

C2

Dens-Rotation between skull and atlas

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Inherited Oral Diseases

Inherited Oral Diseases

Disorders Affecting Periodontium/Gingiva

• Papillon-LeFèvre Syndrome

• Cyclic Neutropenia

Disorders affecting Jaw bones and Facies

• Cherubism

• Cleidocranial dysplasia

• Gardner syndrome

• Mandibulofacial dysostosis(Treacher-Collins syndrome)

• Nevoid basal cell carcinoma syndrome

• Osteogenesis Imperfecta

• Aperts Syndrome

• Crouzon Syndrome

Disorders affecting Oral Mucosa

• Hereditary Hemorrhagic Telangiectasia

• Multiple Endocrine Neoplasia Syndrome IIB

• Neurofibromatosis

• Peutz-Jeghers Syndrome

• White Sponge Nevus

Disorders of Teeth

• Amelogenesis Imperfecta

• Dentinogenesis Imperfecta

• Dentin Dysplasia

• Hypohidrotic ectodermal dysplasia

• Hypophophatasia

• Vitamin D deficient rickets

Papillon-LeFèvre Syndrome

• Autosomal Recessive

• Cathepsin C gene mutation which affects the immune response to infection

• Hyperkeratosis of the palms and feet

• Sometimes elbows and knees

• Dramatic periodontitis (periodontoclasia) of both dentitions

– Floating teeth

– DD: Langerhans’ cell disease

Teeth erupt in normal sequence, position and time

1.5 to 2 years, a severe gingivo-periodontal inflammatory process develops

Edema, bleeding, alveolar bone resorption, and mobility of teeth with consequent exfoliation

Teeth are lost in the sequence they are erupted. After loss of last teeth, gingiva regains a normal appearance

Permanent teeth are lost before 14 years

Peripheral blood neutrophil is depressed in all patients with Papillon-Lefèvre suggesting that neutrophils are important factor in pathogenesis of severe periodontal disease

Treatment

Retinoid therapy:  Improves the skin condition but not the periodontal therapy

Periodontal condition:  No effective treatment

Cherubism

• Autosomal dominant

• Facial appearance similar to “cherub”-like

• 2 – 5 yrs of age

• The clinical alterations typically progress until puberty, stabilize and slowly regress

• Bilateral involvement of the posterior mandible – most common appearance – “cherub”-like (all 4 quadrants)

• “Eyes upturned to heaven” appearance – due to involvement of the infraorbital rim and orbital floor

• Painless bilateral expansion of the post. mand.

• Marked widening and distortion of alveolar ridges

• Tooth displacement and eruption failure

Radiographic features

• Multilocular radiolucency with massive expansion

• Both erupted and unerupted teeth are randomly distributed

• After stabilization, lesions exhibit a “ground glass” appearance

Histopathology

• Similar to giant cell granuloma

• But clinical and radiographic correlation necessary

• Vascular fibrous tissue and giant cells (smaller and more focal)

• Eosinophilic cuffing around blood vessels

Treatment

• Prognosis is unpredictable

• Delayed till after puberty (curettage) 

Cleidocranial Dysplasia

Caused by a defect in Cbfa1/Runx2 gene

Autosomal dominant and sporadic pattern

Bone defects involve the clavicle and skull

Clavicles are absent (unilateral or bilateral) – 10% of cases

Short stature with large heads; ocular hypertelorism; broadbase of nose and depressed nasal bridgebase of nose and depressed nasal bridge

Large heads and parietal bossing

Skull sutures show delayed closure and may remain open

Dental manifestations include narrow, high-arched palate with increased prevalence of cleft palate

Presence of numerous unerupted permanent and supernumery teeth with many distorted crown and root shapes supernumery teeth with many distorted crown and root shapes

Prolonged retention of deciduous teeth and delay or complete failure of eruption of permanent teeth

Histology:

Unerupted permanent teeth lack secondary cementum Unerupted permanent teeth lack secondary cementum

Treatment:

No treatment; full-mouth extractions with denture construction;

removal of primary and supernumery teeth followed by removal by exposure and orthodontic treatment of permanent teeth

Crouzon Syndrome (Craniofacial Dysostosis)

Craniosynostosis: Premature closure of sutures

Mutation in FGFR2; 1 in 65,000 births; AD

Wide variation in clinical presentation: Brachycephaly; scaphocephaly; trigonocephaly; “cloverleaf” skull (kleeblattschädel)

Ocular proptosis: blindness and hearing deficit

Headaches; normal intelligence

Underdeveloped maxilla: Midface hypoplasia; crowding of maxillary teeth; bifid uvula

“Beaten metal” skull in radiographs

Surgical treatment

Aperts Syndrome (Acrocephalosyndactyly)

Craniosynostosis syndrome

Mutation in FGFR2; 1 in 65,000 to 160,000 births, AD

Acrobrachycephaly (tower skull); kleeblattschädel (severe cases)

Ocular proptosis; hypertelorism; vision loss; “beaten metal”radiographs

Midface hypoplasia; ‘V”-shaped arch “open-mouth” feature; hearing loss

SYNDACTYLY of the 2nd, 3rd and 4th digits; MENTAL RETARDATION

Pseudo cleft palate due to swellings (accumulation of glycos-aminoglycans) of the lateral hard palate and crowding of maxillary teeth; bifid uvula

Surgery

Treacher-Collins Syndrome (Mandibulofacial Dysostosis)

Defects of 1st and 2nd BA

AD; 1 in 25,000 to 50,000 births; 60% new mutations

Mutations in the TCOF1 gene

Characteristic face: Hypoplastic zygoma causing narrow face with depressed cheeks and downward slanting palpebral fissures

Coloboma (notch) at the outer portion of lower eyelid

Ears anomalies: Deformed pinnae, extra ear tags, middle ear ossicle defects cause hearing loss

Underdeveloped mandible; condyle and coronoid hypoplasia

Lateral facial clefting and cleft palate

No treatment required in most cases; Cosmetic surgery in severe cases

Neurofibromatosis (von Recklinghausen disease of the skin)

• A.D.; 50% of cases are new mutations; 1:3,000 births

• Many forms

• NF1 most common; chr. 17

• Malignant transformation

• Diagnostic criteria (2 or more needed)

          – Six or more café au lait macules over 5mm in prepubertal and 15mm in postpubertal

          – Two NFs or one plexiform NF

          – Axillary freckles (Crowe’s sign)

          – Optic glioma

         – Lisch nodules (brown pigmented spots of the iris)

         – Distinct osseous lesions (thinning of long bone cortex)

         –1st degree relative with 2 or more of these findings

• Oral lesions

         –NFs anywhere

         – Enlargement of fungiform papillae

         – Enlargement of mandibular foramen

         – Enlargement of the mandibular canal

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Radiographic Anatomy of Facial Bones

Radiographic Anatomy of Facial Bones

Postero-Anterior Caldwell View

Occipito Mental (OM) (Waters) View

Postero-Anterior 30° (Modified Parietocanthial)

Occipito Mental 30° (OM30) View

Submentovertex (SMV) / Slit Basal / Jughandles View

Adult Facial Bones - Lateral View

Slit Townes View

Abnormalities of the Skull and Facial Bones
Cause	Radiological Features
Enlargement of Skull Vault
Children
Hydrocephalus	Sutural  diastasis, increased convoluted markings, “copper beaten skull”
Raised intra cranial pressure	Bulging of fontanelle in infancy.
Adults
Acromegaly	Enlarged frontal sinuses and mandible, erosion and enlargement of sella turcica
Paget’s disease	Thickened skull vault, increased density of vault and facial bones.
Increased Density
Localised
Hyperostosis frontalis	Symmetrical thickening of the inner table of skull vault, usually in women, of no significance.
Meningioma	Area of  localised sclerosis, possible enlarged groove of feeding artery.
Fibrous displasia	Asymmetrical, affecting the facial bones maxilla and base of skull.
Generalised
Paget’s disease	Irregular sclerosis with thickened vault.
Secondary deposits. e.g. prostate & breast	Irregular sclerosis, thickened vault.
Lytic lesions
Childhood
Secondary deposits, neuroblastoma, leukaemi	Variable appearances,  Sutural deposits may mimic sutural diastasis.
Eosinic granuloma, Histiocytosis X	Transradient defect with bevelled edges.
Adults
Myelomatosis	Rounded translucent (2-10mm) multiple ‘holes’
Secondary deposits	Generally ill defined translucent patches.
Hyperparathyroidism	Mottled appearance of ‘pepper pot’ skull.
Paget’s	Sharply defined zones affecting large areas of the vault.

Radiographic Anatomy of Mandible

Mandible - Postero-Anterior View

Mandible - Oblique View

Mandible – Lateral View

Orthopantogram (OPG)

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