CHAPTER III

LITERATURE REVIEW

Anatomy of tongue

The tongue

The tongue consists of a buccal and a pharyngeal portion separated by a V-

shaped groove on its dorsal surface, the sulcus terminalis. At the apex of this groove is a

shallow depression, the foramen caecum, marking thethe sulcus lie a row of large vallate

papilliae. The under aspect of the tongue bears the median frenulum linguae; the mucosa

is thin on this surface and the lingual veins can thus be seen on either side of the frenulum.

The lingual nerve and the lingual artery are medial to the vein but not visible. More laterally

can be seen a fringed fold of mucous membrane termed the plica fimbriata. On either side

of the base of the frenulum can be seen the orifice of the submandibular duct on its papilla.

Inspect this in a mirror and note the discharge of saliva when you press on your

submandibular gland just below the angle of the jaw. (Ellis, 2006)

Structure

1

The thick stratified squamous mucosa of the dorsum of the tongue bears papillae

over the anterior two-thirds back as far as the sulcus terminalis. These papillae (particularly

the vallate) bear the taste buds. The posterior one-third has no papillae but carries

numerous lymphoid nodules which, with the palatine tonsils and adenoids, make up the

lymphoid ring of Waldeyer. (Ellis, 2006)

Small glands are scattered throughout the submucosa of the dorsum; these are

predominantly serous anteriorly and mucous posteriorly.The tongue is divided by a median

vertical fibrous septum, as indicated on the dorsum by a shallow groove. On each side of

this septum are the intrinsic and extrinsic muscles of the tongue.The intrinsic muscles are

disposed in vertical, longitudinal and transverse bundles; they alter the shape of the

tongue. The extrinsic muscles move the tongue as a whole. They pass to the tongue from

the symphysis of the mandible, the hyoid, styloid process and the soft palate, respectively

the genioglossus, hyoglossus, styloglossus andpalatoglossus. The functions of the

individual extrinsic muscles can be deduced from their relative positions. Genioglossus

protrudes the tongue, styloglossus retracts it and hyoglossus depresses it. Palatoglossus

is, in fact, a palatal muscle and helps to narrow the oropharynx in swallowing. (Ellis, 2006)

The mucous membrane on the anterior part of the tongue is rough because of the

presence of numerous small lingual papillae (Moore & Dalley, 2006):

1. Vallate papillae: large and flat topped, they lie directly anterior to the terminal

sulcus and are arranged in a V-shaped row. They are surrounded by deep moat-

like trenches, the walls of which are studded with taste buds. The ducts of the

serous glands of the tongue open into the trenches.

2. Foliate papillae: small lateral folds of the lingual mucosa. They are poorly

developed in humans.

2

3. Filliform papillae: long and numerous, they contain afferent nerve endings that are

sensitive to touch. These scaly, conical projections are pinkish gray and are

arranged in V-shaped rows that are parallel to the terminal sulcus, except at the

apex, where they tend to be arranged transversely.

4. Fungiform papillae: mushroom shaped pink or red spots, they are scattered among

filliform papillae but are most numerous at the apex and margins of the tongue.

Blood supply

Blood is supplied from the lingual branch of the external carotid artery. (Ellis, 2006)

Lymph drainage

The drainage zones of the mucosa of the tongue can be grouped into three: (Ellis, 2006)

1 The tip drains to the submental nodes;

2 The anterior two-thirds drains to the submental and submandibular nodes and

thence to the lower nodes of the deep cervical chain along the carotid sheath;

3 The posterior one-third drains to the upper nodes of the deep cervical chain.

3

Nerve supply

The anterior two-thirds of the tongue receives its sensory supply from the lingual

branch of V which also transmits the gustatory fibres of the chorda tympani (VII). Common

sensation and taste to the posterior one-third, including the vallate papillae, are derived

from IX. Afew fibres of the superior laryngeal nerve (X) carry sensory fibres from the

posterior part of the tongue.All the muscles of the tongue except palatoglossus are

supplied by XII; palatoglossus, a muscle of the soft palate, is innervated by the pharyngeal

branch of X (Ellis, 2006)

Fissured tongue

Definition

Fissured tongue (FT), also termed lingua fissurata, lingua plicata, scrotal tongue

and grooved tongue is recognized clinically by an groove oriented anteroposteriorly, often

with multiple branch fissures extending laterally. The frequency of FT increases with age

and has been associated with psoriasis, acromegaly, and Sjo¨gren’s, Down’s and

Melkerson–Rosenthal syndromes (Zargari, 2005). The fissured tongue (FT) is a condition,

either inherited or acquired, that manifests variable degrees of grooves or fissures on the

tongue dorsum (Silverman et al, 2002). A tongue with fissures on the dorsum (Scully et al,

2010).

Prevalence

About 5% of population. Age mainly affected: More noticeable with increasing age.

Gender mainly affected: M = F (Scully et al, 2010). It is unclear whether FT occurs more

frequently in male or female patients. It has been reported in patients ranging in age from

15 to 84 years (Wood & Goaz, 1997).

4

Etiology

The etiology is uncertain, because the time when the fissures first appeared

cannot be documented with certainty. Whereas there has been some testimonial

association with nutritional and vitamin deficiencies, this has not been frequent or well-

confirmed (Silverman et al, 2002). For years median rhomboid glossitis (MRG) (central

papillary atrophy of the tongue) has been considered a developmental and congenital

defect causing a segment of the tuberculum impar to persist on the dorsal surface of the

tongue, instead of being buried in normal embryonic development. However, the paucity of

cases in children and some cases of remission has diminished support for this theory. It is

thought that a chronic candidal infection plays a leading etiologic role and smoking may

also act as a promoter. Conflicting reports concern a possible role by diabetes (Wood &

Goaz, 1997).

The etiology is unknown but hereditary plays a significant role. The condition may

be congenital, present at birth, or may become apparent during childhood or later in life.

Ajra examined clinical and genetic characteristics of histologically defined fissured tongue

in a familial study and reported that fissured tongue with smooth-surfaced papillae was

transmitted as a dominant characteristic with incomplete penetrance and was preceded by

geographic tongue. The severity of fissured tongue changed with increasing age. Tongue

fissuring with normal appearing filiform papillae was not familial and was not associated

with geographic tongue. Fissuring with normal-appearing structure should be considered

as variation of normal anatomy, whereas fissured tongue and geographical tongue are

clinical and etiological disease entity. Aging and local environmental factors may also

contribute to its development. Fissured tongue may present as an independent

manifestation or associated with certain underlying syndromes or familial

conditions. Conditions associated with fissured tongue include Melkersson-Rosenthal

5

syndrome, Down syndrome, acromegaly, Sjorgen’s syndrome, oro-facial granulomatosis,

psoriasis and geographic tongue (Rathee et al, 2010).

Clinical findings

Usually asymptomatic. However, it is often complicated by geographic tongue, or

the tongue becomes sore for no apparent reason. Multiple fissures on the dorsum of the

tongue. There is such a wide range of fissuring appearances that there is no standard

classification or adequate description (Scully et al, 2010). Occasionally, when a patient

notices a FT for the first time or feels that the fissures are increasing, there is concern over

the significance. In some patients, there are complaints of discomfort, or coincidental

tongue symptoms; these are eventually shown to be unrelated to the fissuring (Silverman

et al, 2002).

The lesion is located on the dorsal surface of the tongue in the midline and anterior

to the circumvallate papillae. The surface is dusky red, completely devoid of filiform

papillae, and usually smooth; however, nodular or fissured surfaces have been noted.

Rarely, there may be some keratosis. The size and shape of the lesion are somewhat

variable, at times causing confusion as to the diagnosis. The lesions are generally

asymptomatic, but pain and ulceration have been reported (Wood & Goaz, 1997).

6

Fissured tongue is characterized by anteroposterior and multiple laterally fissures on the dorsal aspect of the tongue

Histology

Microscopic examination of fissured tongue reveals hyperplasia of the rete ridges

and loss of the keratin " hairs" on the surface of the filiform papillae. The papillae vary in

size and often arc separated by deepgrooves. Polymorphonuclear leukocytes can be seen

migrating into the epithelium. often forming microabscesses in the upper epithelial layers. A

mixed inflammatory cell in filtrate is present in the lamin a propria. (Neville et al, 2002)

Diagnosis

The diagnosis is made by clinical findings and history. If there are indications of a

systemic disease or condition based on signs and symptoms, then the appropriate referral

or laboratory tests should be carried out. By simply stretching the tongue with mild

pressure, the epithelial-lined fissures become obvious (Silverman et al, 2002).

Treatment

7

The prime treatment involves counseling the patient regarding the benign nature,

the common occurrence, and the lack of association with infections or other conditions or

diseases. Management is empirical, including optimal hygiene and mouthrinses. Rarely,

when a fissure is deep and associated with debris and exudate, débridement and closure

of the defect is in order (Silverman et al, 2002). No treatment is indicated or available.

(Scully et al, 2010)

Prognosis

Excellent. (Scully et al, 2010)

Differential Diagnosis : Geographic tongue

Definition

Geographic tongue (benign migratory glossitis) is an entity of unknown cause and

presents clinincally with loss of the filiform papillae on the dorsal and lateral surfaces of the

tongue sometimes accompanied by an advancing white border with or without erythema

(Rathee et al, 2010). GT, also known as benign migratory glossitis or glossitis areata

migrans, is an inflammatory disorder of unknown aetiology caused by the local loss of

filiform papillae. The condition usually presents as asymptomatic erythematous patches

with serpiginous borders. The patches are irregular and sharply demarcated, resembling a

map. These lesions characteristically have a migratory nature, and their colour and shape

change over time. GT is usually an isolated abnormality but has been associated with

psoriasis, atopic diathesis, diabetes mellitus, reactive bronchitis, anaemia, stress,

hormonal disturbances, Reiter’s and Down’s syndromes, and lithium therapy

(Zargari,2005).

8

Prevalence

Geographical tongue occurs in about 1% of general population, and 50% in

association with fissured tongue (Rathee et al, 2010). The reported prevalence is

approximately 1 per cent of the population and there is often a family history. The disorder

occurs over a wide age range and presents both in children and adults. (Soames &

Southam, 2005)

Etiology

The cause has not been clearly identified. It is considered to be an allergic or

hypersensitivity reaction to certain factors to which the tongue is exposed. This could be a

germ that usually lives in the mouth or a foodstuff. This reaction causes excessive

shedding of cells on the surface of the tongue (Scully et al, 2010).

Clinical findings

Irregular, partially depapillated, red areas on the anterior two-thirds of the dorsal

tongue surface and is associated with loss of the filiform papillae, the fungiform papillae

remaining as shiny, dark-red eminences. The margins of the lesions are often outlined by a

thin, white line or band and the disorder is frequently associated with fissured (scrotal)

tongue . The affected areas may begin as small lesions only a few millimetres in diameter

which, after gradually enlarging, heal and then reappear in another location. The condition

may regress for a period and then recur. It is usually symptomless but there may be some

irritation associated with acid and spicy foods. (Soames & Southam, 2005)

9

Geographical tongue. Note the atrophic red patches are sharply demarcated, resembling a map

Histology

Histological examination shows the epithelium at the edges of the lesions to be

acanthotic with a dense, neutrophil leucocyte infiltration throughout the epithelium and the

lamina propria. In the centres of the lesions, the loose desquamating cells on the surface

have been lost and there is underlying chronic inflammatory cell infiltration (Soames &

Southam, 2005)

Histologically, there is thinning of the epithelium in the centre of the lesion with

mild hyperplasia and hyperkeratosis at the periphery. There are chronic inflammatory cells

in the underlying connective tissue. The irregular areas of dekeratinized and desquamated

filliform papillae which is red in colour are surrounded by elevated whitish or yellow

margins due to acantholysis and hyperkeratosis. (Cawson & Odell, 2002)..

Pathophysiology

10

Red patches develop and then over a few days coalesce to form rather large areas

of raw-looking patches (Murtagh, 2010). In this condition, localized areas of filliform

papillae are rapidly lost and replaced by uneven areas of smooth dorsal surface lingual

mucosa that is often erythematous because of hyperemia (Sonis et al., 1995). The cause

of lost papillae is still unknown.

The fungiform papillae are exaggerated (Sonis et al., 1995). The papillae on the

tongue surface rapidly regrow and the affected area returns to normal. The process moves

around to other parts of the tongue with a major change occurring every three weeks. The

process may then subside and go into remission that may be complete or partial. However,

it may return at a later time (Murtagh, 2010).

Diagnosis

The diagnosis is based upon clinical appearance and history. When there is

clinical confusion because of a rather bizarre manifestation, or deep concern on the part of

the patient, a biopsy can be performed. (Scully et al, 2010).

Treatment

Most important, patients must be reassured that although this is a chronic or cyclic

condition, GT does not represent a neoplastic, infectious, or contagious disease. Biopsy is

elective. If a patient has generalized complaints or findings, then a physical examination

should be suggested to rule out a coincidental systemic problem. When a patient is

asymptomatic, no further treatment is necessary. Since some patients may be

uncomfortable or experience considerable pain, identifiable irritants (mainly food types)

should be avoided. Symptoms are treated empirically. Trials can include placebos

(vitamins), mouthrinses, antianxiety medications, and anti-inflammatory drugs. The latter

11

can include nonsteroidal anti-inflammatory drugs (NSAIDs) and topical or systemic

corticosteroids. Analgesic agents are sometimes needed. There is no specific treatment,

drug or process that makes it disappear. However, palliation in the form of sprays,

ointments or rinses may be helpful in symptomatic cases (Sonis et al, 1995 ; Scully et al,

2010).

Prognosis

There are no complications. Spontaneous resolution of the lesion in one area is not

uncommon, but usually another lesion appears in another location. (Scully et al, 2010)

Ulcer

Definition and Terminology

Ulcerative lesions are a group of common oral mucosal disorders. The most

common causes of these lesions are mechanical and reactive factors, infectious diseases,

and neoplasms, as well as autoimmune and hematological disorders. The main clinical

feature in all these conditions is an ulcer, which is defined as loss of all epithelial layers. In

addition, the term “erosion” is used to defined a superficial loss of epithelium. However, at

the clinical level, the terms “ulcer” and “erosion” are usually used interchangeably. In this

chapter, only primary ulcerative lesions are discussed, and not lesions that arise

secondarily fromrupture d bullae.(Laskaris, 2006)

Ulceration is a breach in the oral epithelium, which typically exposes nerve

endings in the underlying lamina propria, resulting in pain or soreness, especially when

eating spicy foods or citrus fruits. Patients vary enormously in the degree to which they

suffer and complain of soreness in relation to oral ulceration. It is always important to

exclude serious disorders such as oral cancer or other serious disease, but not all patients

12

who complain of soreness have discernible organic disease. Conversely, some with

serious disease have no pain. Even in those with detectable lesions, the level of complaint

can vary enormously. Some patients with large ulcers complain little; others with minimal

ulceration complain bitterly of discomfort. Sometimes there is a psychogenic influence.

(Scully, 2005)

Erosion which is the term used for superficial breaches of the epithelium. These

often have a red appearance initially as there is little damage to the underlying

lamina propria, but they typically become covered by a fibrinous exudate which

has a yellowish appearance (Scully, 2005).

Ulcer which is the term usually used where there is damage both to epithelium

and lamina propria. An inflammatory halo, if present, also highlights the ulcer with

a red halo around the yellow or grey ulcer (Scully, 2005).

Etiology

(Scully, 2005)

Trauma

Recurrent aphthous stomatitis (RAS)

Microbial infections

Mucocutaneous diseases

Systemic disorders

Drug therapy

Squamous cell carcinoma

Clinical features

13

Acute reactive ulcers of oral mucous membranes exhibit the clinical signs and

symptoms of acute inflammation, including variable degrees of pain, redness, and swelling

The ulcers are covered by a yellow-white fibrinous exudate and are surrounded by an

erythematous halo. Chronic reactive ulcers may cause little or no pain. They are covered

by a yellow membrane and are surrounded by elevated margins that may show

hyperkeratosis. Induration, often associated with these lesions, is due to star formation and

chronic inflammatory cell infiltration (Regezi, 2003).

Oral ulcer at right buccal

Histology

Acute ulcers show a loss of surface epithelium that is replaced by a fibrin network

containing predominantly neutrophils. The ulcer base contains dilated capillaries and, with

time, granulation tissue. Regeneration of the epithelium begins at the ulcer margins, with

proliferating cells moving over the granulation tissue base and under the fibrin clot. Chronic

ulcers have a granulation tissue base, with scar found deeper in the tissue. A mixed

inflammatory cell infiltrate is seen throughout. Epithelial regeneration occasionally may not

occur because of continued trauma or because of unfavorable local tissue factors. It has

been speculated (hat these factors are related to inappropriate adhesion molecule

expression (integrins) and/or inadequate extracellular matrix receptors for the keratinocyte

integrins. In traumatic granulomas, tissue injury and inflammation extend into subjacent

skeletal muscle. The term granuloma as used here reflects the large numbers of

14

macrophages that dominate the infiltrate, but this is not a typical granuloma as seen in an

infectious process, such as tuberculosis. (Regezi et al,2003)

Histological examination shows an ulcer covered by a thick layer of fibrinous

exudate with a dense, chronic inflammatory cell infiltrate in its base involving underlying

damaged muscle. The deeper parts of the lesion are characterized by an infiltrate rich in

histiocytes and eosinophils (Soames, 2005).

Treatment

Management involves the elimination of the suspected cause and use of an

antiseptic mouthwash (for example, 0.2 per cent chlorhexidine) or a simple covering agent

such as Orabase). Ulcers of local cause usually heal spontaneously within 7–14 days if the

cause is removed. Maintenance of good oral hygiene and the use of hot saline mouthbaths

and 0.2% aqueous chlorhexidine gluconate mouthwash aid healing. Occasionally,

particularly in self-induced trauma, mechanical protection with a plastic guard may help.

Patients should be reviewed within three weeks to ensure healing has occurred. Any

patient with a single ulcer lasting more than 2–3 weeks should be regarded with suspicion

and investigated further; biopsy may be indicated. Most reactive ulcers of oral mucous

membranes arc simply observed. If pain is considerable, topical treatment may be of

benefit. This could be in the form of a topical corticosteroid (Regezi,2003; Scully, 2010 )

15

CHAPTER IV

DISCUSSION

The patient complained that his tongue has crack and groove on surface of his

tongue. Patient said that he never had any discomfort or pain but he finds it difficult to

clean and sometime there are white coatings on the tongue. Patient also complaints of

ulceration on right cheek. The ulcers form around 3 days ago. The patient did not recall

any bitting or traumatizing at the ulcer location and not taking any medication for the ulcers.

Extraoral examination and anemnesis showed no underlying systemic disease of

the patient that may manifest in the oral cavity. After intraoral examination, it is found that

there are fissuring on the dorsum and lateral side of the tongue. According to the patient,

the lesion never caused him any pain or discomfort but sometimes making cleaning the

tongue hard. This is consistent with statement from Silverman et al (2001), Scully et al

(2010), Wood & Goaz (1997) and Neville et al (2002) which state that fissure tongue are

usually asymptomatic. The patient also revealed ulcerations on the buccal right. The ulcer

16

healed 5 days after the first visit. According to Regezi and Scully,ulceration in oral mucosa

usually heal spontaneously within 7-14 days.

The patient was explained about his condition and the nature of fissure tongue.

According to Scully, fissured tongue progress with age. The patient was informed about

this progression of fissured tongue and was advised to not concern himself as long as the

patient does not feel any discomfort or pain and practices good oral hygiene. The patient

was reassure that good oral hygiene is a sufficient way to manage his treatment. The

patient is instructed to maintain a good oral hygiene. In addition to daily brushing, the

patient was instructed to scrape the tongue to ensure torough cleaning of the oral cavity.

This is to make sure that food debris and microorgannism will not accumulate and reside

between the groves and fissure. The treatment prescribed is antiseptic Chlorhexidine

gluconate 0.2% mouthrinse as it has antimicrobial properties to fight against germs and

bacteria. Antiseptic is a solution used to disinfect skin or other living tissue (Burton &

Engelkirk, 1996). Antimicrobial agent is defined as an agent that can kill or inhibit microbial

growth (Prescott, Harley & Klein, 2002). Chlorhexidine is used twice daily with 30 to 60

seconds gargling until the ulcer subsides.. This is also to make sure that there are no

secondary infection at the ulcers. Chlorhexidine gluconate is only advised to be used for 7-

14 days. It is known that prolonged usage or chlorhexidine can cause staining of tongue

and change of oral microflora (Yagiela, Dowd & Neidle, 2007).

Then, the lesion is examined again after 1 week. The ulcer on the buccal right

already healed. The patient has no complaints and has been using tongue scraper to helps

with the cleansing of the tongue surface. There is no specific management and treatment

for fissured tongue. The patient need optimal hygiene and mouthrinses in order to prevent

any progress or occurance of infection (Silverman et al, 2002; Scully et al, 2010).

17

CHAPTER V

CONCLUSSION

Based on the anamnesis and clinical examination, all the patient’s symptoms and the

clinical features of the lesion fulfill the criteria of diagnosing fissure tongue. According to

literature, no specific treatment was stated, the patient was instructed to maintaine good

oral hygine and encourage to scrape his tongue for a better removal of food debris. After a

week the patient is called back for control and the patient didn’t have any complaints.

18

REFERENCES

Better Health Channel, 2010. Tongue. P. 1-4. Available online at www.betterhealth.vic.gov.au.

Burton R and Engelkirk R;1996 Microbiology for the Health Sciences. 5 th ed. Lippincott. p. 125-126

Cawson, R.A. & Odell, E.W., 2006. Essential Pathology and Oral Medicine. 7th edition. Churchill Livingstone.

Ellis H. 2006.Clinical anatomy: applied anatomy for students and junior doctors .Wiley-Blackwell.

John Hopkins, 2008. Symptoms and Remedies: The Complete Home Medical References. Remedy Health Media, LLC.Available online at http://www.johnshopkinshealthalerts.com

Laskaris G, 2006, Pocket Atlas of Oral Diseases. Thieme

Moore & Dalley, 2006. Clinically Oriented Anatomy. 5th edition. Lippincott Williams & Wilkins

Neville B.W. Douglas D. Damm. Terry A Day .2002. Oral and maxillofacial pathology. Saunders/Elsevier

Prescott LM, Harley JP & Klein DA, 2002. Microbiology 5 th Ed. Boston Mc Graw-Hill Higher Education. p. 806-812

Rathee M, A. Hooda & A. Kumar. 2010.Fissured Tongue: A Case Report and Review of Literature. The Internet Journal of Nutrition and Wellness. 10(1)

Regezi, Sciubba, Jordan.2003.Oral Pathology: Clinical Pathologic Correlations 4th ed. Saunders

Scully C. Oslei Paes de Almeida, Jose Bagan, Pedro Diz Dios, Adalberto Mosqueda Taylor. 2010. Oral Medicine and Pathology at a Glance .John Wiley and Sons.

Scully C. Felix DH. 2005.Oral medicine — Update for the dental practitioner Aphthous and other common ulcers, British Dental Journal ; 199:259–264

19

Silverman S, Lewis R.E, Edmond L.T, 2002,Essentials of oral medicine. PMPH-USA

Soames JV, Southam JC .2005.Oral Pathology - 4th Ed.

Sonis, Fazio & Fang 1995, Principles and Practices of Oral Medicine, 2nd ed. W.B. Saunders Company.

Wood NK, Goaz PW. 1997.Differential diagnosis of oral lesions. 5th ed. St. Louis: Mosby,

Yagiela JA,Frank J. Dowd,Bart Johnson,Angelo Mariotti,and Enid A. Neidle,2007. Pharmacology and Therapeutics for Dentistry, 4th Edition

Zargari O.2006. The prevalence and significance of fissured tongue and geographical tongue in psoriatic patients.Clinical and Experimental Dermatology, 31, 192–195