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SEMINAR ON CANCRUM ORIS
AND APTHOUS STOMATITIS
INDIAN DENTAL ACADEMY
Leader in continuing dental education
www.indiandentalacademy.com
www.indiandentalacademy.com
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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PREDISPOSING FACTORS:
 A) undernourished person.
 B)Debilitated person having infections
like Diphtheria,dysentery,measles,
pneumonia,scarlet fever,syphilis,
tuberculosis and blood dyscrasias
including anemia.
www.indiandentalacademy.com
 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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 Selye reported the production of a
noma like condition in rats as a result of
simultaneous administration of
cortisone and clipping of the mandibular
incisor forcing the animals to chew with
their gingiva and thus to cause
excessive mechanical injury to mucosa.
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 Condition usually began around the gingiva
and progressed to destruction of the floor of
the mouth and lower lip.
 Susceptibility to tissue injury which was
produced by cortisone and this can be
eliminated by pituitary growth hormone.
 Selye suggested that Noma may not
necessarily be due to a specific pathogenic
agent but may be due to a pathogenic
situation.
www.indiandentalacademy.com
 Clinical features: Start
with the 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
 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
www.indiandentalacademy.com
out leaving the jaw exposed.
 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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 Palate and tongue can also be involved
by this process.
 High temperature during the Course of
the disease.
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 Mortality rate:75%
 Treatment:Immediate treatment of
malnutrition.
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APTHOUS 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.
Images3.jpg
www.indiandentalacademy.com
 2)Immunologicabnormal
ities:
Lehner:a)autoimmune
response
b)detected IgM
and IgG antibody in
epithelial cell of the
spinous layer of the oral
cavity.
 Addy and dolby:normal
level of complement
and antinuclear factor.
www.indiandentalacademy.com
 Cohen:a) not an
autoimmune
disease.
b)local
immune response
against an
antigenically altered
oral mucosa.
www.indiandentalacademy.com
 results of diffusion of bacterial toxins, food
and other substance acting as allergen.
 Donatsky-elevated gamma globulin level
against sterptococus.
 Recurrent apthous stomatitis-altered immune
response which is directed against non
pathogenic oral flora and host oral tissue.
 4)chemical mediator
www.indiandentalacademy.com
 5)focal release of neuropeptide.
 6)viral infection.
 7)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.
 8)patient with malabsorption condition.
www.indiandentalacademy.com
12)seen in HIVpatients
www.indiandentalacademy.com
 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.
www.indiandentalacademy.com
 Endocrine condition-relationship between
occurrence of the menstrual period and
development of apthous ulcer.
 Related with the level of progesterone
 Woman have remission of disease during
pregnancy.
 Onset of disease associated with menopause
and menarche.
www.indiandentalacademy.com
 Psychic factors-association with acute
psychological problem and stress.
 Allergic factor-association with asthma
hey fever,food or drug allergy.
www.indiandentalacademy.com
 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 treatment.
www.indiandentalacademy.com
 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
 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.
www.indiandentalacademy.com
 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 erythemeatous halo.
www.indiandentalacademy.com
 Generalized edema of the oral cavity.
 Parasthesia
 Low grade fever
 Localized lymphoadenopathy
 Vesicle like lesion containing mucus.
 Difficulties in eating.
www.indiandentalacademy.com
 Common site of occurrence:buccal and
labial mucosa
 Buccal and lingual sulci
 Soft palate,gingiva labial mucosa.
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 Lateral and ventral
surface of the
tongue is also
affected.
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 Heal in 7 to 1o days without scar
formation.
 Oral manifestation include mucosal
fissure,small multiple hyperplastic
nodule on the buccle mucosa produce
cobbel stone appearance.
 Biopsy finding suggest nonceasenting
granuloma.
www.indiandentalacademy.com
www.indiandentalacademy.com
 Major apthous ulcer:most sever expression of
apthous 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
www.indiandentalacademy.com
 Difficulties in eating,pain and
discomfort.
 Show similar lesion in vagina,penis
larynx.
 No particular age group,females
affected more then males.
www.indiandentalacademy.com
 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.
www.indiandentalacademy.com
 Here the ulcer will be preceded by vesicle
and exhibit no virus infected cell.
 Brooke and sapp-numerous small lesion
found in oral mucosa.
 Small pinhead sized erosion that gradually
enlarge and coalesce
 Painful lesion present for one to three years.
 Immediate relief from tetracycline
mouthwash.
www.indiandentalacademy.com
 Laboratory test-no herpes simplex virus
is cultured.
 Absence of multinucleated giant cell.
 No antibodies against herpes virus.
www.indiandentalacademy.com
www.indiandentalacademy.com
www.indiandentalacademy.com
 Histopathology:minor apthous ulcer-
fibrinopurulent membrane covering the
ulcerated area.
 Superficial colonies of microorganism present
in this membrane.
 Inflammatory cell infiltration in connective
tissue.
 Granulation tissue at the base of the lesion.
 Epithelial proliferation at margins.
www.indiandentalacademy.com
 Lesion begin at the excretory duct of
minor salivary gland.
 Wood-anitschkow cell.
 Mononuclear cell in submucosa and in
perivascular tissue in preulcerative
stage.
 In ulcerative stage-CD4and CD8
lymphocyte.
www.indiandentalacademy.com
 Presence of macrophages and mast
cells.
 Differential diagnosis:1)herpes simplex
infection.
 Trauma.
 Pemphigus vulgaris.
 Mucous membrane pemphigoid.
www.indiandentalacademy.com
 Treatment:mouth rinse-sodium bicarbonate in
warm water.
 Drug-prednisone-20 to 40 mg daily for a week
 Topical corticosteroid.
 Intralesional injection of triamicolone.
 Antibiotics-tetracycline suspension.
 Tetracycline mouthwash-250 mg per 5 ml
used 4 times daily for 5 to 7 days .
www.indiandentalacademy.com
 Steroid ointment-1.5 %cortisone
acetate applied locally.
 Hydrocortisone acetate antibiotics
lozenges.
 Chemical cautery.
www.indiandentalacademy.com
 250 mg of capsule in 30 ml of warm
water.(4 times in a day for 4 day)
 Other
drugs:azathioprine,cyclophosphamide.
Thailodomide,pentixyfilline
www.indiandentalacademy.com
www.indiandentalacademy.com
 BEHCETS SYNDROME:Uncertain
etiology.
 Pleuropnumonia like organism.
 Autoimmune etiology.
 Lehner-immunologic similarities
between this syndrome and recurrent
apthous stomatitis.
www.indiandentalacademy.com
 Clinical features: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.
www.indiandentalacademy.com
 Size ranging from several millimeter to
centimeter or more in diameter.
 Ulcer have an erythematous border and
covered by gray or yellow exudates.
 Genital ulcer are small and located on
scortum,root of the penis.
 Ocular lesions-photophobia and
irritation
www.indiandentalacademy.com
 Simple conjunctivitis to finally uveitis
and finally popyon
 Skin lesions –small papules on the
trunk and limbs and around the
genitalia.
 Involvement of CNS and cardiac and
pulmonary involvement is seen.
www.indiandentalacademy.com
www.indiandentalacademy.com
www.indiandentalacademy.com
 Histologic features-similar to recurrent
apthous stomatitis.
 Endothelial proliferation.
 Vasculitis.
 Laboratory findings:
hypergammaglobulinemia
leucocytosis
eosinophilia
elevated sedimentation rate.
www.indiandentalacademy.com
 Treatment and prognosis-supportive
treatment.
 Remission after a period of months to
years.
 Serious complication can lead to death.
www.indiandentalacademy.com
For more details please visit
www.indiandentalacademy.com
www.indiandentalacademy.com

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Cancrum /certified fixed orthodontic courses by Indian dental academy

  • 1. SEMINAR ON CANCRUM ORIS AND APTHOUS STOMATITIS INDIAN DENTAL ACADEMY Leader in continuing dental education www.indiandentalacademy.com www.indiandentalacademy.com
  • 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. www.indiandentalacademy.com
  • 3. PREDISPOSING FACTORS:  A) undernourished person.  B)Debilitated person having infections like Diphtheria,dysentery,measles, pneumonia,scarlet fever,syphilis, tuberculosis and blood dyscrasias including anemia. www.indiandentalacademy.com
  • 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. www.indiandentalacademy.com
  • 5.  Selye reported the production of a noma like condition in rats as a result of simultaneous administration of cortisone and clipping of the mandibular incisor forcing the animals to chew with their gingiva and thus to cause excessive mechanical injury to mucosa. www.indiandentalacademy.com
  • 6.  Condition usually began around the gingiva and progressed to destruction of the floor of the mouth and lower lip.  Susceptibility to tissue injury which was produced by cortisone and this can be eliminated by pituitary growth hormone.  Selye suggested that Noma may not necessarily be due to a specific pathogenic agent but may be due to a pathogenic situation. www.indiandentalacademy.com
  • 7.  Clinical features: Start with the 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
  • 8.  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 www.indiandentalacademy.com
  • 9. out leaving the jaw exposed.  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. www.indiandentalacademy.com
  • 10.  Palate and tongue can also be involved by this process.  High temperature during the Course of the disease. www.indiandentalacademy.com
  • 11.  Mortality rate:75%  Treatment:Immediate treatment of malnutrition. www.indiandentalacademy.com
  • 12. APTHOUS 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. Images3.jpg www.indiandentalacademy.com
  • 13.  2)Immunologicabnormal ities: Lehner:a)autoimmune response b)detected IgM and IgG antibody in epithelial cell of the spinous layer of the oral cavity.  Addy and dolby:normal level of complement and antinuclear factor. www.indiandentalacademy.com
  • 14.  Cohen:a) not an autoimmune disease. b)local immune response against an antigenically altered oral mucosa. www.indiandentalacademy.com
  • 15.  results of diffusion of bacterial toxins, food and other substance acting as allergen.  Donatsky-elevated gamma globulin level against sterptococus.  Recurrent apthous stomatitis-altered immune response which is directed against non pathogenic oral flora and host oral tissue.  4)chemical mediator www.indiandentalacademy.com
  • 16.  5)focal release of neuropeptide.  6)viral infection.  7)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.  8)patient with malabsorption condition. www.indiandentalacademy.com
  • 18.  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. www.indiandentalacademy.com
  • 19.  Endocrine condition-relationship between occurrence of the menstrual period and development of apthous ulcer.  Related with the level of progesterone  Woman have remission of disease during pregnancy.  Onset of disease associated with menopause and menarche. www.indiandentalacademy.com
  • 20.  Psychic factors-association with acute psychological problem and stress.  Allergic factor-association with asthma hey fever,food or drug allergy. www.indiandentalacademy.com
  • 21.  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 treatment. www.indiandentalacademy.com
  • 22.  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
  • 23.  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. www.indiandentalacademy.com
  • 24.  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 erythemeatous halo. www.indiandentalacademy.com
  • 25.  Generalized edema of the oral cavity.  Parasthesia  Low grade fever  Localized lymphoadenopathy  Vesicle like lesion containing mucus.  Difficulties in eating. www.indiandentalacademy.com
  • 26.  Common site of occurrence:buccal and labial mucosa  Buccal and lingual sulci  Soft palate,gingiva labial mucosa. www.indiandentalacademy.com
  • 27.  Lateral and ventral surface of the tongue is also affected. www.indiandentalacademy.com
  • 28.  Heal in 7 to 1o days without scar formation.  Oral manifestation include mucosal fissure,small multiple hyperplastic nodule on the buccle mucosa produce cobbel stone appearance.  Biopsy finding suggest nonceasenting granuloma. www.indiandentalacademy.com
  • 30.  Major apthous ulcer:most sever expression of apthous 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 www.indiandentalacademy.com
  • 31.  Difficulties in eating,pain and discomfort.  Show similar lesion in vagina,penis larynx.  No particular age group,females affected more then males. www.indiandentalacademy.com
  • 32.  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. www.indiandentalacademy.com
  • 33.  Here the ulcer will be preceded by vesicle and exhibit no virus infected cell.  Brooke and sapp-numerous small lesion found in oral mucosa.  Small pinhead sized erosion that gradually enlarge and coalesce  Painful lesion present for one to three years.  Immediate relief from tetracycline mouthwash. www.indiandentalacademy.com
  • 34.  Laboratory test-no herpes simplex virus is cultured.  Absence of multinucleated giant cell.  No antibodies against herpes virus. www.indiandentalacademy.com
  • 37.  Histopathology:minor apthous ulcer- fibrinopurulent membrane covering the ulcerated area.  Superficial colonies of microorganism present in this membrane.  Inflammatory cell infiltration in connective tissue.  Granulation tissue at the base of the lesion.  Epithelial proliferation at margins. www.indiandentalacademy.com
  • 38.  Lesion begin at the excretory duct of minor salivary gland.  Wood-anitschkow cell.  Mononuclear cell in submucosa and in perivascular tissue in preulcerative stage.  In ulcerative stage-CD4and CD8 lymphocyte. www.indiandentalacademy.com
  • 39.  Presence of macrophages and mast cells.  Differential diagnosis:1)herpes simplex infection.  Trauma.  Pemphigus vulgaris.  Mucous membrane pemphigoid. www.indiandentalacademy.com
  • 40.  Treatment:mouth rinse-sodium bicarbonate in warm water.  Drug-prednisone-20 to 40 mg daily for a week  Topical corticosteroid.  Intralesional injection of triamicolone.  Antibiotics-tetracycline suspension.  Tetracycline mouthwash-250 mg per 5 ml used 4 times daily for 5 to 7 days . www.indiandentalacademy.com
  • 41.  Steroid ointment-1.5 %cortisone acetate applied locally.  Hydrocortisone acetate antibiotics lozenges.  Chemical cautery. www.indiandentalacademy.com
  • 42.  250 mg of capsule in 30 ml of warm water.(4 times in a day for 4 day)  Other drugs:azathioprine,cyclophosphamide. Thailodomide,pentixyfilline www.indiandentalacademy.com
  • 44.  BEHCETS SYNDROME:Uncertain etiology.  Pleuropnumonia like organism.  Autoimmune etiology.  Lehner-immunologic similarities between this syndrome and recurrent apthous stomatitis. www.indiandentalacademy.com
  • 45.  Clinical features: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. www.indiandentalacademy.com
  • 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 ulcer are small and located on scortum,root of the penis.  Ocular lesions-photophobia and irritation www.indiandentalacademy.com
  • 47.  Simple conjunctivitis to finally uveitis and finally popyon  Skin lesions –small papules on the trunk and limbs and around the genitalia.  Involvement of CNS and cardiac and pulmonary involvement is seen. www.indiandentalacademy.com
  • 50.  Histologic features-similar to recurrent apthous stomatitis.  Endothelial proliferation.  Vasculitis.  Laboratory findings: hypergammaglobulinemia leucocytosis eosinophilia elevated sedimentation rate. www.indiandentalacademy.com
  • 51.  Treatment and prognosis-supportive treatment.  Remission after a period of months to years.  Serious complication can lead to death. www.indiandentalacademy.com
  • 52. For more details please visit www.indiandentalacademy.com www.indiandentalacademy.com