Diseases of Tongue l Oral medicine MCQs for dental students

Diseases of Tongue : Macroglossia ( Abnormal Large tongue), Lingual thyroid nodule, Fissured tongue, Black hairy tongue and Geographic tongue ( Benign Migratory Glossitis) l Oral medicine MCQ (multiple choice question) for dental student

 

DEVELOPMENTAL DEFECTS OF THE TONGUE

Macroglossia ( Abnormal Large tongue):

• Congenital Macroglossia: in Down's syndrome, Hemangioma & Lymphangioma.
• Acquired Macroglossia: in Edentulism, Amyloidosis, Acromegaly & myesthenia gravis.
• Macroglossia leads to Noisy breathing, Drooling & difficulty in eating.  
• Clinically: Tongue has crenated lateral borders, patient will have open bite & mandibular prognathism.

 

Lingual thyroid nodule:

• thyroid remnant in the region of the thyroid gland origin.
• smooth, sessile mass on mid-posterior dorsum of the tongue in the region of foramen caecum.
• Causes Dysphagia, Dysphonia, Dyspnoea & hypothyroidism.
• Diagnosed by iodine isotopes or Tecnetium -99m with CT or MRI.
• No treatment, periodic follow up

 

Fissured tongue:

• geographic tongue may cause fissured tongue .
• no Treatment required just brush the tongue .

 

Black hairy tongue:

• caused by accumulation of keratin on the filliform papillae on the dorsum  of the tongue + over growth of pigment-producing bacteria or fungi.
• Associated with Antibiotic therapy, poor oral hygeine, use of oxidizing mouth washes, overgrowth of bacteria or fungi.
• Patients may complain of gagging sensation or a bad taste in the mouth.

 

Geographic tongue ( Benign Migratory Glossitis):

• Multiple large, red, atrophic patches on the tongue with white, slightly raised borders on the dorsum of the tongue.
• resolve in days to weeks & papillae regenerate.
• The red areas are devoid of filiform papillae, whereas white areas show hypertrophy of papillae.
• Recurrent issue and the lesion appears to migrate from area to area.
• can be confused with more serious form of glossitis & even premalignant or malignant lesions.

 

vesicullo bullous diseases

Macules:

• small flat area of altered colour or texture

Patch:

• large flat area of altered colour or texture

Papule:

• solid and raised lesion smaller than 1 cm

Plaque:

• solid and raised lesion larger than 1 cm (large papules)

Fissure:

• linear cut in the epithelium

Erosion:

• moist red lesion due to loss of the superficial epithelium

Ulcer:

• circumscribed depressed lesion over which the epithelium is lost

Nodule:

• lesion deep in submucosa, over-which the epithelium can be easily moved

1.                         Exophytic: growing upwards
2.                         Endophytic: growing downwards

 

Vesicle:

• elevated blister containing clear fluid that is under 1 cm in diameter

Bullous:

• elevated blister containing clear fluid that is greater than 1 cm in diameter

Pustule:

• elevated lesion containing purulent material

 

N.B

• difference between macule and patch : size
• difference between vesicle and bullous :  size
• difference between pustule and bullous :  content
• difference between erosion and ulcer : depth
• questions to ask any VB patient :

1. When did you notice the vesicles and how long do they last for and what happens when they rupture
2. Did you see those lesions anywhere else in your body ? [ skin , eyes genitalia] 
3. Drug history + family history 

 : N.B

• to rule out if the vesicles are due to viral infection or not → ask if there are any prodromal symptoms
• to rule out if the vesicles are immune mediated or not → ask if there is involvement of other tissues
• to rule out if the vesicles are hereditary or not → ask about family history + onset [ usually early in childhood]

VIRAL VB DISEASES

Herpes simplex virus

• Known for causing an infection and then staying dormant in the nerve gangilion close by and then get reactivated again later on in life.

 

HSV1 :

• primary infection causes flu like symptoms and sis self limiting in the majority of pts secondary infection has localized prodromal symptoms
• Route = physical contact
• Virus remains dormant in trigeminal gangilion
• Reactivation by : trauma, UV light, cold, stress, immune-suppression, travelling

 

Primary herpetic gingivostomatitis:

1. Caused by HSV 1
2. Children and infants
3. Clinical history :

• child had fever 2 days ago and then stopped eating , distressed and irritable child with pain and fatigue

      4. Clinical picture :

• multiple ulcerations on the attached gingiva + sometimes dorsum of the tongue [ nothing on the buccal mucosa or the soft palate ]
• You will see multiple stages together [ vesicles + ulcers ]
• The main site for primary herpetic gingivostomatitis = the gingiva

Q: why do you see ulcerations in PHG even though it is a VB disease?

• The ulcers are formed when the vesicle rupture

Q: what is the most common misdiagnosis for PHG among pediatricians?

• Candida [ most doctors prescribe anti fungal agents thinking it is candida because they see whitish areas in the mouth ]

Q: why do you see whitish areas in the mouth in cases of PHG?

• The patient cannot swallow because of the painful ulcers → desquamated epithelial cells accumulate in the mouth instead of being swallowed into the GIT → whitish areas

Q: why do you see multiple stages of Primary herpetic gingivostomatitis together ?

• because the virus moves in waves infecting the epithelium at different timings, you will see vesicles and also ulcers after the vesicles rupture
• Most patients show up in the Ulcerative phase because it is painful and lasts for a few days

Treatment of Primary herpetic gingivostomatitis:

• self limiting in 7- 10 days [ just symptomatic Treatment]
• An important clinical feature of ulcers that result from ruptured vesicles due to viral infection is = Coalescence of small ulcers forming large irregular ulcer
• Secondary HSV 1 infection causes herpes labialis [ on the vermilion zone of the lips] - pt will tell you “I feel ants on my lips”

Treatment for HSV infections :

• Primary infection [ PHG ] → symptomatic care
• Severe systematic infections → acyclovir [ activated by thymidine kinase produced by the virus → will inhibit DNA polymerase in infected cells only not healthy cells ] 
• Acyclovir should be used as early as possible to be effective
• CUATION : corticosteroids can only be prescribed after the damage to the cells has already occurred if they are prescribed in the wrong time they will further lower the body’s immunity allowing the virus to spread more

 

Varicella zoster virus:

• Primary infection: varicella or chickenpox
• Secondary (recurrent) infection: zoster or shingles
• Route = airborne

 

Varicella [Chicken pox] :

• Caused by VZV
• Viral symptoms [ fever , malaise etc ]
• Rash → vesicles → pustules → ulcers [ all stages are seen together]
• Highly pruritic [ causes itching]
• Treatment: no treatment – self limitng in few weeks [ only symptomatic care]

 

Zoster [ shingles ] :

• the secondary infection of VZV [ if the latency occurs in CN 7 and CN 8 → RAMSAY HUNT SYNDROME → facial palsy and damage to the ear
• Treatment: acyclovir – for ramsay hunt syndrome [ corticosteroids +/- antiviral agents]

 

Coxsackie virus

Hand Foot and Mouth disease :

• Caused by Coxsackie virus (A16 mainly) – occurs on the hands , feet and mouth
• Route = by airborne and orofecal routes
• Maculopapular rash [ on skin ] + vesicles and ulcers [ in the mouth ] – mostly kids
• Treatment: bland mouthwash + symptomatic care [ self limiting within few days ]

 

Herpangia:

• Caused by Coxsackie virus
• Route = saliva and possibly oro-fecal routes
• Endemic and seasonal (summer and early autumn)
• Ulcers and vesicles at the posterior region of the mouth
• Treatment: symptomatic

 

Measles :

• Caused by Measles virus (Paramyxovirus family)
• Route = Airborne
• Seasonal (winter and spring)
• IP = 7-10 days, after 1-2 days --> Koplik’s spots, then after 1-2 days --> maculopapular rash starting head to trunk to extremities
• Treatment: symptomatic
• Koplik’s spots = white spots on red background [ occur on the buccal mucosa ]