INNERVATIONS

OF TONGUE

DR.SAMEEN RJ
MDS 1ST YEAR
ORAL MEDICINE AND
RADIOLOGY
  INTRODUCTION

 DEVELOPMENT OF TONGUE

SYNOPSIS  PARTS AND SURFACE OF TONGUE

 MUSCLES OF TONGUE

 VASCULAR SUPPLY OF TONGUE

 LYMPHATIC DRAINAGE OF TONGUE

 INNERVATION OF TONGUE

 EXAMINATION OF TONGUE

 CLINICAL CONSIDERATION & DISEASES OF THE

TONGUE

 CONCLUSION

 REFERENCES
INTRODUCTION
 The tongue is fleshy, movable, muscular organ, attached in
most vertebrates to the floor of the mouth.
 It is the principal organ of taste, an aid in chewing and
swallowing.
 In humans, an important organ of speech.

Tongue is barely three inches long but it can kill a

person six feet tall
Development of Tongue
 Starts to develop near the end of fourth
week.
 A median triangular elevation appears in the floor of
the primordium pharynx near the end of 4th week, just
rostral to the foramen cecum

 Thisswelling or median tongue bud is the first

indication of tongue development

 Soon two oval distal tongue buds develop on each

side of the median tongue bud
 The three lingual buds result from the proliferation of
mesenchyme in ventromedial parts of the first pair of
pharyngeal arches

 The distal tongue buds rapidly increase in size, merge with

each other, and overgrow the median tongue bud

 The merged distal tongue buds form the anterior two-thirds

(oral part) of the tongue
  Fusion of the distal tongue buds is indicated
by a middle groove, the median sulcus of the
tongue and internally by the fibrous lingual
septum
 Median tongue bud forms no recognizable part of
the adult tongue

Formation of Posterior third of Tongue

 It is indicated by two elevations that develop caudal to the
foramen cecum

 Copula: Forms by fusion of the ventromedial part of the

second pair of pharyngeal arches

 The hypopharyngeal eminence: Develops caudal to the

copula from mesenchyme in the ventromedial parts of the
third and fourth pairs of arches
 As the tongue develops the copula is gradually overgrown by the
hypopharyngeal eminence and disappear

 As a result, the pharyngeal part of the tongue develops from the

rostral part of the hypopharyngeal eminence

 The line of fusion of the anterior and posterior parts of the tongue is
roughly indicated by a V-shaped groove called terminal sulcus
 Pharyngeal mesenchyme forms the connective tissue and vasculature of the
tongue

 Most of the tongue muscles are derived from myoblasts that migrate from the
occipital myotomes

 The hypoglossal nerve (CN Ⅻ) accompanies the myoblast during their

migration and innervates the tongue muscles as they develop

 The entire tongue is within the mouth at birth, its posterior third descends into
the oropharynx by 4 years of age
 Papillae and Taste Buds
 The most common lingual papillae, known as filiform
papillae because of their threadlike shape, develop
during early fetal period (10-11 weeks)

 They contain afferent nerve endings sensitive to touch

 Taste buds develop during 11-13 weeks

 Most taste buds form on the dorsal surface of the tongue

 Fetalresponses in the face can be induced by bitter
tasting substances at 26-28 weeks, indicating that the
reflex pathways between taste buds and facial muscles
are established by this age
 The development of tongue explains its nerve supply

 The sensory supply to the mucosa of almost the entire

anterior two-thirds of the tongue is from the lingual branch
of the mandibular division of the trigeminal nerve

 This nerve is the nerve of first pharyngeal arch and this

arch forms the median and distal tongue buds
 Facial nerve is the nerve of second pharyngeal arch

 Its chorda tympani branch supplies the taste buds in the

anterior two-thirds of the tongue except the vallate papillae

 The facial nerve does not supply any of the tongue mucosa,
except for taste buds in the oral part of the tongue
 The vallate papillae in the oral part of the tongue are
innervated by glossopharyngeal nerve (CN Ⅸ) of the third
pharyngeal arch

 This is due to the reason that mucosa of posterior two third

of the tongue is pulled slightly anteriorly as the tongue
develops

 The posterior third of the tongue is innervated mainly by the

glossopharyngeal nerve, which is a nerve of third
pharyngeal arch
 The superior laryngeal branch of the vagus nerve (CN Ⅹ)
of the fourth arch supplies small area of the tongue
anterior to the epiglottis

 All muscles of the tongue are supplied by the hypoglossal

nerve (CN Ⅻ), except for palatoglossus, which is supplied
from pharyngeal plexus by fibers arising from the vagus
nerve
PARTS AND SURFACE OF
TONGUE

APEX: The apex is the region of the tongue anterior to the frenulum.

BODY: The body extends from the circumvallate papillae to the

frenulum, the anterior part of the genioglossus muscle. The body is
the largest segment and it convenient to arbitrarily separate the body
into an anterior and posterior part. The anterior body is beneath the
hard palate, the posterior body lies beneath the soft palate.

BASE OR ROOT : The base, or root, is that part of the tongue

posterior to the sulcus terminalis, the line of circumvallate papillae
taste receptors.
 Muscles of tongue
Anatomically ,the tongue formed of two main regions:
Lingual mucosa.
Lingual muscles.
Lingual muscles divided into two main groups:
– Extrinsic muscle: The extrinsic muscles have one
attachment to a bone (mandible, hyoid bone or styloid
process) while the other end inserts within the tongue.
– Intrinsic muscles : Intrinsic muscle originate and insert
within the tongue and have no bony attachments.
Intrinsic muscles –
occupy upper part & are Attached to submucous
fibrous layer and to median fibrous septum
• Superior Longitudinal
• Inferior Longitudinal
• Transverse muscle
• Vertical muscle

Function: Alter the shape of the

tongue
INFERIOR LONGITUDINAL:

Muscle fibers on the underside of

the tongue

Fibers run between genioglossus

and hyoglossus fibers
Course anteriorly from the root

fUNCTION: shorten the tongue, turn tip

downward
Transverse:
Fibers course laterally
Contraction: narrow tongue, elongate
tongue
Vertical:
Course downward (and laterally)
throughout the body of the tongue
Contraction: flattens the tongue

Superior longitudinal:
Most superficial
Longitudinal, oblique fibers
Course anteriorly from the root
Contraction: shorten the tongue, turn tip
upward
Extrinsic Muscles – Five Pair
Connect to
• Genio-glossus (mandible)
• Hyo-glossus (Hyoid)
• Chondro-glossus
• Stylo-glossus (Styloid process)
• Palato-glossus (Palate)

FUNCTION:
Alter position of tongue
Genioglossus
• Fan shaped , form main bulk of tongue

Origin – Sup. Genial tubercles of mandible

Insertion
• Lowest fibers – to body of hyoid
• Intermediate– pass deep to hyoglossus and are
continuous with middle constrictor of pharynx
• Upper – turn forward and upward from root to apex

Action -Protrude tip of tongue and make dorsal

surface concave
Hyoglossus
• Quadrilateral muscle
Origin
• Upper surface of greater cornu and
partly from body of hyoid
• Passes upward & forward under cover
of mylohoid
Insertion
side of tongue b/w styloglossus laterally
and
inferior longitudinal muscle medially
Action
Depresses sides of tongue , make dorsal
surface
Convex
Chondroglossus
detached part of hyoglossus, seperated by genoiglossus
Originate from lesser cornu & attached to side of tongue

Styloglossus

Arise from tip of styloid process & stylomandibular

ligament
Passes downward and forward
Inserted to side of tongue
Oblique fibers interdigitate with hyoglossus
Longitudinal fibres continue with inf. Longitudinal
muscle
Action – retracts tongue backward & upward
Antagonist in action to genioglossus
• Palatoglossus
(glossopalatine):
• Connects soft
palate with the
posterior tongue
• Forms anterior
faucial pillars
• Contraction:
lower soft palate;
raise back of
tongue
INNERVATION OF TONGUE
• 5 primary tastes
– Salty
• Stimulated by chemical salts, especially NaCl
– Sour
• Caused by acids which contain a free hydrogen ion, H+
– Sweet
• Evoked by configuration of glucose
– Bitter
• Brought about by more chemically diverse group of taste
substances
• Examples – alkaloids, toxic plant derivatives, poisonous
substances
– Umami
• Meaty or savory taste/ pleasant taste
Mechanism of stimulation of taste sensation:
– Sweet
G protein activation of adenyl
cyclase c-AMP K conductance

– Bitter
G protein Activatn. of Phospholipase
C IC-insitol(PO4)3 Ca2
release
DENTISTRY AND TONGUE
RELATED DISORDERS
DAVID ET AL 2018
CLASSIFICATION
Developmental disturbances Traumatic lesions of tongue Infections of tongue
Aglossia Physical Bacterial
Microglossia Tongue piercing Tuberculosis
Macroglossia Linea alba Syphilis
Ankyloglossia Scalloped tongue Scarlet fever
Fissured tongue Traumatic ulcer Fungal
Bifid tongue Chemical Candidiasis
Median rhomboid glossitis Thermal Viral
Benign migratory glossitis
Hairy tongue
Lingual thyroid nodule

Immunological conditions of tongue Cysts of tongue Potentially malignant disorders of tongue

Recurrent aphthous stomatitis Dermoid/ Epidermoid Leukoplakia
Lichen planus Lymphoepithelial Erythroplakia
Pemphigus vulgaris Gastric mucosal cyst Lupus erythematous
Mucous cyst Syphilitic glossitis
Neoplastic Malignant
Benign Squamous cell carcinoma
Fibroma Verrucous carcinoma
Giant cell fibroma Kaposi’s sarcoma
Glomus tumor Angiosarcoma
Leiomyoma Mucoepidermoid carcinoma
Rhabdomyoma Malignant lymphoma
Plasmacytoma Malignant melanoma
Neurofibroma
Keratoacanthoma
Syndrome associated with tongue
Papilloma Aglosia–adactylia syndrome
Adenoma Beckwith–Wiedemann syndrome
Hemangioma Burning Mouth syndrome
Lymphangioma Down syndrome
Eagles syndrome
Melkersson–Rosenthal syndrome
Orofacial digital syndrome
Parry–Romberg syndrome
Riley–Day syndrome
Systemic conditions associated with glossitis
Iron deficiency anemia
Pernicious anemia
Niacin deficiency
Folic acid deficiency
Miscellaneous lesion
Lichenoid reaction
Pyogenic granuloma
Dyskeratosis
Taste disorders
Ageusia
Hypogeusia
Hypergeusia
Dysguesia
40
41
KAPOSIS SARCOMA
 Kaposi´s sarcoma (KS) is an angio-proliferative spindle
cell neoplasm of low grade malignancy, described by
Moritz Kaposi in 1872. It may be solitary or multifocal. It
originates almost from lymphatic endothelium and it was
considered rare until the discovery of the Acquired
Immunodeficiency Syndrome (AIDS).
Diagnostic for AIDS in HIV positive individual
Most common oral malignant neoplasm associated with AIDS
Associated with sexually transmitted virus (HHV-8)
Intraoral site is initial presentation in 20- 70% of reported
cases
Biopsy necessary to confirm diagnosis
Appear as macules, patches, nodules or
ulcerations, bluish, brownish, or reddish
Location:
Intra-orally - hard and soft palate and gingiva
Found anywhere - GI tract, skin or viscera

If diagnosed, communication with

physician, dermatologist, oncologist, and
dentist is essential
Currently four types are recognized: classic,
endemic, epidemic and iatrogenic.

Classic
(indolent) KS:

The classic (indolent) KS is seen in white older men of Southern Mediterranean or

Eastern European heritage (over 60 years old in 90% of the cases) and is not related to
HIV infection.
The disease initiates as violaceous or reddish brown maculae and papules on the feet
or hands, progressing to the legs (most common site) and arms. In 10% of the cases there
is involvement of viscera and mucosa.

It progresses over many years and is not often fatal.

Endemic (African) KS :

a. African Cutaneous KS
It develops in middle age adults (25 to 50 years old)
from tropical Africa, can involve bones, causes legs to
swell, and has only local aggressiveness.

b. African Lymphadenopathic KS
It develops mainly children from the “Bantu”
ethnicity less than 10 years old. It is characterized by
generalized lymphadenopathy and has an aggressive
clinical behavior, killing within two years after the
diagnosis.
 Epidemic (AIDS associated) KS:

AIDS was described in 1981, in patients where the KS was the main element of the syndrome, observed in
30 to 40% of them. This form of KS develops predominantly in homosexuals and bisexuals, being rare in
injectable drug users and heterosexuals. Due to the changes on the sexual behavior and the antiretroviral
drugs, its frequency went from 40% at the beginning of the 90ties to 15% nowadays. AIDS associated KS
starts as small, non-itchy, slightly painful, violaceous patches first around the head and neck, trunk, limbs and
oral mucosa, with subsequent progression to plaques and nodules. Visceral lesions are frequent and
gastrointestinal and pulmonary involvements are common. It advances very rapidly, but is not always fatal.
Histopathology shows ill-defined vascular The tumor is composed of proliferating spindle cells with
proliferation in the dermis (H&E, x100). interspersed vascular channels filled with red blood cells.
Note the inflammatory infiltrate, extravasated red blood
cells and the hyaline globules (H&E,x200).
How do diagnose KS?

1. Histopathologic examination of tissue biopsy is mandatory for diagnosis.

2. HHV-8 serostatus determined by detection of antibodies to viral lytic antigens

by indirect immunofluorescence, combined with the detection of specific
antibodies to the K8.1 HHV-8 protein by ELISA.

3. Serum testing for antibodies to HIV, using ELISA and Western Blot.

4. Chest radiography.

5. When clinically indicated, gastrointestinal endoscopy and abdominal

ultrasound or computerized tomography (CT).
There is no officially accepted system for staging
Kaposi sarcoma. However Mitsuyasu classification
system is the most simple and clinicaly acceptable
system which comprises 4 stages:
Stage I: Localized nodular Kaposi sarcoma in elderly
men
Stage II: Localized, invasive, and aggressive Kaposi
sarcoma (mostly seen in Africa)
Stage III: Disseminated mucocutaneous Kaposi
sarcoma in African children and patients who are
homosexual
Stage IV: Stage III with visceral involvement
 How to treat KS?

Even though it often progresses slowly, KS can

ultimately be fatal, so it should always be treated.
There are several ways of treating KS, including:
1.Surgical excision for small single or few localized tumors,
2.Cryotherapy,
3.Electrodessication,
4.Chemotherapy (doxorubicin lipid complex),
5.Interferon (an anti-viral agent), and
6.Radiation (in treating KS when the lesions are not spread
over a large part of the body).
 ORAL
CANDIDIASIS
Proposed revised classification of Oral Candidosis[Primary oral
candidosis (Group I)
•Acute
•Pseudomembranous
•Erythematous
•Chronic
•Erythematous
•Pseudomembranous
•Hyperplastic
•Nodular
•Plaque-like
•Candida-associated lesions
•Angular cheilitis
•Denture stomatitis
•Median rhomboid glossitis
•Keratinized primary lesions superinfected with Candida
•Leukoplakia
•Lichen planus
•Lupus erythematosus.
Secondary oral candidoses (Group II)
Oral manifestations of Systemic mucocutaneous.
Candidosis (due to diseases such as thymic aplasia and candidosis endocrinopathy
syndrome)
These lesions are caused by the yeast Candida albicans.
Candida albicans are one of the components of normal
oral microflora and around 30% to 50% people carry this
organism.
There are many types of Candida species,
which are seen in the oral cavity

Species of oral Candida are: C.

albicans, C. glabrata, C.
guillermondii, C. krusei, C.
parapsilosis, C.
pseudotropicalis, C. stellatoidea, C.
tropicalis.

Candida is a fungus and was first isolated in 1844 from the

sputum of a tuberculosis patient
• Drugs such as inhaled steroids have been shown to increase the risk of oral
candidiasis by possibly suppressing cellular immunity and phagocytosis. The
local mucosal immunity reverts to normal on discontinuation of the inhaled
steroids.

 smoking, diabetes, Cushing's syndrome, immunosuppressive conditions

such as HIV infection, malignancies such as leukemia and nutritional
deficiencies – vitamin B deficiencies have been particularly implicated

•  Drugs such as broad spectrum antibiotics alter the local oral

flora creating a suitable environment for candida to proliferate.

• Immunosuppressive drugs such as the antineoplastic agents

have been shown in several studies to predispose to oral
candidiasis by altering the oral flora, disrupting the mucosal
surface and altering the character of the saliva.
DIAGNOSTIC
ASPECTS
Serological tests for invasive candidiasis
•Detection of antibodies
•Slide agglutination
•Immunodiffusion
•Phytohemagglutination
•Coelectosynersis
•Immunoprecipitation
•A and B immunofluorescence
•Nonspecific Candida Antigens
•Latex agglutination
•Immunobloting
•Cell Wall Components
•Cell Wall Mannoprotein (CWMP)
•b-(1,3)-D-glucan
•Candida Enolase Antigen testing.
 THERAPEUT
ICS
Systemic antifungal medications of oropharyngeal candidiasis Topical antifungal medications
 SOMETHING
NEW?????

DISCUSSION
SESSION
 Lesion Differentiating features

Lichen Lichenoid reactions are associated with the

Planus administration of a drug, contact with a metal
and their resolution when the drug or other
factor was eliminated or when the disease was
treated.
Leukoedema •Characterized by a diffuse, grayish-white milky,
opalescent appearance of the mucosa .
•The surface frequently appears folded.
•Disappears on stretching
 Lesion Differentiating Features
Candidiasis In chemical burns there is acute onset,
pain and focal area of involvement which
is usually not a feature of candidiasis
Tobacco Pouch •Asymptomatic
Keratosis •It is typically a thin gray or gray- white
almost “translucent” plaque with a border
that blends gradually into the surrounding
mucosa
•History will confirm the diagnosis
 Lesion Differentiating Features

Plaque lesions of thrush can be wiped with the

form of help of gauze
Lichen
Planus
Chemical the superficial white material burns of oral
burns mucosa appears thin and delicate as
compared to pseudomembranous candidiasis.

Gangrenous Pseudomembrane
History will confirmis the
darker in color and not
diagnosis
Stomatitis raised above the surface.
 Frictional •Identifiable source of local irritation
Keratosis •Usually there is opaque white
appearance which is homogenous
•It may have sharply delineated
borders
Leukoplakia •• Tissue tag white
Extensive patches present
characterized by raised plaque
formation consisting of single or
group of plaques varying in size
with irregular edges.
 summary

Among the broad-spectrum of lesions that occur on the tongue a few tongue lesions present more
commonly.

The most important thing to remember is that most tongue lesions will resolve spontaneously or
with simple therapy within a week, if they do not, then the lesions will have to be biopsied to rule
out malignancies or serious disorders.

Diagnosing such common tongue lesions will help in the best interest of the patient which is
achieved by both general practitioner and dentists.
 REFERENCES

1. Lodi G, Franchini R, Warnakulasuriya S, Varoni EM, Sardella A, Kerr AR. Interventions

for treating oral leukoplakia to prevent oral cancer. Cochrane Database Syst
Rev. 2016;7:CD001829. [PubMed]
2. Warnakulasuriya S, Johnson NW, van der Waal I. Nomenclature and classification of
potentially malignant disorders of the oral mucosa. J Oral Pathol Med. 2007;36:575–80

3.Flint S, Glick M, Patton L, Tappuni A, Shirlaw P, Robinson P.

Consensus guidelines on quantifying HIV-related oral mucosal
disease. Oral Dis 2002;8 Suppl 2:115-9
4.Hassan Errihani, Narjisse Berrada, Soundouss Raissouni, Fadoi Rais, Hind Mrabti et al.
(2011) Classic Kaposi’s sarcoma in Morocco: Clinico - epidemiological study at the
National Institute Of Oncology. BMC Dermatology; 11:15
5.Investigations for diseases of the tongue: A review Chaya M. David1 , L. K.
Soujanya2 , B. K. Ramnarayan2 , Kanaparthi Alekhya2 , L K Suprith3 , Garima
Karayat2
•6.Malcolm A. Lynch, Vernon J. Brightman, Martin S. Greenberg: Burket’s Oral
Medicine- Diagnosis & Treatment, 8th edition

•7.Shafer, Hine, Levy: Shafer’s Textbook of Oral Pathology, 5th edition

•8.B.D CHAURASIA 3rd volume head and neck anatomy book