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2. NOMA OR CANCRUM ORIS
It is also called as GANGRENOUS
STOMATITIS
Rapidly spreading gangrene.
Occur in debilitated or nutritionally
deficient person.
Mainly seen in children but also occur in
adults.
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3. PREDISPOSING FACTORS
1. Undernourished person.
2. Debilitated person having infections like :
• Diphtheria
• dysentery
• measles
• Pneumonia
• Scarlet fever
• Syphilis
• Tuberculosis
• Blood dyscrasias
including anemia.
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4. • Noma is considered as a secondary
complication rather then a primary
disease.
• Causative organism
a)vincent‘s organism
b)secondary infection by
streptococci,staphylococci and diphtheria
bacilli.
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5. Condition usually began around the
gingiva and progressed to destruction of
the floor of the mouth and lower lip.
Selye suggested that Noma may not
necessarily be due to a specific
pathogenic agent but may be due to a
pathogenic situation.
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6. CLINICAL FEATURES: Starts with a small
ulcer in the gingival mucosa which rapidly
spreads and involves the surroundings
tissue of the jaws, lips ,and cheeks by
gangrenous necrosis.www.indiandentalacademy.com
7. Initial site is an area of stagnation around
a fixed bridge and crown the overlying skin
becomes inflamed, edematous and finally
necrotic.
With the result that a line of demarcation
develops between healthy and dead
tissue,and large masses of the tissue
slough out leaving the jaw exposed.
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8. The commencement of gangrene is
denoted by the appearance of blackening
of the skin.
Necrosis of the buccal fat pad and
subcutaneous fat pad is reported.
Foul odor has arised from gangrenous
tissue.
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9. Palate and tongue can also be involved by
this process.
High temperature during the Course of the
disease.
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10. Mortality rate:75%
Treatment:Immediate treatment of
malnutrition.
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11. APHTHOUS STOMATITIS
Characterized by painful,recurring solitary or
multiple ulceration of the oral mucosa.
Incidence-20 %to 60%.
Prevalence:higher in professional person and
socioeconomic group.
Etiology-1)bacterial infection-L form
streptococus isolated from lesion.
Herpes simplex virus can not be isolated.
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12. 2)Immunologic abnormalities:
Lehner : a)autoimmune response
b)detected IgM and IgG antibody in
epithelial cells of the spinous layer of the oral
cavity.
Addy and dolby :normal level of complement
and antinuclear factor.
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13. Cohen:
a) not an autoimmune
disease.
b) local immune
response against an
antigenically altered
oral mucosa.
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14. results of diffusion of bacterial toxins, food
and other substance acting as allergen.
Donatsky-elevated gamma globulin level
against sterptococus.
Recurrent aphthous stomatitis-altered
immune response which is directed against
non pathogenic oral flora and host oral tissue.
chemical mediator
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15. focal release of neuropeptide.
viral infection.
deficiency of folic acid and iron
Wray reported –after examining 330 patients
47-total deficient person
23 deficient in iron,7 deficient in folic acid,6 in
vitamin B12 deficiency,11 had combined
deficiency.
seen in HIV patients
Patient with malabsorption conditions.
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16. Precipitating factors:Trauma-Graycowaski-
local trauma is an factor in 75% of the
cases.
Self-inflicted bite
Oral surgical procedure
Tooth brushing
Dental procedure,needle injection and
needle trauma.
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17. Endocrine condition-relationship between
occurrence of the menstrual period and
development of aphthous ulcer.
Related with the level of progesterone
Woman have remission of disease during
pregnancy.
Onset of disease associated with menopause
and menarche.
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18. Psychic factors-association with acute
psychological problem and stress.
Allergic factor-association with asthma hey
fever,food or drug allergy.
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19. Clinical features:4 forms
1)minor
2)major
3)herpetiform
4)ulcer associated with Bechets syndrome.
Main difference between 3 groups-clinically
and degree of severity.
Tingling and burning of oral mucosa before
starting the disease.
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20. Minor apthous ulcer-
most commonly
occurred form.
Age-10 to 30 years.
Occurrence early in life.
Disease persist with
recurring attacks.
20% of population
affected.
Mainly in professional
school students.
Familial association.www.indiandentalacademy.com
21. Ulcer will not preceded by vesicles and it
appear on the tongue, buccal mucosa,
floor of the mouth.
Rarely present on hard palate and
attached gingiva.
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22. One or two attacks in a year,one or two
attacks in a month ,never free from lesion.
Appear as a single,painful ulcer,diameter
is less then .5 mm that is covered by
yellow fibrinous membrane and
surrounded by erythematous halo.
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23. Generalized edema of the oral cavity.
Paresthesia
Low grade fever
Localized lymphadenopathy
Vesicle like lesion containing mucus.
Difficulties in eating.
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24. Common site of occurrence:buccal and
labial mucosa
Buccal and lingual sulcus
Soft palate,gingiva labial mucosa.
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25. Lateral and ventral
surface of the
tongue is also
affected.
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26. Heal in 7 to 1o days without scar
formation.
Oral manifestation include mucosal
fissure,small multiple hyperplastic nodule
on the buccal mucosa produce cobble
stone appearance.
Biopsy finding suggest noncaseating
granuloma.
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28. Major aphthous ulcer:most severe expression
of aphthous stomatitis.
1 to 10 in number present in lips,cheeks
tongue, soft palate.
Painful and larger lesion and persist for
longer time
Heal with scar formation.
6 weeks to heal as soon as one disappear
another will appear
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29. Difficulties in eating,pain and discomfort.
Show similar lesion in vagina,penis larynx.
No particular age group,females affected
more then males.
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30. Herpetiform ulcer-present as a crop of
ulcers.
100 in numbers.
Palatal and gingival mucosa are involved.
Pain is present and healing will occur in 1
or 2 weeks.
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31. Here the ulcers will be preceded by vesicles
and exhibit no virus infected cells.
Brooke and Sapp -numerous small lesion
found in oral mucosa.
Small pinhead sized erosions that gradually
enlarge and coalesce
Painful lesions present for one to three years.
Immediate relief from tetracycline
mouthwash.
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32. Laboratory test-no herpes simplex virus
is cultured.
Absence of multinucleated giant cell.
No antibodies against herpes virus.
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35. HISTOPATHOLOGY
minor apthous ulcer-fibrinopurulent
membrane covering the ulcerated area.
Superficial colonies of microorganisms
present in this membrane.
Inflammatory cell infiltration in connective
tissue.
Granulation tissue at the base of the lesion.
Epithelial proliferation at margins.
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36. Lesion begins at the excretory duct of
minor salivary gland.
Wood-anitschkow cell.
Mononuclear cell in submucosa and in
perivascular tissue in pre-ulcerative
stage.
In ulcerative stage-CD4and CD8
lymphocytes are present.
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38. TREATMENT
1. mouth rinse-sodium bicarbonate in warm
water.
2. Drug-prednisone-20 to 40 mg daily for a
week
3. Topical corticosteroid.
4. Intralesional injection of triamicolone.
5. Antibiotics-tetracycline suspension.
6. Tetracycline mouthwash-250 mg per 5 ml
used 4 times daily for 5 to 7 days .
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40. 250 mg of capsule in 30 ml of warm
water.(4 times in a day for 4 day)
Other
drugs:azathioprine,cyclophosphamide.
Thailodomide,pentixyfilline
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44. BEHCETS SYNDROME
Uncertain etiology.
Pleuropnumonia like organism.
Autoimmune etiology.
Lehner-immunologic similarities
between this syndrome and recurrent
apthous stomatitis.
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45. CLINICAL FEATURES
Occurs between 10 to 45 year of age.
Oral and genital ulceration,ocular
lesion,skin lesion.
Oral lesion-first occurrence
Painful and similar in appearance to
recurrent apthous stomatitis.
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46. Size ranging from several millimeter to
centimeter or more in diameter.
Ulcer have an erythematous border and
covered by gray or yellow exudates.
Genital ulcers are small and located on
scrotum,root of the penis.
Ocular lesions-photophobia and
irritation
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47. Simple conjunctivitis to finally uveitis
Skin lesions –small papules on the trunk
and limbs and around the genitalia.
Involvement of CNS and cardiac and
pulmonary involvement is seen.
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50. Histologic features
similar to recurrent apthous stomatitis.
Endothelial proliferation.
Vasculitis.
Laboratory findings:
hypergammaglobulinemia
leucocytosis
eosinophilia
elevated sedimentation rate.
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51. TREATMENT AND PROGNOSIS
1. supportive treatment.
2. Remission after a period of months to
years.
3. Serious complication can lead to death.
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