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Res ORAL PATHOLOGY IN DENTISTRY

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Res This is a lecture on oral pathology in dentistry.
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Oral Pathology/ Medicine

Contents:
1. Terminologies

2. Viral Infections
3. Recurrent apthous ULCERATION

4. Fungal Infection: Oral Candiasis and Denture Stomatitis

5. Vesicullo-Bullous Lesions

6. White Lesions

7. Salivary Gland Disorders

8. Salivary Gland Tumors and Cyst

9. Bacterial Infections

10. Granulomatous Disorders

11. Abnormalities of Tounge

12. Facial Pain

13. Cysts of Jaw

14. Granulomatous Diseases

15. Bullous Disorders

Terminologies:
Vesicles- is a small blister a few millimetre in diameter

Bulla- is a larger blister

Ulcer- is a breach in the mucous membrane

Erosions- are shallower than ULCERS

Papule- is a circumscribed solid elevation of the skin with no visible FLUID , varying in size
from pinhead to 1cm

Macule- is change in surface colour without elevation or DEPRESSION  and therefore non
palpable, well or ill-defined

Cyst- is a epithelial lined cavity fluid with fluid, semi fluid or solid material
Viral Infections: 

 Human herpes virus

 Herpes simplex type I (HHV-1)

 Herpes simplex type II (HHV-2)

 Varicella-zoster virus (VZV/HHV-3)

 Epstein-Barr virus (EBV/HHV-4)

 Cytomegalovirus (CMV/HHV-5)

 Human herpesvirus type 6 (HBLV/HHV-6)

  Human herpesvirus type 7 (HHV-7)

 Kaposi's sarcoma herpesvirus (KSHV/HHV-8)

� DNA virus transmitted through saliva and causes short lived 1� clinical, subclinical
and remain latent afterward

� Seen in Children

� Recurrence of disease in patient with suppressed immune system

1.Herpes Simplex 1 (HSV)

� Causes acute gingivostomatitis in anterior posteror of mouth

� Lymph node enlargement can be seen bilaterally

� Resolves in 10 days without scar

� Remain latent in trigeminal ganglia

     

Manifestations of primary HSV infection

 Systemic infection: eg, fever, sore throat, and lymphadenopathy. It often passes
 unnoticed. If immunocompromised, it may be life-threatening with fever,
lymphadenopathy, pneumonitis, and hepatitis.

 Gingivostomatitis: ulcers filled with yellow slough appear in the mouth.

 Herpetic whitlow: a breach in the skin allows the virus to enter the finger, causing a
vesicle to form. It frequently afflicts children's nurses.

 Traumatic herpes (herpes gladiatorum): vesicles develop at any site where HSV is
ground into the skin by brute force.

 Eczema herpeticum: HSV infection of eczematous skin; usually seen in children.

 Herpes simplex meningitis: this is uncommon and usually self-limiting; typically, HSV-2
in women during a primary attack - see meningitis.

 Genital herpes: usually HSV-2. See the separate article on Herpes Simplex Genital.
  HSV keratitis: manifests with corneal dendritic ulcers. Avoid steroids.

 Herpes simplex encephalitis: usually HSV-1. It spreads centripetally - eg, from cranial
nerve ganglia, to frontal and temporal lobes. Suspect in fever, fits, headaches, odd
behaviour, dysphasia, hemiparesis, or coma or subacute brainstem encephalitis,
meningitis, or myelitis.

Treatment 

Symptomatic relief (nutritious diet, plenty of fluids, bed rest, use of analgesics and anti-
microbial mouthwashes). chlorhexidine MW, 0.2% or hydrogen peroxide 6%.

Acicylovir tablets, 200mg for 5 days or Aciclovir cream, 5% (2g) 

 Apply to lesion every 4 hours (five times daily) for 5 days or Penciclovir cram, 1%. 
2.Varicella Zoster HHV� 3

 Varicella zoster is a neurogenic DNA virus, which causes chicken pox as a 1� infection, and
is a contagious disease caused by air-bourne route.

 Seen below 10 years of age (chicken pox) commonly, shingles is seen in elderly

Clinical Features

 Itchy, vesicular, cutaneous, centripetal rash (from extremity to centre) which sometimes

affect the oral mucosa, diagnosis is by pre eruption pain followed by development of
vesicles.

 Sometimes mouth ulcer can be seen

Rash on trunk or face and passes macular papular, vesicular and pustular stages before
scarring.

Vericella zoster remains latent, with in dorsal root ganglia and do not cause any problem
but if reactivation occurs can lead to shingles.

Shingles occur unilateral.

Can cause Ramsay Hunt�s Syndrome (facial paralysis; vesicular eruptions in oral cavity). 

Zoster of maxillary and mandibular division of trigeminal nerves cause facial rash and
sometimes toothache.

Ophthalmic zoster ulcerate cornea, and needs to be treated urgently.

Treatment 

Seven day regimen of: Aciclovir Tablet, 800mg 1 tab five times daily. 

3. HHV-4 Glandular Fever

 EPSTEIN-BARR VIRUS is main causative agent

Causes infectious mononucleosis

Seen mostly in children and young adults.

Clinical Features

Fever, generalised lymphadenopathy and often maculo-papular rash.

Sore throat with soft palate petchiae and whitish exudate on tonsils, pharyngeal oedema

petechial haemorrhages at the junction of hard and soft palate (pathogen microbe). 

Serological changes
 Monospot test

Paul- Bunnell test 

Ig M antibodies are seen first.

CMV associated ulcers are non specific but cells with typical owl-eye intranuclear inclusions
can be seen in the inflammatory in the ulcer floor.
* Ampicillin should not be given to patients with a sore throat who may have glandular
fever, may cause a rash to anaphylaxis.

* Hairy Leukoplakia can be caused by the proliferation of HSV-4. Normally associated with
HIV-infection. 

4.Cytomegalo Virus HHV � 5

Cytomegalo virus is a ubiquitous found in saliva and urine of infected person

Primary infection is asymptomatic but can cause glandular fever like illness
CMV remains latent in oropharyngeal and epithelial cells and can be reactivated by
immunosuppression. 

Disseminated infection can lead to CMV retinitis in particular leading to blindness.

5.Human Herpes Virus 6 (Red Baby syndrome/ exanthema subitum)

It�s a T-cell lymphotropic herpes virus contracted with in first 2 years of life through
oropharyngeal secretions.

C/F:
Febrile illness

Macular or papular rash on face

Diarrhoea

Cough

Lesions seen mostly on soft palate/ uvula

6.Human Herpes Virus 7

  HHV-7 infects almost all children by the age of three years and persists lifelong, with
the shedding of infectious virus in saliva.

 It is similar to human herpesvirus 6 (HHV-6) in its genetic content and many of its
biological properties, including the ability to cause at least some cases of rosela
infantum

7.Human Herpes Virus 8

It�s B-lymphotropic DNA-virus, transmitted through sexual contact

Associated with KAPOSIS SARCOMA

    Kaposis Sarcoma

Flat-brown lesions initially and raised plaque and then seen as purple-red lesion,
seen on plalate, retromolar area and gingivae
 Purple swelling of hard palate that does not blanch on pressure. 

II Coxsackie Virus (RNA Virus)

A)Herpangina (coxsackie virus A)

Incubation period of 2-9 days

C/F:
Pharyngeal ulcers like herpetic ulcers but affecting posterior mouth (soft palate and
uvula) 

Vesicular formation

Patient have difficulty swallowing

seen only in children

D/D - teething, herpetic stomatitis

B)Hand, Foot and Mouth Disease

Caused by COXSACKIE Virus  usually A16, rarely type 5 and 10.

Highly infectious 

seen only in children

Clinical Features

 papular vesicular rash on extremities and oral mucosa, break down to leave painful ulcers,
particularly on the palate

III  Paramyxovirus
RNA virus
MEASLES
Acute infection of measles transmitted by droplet infection

Incubation period: 10-14 days

C/F:
First manifestation is Koplik�s Spot (whitish) in colour seen in buccal mucosa

Fever

          Rhinitis, Conjunctivitis

Maculopapular rash

Complication

Pneumonia 

Encephalitis
Rubella

Also known as German Measles

C/F:

In children, it causes macular rash starting from face and behind ears

Mild fever

Sore throat and enlarged lymph nodes. 

  

Recurrent Oral ulceration 

Ulceration is defined as a break in the continuity of an epithelial lining.

Recurrent Apthous Stomatitis 

Common oral condition affecting 20% of the population

Aetiology Factors
Genetic 

Nutritional deficiencies 

Systemic diseases

Endocrine

Stress

Trauma 

Allergy 

Infection

Smoking cessation

C/F: 
MINOR APTHOUS

Minor Major Herpetifor

Sex Ratio M=F M=F M�

M=F

Age of Onset 10 - 19 10 � 19 20 � 29

No. Of Ulcers
<10 <5 10 � 100

Size of Ulcers

<10 mm > 10 mm 1-2 mm larger if

ulcers coalese
Duration
> 30 days

Recurrence 4 � 14 days > 30 days < Monthly

Sites Affected Labial and

 1 � 4 months < Monthly buccal mucosa,
soft palate,
Labial and Labial, buccal floor of mouth
buccal mucosa, mucosa,
tongue tongue, palate
Scarring and pharynx Possible if
ulcers colease
Common
Uncommon

MAJOR APTHOUS

Treatment 
Antimicrobial mouthwash

 Chlorhexidine mouthwash, 0.2%

Hydrogen Peroxide mouthwash, 6%

Local Analgesics

 Benzydamine mouthwash, 0.15% . Rinse or gargle using 15 ml every 1� hour as required

 
Lignocaine ointment 5% or spray 10%

Hydrocortisone oromucosal tablets 2.5mg

Traumatic Ulceration

Often seen in buccal or lingual sulcus, lateral tongue

Mostly tender, yellowish- floor, red-margins and no induration

 Should eliminate in 7 � 10 days.

Aetiology

         Mechanical 

Chemical
 Thermal

Factitious injury

Radiation

Oral Candidiasis

Candida Albicans and Candida Dubliniensis are the Candidial species causing Oral
Candidosis. 

Acute Candidosis Chronic Candidosis

- Pseudomembranou  Chronic atrophic

s Candidosis (Thrush) candidosis/ Denture
stomatitis
- Erythematous
candidosis ( formerly  Angular chelitis
called denture sore
mouth)  Chronic
hyperplastic
candidosis(candidal
leukoplakia)
  Median rhomboid
glossitis

Predisposing Factors 
Immunodeficiency

Anaemia 

         antibacterial drugs being taken over a long time

Xerostomia 

Smoking

High carbohydrate diet

Nutritional deficiency (Iron, folate, and vitamin B12)

         steroid inhaler

Thrush/ Acute Pseudomembranous Candidiasis

 Creamy light adherent plaque or erythematous oral mucosa (usually cheek, palate or
oropharynx)

Can be easily wiped off

Commonly seen in HIV patients. 

Denture-Induced Stomatitis 

Prompted by ill fitting dentures, poor denture hygiene, wearing of dentures at night

Enclosed mucosa is cut from protective action of saliva

Mucosal erythema restricted to area cover by denture

Acute Antibiotic Stomatitis

Overuse of antibiotics especially tetracycline suppressing normal oral mucosa

Whole mucosa is red and sore

Erythematous Candidiosis 

 red, shiny, atrophic appearance

Angular Chelitis 

In denture wearing patients, it is caused by infection with candida species.

Iron deficiency is a significant etiology in angular chelitis.

Without denture, it is more likely to be cause by infection with streptococcus species

or staphylococcus species.

unless the classic golden crust associated with S.aureus are present , treatment should be
commenced with azole's.
MEDIAN RHOMBOID GLOSSITIS
-  seen in patients using inhaled steroids and smokers
-lesions are in centre of dorsum of tongue and palate (kissing lesion)
- lozenge shaped erythematous patch on the midline dorsal tongue
-H/P epithelial hyperplasia with neutrophils in the parakeratin layer.

CHRONIC HYPERPLASTIC CANDIDOSIS

-  white patch on the oral commissural buccal mucosa bilaterally or dorsum of tongue
- increased risk of malignant change
H/P candida hyphae can be seen in the superficial layers of the epidermis.
-blunt rete pegs
-neutrophils form microabscesses in the parakeratin
-if dysplasia fount then the lesion may be clinically classified as candida leukoplakia

TREATMENT

Miconazole, 2% 20g tube for Candida gram positive bacteria � apply to angle of mouth
twice daily. Advice patient to continue use for 10 days after lesions have healed OR Sodium
fusidate ointment, 2% 15 g tube � apply to angles of mouth four times daily (if bacterial)

For unresponsive cases: Miconazole 2% and Hydrocortisone 1% cream. 

Treatment 

Local measures to be used in the first instance

Advice patients to who use corticosteroid inhaler to rinse their mouth with water or
brush teeth immediately after using the inhaler

Fluconazole capsule, 50 mg 1 capsule for 7 days.

DO NOT PRESCRIBE azoles for patients taking Warfarin or Statins

OR 

Miconazole oro-mucosa gel, 24mg/ ml 80g tube.

Apply pea-size amount after food four times daily. Advice patient to continue use for
48hours after lesion have healed

         If azole's are contraindicated, Nystatin oral suspension, 1,00 ,000 unit/ml
  1 ml after food four times daily for 7 days. 

VESICULO-BULLOUS LESIONS

A)Angina Bullosa Haemorrhagica 

C/F:
Appearance of recurrent blood blisters in oral mucosa

Most commonly seen in posterior hard and soft palate

Blisters ruptures to leave a superficial ulcer, which is entirely self-limiting.

Investigations

Check clotting screen and full blood count to ensure normal haemostatic
components

Treatment 

Analgesics, mouthwash such as benzydamine hydrochloride 

B) Pemphigus 

Rare autoimmune skin disease with several different variants:

Pemphigus vulgaris

Pemphigus vegetans

Pemphigus foliaceous

Pemphigus erythematosus 
It�s a group of disorders in which autoantibodies directed against component of
desmosomes that enable kertinocytes to adhere one to another. 

P. vulgaris is most common variant. 

Age: 40-60 years old, commonly in females

Lesion often first in mouth but spread to skin widely 

Nikolsky�s sign may be positive (gentle stroking the mucosa can cause a vesicle or
bulla to appear). 

Autoantibodies most commonly Ig G, react with a component of desmosomes called

desmogleins in particularly desmoglein 3 and 1.

Diagnosis is made by direct immunofluorescence on fresh biopsy or cytological material.

Histopathology
Intra-epithelial clefting above basal cell layer

Cells have tombstone appearance (desmosomes)

 Acantholysis is seen (loss of intercellular adherence of suprabasal spinous cells.)

C)Pemphigoid:

Benign Mucous Membrane Pemphigiod/ CICATRICIAL PEMPHIGOID

autoimmune disorder

 characterised by blisters ad erythematous lesions affecting the oral mucosa, conjunctiva

and vulvovaginal region

May also be present as desquamative gingivitis 

may lead to blindness if conjunctiva is involved

Autoantibodies commonly Ig G.

diagnosis is based on direct immunofluorescence testing on a fresh biopsy of perilesional

mucosa.
Histopathology

Separation of connective tissue epithelial from connective tissue at basement

membrane 

Hemidesmosomes are seen intact

Heals with scarring

Bullous Pemphigoid 

Skin lesions on limbs and trunk begin as non-specific urticarial rash. 

TREATMENT:
- Oral steroids. If oral steroids are unresponsive there is evidence for efficacy of DAPSONE
and drugs from SULPHONAMIDE group, like sulfapyridine and sulfamethoxypyridazine.

Immunopathological Features of Vesicullobullous Disorders

Disease Direct Indirect

 Immunoflouroscence Immunoflouroscence
Pemphigus Intercellular IgG C3 Titre correlates with
disease severity 
Mucous Membrane Linear IgG and C3 at Essentially negative
Pemphigiod basement membrane
zone
Bullous Pemphigiod Linear IgG and C3 at Positive in 75% of cases
basement membrane
zone
Linear IgA Disease Linear IgA and c3 at Negative
basement membrane
zone
Dermatitis Granular deposits of IgA Negative
Herpetiformis and C3 at tips of dermal
papillae

rythema Multiforme 
C/F:
Occasionally triggered by herpetic infection or drugs

Mild fever and systemic upset may be associated

Lips frequently grossly swollen, split, crusted and bleeding

Widespread irregular fibrin covered erosions and erythema in the mouth

Cutaneous lesions consist of widespread erythema or characteristic target lesion

Target lesion are red macules a centimetre or more in diameter with a bluish cyanotic
centre.
Self-limiting
 

Investigations and Diagnosis

Diagnosis usually based on clinical picture but can be confirmed with biopsy.

Treatment:

Eliminate precipitating factors

 Prevent dehydration

Systemic steroid (+/- azathioprine) 

White Lesions

White Lesions are white due to  

Hyperplasia of epithelium

Loss of normal vascularity

Hyperkeratosis

Different diagnosis (TINNED VIM)

    1) Trauma 

frictional keratosis
 chemical burns

skin grafts

scars

2) Infective

Candidosis (acute, chronic, mucocutaneous, chronic hyperplastic leukoplakia)

hairy Leukoplakia

Condyloma Acuminata

Papilloma and other HPV lesions

pailloma and other HPV lesions

syphilitic Leukoplakia
 Kopliks spots (measles)

3) Neoplastic 

a. Carcinoma (Squamous cell)

4) Endocrine

5) Developmental

a Fordyces spots

b White sponge Naevus

c Dyskeratosis Congentita

d  Tylosis

e Dariers Disease

6) Vascular

7) Immunological

a Lichenoid
 b Lichen Planus

c Lichen Sclerosis

d Lupus erythematosus

e Pyostomatitis vegetans

f Xanthomatosis

g Dermatomyositis

8) Idiopathic
 
a Leukoplakia

b sublingual Keratoses

9) Medication

a Tobacco related keratoses

b Oral submucous Fibrosis (betel quid)

10) Metabolic

A)Dysplasia
Disturbance of differentiation in epithelium in a premalignant way- ranges
from mild atypic to severe dysplas

Abnormal and increased mitoses

Loss of basal cell polarity

Cell pleomorphism

Drop shaped rete processes

Deep cell cohesion

Irregular hyperplasia/atrophy

Irregular stratification

Loss of differentiation

Nuclear hyperchromatism

B)Carcinoma in situ:

Neoplasm that shows all the features os a carcinoma but hasn�t invaded the basement
membrane 

Risk Factors

History- Betel Quid Usage,

     Tobacco smoking

    High alcohol intake

     Genetic Disorders

    Large persistent lesions

    Change in existing lesion

Site  1) Posterolateral tongue

         2) Floor of mouth

         3)Retromolar region

         4) Anterior pillar of fauces

C)Fordyces spots
 -appear after the age of 3

-sebacous glands seen as creamy yellow dots along border between vermillion and
oral mucosa

D)White Sponge Naevus

Incidence: rare,
Age: 2nd decade

Clinical Features
Shaggy spongy folded white lesion at several mucosal sites
Asymptomatic diffuse bilateral lesions

Mostly seen on buccal mucosa

No malignant potential therefore reassurance is only tx needed