Diseases of oral cavity and ludwig’s angina ug,18.07.16 dr.davis thomas

1. DR. DAVISTHOMAS P.

2.  Oral cavity
 Lips
 Tongue
 Floor of Mouth
 Buccal mucosa
 Palate
 Retromolar trigone

3.  Reactive lesions
 Inflammatory lesions
 Oral cancer
 Precancerous lesions (Leukoplakia &
erythroplakia)
 Benign Tumors of Oral Cavity

4. 1-Irritation fibroma :
 Most common
 61 % of all the
reactive lesions
 Can occur throughout
the oral cavity
 Most common along
the "bite line."
 Microscopically:
fibrous tissue covered
by squamous mucosa.

6. 2-Pyogenic granulomas
 12 %
 Highly vascular lesions similar
to granulation tissue.
3-Peripheral giant cell granuloma
(giant cell epulis)
 5%
 Aggregation of multinucleated
foreign body-like giant cells
 Separated by fibroangiomatous
stroma.
Giant cell epulis

7.  Epulis is a clinical
term applied to
swellings at the
gum margin.
 Most of them are
granulomas
associated with
chronic gingivitis
 A few are true
neoplasms

8.  Reactive lesions
 Inflammatory lesions
 Oral cancer
 Precancerous lesions (Leukoplakia &
erythroplakia)
 Benign Tumors of Oral Cavity

9. 1. Viral infection
2. Fungal infection
3. Bacterial infection
A - Vincent’s angina
B - Syphilis
C - Oral tuberculosis
4. Aphthous ulcers (aphthous stomatitis)
5. Dermatoses

10.  Inflammation of the mouth (Stomatitis)(Stomatitis)
 Inflammation of the Lips (Cheilitis)(Cheilitis)
 Inflammation of the soft tissues around teeth typically
resulting from inadequate oral hygiene (Gingivitis)(Gingivitis)
 Inflammmation of the tongue (Glossitis).(Glossitis).
 GlossitisGlossitis more commonly applied to the "beefy-red" tongues"beefy-red" tongues of
certain deficiency states (e.g.; vitamin B12, and iron, deficiencies).(e.g.; vitamin B12, and iron, deficiencies).
 Other causes of glossitis:Other causes of glossitis: hot and spicy foods, chronic irritation by
excessive smoking, ragged tooth or syphilitic inflammation

11.  Herpes simplex virus (usually
type 1) infection causes "cold
sores"
 The virus infects the mouth in
children.
 Most adults have had HSV1
infection, but it remains latent and
produces this small sore:
 During periods of stress
 From local trauma
 Environmental changes
 Cold sores consist of
numerous vesicles and
shallow ulcerations.
Cold sore of lower lip (herpes labialis)
Sore = abraded or painful area of the body

13.  Treatment
 Antipyretics, analgesics, hydration
 Valacyclovir and famciclovir inhibit viral DNA
polymerase – help to suppress and controlhelp to suppress and control
symptoms,symptoms, but does not curebut does not cure (given for 1 week)
 If catch in the prodrome - 5% acyclovir cream for 1
week has shown to shorten course or completely
abort reactivation altogether
 KEY TO DIAGNOSIS – Clinical + Fluid analysis (PCR)Clinical + Fluid analysis (PCR)
and/or serology (Elisa, Western Blot)and/or serology (Elisa, Western Blot)

14.  Coxackie A virus causes
herpangia
 Acute vesiculo-ulcertaive
mucosal lesion
 Occurs in epidemics
 Affects children
 Begins in tonsils, soft palate &tonsils, soft palate &
uvulauvula
 Painful
 Heal spontaneously within few
days
 Koplik’s spots are a feature of
measles
Koplik’s spots
Herpangia

16. Herpangina

17.  Candida albicans is an oral commensal in 20-40%oral commensal in 20-40% of
population.
 Infection occurs in:
 Infants
 Patients on broad spectrum antibiotics, steriod or cytotoxic therapy
 Diabetes
 Neutropenia
 Immunodeficiency (AIDS)
 Presents as superficial gray-white inflammatory
membranes comprising fungus in a fibrinosuppurative
exudate.
 White exudate can be removed by scraping
 Exudate bleeds on removal

18. Erythematous Candidiasis

19.  Treatment
 Mild, acute formsMild, acute forms – topical Nystatin
 Mild, chronicMild, chronic – topical Nystatin + Clotrimazole
troches (troche=lozenge)
 Refractory or immunocomprimised WITHOUTRefractory or immunocomprimised WITHOUT
systemic involvementsystemic involvement – add oral Fluconazole
 Severe forms (systemicsystemic) – IV Amphotericin B
with or without Fluconazole
 KEY TO DIAGNOSIS: Clinical + KOH Prep;
culture and serum (1,3)β-D-glucan detection
assay if unclear

20.  Caused by Borellia vincenti and
fusiform bacilli
 Both are normal inhabitants of oral
cavity
 Decreased resistance (inadequate
nutrition, immunofeciency) is a
predisposing factor to infection
 Punched out erosions ulceration→
spreads invovles all gingival→ →
margin, which become covered by
a necrotic pseudomembrane

22. A-Ulcerated chancre B-Ulcerated mucous
patches (snail track ulcers)
C-Gummatous ulcer
C - Tuberculosis of
The Tongue

25.  Apthous ulcers are
extremely common lesions
(up to 20% of population)
 They are painful, multiple,
small, shallow, recurrent
ulcerations
 Presented clinically as
white lesions (1<,1> CM)
 Etiology is unknown
Aphtha = Whitish spot

26. ○ Most common cause of non-traumatic ulcerations of the oral cavity
○ Etiology unclear
○ 10-20% of general population
○ Diagnosis of exclusion
○ Classifications
 Minor aphthous ulcerMinor aphthous ulcer
- < 1cm< 1cm in diameter
- Located on freely mobile oral mucosa
- Appears as a well-delineated white lesion with an erythematous halo
- Prodrome of burning or tingling in area prior to ulcer’s appearance
- Resolve in 7-10 days
- Never scars
 Major aphthous ulcerMajor aphthous ulcer
- > 1cm> 1cm in diameter
- Involves freely mobile mucosa, tongue, and palate
- Last much longer – 6 weeks or more
- Typically scar upon healing

27. Herpetiform ulcers
- Small, 1-3mm in diameter ulcerations appearing in crops of 20-200
ulcers
- Typically located on mobile oral mucosa, tongue, and palate
- Last 1-2 weeks
- Called herpetiform because ulcerations resemble those of HSV,Called herpetiform because ulcerations resemble those of HSV,
but there isbut there is no vesicular phaseno vesicular phase
 Treatment
 Topical tetracycline solution for 5-7 days has shown good results
 Topical steroids shown to shorten disease duration
 Sucralfate suspension shown to improve pain as well as shorten
disease duration
 Major aphthous ulcers or more severe forms of disease require 2Major aphthous ulcers or more severe forms of disease require 2
week course of systemic steroidsweek course of systemic steroids
 KEY TO DIAGNOSIS: Diagnosis of exclusion; clinical
appearance/course

29.  Lichen planus
White plaques

30. whitish linear lesions in lacy patternwhitish linear lesions in lacy pattern

31.  Reactive lesions
 Inflammatory lesions
 Oral cancer
 Precancerous lesions (Leukoplakia &
erythroplakia)
 Benign Tumors of Oral Cavity

32.  Incidence:
 Geographic variation:
 Accounts for 2% of cancers in UK
 Commoner in S. East Asia
 Ages & sex :
 Old Men (50-60 years)
• Site :
1.Lip (lower lip)
2.Tongue (anterior )⅔
3.Mouth floor
4.Tonsil and Fauces
Squamous Cell Carcinoma
constitutes 95% of oral cancers

33. Aetiology:
1-Tobacco and alcohol are the most common
associations:
 Smokers can have 15-fold greater risk ( than nonsmokers ) of
malignancy.
 Chewing tobacco and betel nuts are important causes in India and
parts of Asia.
2- Leukoplakia and Erythroplakia
3- Human papilloma virus (HPV) (type16)
4- Genetic factors may also play a role
 (deletions in chromosomes 18q, lap, 8p, and 3p are implicated).
5- Exposure to ultra-violet light (cancer of the lip).

34. Gross:
 Ulcerated nodule with
raised everted edges
 Often on lower lip
Histologically:
 Well differentiated
squamous carcinomas
Spread:
 Growth is relatively
slow
 Submandibular nodes
 Deeper cervical lymph
nodes

35.  More aggressive than tumors of the lips
 Grossly starts as a nodule malignant ulcer→
 Spread:
1-Local
Local infiltration to floor of the mouth,
facuces and pharynx leads to fixation the
tongue, interfering with speech and
swallowing.
Local spreads into the medullary cavity of the
mandible.
2-lymphatic spread (occurs early) → deep
cervical lymph nodes.

36. Perform incisional Bx in any oral lesion persist for more than 2wks

37.  Prognosis is best with lip lesions
 Poorest with mouth floor and tongue base
lesions (20%-30% 5-year survival rate ).

38.  Malignant melanoma
 Lymphomas
 Leukemic infiltration
 Adenocarcinoma of
minor salivary glands
 Sarcomas
Acute Leukemia: gum involvement

39.  Reactive lesions
 Inflammatory lesions
 Oral cancer
 Precancerous lesions
 Benign Tumors of Oral Cavity

40. Premalignant lesions
○ Leukoplakia
 Whitish plaque that cannot be scrapped off
 5-20% malignant potential5-20% malignant potential
 Microscopic examination reveals hyperkeratosis and atypia
 Lesions on lateral tongue, lower lip, and floor of mouth more
likely to progress to malignancy
○ Erythroplakia
 Red patch or macule with soft, velvety texture
 Much higher chance of harboring malignancy – 60-90%– 60-90% of
untreated cases
 Treatment is surgical excision or laser ablation

41.  Causes include:
1- Chronic tobacco
use (pipe -
smoking).
2- Chronic irritation
(e.g.; dentures).
2- Alcohol abuse.

42.  An oral lesion seen in
HIV infected, AIDS
patients
 Caused by Epstein-Barr
virus (EBV) infection,
often with
superimposed candida
 Lesions are white
patches of fluffy
("hairy") hyperkeratosis
on tongue lateral
borders.

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44. It is an insidious chronic disease affecting any part of the oral cavity and
sometimes the pharynx.
Although occasionally preceded by and /or associated with vesicle
formation ,it is always associated with juxta-epithelial inflammatory reaction
followed by a fibro-elastic changes of the lamina propria with epithelial
atrophy leading to stiffness of the oral mucosa and causing trismus and
inability to eat.
DEFINITION

45. Etiology of OSMF:
Exact etiology is unknown. The suggested factors are,
1. Chronic Irritation
Chilies
Lime
Betel nut
Tobacco Chewing
2. Deficiency disease.
3. Defective iron metabolism
4. Bacterial Infection
5. Collagen disorder
6. Immunological disorders
7. Genetic disorder.

46. MULTIFACTORIAL PATHOGENESIS
ARECANUT TOBACCO LIME VOLATILE OILSVOLATILE LIQUIDS
TANNIN&
AFLOTOXIN
ARECOLINE
DEGRADATION
OF COLLAGEN
INCREASED SYNTHESIS
OF COLLAGEN
MECHANICAL
TRAUMA
CHEMICAL BURN HYPERSENSITIVITY
ALTERED IMMUNITY
GENETIC
REDISPOSITION
FIBROBLAST
FORMATION
IRREVERSIBLE FIBROSIS
CACINOMAEXPOSURE CONTINOUS

47. Prodromal symptoms :
 Onset is insidious. The most common
initial symptoms are:
 Burning sensation on eating spicy food
 Blisters on the palate
 Ulceration or recurrent stomatitis
 Excessive salivation
 Defective gustatory sensation
 Dryness of mouth.

48. Later,
 Difficulty in opening mouth
 Inability to whistle, blow
 Difficulty in swallowing
 When fibrosis involves pharynx- referred pain to the ear.
 Changes in tone of the voice due to vocal cord involvement
 Some times deafness due to occlusion of eustachian tubes

49. COMMON SITES INVOLVED
 Buccal mucosa, faucial pillars ,soft palate, lips and hard
palate.
 The fibrous bands in the buccal mucosa run in a vertical
direction ,sometimes so marked that the cheeks are
almost immovable.
 In the soft palate the fibrous bands radiate from the
pterygomandibular raphe or the faucial pillars and have a
sear like appearance

50.  The uvula is markedly involved , shrinks and appears as a
small fibrous bud.
 The faucial pillars become thick , short, and extremely
hard.
 The tonsils may be pressed between the fibrosed pillars
 The lips are often affected and upon palpation , a circular
band can be felt around the entire rima oris
 When gingiva is affected , it is fibrotic, blanched and
devoid of its normal stippled appearance.

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58. MANAGEMENT
 Various modalities of treatment have
been tried.
1.Restriction of habits/ Behavioral therapy
2.Medicinal therapy
3.Surgical therapy.
4.Oral Physiotherapy

59.  Reactive lesions
 Inflammatory lesions
 Oral cancer
 Precancerous lesions (Leukoplakia &
erythroplakia)
 Benign Tumors of Oral Cavity

60. 1-Squamous cell
papilloma.****
2-Capillary hemangioma
3-Cavernous hemangioma &
lymphangioma →
macrochelia &
macroglossia
4-leiomyoma
5-Schwannoma
Cavernous hemangioma

62.  Extension of localized periapical infection
 Anterior mandibular → Sublingual
 Posterior mandibular (molar) → Submandibular
 Fascial planes

63.  Recent dental extraction or work
 Dental caries
 Fever
 Swelling of mouth, face, neck
 Compromised host
 Co-morbidities (diabetes)

64.  Toxicity
 Brawny bilateral boardlike edema
 Submandibular, submental, sublingual
 Trismus
 Tongue elevation
 No fluctuance

65. A, Ludwig angina may initially appear benign. B, In Ludwig angina, rapid progression may
compromise the airway in a few hours.

66.  Streptococcus
 Staphylococcus
 Mixed aerobic/anaerobic infection
 B. Fragilis
 ß-lactamase resistance (<= 40%)

67.  Clinical
 CT scan

68.  Airway control - EARLY
 Fiberoptic
 Deterioration may be rapid
 Cricothyrotomy or tracheostomy may be necessary
 Surgical consultation mandatory
 Oral maxillofacial surgeon or ENT
 Definitive surgical drainage and debridement
 ICU

69.  Extended spectrum penicillins
 Ampicillin/Sulbactam (Unasyn)
 Ticarcillin/Clauvulate (Timentin)
 Piperacillin/Tazobactam (Zosyn)
 Clindamycin + Cipro (PCN allergy)
 Flagyl (B. Fragilis)

70.  Reduce edema
 “Used routinely when airway compromise
suspected” (Larawin et al.)
 Dexamethasone 10-20 mg IV
 Then 4-6 mg Q6 for 8 doses (Busch)

71.  Serious deep space infection
 Potentially fatal
 Aggressive manage airway as indicated
 Surgical consultation
 Antibiotics and steroids
 ICU