orl Flashcards
acute atrophic candidiasis
erythematous or stomatitis following antibiotic therapy
clinical signs: red congested swallon mucosa covered by small white zones (pseudomembranous )
located mainly on the tongue and hard palate
{depapilation of the tongue is prsent }
C.T: direct microscopic examination , culture media
treatment: topical or systemic anti fungal therapy
PEMPHIGUS VEGETANTS
resents two clinical features: 1. evolutionary-nature; 2. appearance of grain or hypertrophic vegetationon the surface of post-bullous erosive lesions.
The initial rash is identical with that of pemphigus vulgaris.
The involvement of the oral mucosa is rare,
but vegetating lesions occur mainly on the vermillion and commissures. .
c. t: Immunofluorescence tests are identical to those of pemphigus vulgaris.
treatment: same as pemphigus vulgaris
major aphthous
reticular lichen planus
reticularform of lichen planus
reticular lichen planus
most common tupe of planus
common location: jugal mucosa bilateral , but also on lips tongue , gingiva
clinical aspect: keratotic lesions called wicham straiae (so many)
C.test: histopathalogical test
immunofluorocense tet
treatment: assymptomatic lesion>>no treatment needed
symptomatic lesion>>>> systemic cyclosporine
major aphthous
primary tuberculosis
Ulceration appears as a little deep lesion with thin borders, red-purple surface and painful.It is mainly located on the:-gingiva-vestibular cavities-sore mucosa surrounding the teeth-post-extraction area.
Complementary examinations histopathologicexamination tuberculin I.D.R.inoculation on culture mediathoracic radiography showing pulmonary lesions
- and biopsy and Tuberculin intradermaltest turns out positive after 20 days of disease evolution
Primary tuberculosis-ulceration+lymphadenopathy
General treatment :contains anti inflammatory drugs, painkillers and tuberculostatic medication
ACTINOMYCOSIS
More than 50% of cases are located on the cervical-facial part of the body
from a small circumscribed noduleto swellings that affect large areas of tissue and even pseudo-tumoral forms
clinical aspects, microbiologic and histologicalexamination
treatment: antibiotic therapy associated with surgical intervention
minus aphthae
frictional hyperplasia
actinic chelitis
SECONDARY TUBERCLUSIS……….Tuberculosis gumma is mainly located on the anterior half of the tongue.As in syphilitic gumma there are four stages: rawness, softening, ulceration and healing.During the first stage it can be shallow or profound and it may have a tumor like aspect.Later, it shows on the dorsal part of the tongue. After the softening stage it ulcerates and it eliminates the yellow-green purulent content.
Treatment is surgical during the first stage and it consists of excisionand suture; during the cold abscess stage it is preferred to drain the content of the lesion and to undergo a specific tuberculostatic medication
gumma
TERTIARY SYPHILIS
1/3 OF 1/3 cases of syphilis will develop the third
It is mainly characterized by:
neurological manifestations
cardiovascular lesions
lesions of the skin and mucosa
bone lesions
3 LESIONS
GUMA >>>> HARD PALATE FISTUA
From an evolution point of view, gumma knows 4 stages:-rawness-softening-ulceration-healing
The size of the lesion varies from 1 to 10 cm.It is most frequently located on the hard palate
ATROPHIC GLOSITIS
is the consequence of a vasculitis that evolves into an obliteratingendarteritis, causing the atrophy of both the mucosa and the muscle of the tongue. Consequently, the dorsal part of the tongue becomes neat and atrophic.
SCLROTIC GLLOSITIS
is the result of tongue becoming deformed once a gumma has healed. Consequently, the tongue has a lobulated appearancewith deep and irregular ditches
Herpangina
ZahorskyDisease
The characteristic lesions affect:soft palateuvulatonsilsanterior pillarsposterior pharynxVesicles are small and numerous and they break down into painful ulcerations, not very deep, that will heal in 7-12 days.The absence of lesions on lips, gums and palate is significant for this disease and for the consequent diagnosis.
Positive diagnosisis based on unique clinical criteria and no further complementary examinations are required.
Treatment: is supportive.
Varicella (chickenpox)
Oral lesionsare common and mostly located on the palate and lips and sometimes they precede the skin
lesions. Vesicles are small (3-4 mm) and quickly turn into erosions surrounded by an erythematous halo.
Positive diagnosisis based on epidemiologic data and clinical manifestations.
Treatmentis supportive: rigorous body hygiene, mint alcohol 1% or mint talcwill help prevent pruritus, antihistamines and antipyretics.Children and teenagers will not be treated with aspirin because of the high risk of developing Reye syndrome(a rare, yet severe condition causing irreversible lesions such as acute encephalopathyand hepatic fatty degeneration).Antiseptic solutions are recommended for oral lesions.Antiviral medication including Acyclovir, Vidarabine or Interferonis recommended only in patients with immunodeficiency.Prevention of chickenpox can be obtained with the varicella vaccine that gives 100% protection to the virus
labial herpes
Clinical aspect:-a discrete congestion and an edema of the vermilion border and the surrounding skin, -vesicle eruption, vesicle has 1-3 mm diameter, while the lesion reaches 1 –2 cm,-people with immunodeficiency will present larger lesions associated with discomfort and physiognomic alterations.The vesicles break down into ulcerations that will get covered by dry scabs and eventually heal in the course of 1 –2 weeks
Positive diagnosis -is based on clinical examination
TreatmentLocal therapy –acyclovir (Zovirax,Euvirox) 5%-ointment x5/day-penciclovir(Denavir)1% ,at 2h,4days-vidarabine3%-idoxuridine3%Systemic -valacyclovir(Valtrex) 4 g ( 2gx2)one doseProphylactic –ointments based on zinc oxide or titanium dioxide
BULLOUS PEMPHIGOID
Oral lesions usually occur after the skin ones and they can not be distinguished clinically from those of scarring pemphigoid. The bullas and erosion generally occur on the fixed gums, but may also involve othermucosal areas (soft palate, buccal mucosa, oral floor). Healing is without scars
Complementary tests:Histopatological examDirectimmunofluorescenceIndirect immunofluorescence
Treatament:systemic corticosteroidssulfones, sulfonamides and antibiotics (tetracycline, erythromycin)corticosteroids + immunosuppressives
MECHANICAL ULCER
ATIONS:
Most ulcers occurring on the soft parts of the oral cavity are of mechanical nature and are
located on the
lower lip, tongue, buccal mucosa and oral floor
. These ulcers are not related to genderor age.
In newborns with natal or neonatal teeth the traumatic ulceration that usually occurs on the ventral surface of the tongue 1/3 anterior is called Riga Fede disease
.Root residues, sharp edges of the teeth,periodontal carious lesions, crochets from partial dental prosthesis, malpositioned teeth, unstable full dental prosthesis, etc could determine acute or chronic traumatic ulcerations.
In less common circumstances in people suffering from psychic conditions, lesions can be
selfinduced by abnormal
behaviours such as lip, tongue or cheek biting. Traumatic ulcerations can also be iatrogenic. Thus, ulcerations of mucosa could be caused while removing cotton rolls or compresses from the mucosa, while pressing too hard the saliva vacuum or by accidental injury of soft mucosa with mills or disks.
SECONDARY TUBERCLUSIS……….Tuberculosis gumma is mainly located on the anterior half of the tongue.As in syphilitic gumma there are four stages: rawness, softening, ulceration and healing.During the first stage it can be shallow or profound and it may have a tumor like aspect.Later, it shows on the dorsal part of the tongue. After the softening stage it ulcerates and it eliminates the yellow-green purulent content.
Treatment is surgical during the first stage and it consists of excisionand suture; during the cold abscess stage it is preferred to drain the content of the lesion and to undergo a specific tuberculostatic medication
TERTIARY SYPHILIS
1/3 OF 1/3 cases of syphilis will develop the third
It is mainly characterized by:
neurological manifestations
cardiovascular lesions
lesions of the skin and mucosa
bone lesions
3 LESIONS
GUMA >>>> HARD PALATE FISTUA
From an evolution point of view, gumma knows 4 stages:-rawness-softening-ulceration-healing
The size of the lesion varies from 1 to 10 cm.It is most frequently located on the hard palate
ATROPHIC GLOSITIS
is the consequence of a vasculitis that evolves into an obliteratingendarteritis, causing the atrophy of both the mucosa and the muscle of the tongue. Consequently, the dorsal part of the tongue becomes neat and atrophic.
SCLROTIC GLLOSITIS
is the result of tongue becoming deformed once a gumma has healed. Consequently, the tongue has a lobulated appearancewith deep and irregular ditches
SECONDARY TUBERCULOSIS
herpetiform aphtus ulceration
dooo nooot confuse this and primary herpes simplex since the lesions are not like vesicles with borders!!!
Erythema multiforme –minor form
ERYTHEMA MULTIFORME(minor form)
initially flat, round, having a dark red color. Later,these can develop into a bullawith a necrotic center. Sometimes, skin lesions appear with characteristic appearance „in target” or „herpes iris.
In oral cavity, lesions appear as erythematous patches, which subsequently by epithelial necrosis, , with irregular edges. Hemorrhagic crusts appear on vermillion, often with symmetrical distribution include: labial mucosal side, buccal mucosa, oral floor, soft palate, tongue. Painful ulcerative lesionsmay appear in relapsessimilarto the initial episode or erythematous patches with limited ulceration and reduced symptoms.
Positive diagnosis isbased on clinical data.The histopathological exam and the immunopathological tests are not specificfor erythema multiforme. However, the presence of Ig M, the complement and fibrin in dermal vessel walls, is an indication of immune-complex vasculitis and implicitly is the cause of erythema multiforme.
Treatment: in common forms of the disease, the topical administration of corticosteroids, antibiotics, analgesics, antifungals has been recommended. In severe cases, average doses of systemic corticosteroidsand high doses of antibiotics are recommended. The treatment is the prerogative of the dermatologist
hairy tongue,
heredity, emotional stress, imunodeficiecy
its benign and its dekeratinization of the tongue
Usually the condition is located on the 2/3 dorsal and the lateral sides of the tongue
round ovale , erythematous border with white peripheral zone…….. more importantly it changes its appearance every 12-24 hours
no complementary test
treatmnt: just inform the patient that its a benign situation/ in caseof painful fissures use antifungal and topical steroids
acute pseudomembranous candidiasis
in this situation the mouth is dry and burning with dysphagia
white or white yellowish patches that can be easily wiped away to reveal the erythematous beneath
located : can be seen everywhere in oral cavity but mostly palate , tongue , jugal mucosa
C.T: based on clinical examination and culture media on different media and direct microscopic examination
hand foot mouth disease
it is caused by Coxsackie virus
Intra-oral eruption is characterized by the occurrence of small vesicles, not more than 5 –10, that blister into superficial ulcerations with 2-4 mm diameter and are circumscribed by an erythematous halo. eventually be covered by dry scabs.
Most common locations are:tonguepalatebuccal mucosalips.
Positive diagnosisis based on clinical data
Treatmentis supportive(antipyretics and topic anesthetics
actinic chelitis
pernicious anemia (fatal)
mostly happens on the tongue associated with pain,burning sensation , loss of taste, red glossy aspect and smooth depapillated <<hunter-glossitis>> aspect
the rst of the oral mucosa is pale.
C,T : haemoglubin and serum vit b12 test
myelogram (bone marrow)
erythrocytes
treatment:topical applications of benadryl or viscous xylocaine 2% rinse , several times a day
ACTINOMYCOSIS
More than 50% of cases are located on the cervical-facial part of the body
from a small circumscribed noduleto swellings that affect large areas of tissue and even pseudo-tumoral forms
clinical aspects, microbiologic and histologicalexamination
treatment: antibiotic therapy associated with surgical intervention
NOMA (cancrum oris, gangrenous stomatitis, necrotic stomatitis)
ask if the patient can have AIDS ? since the clinical aspects are very much like the acute and chronic lukemia….
From a clinical point of view, the disease can start as an acute ulcerative-necrotic gingivitis
Necrotic areas could also occur on the soft areas as a consequence of traumatic lesions without any continuity to the gingiva
Gangrenous ulcerations are covered by fibrinoid white-grey deposits
Treatment: consists of preventing and eliminating the predisposing factors, diet rebalancing,
hydration and antibiotic therapy (penicillin and metronidazole). Locally, the necrotic tissue will be removed and reconstructive surgery will be performed one year later
In the absence of any treatment, mortality rate reaches 95%,
c.t : based on clinical aspect and culture media since the etiology of the disease is bacterial
Varicella (chickenpox)
Oral lesionsare common and mostly located on the palate and lips and sometimes they precede the skin
lesions. Vesicles are small (3-4 mm) and quickly turn into erosions surrounded by an erythematous halo.
Positive diagnosisis based on epidemiologic data and clinical manifestations.
Treatmentis supportive: rigorous body hygiene, mint alcohol 1% or mint talcwill help prevent pruritus, antihistamines and antipyretics.Children and teenagers will not be treated with aspirin because of the high risk of developing Reye syndrome(a rare, yet severe condition causing irreversible lesions such as acute encephalopathyand hepatic fatty degeneration).Antiseptic solutions are recommended for oral lesions.Antiviral medication including Acyclovir, Vidarabine or Interferonis recommended only in patients with immunodeficiency.Prevention of chickenpox can be obtained with the varicella vaccine that gives 100% protection to the virus
white sponge nevous
discoid lupus erythematosous
herpetiform aphtous ulcers
minus aphthae
chronic atrophic candidiasis (prosthesis candidiasis)
LOCATED MAINLY ON THE HARD PALATE
HAS 3 stages: 1st:red hyperemic punctiform zones on the salivary glandsholes 2nd:diffuse erythema on the hard palate 3rd: papilary hyperplasia
pain and burning is common
C.T : immunofluorocense examination
treatment: nystatin sol 100.000u/ml 4times a day
amphotericin B suspension 100mg/ml 4 times a day
miconazole gel 2% 4*aday
new prosthetic device , rigorous oral hygiene
remove the prosthetic at nights
hand foot mouth disease
it is caused by Coxsackie virus
Intra-oral eruption is characterized by the occurrence of small vesicles, not more than 5 –10, that blister into superficial ulcerations with 2-4 mm diameter and are circumscribed by an erythematous halo. eventually be covered by dry scabs.
Most common locations are:tonguepalatebuccal mucosalips.
Positive diagnosisis based on clinical data
Treatmentis supportive(antipyretics and topic anesthetics
pigmented lichen planus lesions
pigmented papules with keratotic white lesions disposed in a reticular pattern.
C.T : histopathalogical
immunofluorescense can be useful
treatment: has no specific treatment
SECONDARY SYPHILIS
reticular lichen planus
most common tupe of planus
common location: jugal mucosa bilateral , but also on lips tongue , gingiva
clinical aspect: keratotic lesions called wicham straiae (so many)
C.test: histopathalogical test
immunofluorocense tet
treatment: assymptomatic lesion>>no treatment needed
symptomatic lesion>>>> systemic cyclosporine
acute atrophic candida
acute atrophic candidiasis
erythematous or stomatitis following antibiotic therapy
clinical signs: red congested swallon mucosa covered by small white zones (pseudomembranous )
located mainly on the tongue and hard palate
{depapilation of the tongue is prsent }
C.T: direct microscopic examination , culture media
treatment: topical or systemic anti fungal therapy
chronic leukemia
clinical: less severe than the acute form
pale oral mucosa , sometimes associated with ulcerated causes, gingival hyperplasia
leukemic nodules can be observed on the palatinenfiber-mucosa
C,T : peripheral blood analysis
medulograma>>>bone marrow analysis tosee if there is any leukemic cells
also send the patient to th haemotologist
treatment:like the acute one >>>>
send tohaemotologist
thrombin sponge in case of bleeding
2ND syphilis
2ND SYPHiLIS
dark-red macular eruption -syphilitic rosella, located mainly on the posterior side of the oral cavity. Further on, there will appearmucous plaquesrepresenting the most frequent manifestation of thisstage. From a clinical point of view, they are oval, slightly bolded and turning into opalescent, white-grey plaques and surrounded by an erythematous margin. The superficial layer is removed and slightly painful, possibly bleeding ulcers are revealed
Laboratory examinations-serologic tests are positive-dark field microscopic examination and immunofluorescence examination
treatment : same as other syphilises
behcet syndrome
acute pseudomembranous candidiasis
in this situation the mouth is dry and burning with dyphagia
white or white yellowish patches that can be easily wiped away to reveal the erythematous beneath
located : can be seen everywhere in oral cavity but mostly palate , tongue , jugal mucosa
C.T: based on clinical examination and culture media on different media and direct microscopic examination
Pemphigus vulgaris
Vesicles or bullaspainful erosions that tend to peripheral expansion Eruptions.
Characteristic signs: Nicolsky, Asboe-Hansen
Lesions can be found in any area of the oral mucosa, with a predilection for:-palate -jugalmucosa -lower lip -oral floor
complementary test: Cytological examination -shows the presence of typical acantholyticcells(Tzanckcells) with large, hyperchromaticnuclei.Histopathologicalexaminationfrom a biopsytaken from a perilesionalskin shows the integrity of basal layer and the acantholysisof the spinouslayer.Direct immunofluorescenceIndirect immunofluorescence
Treatament :
sistemic: high doses of prednisone(Prednison) on alternate days with immunosuppressants:Azathioprine, Methotrexate, Cyclophosphamideparenteral administration of gold salts, etretinate, dapsoneand plasmapheresis( in patients refractory to corticosteroid therapy)
local: a rigorous local hygiene ,
mouth rinses with antiseptic solutions-Clorhexidine-0,2%
Topical anesthetics(Lidocaine 5%)
Topical steroids:ELOCOM-crème:3,4 apl./day
NOMA (cancrum oris, gangrenous stomatitis, necrotic stomatitis)
ask if the patient can have AIDS ? since the clinical aspects are very much like the acute and chronic lukemia….
From a clinical point of view, the disease can start as an acute ulcerative-necrotic gingivitis
Necrotic areas could also occur on the soft areas as a consequence of traumatic lesions without any continuity to the gingiva
Gangrenous ulcerations are covered by fibrinoid white-grey deposits
Treatment: consists of preventing and eliminating the predisposing factors, diet rebalancing,
hydration and antibiotic therapy (penicillin and metronidazole). Locally, the necrotic tissue will be removed and reconstructive surgery will be performed one year later
In the absence of any treatment, mortality rate reaches 95%,
c.t : based on clinical aspect and culture media since the etiology of the disease is bacterial
behcet syndrom
plummer-vinson Iron def anemia
angular chelitis can be present mostly
general signs: weight loss
pale face , dysponea , headache, hair and nail fragility
oral signs:burning sensation of the tongue, atrophy of filliform and fungiform papilla , dorsal surface of the tongue becomes red-glossy and smooth
*******
in case of plummer-vinson syndrom and hyperchromic anemia oral manifestations are accompanied by dysphagia caused by painful erosions of esophagus
C.T srium iron test
haemoglubin
hematocrit(low level)
treatment:m increasing the iron through supplements and real food
major aphtae
ertholeukoplakia
verroucous lekoplakia
FRICTIONAL HYPERPLASIA (traumatic keratosis)
: lips, lateral margins of tongue, jugal mucosa along the occlusion plane of teeth
an isolated, white and thickened patch on the mucosa due to orthodontic appliance , eating with odontholous spaces , cheek biting
no complementary test
no treatment needed
acute pseudomembranous candidiasis
in this situation the mouth is dry and burning with dyphagia
white or white yellowish patches that can be easily wiped away to reveal the erythematous beneath
located : can be seen everywhere in oral cavity but mostly palate , tongue , jugal mucosa
C.T: based on clinical examination and culture media on different media and direct microscopic examination
frictional hyperplasia
Primary Herpetic Gingivostomatitis
The oral mucosa is congested and edematous with many vesicles grouped in bunches. These vesicles will break down the next 24 hours into superficial, painful ulcerations covered by dark grey pseudo-membranes surrounded by an erythematous halo , Ulcerations will heal in 10 –14 days, leaving no marks.
Histopathologic examination: .Culture Antibodies titer .Immunologic testing using DNA hybridization
TreatmentSevere casesAcyclovir-systemic or suspension-200mg/5mlRodilemidi.m. 10 days/ month -3 monthsMild and medium forms-symptomaticAntipyreticsLiquid diet (for hydration and electrolyte balance)Topic anesthetics(dyclorinehydrochloride 0,5-1%,benzocainegel 20%, xylocaineviscous 2%, lidocaine5%).Rigorous oral hygiene with antiseptic solutions (Clorhexidine0, 4%) or local application with gentian violet 2% or methyleneblue 1%.
MECHANICAL ULCER
ATIONS:
Most ulcers occurring on the soft parts of the oral cavity are of mechanical nature and are
located on the
lower lip, tongue, buccal mucosa and oral floor
. These ulcers are not related to genderor age.
In newborns with natal or neonatal teeth the traumatic ulceration that usually occurs on the ventral surface of the tongue 1/3 anterior is called Riga Fede disease
.Root residues, sharp edges of the teeth,periodontal carious lesions, crochets from partial dental prosthesis, malpositioned teeth, unstable full dental prosthesis, etc could determine acute or chronic traumatic ulcerations.
In less common circumstances in people suffering from psychic conditions, lesions can be
selfinduced by abnormal
behaviours such as lip, tongue or cheek biting. Traumatic ulcerations can also be iatrogenic. Thus, ulcerations of mucosa could be caused while removing cotton rolls or compresses from the mucosa, while pressing too hard the saliva vacuum or by accidental injury of soft mucosa with mills or disks.
2NDARY SYPHILIS
2ND SYPHiLIS
dark-red macular eruption -syphilitic rosella, located mainly on the posterior side of the oral cavity. Further on, there will appearmucous plaquesrepresenting the most frequent manifestation of thisstage. From a clinical point of view, they are oval, slightly bolded and turning into opalescent, white-grey plaques and surrounded by an erythematous margin. The superficial layer is removed and slightly painful, possibly bleeding ulcers are revealed
Laboratory examinations-serologic tests are positive-dark field microscopic examination and immunofluorescence examination
treatment : same as other syphilises
scarlet fever
cold seasons and children
General symptoms: shiver, vomiting, nausea, headache
fver, lymph adenopathy
two stages: 1” Enanthema : exfoliating glossitis with angina ( suffocative pain) associated with erythema of tonsills pillars , ovula, soft palate, not on the hard palate.<< tongue becomes extremely congested and it gets redwith glossy aspect and shows the CAT TONGUE aspect. heals in10-12 days
2” Exanthema : dyfussed erythema on the skin giving skin a harsh aspect .
complementary test : culture of type A streptococcus
treatment: antibiotics erythromycin , penicillin
nicotinic stomatitis
verroucous leukoplakia
secondary tuberculosis
Kaposi’s sarcoma
its an endothelial cells malignancy
4 types: classic kaposi’s sarcoma (skin lesion)
african kaposi’s sarcoma(skin lesions)
aquired kaposi’s sarcoma (skin)
EPIDEMIC KAPOSI’S SARCOMA :OVER 50% of the patients showed oral manifestation
lesion has 3 stages>>> first its assymptomatic erythematous that dont disappear after pressure >>>then it gets bigger and it will turn into red-blue or purple papular lesion>>> and at the advanced stages sarcoma appears purplish,blue nodules that can bleed and its painful.
located on jugal mucosa, dorsal face of the tongue, half of the palate, on the gingiva
C.T is biopsy
treatment: radiotherapy surgery, chemotherapy Co2 laser
MECHANICAL ULCER
ATIONS:
Most ulcers occurring on the soft parts of the oral cavity are of mechanical nature and are
located on the
lower lip, tongue, buccal mucosa and oral floor
. These ulcers are not related to genderor age.
In newborns with natal or neonatal teeth the traumatic ulceration that usually occurs on the ventral surface of the tongue 1/3 anterior is called Riga Fede disease
.Root residues, sharp edges of the teeth,periodontal carious lesions, crochets from partial dental prosthesis, malpositioned teeth, unstable full dental prosthesis, etc could determine acute or chronic traumatic ulcerations.
In less common circumstances in people suffering from psychic conditions, lesions can be
selfinduced by abnormal
behaviours such as lip, tongue or cheek biting. Traumatic ulcerations can also be iatrogenic. Thus, ulcerations of mucosa could be caused while removing cotton rolls or compresses from the mucosa, while pressing too hard the saliva vacuum or by accidental injury of soft mucosa with mills or disks.
acute atrophic candidiasis
acute atrophic candidiasis
erythematous or stomatitis following antibiotic therapy
clinical signs: red congested swallon mucosa covered by small white zones (pseudomembranous )
located mainly on the tongue and hard palate
{depapilation of the tongue is prsent }
C.T: direct microscopic examination , culture media
treatment: topical or systemic anti fungal therapy
chronic atrophic candidiasis (prosthesis candidiasis)
LOCATED MAINLY ON THE HARD PALATE
HAS 3 stages: 1st:red hyperemic punctiform zones on the salivary glandsholes 2nd:diffuse erythema on the hard palate 3rd: papilary hyperplasia
pain and burning is common
C.T : immunofluorocense examination
treatment: nystatin sol 100.000u/ml 4times a day
amphotericin B suspension 100mg/ml 4 times a day
miconazole gel 2% 4*aday
new prosthetic device , rigorous oral hygiene
remove the prosthetic at nights
infectious mono neucleosis(kissing disease)
Epstain barr virus
transmitted through saliva
generally it has fever, pharyngitis , tonsilitis, lymh adenopathy, weakness , malaise
orally : petechiae (dark red dots ) in purpura is like rash or dark red bleeding dots
on the SOFT and HARD palate
can be associated with necrotsing acute gingivitis
diffused erythema of the oram mucosa
C,T test of specific antibodies
treatment: antiseptic adn topical anesthetic agents (supportive)
The Stevens-Johnson Syndrome
is a severe form of erythema multiforme caused by drugs
Oral mucosaisconstantly involved. Extensive superficial ulcers, painful, covered by gray-white or bleeding pseudomembranes are preceded by bubbles. Lips are covered by characteristic hemorrhagic crusts. Erosions of other mucosal membranes can appear simultaneously. Ocular lesionsmanifested by conjunctivitis, corneal ulceration, anterior uveitis can cause corneal opacity, symblepharons and even blindness. Cutaneous manifestationsmay occur as a typical maculopapular rash of erythema multiforme, but more frequently bullous lesions or ulcers are met. Evolution and prognosis: there is a 5-15% mortality in the absence of treatment
Positive diagnosis is based on clinical data
Treatment-common forms: topical administration of corticosteroids, antibiotics, analgesics, antifungals-severe cases :high doses of systemic corticosteroids and antibiotics.
nodular leukoplakia
Herpangina
ZahorskyDisease
The characteristic lesions affect:soft palateuvulatonsilsanterior pillarsposterior pharynxVesicles are small and numerous and they break down into painful ulcerations, not very deep, that will heal in 7-12 days.The absence of lesions on lips, gums and palate is significant for this disease and for the consequent diagnosis.
Positive diagnosisis based on unique clinical criteria and no further complementary examinations are required.
Treatment: is supportive.
major aphthous
Herpes panaritium
acute primary or secondary infection of finger (fingers) with HSV-The vesicle-ulcerative eruption is associated with pain, congestion and swelling, and eventually with axillaryor epitrocheallymphadenopathy.-The duration of such lesion lasts from 4 to 6 week
wearing surgical gloves,will prevent the risk of contacting theinfection
PRIMARY SYPHILIS
Treponema pallidum(etyiology)
after lips and commissures, are:-tongue-palate-gingiva (the incisive –caninearea)-tonsils
From a clinical point of view, chancre first resembles a macula that progressively turns into an inflammatory papule that quickly erodes and becomes a painless, neat lesion with slightly bold
margins, hard base and surrounded by a red line. The surface of the sore is covered by a grey
exudate that contains numerous treponemes; the sore is highly contagious.
- Chancre usually occurs as a singular sore, although multiple sores are possible
- direct immunofluorescence staining
- .During primary stage of syphilis, serologic tests can turn out negative.
- At the end of the primary stage of syphilis (about a month after inoculation) VDRL (VenerealDisease Research Laboratory), immunofluorescence reaction –FTA –Abs (Fluorescent Treponemal Antibody Absorption) or the TPHA (Treponema palladium haemaglutination assay) turn out positive.
- Treatment:penicillin is the treatment of choice in all stages of syphilis. When there is a case of allergy to penicillin, other types of antibiotics can be prescribed (erythromycin, cephalosporin, tetracycline, and doxycycline)
idiopathic leukoplakia non homo/ erythroleukoplakia
SOLAR CHEILITIS (actinic cheilitis)
scarlet fever
cold seasons and children
General symptoms: shiver, vomiting, nausea, headache
fver, lymph adenopathy
two stages: 1” Enanthema : exfoliating glossitis with angina ( suffocative pain) associated with erythema of tonsills pillars , ovula, soft palate, not on the hard palate.<< tongue becomes extremely congested and it gets redwith glossy aspect and shows the CAT TONGUE aspect. heals in10-12 days
2” Exanthema : dyfussed erythema on the skin giving skin a harsh aspect .
complementary test : culture of type A streptococcus
treatment: antibiotics erythromycin , penicillin
acute pseudomembranous candidiasis
acute pseudomembranous candidiasis
in this situation the mouth is dry and burning with dyphagia
white or white yellowish patches that can be easily wiped away to reveal the erythematous beneath
located : can be seen everywhere in oral cavity but mostly palate , tongue , jugal mucosa
C.T: based on clinical examination and culture media on different media and direct microscopic examination
measles
Koplik’s spots. This is pathognomonic for measles and it consists of 10-12 isolated or grouped lesions on the buccal mucosa (in the region of the last molars); these lesions are very small, slightly bold, they have a white-bluish colour and are surrounded by a red halo. These formations occur 24-48 hours before the exanthema and quickly disappear leaving hemorrhagic spots on the congested mucosa.
Cutaneous rash occurs 3 –4 days after prodromal phase and it is characterisedby a maculo-papular eruption that starts behind the back of the ears and the frontal region; duringthe next 24 hoursit quickly spreadsto cover the rest of the face, neck, torso and extremities
Positive diagnosisis based on clinical symptoms and signs
Treatmentis supportive and it includes:-hygiene and diet regime-antipyretics-painkillers-cough remediesAntibiotics are recommended only when complications occur.
ACTINOMYCOSIS
More than 50% of cases are located on the cervical-facial part of the body
from a small circumscribed noduleto swellings that affect large areas of tissue and even pseudo-tumoral forms
clinical aspects, microbiologic and histologicalexamination
treatment: antibiotic therapy associated with surgical intervention
chronic leukemia
clinical: less severe than the acute form
pale oral mucosa , sometimes associated with ulcerated causes, gingival hyperplasia
leukemic nodules can be observed on the palatinenfiber-mucosa
C,T : peripheral blood analysis
medulograma>>>bone marrow analysis tosee if there is any leukemic cells
also send the patient to th haemotologist
treatment:like the acute one >>>>
send tohaemotologist
thrombin sponge in case of bleeding
2ND SYPHiLIS
dark-red macular eruption -syphilitic rosella, located mainly on the posterior side of the oral cavity. Further on, there will appearmucous plaquesrepresenting the most frequent manifestation of thisstage. From a clinical point of view, they are oval, slightly bolded and turning into opalescent, white-grey plaques and surrounded by an erythematous margin. The superficial layer is removed and slightly painful, possibly bleeding ulcers are revealed
Laboratory examinations-serologic tests are positive-dark field microscopic examination and immunofluorescence examination
treatment : same as other syphilises
behcet syndrom
hand foot mouth disease
it is caused by Coxsackie virus
Intra-oral eruption is characterized by the occurrence of small vesicles, not more than 5 –10, that blister into superficial ulcerations with 2-4 mm diameter and are circumscribed by an erythematous halo. eventually be covered by dry scabs.
Most common locations are:tonguepalatebuccal mucosalips.
Positive diagnosisis based on clinical data
Treatmentis supportive(antipyretics and topic anesthetics
The Stevens-Johnson Syndrome
is a severe form of erythema multiforme caused by drugs
Oral mucosaisconstantly involved. Extensive superficial ulcers, painful, covered by gray-white or bleeding pseudomembranes are preceded by bubbles. Lips are covered by characteristic hemorrhagic crusts. Erosions of other mucosal membranes can appear simultaneously. Ocular lesionsmanifested by conjunctivitis, corneal ulceration, anterior uveitis can cause corneal opacity, symblepharons and even blindness. Cutaneous manifestationsmay occur as a typical maculopapular rash of erythema multiforme, but more frequently bullous lesions or ulcers are met. Evolution and prognosis: there is a 5-15% mortality in the absence of treatment
Positive diagnosis is based on clinical data
Treatment-common forms: topical administration of corticosteroids, antibiotics, analgesics, antifungals-severe cases :high doses of systemic corticosteroids and antibiotics.
acute pseudomembranous candidiasis
in this situation the mouth is dry and burning with dyphagia
white or white yellowish patches that can be easily wiped away to reveal the erythematous beneath
located : can be seen everywhere in oral cavity but mostly palate , tongue , jugal mucosa
C.T: based on clinical examination and culture media on different media and direct microscopic examination
ACUTE PSEUDOMEM CANDIDI
PEMPHIGUS VEGETANTS
resents two clinical features: 1. evolutionary-nature; 2. appearance of grain or hypertrophic vegetationon the surface of post-bullous erosive lesions.
The initial rash is identical with that of pemphigus vulgaris.
The involvement of the oral mucosa is rare,
but vegetating lesions occur mainly on the vermillion and commissures. .
c.t: Immunofluorescence tests are identical to those of pemphigus vulgaris.
treatment: same as pemphigus vulgaris
HERPES zoster
Intraoral eruption is preceded by pain that can mimic pulpitis. Vesicles are grouped in bunches, breaking down after 2-3 days into ulcerations circumscribed by an erithematousborder.Healing process will take 2 –3 weeks leaving no marks.The location of the lesions on one side only is the main clinical sign of herpes zoster
The most frequent complication of this condition is residual trigeminal neuralgia that can last for weeks or months
Positive diagnosis of oral lesions is established following clinical criteria.
TreatmentTargetsthe reduction of the duration of disease,preventing post-herpetic neuralgia the dissemination in patients with immunodeficiency.Acyclovir<50 years old-200 mg x 5/day, 7-10 days>50 years old-800 mg x 5 /day, 7-10 daysCapsaicina–local therapy Xylineor Novocain infiltration on the affected nerve.
SECONDARY SYPHLIS
hairy tongue
hairy tongue,
heredity, emotional stress, imunodeficiecy
its benign and its dekeratinization of the tongue
Usually the condition is located on the 2/3 dorsal and the lateral sides of the tongue
round ovale , erythematous border with white peripheral zone…….. more importantly it changes its appearance every 12-24 hours
no complementary test
treatmnt: just inform the patient that its a benign situation/ in caseof painful fissures use antifungal and topical steroids
Pemphigus vulgaris
Vesicles or bullaspainful erosions that tend to peripheral expansion Eruptions.
Characteristic signs: Nicolsky, Asboe-Hansen
Lesions can be found in any area of the oral mucosa, with a predilection for:-palate -jugalmucosa -lower lip -oral floor
complementary test: Cytological examination -shows the presence of typical acantholyticcells(Tzanckcells) with large, hyperchromaticnuclei.Histopathologicalexaminationfrom a biopsytaken from a perilesionalskin shows the integrity of basal layer and the acantholysisof the spinouslayer.Direct immunofluorescenceIndirect immunofluorescence
Treatament :
sistemic: high doses of prednisone(Prednison) on alternate days with immunosuppressants:Azathioprine, Methotrexate, Cyclophosphamideparenteral administration of gold salts, etretinate, dapsoneand plasmapheresis( in patients refractory to corticosteroid therapy)
local: a rigorous local hygiene ,
mouth rinses with antiseptic solutions-Clorhexidine-0,2%
Topical anesthetics(Lidocaine 5%)
Topical steroids:ELOCOM-crème:3,4 apl./day
herpes zoster
Intraoral eruption is preceded by pain that can mimic pulpitis. Vesicles are grouped in bunches, breaking down after 2-3 days into ulcerations circumscribed by an erithematousborder.Healing process will take 2 –3 weeks leaving no marks.The location of the lesions on one side only is the main clinical sign of herpes zoster
The most frequent complication of this condition is residual trigeminal neuralgia that can last for weeks or months
Positive diagnosis of oral lesions is established following clinical criteria.
TreatmentTargetsthe reduction of the duration of disease,preventing post-herpetic neuralgia the dissemination in patients with immunodeficiency.Acyclovir<50 years old-200 mg x 5/day, 7-10 days>50 years old-800 mg x 5 /day, 7-10 daysCapsaicina–local therapy Xylineor Novocain infiltration on the affected nerve.
thrombocytopenic purpura
petechiae, ecchymoses and haematoma on the buccal mucosa and palate associated with spontanious bleeding from the gingiva
C.T: MYELOGRAM
PLATELET TEST
COAGULATION TIME
TREATMENT: systematic steroids
splenectomy
platelet transfusion
herpetiform aphtous ulcers
ERYTHEMA MULTIFORME(minor form)
initially flat, round, having a dark red color. Later,these can develop into a bullawith a necrotic center. Sometimes, skin lesions appear with characteristic appearance „in target” or „herpes iris.
In oral cavity, lesions appear as erythematous patches, which subsequently by epithelial necrosis, , with irregular edges. Hemorrhagic crusts appear on vermillion, often with symmetrical distribution include: labial mucosal side, buccal mucosa, oral floor, soft palate, tongue. Painful ulcerative lesionsmay appear in relapsessimilarto the initial episode or erythematous patches with limited ulceration and reduced symptoms.
Positive diagnosis isbased on clinical data.The histopathological exam and the immunopathological tests are not specificfor erythema multiforme. However, the presence of Ig M, the complement and fibrin in dermal vessel walls, is an indication of immune-complex vasculitis and implicitly is the cause of erythema multiforme.
Treatment: in common forms of the disease, the topical administration of corticosteroids, antibiotics, analgesics, antifungals has been recommended. In severe cases, average doses of systemic corticosteroidsand high doses of antibiotics are recommended. The treatment is the prerogative of the dermatologist
major aphtae
. Secondary tuberculosis :ulcerationgummatuberculosis lupus
Ulceration occurs once the infection has spread through saliva. The most frequent location is on the dorsal part of the tongue, followed by the palate, buccal mucosa, gingiva and lips.Typical lesions have 1 -5cm diameter, irregular borders andgranular surface and are covered by a yellow deposit. Sometimes, at the border of the lesions small yellow nodules are visible (representing calcified tubercles) and are called Trélat granulations.
Histopathologicexamination .Tuberculin I.D.R.-Inoculation on culture media-Thoracic radiography
Localtreatment consists of:-hygiene of oral cavity-anti inflammatory drugs-painkillers
a dark-red macular eruption -syphilitic rosella, located mainly on the posterior side of the oral cavity
dark field microscopic examination and immunofluorescence examination
TREATMENT PENICILIN
2NDSARYSYPHILIS
2ND SYPHiLIS
dark-red macular eruption -syphilitic rosella, located mainly on the posterior side of the oral cavity. Further on, there will appearmucous plaquesrepresenting the most frequent manifestation of thisstage. From a clinical point of view, they are oval, slightly bolded and turning into opalescent, white-grey plaques and surrounded by an erythematous margin. The superficial layer is removed and slightly painful, possibly bleeding ulcers are revealed
Laboratory examinations-serologic tests are positive-dark field microscopic examination and immunofluorescence examination
treatment : same as other syphilises
discoid lupus erythematosous
major aphthous
sclerotic glossitis >>>>>median rhomboid glossitis
median rhomboid glositis
is a kind of chronic candidiasis
central papillary atrophy of the tongue
clinicalfeatures: first soft red denudated patch located on the median line of the dorsal side of the tongue ,,,,,,,,,,,,,,,,,later it gets hard and lobulated ,,,,,it is - cm oval or rhombic with rounded borders
sclerotic glossitis
minor aphthae
female population and young adults
burning sensations, paresthesia or local hyperesthesia 24-48 hours prior
round or oval shape and less than 1 cm
very painful, covered by a white-yellowish necrotic tissue/ well circumscribed, with a specific erythematous hallo
Their most common locations are: - labial mucosa - the margins and ventral surface of the tongue - buccal mucosa - vestibule of the mouth - floor of the mouth
Treatment: anti-inflammatory agents kenlog
oral antiseptic solutions LISTERINE®
antibiotic with tetracyline >>>> achromycine
analgesic>>>xylocaine
mandatory to eliminate all local sources of irritation and a thorough oral hygiene will be instituted, together with complete avoidance of spicy, acid or irritating foods and allergenic agents
acute atrophic candidiasis
erythematous or stomatitis following antibiotic therapy
clinical signs: red congested swallon mucosa covered by small white zones (pseudomembranous )
located mainly on the tongue and hard palate
{depapilation of the tongue is prsent }
C.T: direct microscopic examination , culture media
treatment: topical or systemic anti fungal therapy
scarlet fever
cold seasons and children
General symptoms: shiver, vomiting, nausea, headache
fver, lymph adenopathy
two stages: 1” Enanthema : exfoliating glossitis with angina ( suffocative pain) associated with erythema of tonsills pillars , ovula, soft palate, not on the hard palate.<< tongue becomes extremely congested and it gets redwith glossy aspect and shows the CAT TONGUE aspect. heals in10-12 days
2” Exanthema : dyfussed erythema on the skin giving skin a harsh aspect .
complementary test : culture of type A streptococcus
treatment: antibiotics erythromycin , penicillin
BULLOUS PEMPHIGOID
Oral lesions usually occur after the skin ones and they can not be distinguished clinically from those of scarring pemphigoid. The bullas and erosion generally occur on the fixed gums, but may also involve othermucosal areas (soft palate, buccal mucosa, oral floor). Healing is without scars
Complementary tests:Histopatological examDirectimmunofluorescenceIndirect immunofluorescence
Treatament:systemic corticosteroidssulfones, sulfonamides and antibiotics (tetracycline, erythromycin)corticosteroids + immunosuppressives
secondary herpetic stomatitis
numerous vesicles grouped in bunches, most commonly located on the hard palate and the gingival fiber-mucosa During the next few hours vesicles will break down into ulcerations (1-3 mm diameter) that will spontaneously heal the next 7-10 days, leaving no visible marks.
Differential diagnosisincludes:Recurrent aphthae(recurrent herpetic aphthous stomatitis)
Treatmentis supportive. Acyclovir is efficient when administered systematically(200mg x5/7 days)and it prevents recurrence, although it is not to be used in occasional or minor manifestations of the condition.Antiseptic solutions (Clorhexidine0, 2%)
c.t : no need, based on clinical examination
bechet syndrome
white necrotic ulcers covered by serous exudates, oval ulcers, can be supeficial or profoud,bright red margins
frequent location is on: - lips - gingiva - buccal mucosa - tongue
without leaving any scars,
complementary test:Histopathologic examination
serological examinations
One particularity of Behçet disease is the hypersensitivity of the skin to needle sting that manifests as an erythemal-papular reaction, followed by the formation of a sterile pustule.
treatment: minor>>>>>>s topic steroids administration, painkillers and non-steroid anti-inflammatory medication.
major>>>>>>>>>>>immunosupression meds like corticosteroids(levamisol)
Primary Herpetic Gingivostomatitis
The oral mucosa is congested and edematous with many vesicles grouped in bunches. These vesicles will break down the next 24 hours into superficial, painful ulcerations covered by dark grey pseudo-membranes surrounded by an erythematous halo , Ulcerations will heal in 10 –14 days, leaving no marks.
Histopathologic examination: .Culture Antibodies titer .Immunologic testing using DNA hybridization
TreatmentSevere casesAcyclovir-systemic or suspension-200mg/5mlRodilemidi.m. 10 days/ month -3 monthsMild and medium forms-symptomaticAntipyreticsLiquid diet (for hydration and electrolyte balance)Topic anesthetics(dyclorinehydrochloride 0,5-1%,benzocainegel 20%, xylocaineviscous 2%, lidocaine5%).Rigorous oral hygiene with antiseptic solutions (Clorhexidine0, 4%) or local application with gentian violet 2% or methyleneblue 1%.
erythroleukoplakia
nodular leukoplakia
Primary Herpetic Gingivostomatitis
The oral mucosa is congested and edematous with many vesicles grouped in bunches. These vesicles will break down the next 24 hours into superficial, painful ulcerations covered by dark grey pseudo-membranes surrounded by an erythematous halo , Ulcerations will heal in 10 –14 days, leaving no marks.
Histopathologic examination: .Culture Antibodies titer .Immunologic testing using DNA hybridization
TreatmentSevere casesAcyclovir-systemic or suspension-200mg/5mlRodilemidi.m. 10 days/ month -3 monthsMild and medium forms-symptomaticAntipyreticsLiquid diet (for hydration and electrolyte balance)Topic anesthetics(dyclorinehydrochloride 0,5-1%,benzocainegel 20%, xylocaineviscous 2%, lidocaine5%).Rigorous oral hygiene with antiseptic solutions (Clorhexidine0, 4%) or local application with gentian violet 2% or methyleneblue 1%.
Kaposi’s sarcoma
its an endothelial cells malignancy
4 types: classic kaposi’s sarcoma (skin lesion)
african kaposi’s sarcoma(skin lesions)
aquired kaposi’s sarcoma (skin)
EPIDEMIC KAPOSI’S SARCOMA :OVER 50% of the patients showed oral manifestation
lesion has 3 stages>>> first its assymptomatic erythematous that dont disappear after pressure >>>then it gets bigger and it will turn into red-blue or purple papular lesion>>> and at the advanced stages sarcoma appears purplish,blue nodules that can bleed and its painful.
located on jugal mucosa, dorsal face of the tongue, half of the palate, on the gingiva
C.T is biopsy
treatment: radiotherapy surgery, chemotherapy Co2 laser
discoid lupus erythematosous
acute leukemia
clinical signs: hyperplastic swelling of vestibular and oral side of the mouth , pale or purplish gingiva , gingival hyperplasia, dental mobility , tonsil hypertrophy
C.T lab examination of the peripheral blood and bone marrow myelogram or medulogram >>>leukemic cells differentiation
treatment: send the patient to a haemotologist …. any dental procedure needs the approval or presence of the haemotologist.
thrombin sponges in case of gingival bleeding.
Late congenital syphilis occurs in children aged between 6 and 15
ogival palatesaddle nosefrontal bossingHutchinson’s triad is characterized by:interstitial keratitislabyrinthine deafnessdental dysplasia or hypoplasia
From a clinical point of view, the permanent upper central incisors have a conical shape, while the margin is peg-shaped. Lateral incisors can present the same abnormalities, although less severe.The orientation on the arcade is also abnormal and the longitudinal axis is convergent towards the free margin.Hypoplasia of the enamel can equally interestthe permanent molars, especially the first inferior molars that present multiple cusps and thus resulting a mulberry-like aspect (Moon molars).
Positive diagnosis is based on the clinical examinationand serologic testing
treatment: Penicilin G
secondary tuberculosis
hairy tongue
hairy tongue,
heredity, emotional stress, imunodeficiecy
its benign and its dekeratinization of the tongue
Usually the condition is located on the 2/3 dorsal and the lateral sides of the tongue
round ovale , erythematous border with white peripheral zone…….. more importantly it changes its appearance every 12-24 hours
no complementary test
treatmnt: just inform the patient that its a benign situation/ in caseof painful fissures use antifungal and topical steroids
???? Homogenous leukoplakia !!!!
idiopathic leukoplakia{thickening of the mucosal layer, hyperkeratinization)
etiology:alcohol, candida albikans60%, mecha, chemic, anemia
Location: jugal mucosa , lips, lateral of tongu, retromolar areas , palate
clicical aspect:assymptomatic burning sensationby irritants, keratotic lesions ……>>>> homogenous: white flat patches..>>> less malignancy
Non-homogenous: white, whiteyellow, gray lesions or white red mixed ……… can be nodular or spicky …..more ratio of dysplasia or malignancy…..>>>>types: verrucous leukoplakia {spicky one} , erytholeukoplakia, nodular leukoplakia
treatment: with dysplasia >>>> co2 laser, surgical crayotherapy
without dysplasia>>>>> retinoid compounds , BETA CAROTHEN
white sponge nevous
PRIMARY syphilis
PRIMARY SYPHILIS
after lips and commissures, are:-tongue-palate-gingiva (the incisive –caninearea)-tonsils
Treponema pallidum(etyiology)
From a clinical point of view, chancre first resembles a macula that progressively turns into an inflammatory papule that quickly erodes and becomes a painless, neat lesion with slightly bold
margins, hard base and surrounded by a red line. The surface of the sore is covered by a grey
exudate that contains numerous treponemes; the sore is highly contagious.
Chancre usually occurs as a singular sore, although multiple sores are possible
direct immunofluorescence staining
.During primary stage of syphilis, serologic tests can turn out negative.
At the end of the primary stage of syphilis (about a month after inoculation) VDRL (VenerealDisease Research Laboratory), immunofluorescence reaction –FTA –Abs (Fluorescent Treponemal Antibody Absorption) or the TPHA (Treponema palladium haemaglutination assay) turn out positive.
Treatment:penicillin is the treatment of choice in all stages of syphilis. When there is a case of allergy to penicillin, other types of antibiotics can be prescribed (erythromycin, cephalosporin, tetracycline, and doxycycline)
CICATRICIAL PEMPHIGOID
oral cavity; in 95% of cases it is the very first location of the disease and it may be the only affected location. Another feature is the tendency of lesions to remain localized in an area of the mucosa, most commonly on the gum, taking the look of a desquamativegingivitis
Oral lesions of cicatricial pemphigoid appear at onset as erosions similar tothose of pemphigus or as bullasor intact blisters. The ability to notice blisters or intact bullas is higher in this disease, compared to pemphigus because the lesions being subepithelial have a thicker coating.
Ocular lesionsare the second location in frequency after oral mucosa and they may cause the appearance of symblepharons, corneal opacities and even blindness
Complementary tests: Histopatological examDirectimmunofluorescenceDifferentialDiagnostic:Pemphigus vulgarisPemphigoid bullousBullousLichen planus
Treatament-depends on the severity of symptomstopical treatment with steroids (Clobetasol, Fluocinonide)therapy with Dapsonecorticosteroids combination + immunosuppressives( in severe cases)
nicotinic stomatitis
Primary Herpetic Gingivostomatitis
The oral mucosa is congested and edematous with many vesicles grouped in bunches. These vesicles will break down the next 24 hours into superficial, painful ulcerations covered by dark grey pseudo-membranes surrounded by an erythematous halo , Ulcerations will heal in 10 –14 days, leaving no marks.
Histopathologic examination: .Culture Antibodies titer .Immunologic testing using DNA hybridization
TreatmentSevere casesAcyclovir-systemic or suspension-200mg/5mlRodilemidi.m. 10 days/ month -3 monthsMild and medium forms-symptomaticAntipyreticsLiquid diet (for hydration and electrolyte balance)Topic anesthetics(dyclorinehydrochloride 0,5-1%,benzocainegel 20%, xylocaineviscous 2%, lidocaine5%).Rigorous oral hygiene with antiseptic solutions (Clorhexidine0, 4%) or local application with gentian violet 2% or methyleneblue 1%.
reticular form of lichen planus
reticularform of lichen planus
reticular lichen planus
most common tupe of planus
common location: jugal mucosa bilateral , but also on lips tongue , gingiva
clinical aspect: keratotic lesions called wicham straiae (so many)
C.test: histopathalogical test
immunofluorocense tet
treatment: assymptomatic lesion>>no treatment needed
symptomatic lesion>>>> systemic cyclosporine
ERYTHEMA MULTIFORME(minor form)
initially flat, round, having a dark red color. Later,these can develop into a bullawith a necrotic center. Sometimes, skin lesions appear with characteristic appearance „in target” or „herpes iris.
In oral cavity, lesions appear as erythematous patches, which subsequently by epithelial necrosis, , with irregular edges. Hemorrhagic crusts appear on vermillion, often with symmetrical distribution include: labial mucosal side, buccal mucosa, oral floor, soft palate, tongue. Painful ulcerative lesionsmay appear in relapsessimilarto the initial episode or erythematous patches with limited ulceration and reduced symptoms.
Positive diagnosis isbased on clinical data.The histopathological exam and the immunopathological tests are not specificfor erythema multiforme. However, the presence of Ig M, the complement and fibrin in dermal vessel walls, is an indication of immune-complex vasculitis and implicitly is the cause of erythema multiforme.
Treatment: in common forms of the disease, the topical administration of corticosteroids, antibiotics, analgesics, antifungals has been recommended. In severe cases, average doses of systemic corticosteroidsand high doses of antibiotics are recommended. The treatment is the prerogative of the dermatologist
WHITE SPONGE NEVUS (Canon disease)
symetrical lesions ,asymptomatic, white and spongy , on jugal mucosa , lateral of the tongue, labial mucosa, floor of the mouth
Histopathologic examination
no treatment required
herpetiform aphtous ulcers
numourous ulcers, sizes 1-3 mm, not very deep,invisible scars,
location:ventral side of the tongue (fig. 47) - buccal mucosa - floor of the mouth
treatment: corticosteroids (15-40
mg/day for a period of 7 days
and
tetracyclines
chemical ulcer
1**chemical substances used in dental practice could cause iatrogenic ulcerative lesions of
the oral mucosa when applied incorrectly. Thus,
phenol, trichloroacetic acid eugenol, silver nitrate, formaldehyde, sodium hypochlorite,
etc could cause burns of the oral mucosa and
superficial ulcerations that will heal spontaneously within 4 to 7 days. chemistry
2**there are cases of lesions of the mucosa caused by aspirin or alcohol applied by the patient on the painful tooth. Thus, a tissue necrosis with painful erosions occurs on that specific spot and it will heal in a week time.
CICATRICIAL PEMPHIGOID
oral cavity; in 95% of cases it is the very first location of the disease and it may be the only affected location. Another feature is the tendency of lesions to remain localized in an area of the mucosa, most commonly on the gum, taking the look of a desquamativegingivitis
Oral lesions of cicatricial pemphigoid appear at onset as erosions similar tothose of pemphigus or as bullasor intact blisters. The ability to notice blisters or intact bullas is higher in this disease, compared to pemphigus because the lesions being subepithelial have a thicker coating.
Ocular lesionsare the second location in frequency after oral mucosa and they may cause the appearance of symblepharons, corneal opacities and even blindness
Complementary tests: Histopatological examDirectimmunofluorescenceDifferentialDiagnostic:Pemphigus vulgarisPemphigoid bullousBullousLichen planus
Treatament-depends on the severity of symptomstopical treatment with steroids (Clobetasol, Fluocinonide)therapy with Dapsonecorticosteroids combination + immunosuppressives( in severe cases)
scarlet fever
cold seasons and children
General symptoms: shiver, vomiting, nausea, headache
fver, lymph adenopathy
two stages: 1” Enanthema : exfoliating glossitis with angina ( suffocative pain) associated with erythema of tonsills pillars , ovula, soft palate, not on the hard palate.<< tongue becomes extremely congested and it gets redwith glossy aspect and shows the CAT TONGUE aspect. heals in10-12 days
2” Exanthema : dyfussed erythema on the skin giving skin a harsh aspect .
complementary test : culture of type A streptococcus
treatment: antibiotics erythromycin , penicillin
hand foot mouth disease
it is caused by Coxsackie virus
Intra-oral eruption is characterized by the occurrence of small vesicles, not more than 5 –10, that blister into superficial ulcerations with 2-4 mm diameter and are circumscribed by an erythematous halo. eventually be covered by dry scabs.
Most common locations are:tonguepalatebuccal mucosalips.
Positive diagnosisis based on clinical data
Treatmentis supportive(antipyretics and topic anesthetics
acute pseudomembranous candidiasis
in this situation the mouth is dry and burning with dyphagia
white or white yellowish patches that can be easily wiped away to reveal the erythematous beneath
located : can be seen everywhere in oral cavity but mostly palate , tongue , jugal mucosa
C.T: based on clinical examination and culture media on different media and direct microscopic examination
NOMA (cancrum oris, gangrenous stomatitis, necrotic stomatitis)
ask if the patient can have AIDS ? since the clinical aspects are very much like the acute and chronic lukemia….
From a clinical point of view, the disease can start as an acute ulcerative-necrotic gingivitis
Necrotic areas could also occur on the soft areas as a consequence of traumatic lesions without any continuity to the gingiva
Gangrenous ulcerations are covered by fibrinoid white-grey deposits
Treatment: consists of preventing and eliminating the predisposing factors, diet rebalancing,
hydration and antibiotic therapy (penicillin and metronidazole). Locally, the necrotic tissue will be removed and reconstructive surgery will be performed one year later
In the absence of any treatment, mortality rate reaches 95%,
c.t : based on clinical aspect and culture media since the etiology of the disease is bacterial
Herpangina
ZahorskyDisease
The characteristic lesions affect:soft palateuvulatonsilsanterior pillarsposterior pharynxVesicles are small and numerous and they break down into painful ulcerations, not very deep, that will heal in 7-12 days.The absence of lesions on lips, gums and palate is significant for this disease and for the consequent diagnosis.
Positive diagnosisis based on unique clinical criteria and no further complementary examinations are required.
Treatment: is supportive.
hand foot mouth disease
it is caused by Coxsackie virus
Intra-oral eruption is characterized by the occurrence of small vesicles, not more than 5 –10, that blister into superficial ulcerations with 2-4 mm diameter and are circumscribed by an erythematous halo. eventually be covered by dry scabs.
Most common locations are:tonguepalatebuccal mucosalips.
Positive diagnosisis based on clinical data
Treatmentis supportive(antipyretics and topic anesthetics
hand foot mouth disease
it is caused by Coxsackie virus
Intra-oral eruption is characterized by the occurrence of small vesicles, not more than 5 –10, that blister into superficial ulcerations with 2-4 mm diameter and are circumscribed by an erythematous halo. eventually be covered by dry scabs.
Most common locations are:tonguepalatebuccal mucosalips.
Positive diagnosisis based on clinical data
Treatmentis supportive(antipyretics and topic anesthetics
hand foot mouth disease
it is caused by Coxsackie virus
Intra-oral eruption is characterized by the occurrence of small vesicles, not more than 5 –10, that blister into superficial ulcerations with 2-4 mm diameter and are circumscribed by an erythematous halo. eventually be covered by dry scabs.
Most common locations are:tonguepalatebuccal mucosalips.
Positive diagnosisis based on clinical data
Treatmentis supportive(antipyretics and topic anesthetics
hairy tongue
keratin deposit on the tongue (appears in a hypertrophic form )
etiology:severe smoking candida albikans , low immune , poor hygine, long term use of antibiotics, metronidazol, systemic corticosteroids
clinicalaspect : hypertrophic lesion of the tongue in diff colors like white gray, yellow , brown it starts from foramen cecum of the tongue to lateral and anterir side of the tongue
no complementary test
treatment: nystatine if candida, palleteknife in moderate cases, brushing, keratolytic agents like salicilic acid
labial herpes
Clinical aspect:-a discrete congestion and an edema of the vermilion border and the surrounding skin, -vesicle eruption, vesicle has 1-3 mm diameter, while the lesion reaches 1 –2 cm,-people with immunodeficiency will present larger lesions associated with discomfort and physiognomic alterations.The vesicles break down into ulcerations that will get covered by dry scabs and eventually heal in the course of 1 –2 weeks
Positive diagnosis -is based on clinical examination
TreatmentLocal therapy –acyclovir (Zovirax,Euvirox) 5%-ointment x5/day-penciclovir(Denavir)1% ,at 2h,4days-vidarabine3%-idoxuridine3%Systemic -valacyclovir(Valtrex) 4 g ( 2gx2)one doseProphylactic –ointments based on zinc oxide or titanium dioxide
major aphtae
NOMA (cancrum oris, gangrenous stomatitis, necrotic stomatitis)
ask if the patient can have AIDS ? since the clinical aspects are very much like the acute and chronic lukemia….
From a clinical point of view, the disease can start as an acute ulcerative-necrotic gingivitis
Necrotic areas could also occur on the soft areas as a consequence of traumatic lesions without any continuity to the gingiva
Gangrenous ulcerations are covered by fibrinoid white-grey deposits
Treatment: consists of preventing and eliminating the predisposing factors, diet rebalancing,
hydration and antibiotic therapy (penicillin and metronidazole). Locally, the necrotic tissue will be removed and reconstructive surgery will be performed one year later
In the absence of any treatment, mortality rate reaches 95%,
c.t : based on clinical aspect and culture media since the etiology of the disease is bacterial
Discoid lupus erythematosus (DLE)
Skin lesions develop on sun-exposure
purplish patches on the skin
specific aspect of “butterfly wings” on the face.
The favoured locations of the lesions are: - buccal mucosa - lower lip - gingival fibre-mucosa - tongue
central atrophic red patch with whitish lines disposed as sunrays.
Complementary examinations: direct immunofluorescence test and histopathologic
Treatment :Oral lesions are treated with topical steroid medication
oral administration of corticosteroids or anti-malaria medication.
NOMA (cancrum oris, gangrenous stomatitis, necrotic stomatitis)
ask if the patient can have AIDS ? since the clinical aspects are very much like the acute and chronic lukemia….
From a clinical point of view, the disease can start as an acute ulcerative-necrotic gingivitis
Necrotic areas could also occur on the soft areas as a consequence of traumatic lesions without any continuity to the gingiva
Gangrenous ulcerations are covered by fibrinoid white-grey deposits
Treatment: consists of preventing and eliminating the predisposing factors, diet rebalancing,
hydration and antibiotic therapy (penicillin and metronidazole). Locally, the necrotic tissue will be removed and reconstructive surgery will be performed one year later
In the absence of any treatment, mortality rate reaches 95%,
c.t : based on clinical aspect and culture media since the etiology of the disease is bacterial
frictional hyperplasia
reticularform of lichen planus
reticular lichen planus
most common tupe of planus
common location: jugal mucosa bilateral , but also on lips tongue , gingiva
clinical aspect: keratotic lesions called wicham straiae (so many)
C.test: histopathalogical test
immunofluorocense tet
treatment: assymptomatic lesion>>no treatment needed
symptomatic lesion>>>> systemic cyclosporine
major aphthous
unilateral , the lesion is profound and it appears crater shape with irreguar bottom , size 1-5cm -necrotic center,no bleed , painful,dysphagia and dysphonia
**** leaves scar>>>exclude malignency
location: lateral and ventral side of the tongue , buccal, labial , palatin tonsil
*treatment: if its gigantic >> bacidracin tablets
*dexametazone
*systemic steroids hydrocortizon
prednizone
all minor treatments
surgical removal
scarlet fever
cold seasons and children
General symptoms: shiver, vomiting, nausea, headache
fver, lymph adenopathy
two stages: 1” Enanthema : exfoliating glossitis with angina ( suffocative pain) associated with erythema of tonsills pillars , ovula, soft palate, not on the hard palate.<< tongue becomes extremely congested and it gets redwith glossy aspect and shows the CAT TONGUE aspect. heals in10-12 days
2” Exanthema : dyfussed erythema on the skin giving skin a harsh aspect .
complementary test : culture of type A streptococcus
treatment: antibiotics erythromycin , penicillin
atrophic chronic candidiasis
chronic atrophic candidiasis (prosthesis candidiasis)
LOCATED MAINLY ON THE HARD PALATE
HAS 3 stages: 1st:red hyperemic punctiform zones on the salivary glandsholes 2nd:diffuse erythema on the hard palate 3rd: papilary hyperplasia
pain and burning is common
C.T : immunofluorocense examination
treatment: nystatin sol 100.000u/ml 4times a day
amphotericin B suspension 100mg/ml 4 times a day
miconazole gel 2% 4*aday
new prosthetic device , rigorous oral hygiene
remove the prosthetic at nights
secondary herpetic stomatitis
numerous vesicles grouped in bunches, most commonly located on the hard palate and the gingival fiber-mucosa During the next few hours vesicles will break down into ulcerations (1-3 mm diameter) that will spontaneously heal the next 7-10 days, leaving no visible marks.
Differential diagnosisincludes:Recurrent aphthae(recurrent herpetic aphthous stomatitis)
Treatmentis supportive. Acyclovir is efficient when administered systematically(200mg x5/7 days)and it prevents recurrence, although it is not to be used in occasional or minor manifestations of the condition.
c.t : no need, based on clinical examination
acute leukemia
clinical signs: hyperplastic swelling of vestibular and oral side of the mouth , pale or purplish gingiva , gingival hyperplasia, dental mobility , tonsil hypertrophy
C.T lab examination of the peripheral blood and bone marrow myelogram or medulogram >>>leukemic cells differentiation
treatment: send the patient to a haemotologist …. any dental procedure needs the approval or presence of the haemotologist.
thrombin sponges in case of gingival bleeding.
Primary Herpetic Gingivostomatitis
The oral mucosa is congested and edematous with many vesicles grouped in bunches. These vesicles will break down the next 24 hours into superficial, painful ulcerations covered by dark grey pseudo-membranes surrounded by an erythematous halo , Ulcerations will heal in 10 –14 days, leaving no marks.
Histopathologic examination: .Culture Antibodies titer .Immunologic testing using DNA hybridization
TreatmentSevere casesAcyclovir-systemic or suspension-200mg/5mlRodilemidi.m. 10 days/ month -3 monthsMild and medium forms-symptomaticAntipyreticsLiquid diet (for hydration and electrolyte balance)Topic anesthetics(dyclorinehydrochloride 0,5-1%,benzocainegel 20%, xylocaineviscous 2%, lidocaine5%).Rigorous oral hygiene with antiseptic solutions (Clorhexidine0, 4%) or local application with gentian violet 2% or methyleneblue 1%.
erosive form of lichenplanus
clinical aspect: burning and pain sensation more red than white compare to reticular form , erythematous lesion with some straia but the straia is not as white
retrocomissural (where mandible and maxila meet intraorally)
lower buccal vestibule(buccal mucosa) near the molar >>>> lower means mandible side
comlementary test: histo+ immunofluorosens
treatment
general:cyclosporine , nystatin in candida associated and cortico steroids cream and injection intra lesional
Iron def anemia
angular chelitis can be present mostly
general signs: weight loss
pale face , dysponea , headache, hair and nail fragility
oral signs:burning sensation of the tongue, atrophy of filliform and fungiform papilla , dorsal surface of the tongue becomes red-glossy and smooth
*******
in case of plummer-vinson syndrom and hyperchromic anemia oral manifestations are accompanied by dysphagia caused by painful erosions of esophagus
C.T srium iron test
haemoglubin
hematocrit(low level)
treatment:m increasing the iron through supplements and real food
allergic reaction
edema of the lips and edema of the neck area that might cause airways blockage
diagnosis is based on the history of those allergic reactions, presence of edema, hereditary history of the disease
treatment: Anti-histamines
i. m adrenaline
i. v corticosteroids
NOMA (cancrum oris, gangrenous stomatitis, necrotic stomatitis)
ask if the patient can have AIDS ? since the clinical aspects are very much like the acute and chronic lukemia….
From a clinical point of view, the disease can start as an acute ulcerative-necrotic gingivitis
Necrotic areas could also occur on the soft areas as a consequence of traumatic lesions without any continuity to the gingiva
Gangrenous ulcerations are covered by fibrinoid white-grey deposits
Treatment: consists of preventing and eliminating the predisposing factors, diet rebalancing,
hydration and antibiotic therapy (penicillin and metronidazole). Locally, the necrotic tissue will be removed and reconstructive surgery will be performed one year later
In the absence of any treatment, mortality rate reaches 95%,
c.t : based on clinical aspect and culture media since the etiology of the disease is bacterial
Kaposi’s sarcoma
its an endothelial cells malignancy
4 types:1* classic kaposi’s sarcoma (skin lesion)
2*african kaposi’s sarcoma(skin lesions)
3*aquired kaposi’s sarcoma (skin)
4*EPIDEMIC KAPOSI’S SARCOMA :OVER 50% of the patients showed oral manifestation
lesion has 3 stages>>> first its assymptomatic erythematous that dont disappear after pressure >>>then it gets bigger and it will turn into red-blue or purple papular lesion>>> and at the advanced stages sarcoma appears purplish,blue nodules that can bleed and its painful.
located on jugal mucosa, dorsal face of the tongue, half of the palate, on the gingiva
C.T is biopsy
treatment: radiotherapy surgery, chemotherapy Co2 laser
Primary Herpetic Gingivostomatitis
The oral mucosa is congested and edematous with many vesicles grouped in bunches. These vesicles will break down the next 24 hours into superficial, painful ulcerations covered by dark grey pseudo-membranes surrounded by an erythematous halo , Ulcerations will heal in 10 –14 days, leaving no marks.
Histopathologic examination: .Culture Antibodies titer .Immunologic testing using DNA hybridization
TreatmentSevere casesAcyclovir-systemic or suspension-200mg/5mlRodilemidi.m. 10 days/ month -3 monthsMild and medium forms-symptomaticAntipyreticsLiquid diet (for hydration and electrolyte balance)Topic anesthetics(dyclorinehydrochloride 0,5-1%,benzocainegel 20%, xylocaineviscous 2%, lidocaine5%).Rigorous oral hygiene with antiseptic solutions (Clorhexidine0, 4%) or local application with gentian violet 2% or methyleneblue 1%.
herpes zoster
Intraoral eruption is preceded by pain that can mimic pulpitis. Vesicles are grouped in bunches, breaking down after 2-3 days into ulcerations circumscribed by an erithematousborder.Healing process will take 2 –3 weeks leaving no marks.The location of the lesions on one side only is the main clinical sign of herpes zoster
The most frequent complication of this condition is residual trigeminal neuralgia that can last for weeks or months
Positive diagnosis of oral lesions is established following clinical criteria.
TreatmentTargetsthe reduction of the duration of disease,preventing post-herpetic neuralgia the dissemination in patients with immunodeficiency.Acyclovir<50 years old-200 mg x 5/day, 7-10 days>50 years old-800 mg x 5 /day, 7-10 daysCapsaicina–local therapy Xylineor Novocain infiltration on the affected nerve.
nicotinic stomatitis
major aphtae
THERMAL ULCERATIONS:
Intraoral thermal burns are quite rare. They can be caused by hot liquids or food and they are mostly located on the lips, tongue and mouth floor Also, acrylic resins resulting from polymerization or monomer excess as well as some blueprints materials (wax, hydrocolloids) could cause burns on the oral mucosa. All lesions caused by erythema, erosions or vesicles will heal within a week.
Pemphigus vulgaris
Vesicles or bullaspainful erosions that tend to peripheral expansion Eruptions.
Characteristic signs: Nicolsky, Asboe-Hansen
Lesions can be found in any area of the oral mucosa, with a predilection for:-palate -jugalmucosa -lower lip -oral floor
complementary test: Cytological examination -shows the presence of typical acantholyticcells(Tzanckcells) with large, hyperchromaticnuclei.Histopathologicalexaminationfrom a biopsytaken from a perilesionalskin shows the integrity of basal layer and the acantholysisof the spinouslayer.Direct immunofluorescenceIndirect immunofluorescence
Treatament :
sistemic: high doses of prednisone(Prednison) on alternate days with immunosuppressants:Azathioprine, Methotrexate, Cyclophosphamideparenteral administration of gold salts, etretinate, dapsoneand plasmapheresis( in patients refractory to corticosteroid therapy)
local: a rigorous local hygiene ,
mouth rinses with antiseptic solutions-Clorhexidine-0,2%
Topical anesthetics(Lidocaine 5%)
Topical steroids:ELOCOM-crème:3,4 apl./day
median rhomboid glositis
is a kind of chronic candidiasis
central papillary atrophy of the tongue
clinicalfeatures: first soft red denudated patch located on the median line of the dorsal side of the tongue ,,,,,,,,,,,,,,,,,later it gets hard and lobulated ,,,,,it is - cm oval or rhombic with rounded borders
scarlet fever
cold seasons and children
General symptoms: shiver, vomiting, nausea, headache
fver, lymph adenopathy
two stages: 1” Enanthema : exfoliating glossitis with angina ( suffocative pain) associated with erythema of tonsills pillars , ovula, soft palate, not on the hard palate.<< tongue becomes extremely congested and it gets redwith glossy aspect and shows the CAT TONGUE aspect. heals in10-12 days
2” Exanthema : dyfussed erythema on the skin giving skin a harsh aspect .
complementary test : culture of type A streptococcus
treatment: antibiotics erythromycin , penicillin
Varicella (chickenpox)
Oral lesionsare common and mostly located on the palate and lips and sometimes they precede the skin
lesions. Vesicles are small (3-4 mm) and quickly turn into erosions surrounded by an erythematous halo.
Positive diagnosisis based on epidemiologic data and clinical manifestations.
Treatmentis supportive: rigorous body hygiene, mint alcohol 1% or mint talcwill help prevent pruritus, antihistamines and antipyretics.Children and teenagers will not be treated with aspirin because of the high risk of developing Reye syndrome(a rare, yet severe condition causing irreversible lesions such as acute encephalopathyand hepatic fatty degeneration).Antiseptic solutions are recommended for oral lesions.Antiviral medication including Acyclovir, Vidarabine or Interferonis recommended only in patients with immunodeficiency.Prevention of chickenpox can be obtained with the varicella vaccine that gives 100% protection to the virus
acute leukemia
clinical signs: hyperplastic swelling of vestibular and oral side of the mouth , pale or purplish gingiva , gingival hyperplasia, dental mobility , tonsil hypertrophy
C.T lab examination of the peripheral blood and bone marrow myelogram or medulogram >>>leukemic cells differentiation
treatment: send the patient to a haemotologist …. any dental procedure needs the approval or presence of the haemotologist.
thrombin sponges in case of gingival bleeding.
PRIMARY SYPHILIS
after lips and commissures, are:-tongue-palate-gingiva (the incisive –caninearea)-tonsils
Treponema pallidum(etyiology)
From a clinical point of view, chancre first resembles a macula that progressively turns into an inflammatory papule that quickly erodes and becomes a painless, neat lesion with slightly bold
margins, hard base and surrounded by a red line. The surface of the sore is covered by a grey
exudate that contains numerous treponemes; the sore is highly contagious.
Chancre usually occurs as a singular sore, although multiple sores are possible
direct immunofluorescence staining
.During primary stage of syphilis, serologic tests can turn out negative.
At the end of the primary stage of syphilis (about a month after inoculation) VDRL (VenerealDisease Research Laboratory), immunofluorescence reaction –FTA –Abs (Fluorescent Treponemal Antibody Absorption) or the TPHA (Treponema palladium haemaglutination assay) turn out positive.
Treatment:penicillin is the treatment of choice in all stages of syphilis. When there is a case of allergy to penicillin, other types of antibiotics can be prescribed (erythromycin, cephalosporin, tetracycline, and doxycycline)
chemical ulcer
1**chemical substances used in dental practice could cause iatrogenic ulcerative lesions of
the oral mucosa when applied incorrectly. Thus,
phenol, trichloroacetic acid eugenol, silver nitrate, formaldehyde, sodium hypochlorite,
etc could cause burns of the oral mucosa and
superficial ulcerations that will heal spontaneously within 4 to 7 days. chemistry
2**there are cases of lesions of the mucosa caused by aspirin or alcohol applied by the patient on the painful tooth. Thus, a tissue necrosis with painful erosions occurs on that specific spot and it will heal in a week time.
sloar chelitis /actinic chelitis
premalignant esion / mostly on lower lips ,/ workers / white population
early stage we see mild keratinisation that causes the disappearance of the line between the edge of vermillion and the surrounding skin, then becomes chronic and white patches appear , deffused margins,swallon crustand lips loss their elassticity.
complementary tests: biopsy and histopathalogical examinatins
treatment: prevenntive: sunscreen and ZINC OXIDE based cream
CRYOTHERAPY (FREZZING STUFF)
reticular form of lichnplanus
reticularform of lichen planus
reticular lichen planus
most common tupe of planus
common location: jugal mucosa bilateral , but also on lips tongue , gingiva
clinical aspect: keratotic lesions called wicham straiae (so many)
C.test: histopathalogical test
immunofluorocense tet
treatment: assymptomatic lesion>>no treatment needed
symptomatic lesion>>>> systemic cyclosporine
Primary Herpetic Gingivostomatitis
The oral mucosa is congested and edematous with many vesicles grouped in bunches. These vesicles will break down the next 24 hours into superficial, painful ulcerations covered by dark grey pseudo-membranes surrounded by an erythematous halo , Ulcerations will heal in 10 –14 days, leaving no marks.
Histopathologic examination: .Culture Antibodies titer .Immunologic testing using DNA hybridization
TreatmentSevere casesAcyclovir-systemic or suspension-200mg/5mlRodilemidi.m. 10 days/ month -3 monthsMild and medium forms-symptomaticAntipyreticsLiquid diet (for hydration and electrolyte balance)Topic anesthetics(dyclorinehydrochloride 0,5-1%,benzocainegel 20%, xylocaineviscous 2%, lidocaine5%).Rigorous oral hygiene with antiseptic solutions (Clorhexidine0, 4%) or local application with gentian violet 2% or methyleneblue 1%.
major aphthous
reticular lichen planus
reticularform of lichen planus
reticular lichen planus
most common tupe of planus
common location: jugal mucosa bilateral , but also on lips tongue , gingiva
clinical aspect: keratotic lesions called wicham straiae (so many)
C.test: histopathalogical test
immunofluorocense tet
treatment: assymptomatic lesion>>no treatment needed
symptomatic lesion>>>> systemic cyclosporine
sloar chelitis or actinic chelitis
ATrophic glossitis
TERTIARY SYPHILIS
1/3 OF 1/3 cases of syphilis will develop the third
It is mainly characterized by:
neurological manifestations
cardiovascular lesions
lesions of the skin and mucosa
bone lesions
3 LESIONS
GUMA >>>> HARD PALATE FISTUA
From an evolution point of view, gumma knows 4 stages:-rawness-softening-ulceration-healing
The size of the lesion varies from 1 to 10 cm.It is most frequently located on the hard palate
ATROPHIC GLOSITIS
is the consequence of a vasculitis that evolves into an obliteratingendarteritis, causing the atrophy of both the mucosa and the muscle of the tongue. Consequently, the dorsal part of the tongue becomes neat and atrophic.
SCLROTIC GLLOSITIS
is the result of tongue becoming deformed once a gumma has healed. Consequently, the tongue has a lobulated appearancewith deep and irregular ditches
verrucous leukoplakia
angular chelitis
is a type of chronic candidiasis
bilateral , painful, can be seen yellow-brownish granular nodules or an erythematous cracked zones with peripheral crusts
C.T NO NEED
TREATMENT:MICONAZOLE GEL 2% 4-6 APPLICATIONS A DAY BOTH ON TH MUCOSA and the prosthetic field
antifungal antibiotic therapy
The Lyell syndrome(toxic epidermal necrolysis)
It is the most serious form of erythema multiforme, sometimes fatal,
Clinically, it is characterized by bullous lesions that may involve the entiresurface of skin and mucous membranes. If the patient survives, cutaneous manifestations subside in 2-4 weeks. Oral lesions heal much slowerand the ocular ones, causing disability are found in½ of the patients.Positive diagnosis isbased on clinical data.The histopathological exam and the immunopathological tests are not specificfor erythema multiforme. However, the presence of Ig M, the complement and fibrin in dermal vessel walls, is an indication of immune-complex vasculitis and implicitly is the cause of erythema multiforme.
Treatment: in common forms of the disease, the topical administration of corticosteroids, antibiotics, analgesics, antifungals has been recommended. In severe cases, average doses of systemic corticosteroidsand high doses of antibiotics are recommended. The treatment is the prerogative of the dermatologist.
acute pseudomembranous candidiasis
acute pseudomembranous candidiasis
in this situation the mouth is dry and burning with dyphagia
white or white yellowish patches that can be easily wiped away to reveal the erythematous beneath
located : can be seen everywhere in oral cavity but mostly palate , tongue , jugal mucosa
C.T: based on clinical examination and culture media on different media and direct microscopic examination
CICATRICIAL PEMPHIGOID
oral cavity; in 95% of cases it is the very first location of the disease and it may be the only affected location. Another feature is the tendency of lesions to remain localized in an area of the mucosa, most commonly on the gum, taking the look of a desquamativegingivitis
Oral lesions of cicatricial pemphigoid appear at onset as erosions similar tothose of pemphigus or as bullasor intact blisters. The ability to notice blisters or intact bullas is higher in this disease, compared to pemphigus because the lesions being subepithelial have a thicker coating.
Ocular lesionsare the second location in frequency after oral mucosa and they may cause the appearance of symblepharons, corneal opacities and even blindness
Complementary tests: Histopatological examDirectimmunofluorescenceDifferentialDiagnostic:Pemphigus vulgarisPemphigoid bullousBullousLichen planus
Treatament-depends on the severity of symptomstopical treatment with steroids (Clobetasol, Fluocinonide)therapy with Dapsonecorticosteroids combination + immunosuppressives( in severe cases)
Primary Herpetic Gingivostomatitis
The oral mucosa is congested and edematous with many vesicles grouped in bunches. These vesicles will break down the next 24 hours into superficial, painful ulcerations covered by dark grey pseudo-membranes surrounded by an erythematous halo , Ulcerations will heal in 10 –14 days, leaving no marks.
Histopathologic examination: .Culture Antibodies titer .Immunologic testing using DNA hybridization
TreatmentSevere casesAcyclovir-systemic or suspension-200mg/5mlRodilemidi.m. 10 days/ month -3 monthsMild and medium forms-symptomaticAntipyreticsLiquid diet (for hydration and electrolyte balance)Topic anesthetics(dyclorinehydrochloride 0,5-1%,benzocainegel 20%, xylocaineviscous 2%, lidocaine5%).Rigorous oral hygiene with antiseptic solutions (Clorhexidine0, 4%) or local application with gentian violet 2% or methyleneblue 1%.
gumma
TERTIARY SYPHILIS
1/3 OF 1/3 cases of syphilis will develop the third
It is mainly characterized by:
neurological manifestations
cardiovascular lesions
lesions of the skin and mucosa
bone lesions
3 LESIONS
GUMA >>>> HARD PALATE FISTUA
From an evolution point of view, gumma knows 4 stages:-rawness-softening-ulceration-healing
The size of the lesion varies from 1 to 10 cm.It is most frequently located on the hard palate
ATROPHIC GLOSITIS
is the consequence of a vasculitis that evolves into an obliteratingendarteritis, causing the atrophy of both the mucosa and the muscle of the tongue. Consequently, the dorsal part of the tongue becomes neat and atrophic.
SCLROTIC GLLOSITIS
is the result of tongue becoming deformed once a gumma has healed. Consequently, the tongue has a lobulated appearancewith deep and irregular ditches
acute leukemia
clinical signs: hyperplastic swelling of vestibular and oral side of the mouth , pale or purplish gingiva , gingival hyperplasia, dental mobility , tonsil hypertrophy
C.T lab examination of the peripheral blood and bone marrow myelogram or medulogram >>>leukemic cells differentiation
treatment: send the patient to a haemotologist …. any dental procedure needs the approval or presence of the haemotologist.
thrombin sponges in case of gingival bleeding.
MECHANICAL ULCER
ATIONS:
Most ulcers occurring on the soft parts of the oral cavity are of mechanical nature and are
located on the
lower lip, tongue, buccal mucosa and oral floor
. These ulcers are not related to genderor age.
In newborns with natal or neonatal teeth the traumatic ulceration that usually occurs on the ventral surface of the tongue 1/3 anterior is called Riga Fede disease
.Root residues, sharp edges of the teeth,periodontal carious lesions, crochets from partial dental prosthesis, malpositioned teeth, unstable full dental prosthesis, etc could determine acute or chronic traumatic ulcerations.
In less common circumstances in people suffering from psychic conditions, lesions can be
selfinduced by abnormal
behaviours such as lip, tongue or cheek biting. Traumatic ulcerations can also be iatrogenic. Thus, ulcerations of mucosa could be caused while removing cotton rolls or compresses from the mucosa, while pressing too hard the saliva vacuum or by accidental injury of soft mucosa with mills or disks.
ATrophic glossitis
TERTIARY SYPHILIS
1/3 OF 1/3 cases of syphilis will develop the third
It is mainly characterized by:
neurological manifestations
cardiovascular lesions
lesions of the skin and mucosa
bone lesions
3 LESIONS
GUMA >>>> HARD PALATE FISTUA
From an evolution point of view, gumma knows 4 stages:-rawness-softening-ulceration-healing
The size of the lesion varies from 1 to 10 cm.It is most frequently located on the hard palate
ATROPHIC GLOSITIS
is the consequence of a vasculitis that evolves into an obliteratingendarteritis, causing the atrophy of both the mucosa and the muscle of the tongue. Consequently, the dorsal part of the tongue becomes neat and atrophic.
SCLROTIC GLLOSITIS
is the result of tongue becoming deformed once a gumma has healed. Consequently, the tongue has a lobulated appearancewith deep and irregular ditches
acute leukemia
clinical signs: hyperplastic swelling of vestibular and oral side of the mouth , pale or purplish gingiva , gingival hyperplasia, dental mobility , tonsil hypertrophy
C.T lab examination of the peripheral blood and bone marrow myelogram or medulogram >>>leukemic cells differentiation
treatment: send the patient to a haemotologist …. any dental procedure needs the approval or presence of the haemotologist.
thrombin sponges in case of gingival bleeding.
chronic atrophic candidiasis (prosthesis candidiasis)
LOCATED MAINLY ON THE HARD PALATE
HAS 3 stages: 1st:red hyperemic punctiform zones on the salivary glandsholes 2nd:diffuse erythema on the hard palate 3rd: papilary hyperplasia
pain and burning is common
C.T : immunofluorocense examination
treatment: nystatin sol 100.000u/ml 4times a day
amphotericin B suspension 100mg/ml 4 times a day
miconazole gel 2% 4*aday
new prosthetic device , rigorous oral hygiene
remove the prosthetic at nights
idiopathic leukoplakia
erythroleukoplakia/ non homogenous
PRIMARY SYPHILIS
PRIMARY SYPHILIS
after lips and commissures, are:-tongue-palate-gingiva (the incisive –caninearea)-tonsils
Treponema pallidum(etyiology)
From a clinical point of view, chancre first resembles a macula that progressively turns into an inflammatory papule that quickly erodes and becomes a painless, neat lesion with slightly bold
margins, hard base and surrounded by a red line. The surface of the sore is covered by a grey
exudate that contains numerous treponemes; the sore is highly contagious.
Chancre usually occurs as a singular sore, although multiple sores are possible
direct immunofluorescence staining
.During primary stage of syphilis, serologic tests can turn out negative.
At the end of the primary stage of syphilis (about a month after inoculation) VDRL (VenerealDisease Research Laboratory), immunofluorescence reaction –FTA –Abs (Fluorescent Treponemal Antibody Absorption) or the TPHA (Treponema palladium haemaglutination assay) turn out positive.
Treatment:penicillin is the treatment of choice in all stages of syphilis. When there is a case of allergy to penicillin, other types of antibiotics can be prescribed (erythromycin, cephalosporin, tetracycline, and doxycycline)
pseudomembranous candida
acute pseudomembranous candidiasis
in this situation the mouth is dry and burning with dyphagia
white or white yellowish patches that can be easily wiped away to reveal the erythematous beneath
located : can be seen everywhere in oral cavity but mostly palate , tongue , jugal mucosa
C.T: based on clinical examination and culture media on different media and direct microscopic examination
. Secondary tuberculosis :ulcerationgummatuberculosis lupus
Ulceration occurs once the infection has spread through saliva. The most frequent location is on the dorsal part of the tongue, followed by the palate, buccal mucosa, gingiva and lips.Typical lesions have 1 -5cm diameter, irregular borders andgranular surface and are covered by a yellow deposit. Sometimes, at the border of the lesions small yellow nodules are visible (representing calcified tubercles) and are called Trélat granulations.
Histopathologic examination .Tuberculin I.D.R.-Inoculation on culture media-Thoracic radiography
Localtreatment consists of:-hygiene of oral cavity-anti inflammatory drugs-painkillers
minus aphthae
Herpangina
ZahorskyDisease
The characteristic lesions affect:soft palateuvulatonsilsanterior pillarsposterior pharynxVesicles are small and numerous and they break down into painful ulcerations, not very deep, that will heal in 7-12 days.The absence of lesions on lips, gums and palate is significant for this disease and for the consequent diagnosis.
Positive diagnosisis based on unique clinical criteria and no further complementary examinations are required.
Treatment: is supportive.
homogenous erythroplakia
red patches ,can be anywhere in the oral cavity ***common loc : tongue , soft palate, pillars, floor of the mouth
C.T: BIOPSY IS MANDATORY IN ALL CASES OF ERYTHROPLAKIA SINCE THEY HAVE A 90% POTENTIAL TOBECOME SQUAMOUS CELL CARCINOMA
HISTOPATHALOGICAL EXAMINATION
treatment : same principle as in the case of leukoplakia eliminate the irritating factor and monitor the lesion for 1-2 weeks then performing TOLUIDINE BLUE staining test.
plaque form lichen planus
similar clinical aspect with leukoplakia,
the hyper-keratotic area can be neat or slightly harsh
. introduced retinoid treatment (Etretinate) with anti-keratinized
It is more frequently found on the dorsal part of the tongue and it usually expands in a centrifugal pattern
second jugal mucosa
complementary test : florocense , histopathalogocal
Kaposi’s sarcoma
its an endothelial cells malignancy
4 types: classic kaposi’s sarcoma (skin lesion)
african kaposi’s sarcoma(skin lesions)
aquired kaposi’s sarcoma (skin)
EPIDEMIC KAPOSI’S SARCOMA :OVER 50% of the patients showed oral manifestation
lesion has 3 stages>>> first its assymptomatic erythematous that dont disappear after pressure >>>then it gets bigger and it will turn into red-blue or purple papular lesion>>> and at the advanced stages sarcoma appears purplish,blue nodules that can bleed and its painful.
located on jugal mucosa, dorsal face of the tongue, half of the palate, on the gingiva
C.T is biopsy
treatment: radiotherapy surgery, chemotherapy Co2 laser
secondary herpetic stomatitis
numerous vesicles grouped in bunches, most commonly located on the hard palate and the gingival fiber-mucosa During the next few hours vesicles will break down into ulcerations (1-3 mm diameter) that will spontaneously heal the next 7-10 days, leaving no visible marks.
Differential diagnosisincludes:Recurrent aphthae(recurrent herpetic aphthous stomatitis)
Treatmentis supportive. Acyclovir is efficient when administered systematically(200mg x5/7 days)and it prevents recurrence, although it is not to be used in occasional or minor manifestations of the condition.
c.t : no need, based on clinical examination
chronic leukemia
clinical: less severe than the acute form
pale oral mucosa , sometimes associated with ulcerated causes, gingival hyperplasia
leukemic nodules can be observed on the palatinenfiber-mucosa
C,T : peripheral blood analysis
medulograma>>>bone marrow analysis tosee if there is any leukemic cells
also send the patient to th haemotologist
treatment:like the acute one >>>>
send tohaemotologist
thrombin sponge in case of bleeding
discoid lupus erythematosous
secondary tuberculosis
chemical ulcer
1**chemical substances used in dental practice could cause iatrogenic ulcerative lesions of
the oral mucosa when applied incorrectly. Thus,
phenol, trichloroacetic acid eugenol, silver nitrate, formaldehyde, sodium hypochlorite,
etc could cause burns of the oral mucosa and
superficial ulcerations that will heal spontaneously within 4 to 7 days. chemistry
2**there are cases of lesions of the mucosa caused by aspirin or alcohol applied by the patient on the painful tooth. Thus, a tissue necrosis with painful erosions occurs on that specific spot and it will heal in a week time.
acute atrophic candidiasis
erythematous or stomatitis following antibiotic therapy
clinical signs: red congested swallon mucosa covered by small white zones (pseudomembranous )
located mainly on the tongue and hard palate
{depapilation of the tongue is prsent }
C.T: direct microscopic examination , culture media
treatment: topical or systemic anti fungal therapy
Pemphigus vulgaris
Vesicles or bullaspainful erosions that tend to peripheral expansion Eruptions.
Characteristic signs: Nicolsky, Asboe-Hansen
Lesions can be found in any area of the oral mucosa, with a predilection for:-palate -jugalmucosa -lower lip -oral floor
complementary test: Cytological examination -shows the presence of typical acantholyticcells(Tzanckcells) with large, hyperchromaticnuclei.Histopathologicalexaminationfrom a biopsytaken from a perilesionalskin shows the integrity of basal layer and the acantholysisof the spinouslayer.Direct immunofluorescenceIndirect immunofluorescence
Treatament :
sistemic: high doses of prednisone(Prednison) on alternate days with immunosuppressants:Azathioprine, Methotrexate, Cyclophosphamideparenteral administration of gold salts, etretinate, dapsoneand plasmapheresis( in patients refractory to corticosteroid therapy)
local: a rigorous local hygiene ,
mouth rinses with antiseptic solutions-Clorhexidine-0,2%
Topical anesthetics(Lidocaine 5%)
Topical steroids:ELOCOM-crème:3,4 apl./day
BULLOUS PEMPHIGOID
Oral lesions usually occur after the skin ones and they can not be distinguished clinically from those of scarring pemphigoid. The bullas and erosion generally occur on the fixed gums, but may also involve othermucosal areas (soft palate, buccal mucosa, oral floor). Healing is without scars
Complementary tests:Histopatological examDirectimmunofluorescenceIndirect immunofluorescence
Treatament:systemic corticosteroidssulfones, sulfonamides and antibiotics (tetracycline, erythromycin)corticosteroids + immunosuppressives
secondary tuberculosis
PRIMARY SYPHILIS
after lips and commissures, are:-tongue-palate-gingiva (the incisive –caninearea)-tonsils
Treponema pallidum(etyiology)
From a clinical point of view, chancre first resembles a macula that progressively turns into an inflammatory papule that quickly erodes and becomes a painless, neat lesion with slightly bold
margins, hard base and surrounded by a red line. The surface of the sore is covered by a grey
exudate that contains numerous treponemes; the sore is highly contagious.
Chancre usually occurs as a singular sore, although multiple sores are possible
direct immunofluorescence staining
.During primary stage of syphilis, serologic tests can turn out negative.
At the end of the primary stage of syphilis (about a month after inoculation) VDRL (VenerealDisease Research Laboratory), immunofluorescence reaction –FTA –Abs (Fluorescent Treponemal Antibody Absorption) or the TPHA (Treponema palladium haemaglutination assay) turn out positive.
Treatment:penicillin is the treatment of choice in all stages of syphilis. When there is a case of allergy to penicillin, other types of antibiotics can be prescribed (erythromycin, cephalosporin, tetracycline, and doxycycline)
Pemphigus vulgaris
Vesicles or bullaspainful erosions that tend to peripheral expansion Eruptions.
Characteristic signs: Nicolsky, Asboe-Hansen
Lesions can be found in any area of the oral mucosa, with a predilection for:-palate -jugalmucosa -lower lip -oral floor
complementary test: Cytological examination -shows the presence of typical acantholyticcells(Tzanckcells) with large, hyperchromaticnuclei.Histopathologicalexaminationfrom a biopsytaken from a perilesionalskin shows the integrity of basal layer and the acantholysisof the spinouslayer.Direct immunofluorescenceIndirect immunofluorescence
Treatament :
sistemic: high doses of prednisone(Prednison) on alternate days with immunosuppressants:Azathioprine, Methotrexate, Cyclophosphamideparenteral administration of gold salts, etretinate, dapsoneand plasmapheresis( in patients refractory to corticosteroid therapy)
local: a rigorous local hygiene ,
mouth rinses with antiseptic solutions-Clorhexidine-0,2%
Topical anesthetics(Lidocaine 5%)
Topical steroids:ELOCOM-crème:3,4 apl./day
Herpangina
ZahorskyDisease
The characteristic lesions affect:soft palateuvulatonsilsanterior pillarsposterior pharynxVesicles are small and numerous and they break down into painful ulcerations, not very deep, that will heal in 7-12 days.The absence of lesions on lips, gums and palate is significant for this disease and for the consequent diagnosis.
Positive diagnosisis based on unique clinical criteria and no further complementary examinations are required.
Treatment: is supportive.
pseudomembranous candidiasis
acute pseudomembranous candidiasis
in this situation the mouth is dry and burning with dyphagia
white or white yellowish patches that can be easily wiped away to reveal the erythematous beneath
located : can be seen everywhere in oral cavity but mostly palate , tongue , jugal mucosa
C.T: based on clinical examination and culture media on different media and direct microscopic examination
behcet syndrom
thrombocytopenic purpura
petechiae, ecchymoses and haematoma on the buccal mucosa and palate associated with spontanious bleeding from the gingiva
C.T: MYELOGRAM
PLATELET TEST
COAGULATION TIME
TREATMENT: systematic steroids
splenectomy
platelet transfusion
NOMA (cancrum oris, gangrenous stomatitis, necrotic stomatitis)
ask if the patient can have AIDS ? since the clinical aspects are very much like the acute and chronic lukemia….
From a clinical point of view, the disease can start as an acute ulcerative-necrotic gingivitis
Necrotic areas could also occur on the soft areas as a consequence of traumatic lesions without any continuity to the gingiva
Gangrenous ulcerations are covered by fibrinoid white-grey deposits
Treatment: consists of preventing and eliminating the predisposing factors, diet rebalancing,
hydration and antibiotic therapy (penicillin and metronidazole). Locally, the necrotic tissue will be removed and reconstructive surgery will be performed one year later
In the absence of any treatment, mortality rate reaches 95%,
c.t : based on clinical aspect and culture media since the etiology of the disease is bacterial
Pemphigus vulgaris
Vesicles or bullaspainful erosions that tend to peripheral expansion Eruptions.
Characteristic signs: Nicolsky, Asboe-Hansen
Lesions can be found in any area of the oral mucosa, with a predilection for:-palate -jugalmucosa -lower lip -oral floor
complementary test: Cytological examination -shows the presence of typical acantholyticcells(Tzanckcells) with large, hyperchromaticnuclei.Histopathologicalexaminationfrom a biopsytaken from a perilesionalskin shows the integrity of basal layer and the acantholysisof the spinouslayer.Direct immunofluorescenceIndirect immunofluorescence
Treatament :
sistemic: high doses of prednisone(Prednison) on alternate days with immunosuppressants:Azathioprine, Methotrexate, Cyclophosphamideparenteral administration of gold salts, etretinate, dapsoneand plasmapheresis( in patients refractory to corticosteroid therapy)
local: a rigorous local hygiene ,
mouth rinses with antiseptic solutions-Clorhexidine-0,2%
Topical anesthetics(Lidocaine 5%)
Topical steroids:ELOCOM-crème:3,4 apl./day
Early congenital syphilis (neonatal)
When affecting the facial area, it is most commonly met in the perioral, pathognomonic part and it is characterized by rhagades(Parrot’s radial scars). The line between skin and vermillion is not clear.
Syphilitic coryzamanifests with swelling, congestion and erosion of the nasal mucosa that is covered by a sero-sanguineous exudate forming crusts and obliterating the nasal cavity.
Positive diagnosis is based on the clinical examinationand serologic testing
treatment: penicillin G
acute pseudomembranous candid
acute pseudomembranous candidiasis
in this situation the mouth is dry and burning with dyphagia
white or white yellowish patches that can be easily wiped away to reveal the erythematous beneath
located : can be seen everywhere in oral cavity but mostly palate , tongue , jugal mucosa
C.T: based on clinical examination and culture media on different media and direct microscopic examination
CONTACT ALLERGIC STOMATITIS
Etiology: denture matterials, restorative matterials and mouth washes
Clinically, in the acute form, the affected
mucosa presents with diffuse erythema and edema, and occasionally small vesicles and erosions (Fig. 65). A burning sensation is a common symptom. In the chronic form, hyperkeratotic white lesions may be seen in addition to erythema
.Laboratory tests
Mucosal and skin patch tests
Treatment:
Removal of suspected allergens, topical or systemic steroids,antihistamines.
Iron def anemia
angular chelitis can be present mostly
general signs: weight loss
pale face , dysponea , headache, hair and nail fragility
oral signs:burning sensation of the tongue, atrophy of filliform and fungiform papilla , dorsal surface of the tongue becomes red-glossy and smooth
*******
in case of plummer-vinson syndrom and hyperchromic anemia oral manifestations are accompanied by dysphagia caused by painful erosions of esophagus
C.T srium iron test
haemoglubin
hematocrit(low level)
treatment:m increasing the iron through supplements and real food
secondary herpetic stomatitis
numerous vesicles grouped in bunches, most commonly located on the hard palate and the gingival fiber-mucosa During the next few hours vesicles will break down into ulcerations (1-3 mm diameter) that will spontaneously heal the next 7-10 days, leaving no visible marks.
Differential diagnosisincludes:Recurrent aphthae(recurrent herpetic aphthous stomatitis)
Treatmentis supportive. Acyclovir is efficient when administered systematically(200mg x5/7 days)and it prevents recurrence, although it is not to be used in occasional or minor manifestations of the condition.
c.t : no need, based on clinical examination
Varicella (chickenpox)
Oral lesionsare common and mostly located on the palate and lips and sometimes they precede the skin
lesions. Vesicles are small (3-4 mm) and quickly turn into erosions surrounded by an erythematous halo.
Positive diagnosisis based on epidemiologic data and clinical manifestations.
Treatmentis supportive: rigorous body hygiene, mint alcohol 1% or mint talcwill help prevent pruritus, antihistamines and antipyretics.Children and teenagers will not be treated with aspirin because of the high risk of developing Reye syndrome(a rare, yet severe condition causing irreversible lesions such as acute encephalopathyand hepatic fatty degeneration).Antiseptic solutions are recommended for oral lesions.Antiviral medication including Acyclovir, Vidarabine or Interferonis recommended only in patients with immunodeficiency.Prevention of chickenpox can be obtained with the varicella vaccine that gives 100% protection to the virus
Primary Herpetic Gingivostomatitis
The oral mucosa is congested and edematous with many vesicles grouped in bunches. These vesicles will break down the next 24 hours into superficial, painful ulcerations covered by dark grey pseudo-membranes surrounded by an erythematous halo , Ulcerations will heal in 10 –14 days, leaving no marks.
Histopathologic examination: .CultureAntibodies titer.Immunologic testingusingDNA hybridization
TreatmentSevere casesAcyclovir-systemic or suspension-200mg/5mlRodilemidi.m. 10 days/ month -3 monthsMild and medium forms-symptomaticAntipyreticsLiquid diet (for hydration and electrolyte balance)Topic anesthetics(dyclorinehydrochloride 0,5-1%,benzocainegel 20%, xylocaineviscous 2%, lidocaine5%).Rigorous oral hygiene with antiseptic solutions (Clorhexidine0, 4%) or local application with gentian violet 2% or methyleneblue 1%.
major aphthous
chemical ulcer
1**chemical substances used in dental practice could cause iatrogenic ulcerative lesions of
the oral mucosa when applied incorrectly. Thus,
phenol, trichloroacetic acid eugenol, silver nitrate, formaldehyde, sodium hypochlorite,
etc could cause burns of the oral mucosa and
superficial ulcerations that will heal spontaneously within 4 to 7 days. chemistry
2**there are cases of lesions of the mucosa caused by aspirin or alcohol applied by the patient on the painful tooth. Thus, a tissue necrosis with painful erosions occurs on that specific spot and it will heal in a week time.
caused by asprin this pic!!!
NOMA (cancrum oris, gangrenous stomatitis, necrotic stomatitis)
ask if the patient can have AIDS ? since the clinical aspects are very much like the acute and chronic lukemia….
From a clinical point of view, the disease can start as an acute ulcerative-necrotic gingivitis
Necrotic areas could also occur on the soft areas as a consequence of traumatic lesions without any continuity to the gingiva
Gangrenous ulcerations are covered by fibrinoid white-grey deposits
Treatment: consists of preventing and eliminating the predisposing factors, diet rebalancing,
hydration and antibiotic therapy (penicillin and metronidazole). Locally, the necrotic tissue will be removed and reconstructive surgery will be performed one year later
In the absence of any treatment, mortality rate reaches 95%,
c.t : based on clinical aspect and culture media since the etiology of the disease is bacterial
Pemphigus vulgaris
Vesicles or bullaspainful erosions that tend to peripheral expansion Eruptions.
Characteristic signs: Nicolsky, Asboe-Hansen
Lesions can be found in any area of the oral mucosa, with a predilection for:-palate -jugalmucosa -lower lip -oral floor
complementary test: Cytological examination -shows the presence of typical acantholyticcells(Tzanckcells) with large, hyperchromaticnuclei.Histopathologicalexaminationfrom a biopsytaken from a perilesionalskin shows the integrity of basal layer and the acantholysisof the spinouslayer.Direct immunofluorescenceIndirect immunofluorescence
Treatament :
sistemic: high doses of prednisone(Prednison) on alternate days with immunosuppressants:Azathioprine, Methotrexate, Cyclophosphamideparenteral administration of gold salts, etretinate, dapsoneand plasmapheresis( in patients refractory to corticosteroid therapy)
local: a rigorous local hygiene ,
mouth rinses with antiseptic solutions-Clorhexidine-0,2%
Topical anesthetics(Lidocaine 5%)
Topical steroids:ELOCOM-crème:3,4 apl./day
The Lyell syndrome(toxic epidermal necrolysis)
It is the most serious form of erythema multiforme, sometimes fatal,
Clinically, it is characterized by bullous lesions that may involve the entiresurface of skin and mucous membranes. If the patient survives, cutaneous manifestations subside in 2-4 weeks. Oral lesions heal much slowerand the ocular ones, causing disability are found in½ of the patients.Positive diagnosis isbased on clinical data.The histopathological exam and the immunopathological tests are not specificfor erythema multiforme. However, the presence of Ig M, the complement and fibrin in dermal vessel walls, is an indication of immune-complex vasculitis and implicitly is the cause of erythema multiforme. The differential diagnosis includes: -Primary herpetic gingivostomatitis -Pemphigus vulgaris -Cicatricial and bullous pemphigoid-Erosive lichen planus -Recurrent aphthous ulcersTreatment: in common forms of the disease, the topical administration of corticosteroids, antibiotics, analgesics, antifungals has been recommended. In severe cases, average doses of systemic corticosteroidsand high doses of antibiotics are recommended. The treatment is the prerogative of the dermatologist.
angular chelitis
angular chelitis
is a type of chronic candidiasis
bilateral , painful, can be seen yellow-brownish granular nodules or an erythematous cracked zones with peripheral crusts
C.T NO NEED
TREATMENT:MICONAZOLE GEL 2% 4-6 APPLICATIONS A DAY BOTH ON TH MUCOSA and the prosthetic field
antifungal antibiotic therapy
Varicella (chickenpox)
Oral lesionsare common and mostly located on the palate and lips and sometimes they precede the skin
lesions. Vesicles are small (3-4 mm) and quickly turn into erosions surrounded by an erythematous halo.
Positive diagnosisis based on epidemiologic data and clinical manifestations.
Treatmentis supportive: rigorous body hygiene, mint alcohol 1% or mint talcwill help prevent pruritus, antihistamines and antipyretics.Children and teenagers will not be treated with aspirin because of the high risk of developing Reye syndrome(a rare, yet severe condition causing irreversible lesions such as acute encephalopathyand hepatic fatty degeneration).Antiseptic solutions are recommended for oral lesions.Antiviral medication including Acyclovir, Vidarabine or Interferonis recommended only in patients with immunodeficiency.Prevention of chickenpox can be obtained with the varicella vaccine that gives 100% protection to the virus
CICATRICIAL PEMPHIGOID
oral cavity; in 95% of cases it is the very first location of the disease and it may be the only affected location. Another feature is the tendency of lesions to remain localized in an area of the mucosa, most commonly on the gum, taking the look of a desquamativegingivitis
Oral lesions of cicatricial pemphigoid appear at onset as erosions similar tothose of pemphigus or as bullasor intact blisters. The ability to notice blisters or intact bullas is higher in this disease, compared to pemphigus because the lesions being subepithelial have a thicker coating.
Ocular lesionsare the second location in frequency after oral mucosa and they may cause the appearance of symblepharons, corneal opacities and even blindness
Complementary tests: Histopatological examDirectimmunofluorescenceDifferentialDiagnostic:Pemphigus vulgarisPemphigoid bullousBullousLichen planus
Treatament-depends on the severity of symptomstopical treatment with steroids (Clobetasol, Fluocinonide)therapy with Dapsonecorticosteroids combination + immunosuppressives( in severe cases)
CONTACT ALLERGIC STOMATITIS
Etiology: denture matterials, restorative matterials and mouth washes
Clinically, in the acute form, the affected
mucosa presents with diffuse erythema and edema, and occasionally small vesicles and erosions (Fig. 65). A burning sensation is a common symptom. In the chronic form, hyperkeratotic white lesions may be seen in addition to erythema
.Laboratory tests
Mucosal and skin patch tests
Treatment:
Removal of suspected allergens, topical or systemic steroids,antihistamines.
measles
Koplik’s spots. This is pathognomonic for measles and it consists of 10-12 isolated or grouped lesions on the buccal mucosa (in the region of the last molars); these lesions are very small, slightly bold, they have a white-bluish colour and are surrounded by a red halo. These formations occur 24-48 hours before the exanthema and quickly disappear leaving hemorrhagic spots on the congested mucosa.
Cutaneous rash occurs 3 –4 days after prodromal phase and it is characterisedby a maculo-papular eruption that starts behind the back of the ears and the frontal region; duringthe next 24 hoursit quickly spreadsto cover the rest of the face, neck, torso and extremities
Positive diagnosisis based on clinical symptoms and signs
Treatmentis supportive and it includes:-hygiene and diet regime-antipyretics-painkillers-cough remediesAntibiotics are recommended only when complications occur.
gumma
TERTIARY SYPHILIS
1/3 OF 1/3 cases of syphilis will develop the third
It is mainly characterized by:
neurological manifestations
cardiovascular lesions
lesions of the skin and mucosa
bone lesions
3 LESIONS
GUMA >>>> HARD PALATE FISTUA
From an evolution point of view, gumma knows 4 stages:-rawness-softening-ulceration-healing
The size of the lesion varies from 1 to 10 cm.It is most frequently located on the hard palate
ATROPHIC GLOSITIS
is the consequence of a vasculitis that evolves into an obliteratingendarteritis, causing the atrophy of both the mucosa and the muscle of the tongue. Consequently, the dorsal part of the tongue becomes neat and atrophic.
SCLROTIC GLLOSITIS
is the result of tongue becoming deformed once a gumma has healed. Consequently, the tongue has a lobulated appearancewith deep and irregular ditches
acute pseudomembranous candidiasis
in this situation the mouth is dry and burning with dyphagia
white or white yellowish patches that can be easily wiped away to reveal the erythematous beneath
located : can be seen everywhere in oral cavity but mostly palate , tongue , jugal mucosa
C.T: based on clinical examination and culture media on different media and direct microscopic examination
Recurrent aphthae(recurrent herpetic aphthousstomatitis)
becareful not to confuse this and secondary herpes
discoid lupus erythematosous
angular chelitis
is a type of chronic candidiasis
bilateral , painful, can be seen yellow-brownish granular nodules or an erythematous cracked zones with peripheral crusts
C.T NO NEED
TREATMENT:MICONAZOLE GEL 2% 4-6 APPLICATIONS A DAY BOTH ON TH MUCOSA and the prosthetic field
antifungal antibiotic therapy
acute pseudomembranous candidiasis
in this situation the mouth is dry and burning with dyphagia
white or white yellowish patches that can be easily wiped away to reveal the erythematous beneath
located : can be seen everywhere in oral cavity but mostly palate , tongue , jugal mucosa
C.T: based on clinical examination and culture media on different media and direct microscopic examination
nicotinic stomatitis
heavy smokers pipe smokers no prosthesis appliance starts with deussed erythema and then epithelium gets hyperkeratinazed and become thick . small red dots are covering the orifficess of the salivary glands////location mainly palatin veil
histopathalogical examination
stopsmoking
NOMA (cancrum oris, gangrenous stomatitis, necrotic stomatitis)
ask if the patient can have AIDS ? since the clinical aspects are very much like the acute and chronic lukemia….
From a clinical point of view, the disease can start as an acute ulcerative-necrotic gingivitis
Necrotic areas could also occur on the soft areas as a consequence of traumatic lesions without any continuity to the gingiva
Gangrenous ulcerations are covered by fibrinoid white-grey deposits
Treatment: consists of preventing and eliminating the predisposing factors, diet rebalancing,
hydration and antibiotic therapy (penicillin and metronidazole). Locally, the necrotic tissue will be removed and reconstructive surgery will be performed one year later
In the absence of any treatment, mortality rate reaches 95%,
c.t : based on clinical aspect and culture media since the etiology of the disease is bacterial
atrophic form of lichen planus
red, atrophic not ulcerative
loc: gingiva
c. t general stuff
non -specific clinical aspect is desquamated gingivitis”(fig. 89) and it interests symmetrically each of the four quarters
The symptoms accompanying this condition are irritation, burns or dryness of the mucosa.
treatment :cyclosporine, coricoid creams,TACROLIMUS
chronic leukemia
clinical: less severe than the acute form
pale oral mucosa , sometimes associated with ulcerated causes, gingival hyperplasia
leukemic nodules can be observed on the palatinenfiber-mucosa
C,T : peripheral blood analysis
medulograma>>>bone marrow analysis tosee if there is any leukemic cells
also send the patient to th haemotologist
treatment:like the acute one >>>>
send tohaemotologist
thrombin sponge in case of bleeding
Bullous lichen planus
bulla or vesicles can be from mm tocm
they will burst into painfull erosions located normally on the juggal mucosa near the wisdom tooth.
Reticular Striae are presents at the peripheral area of the lesion.
C.T histopathalogical
Treatment : no specific treatment
secondary herpetic stomatitis
numerous vesicles grouped in bunches, most commonly located on the hard palate and the gingival fiber-mucosa During the next few hours vesicles will break down into ulcerations (1-3 mm diameter) that will spontaneously heal the next 7-10 days, leaving no visible marks.
Differential diagnosisincludes:Recurrent aphthae(recurrent herpetic aphthous stomatitis)
Treatmentis supportive. Acyclovir is efficient when administered systematically(200mg x5/7 days)and it prevents recurrence, although it is not to be used in occasional or minor manifestations of the condition.
c.t : no need, based on clinical examination
herpes zoster
Intraoral eruption is preceded by pain that can mimic pulpitis. Vesicles are grouped in bunches, breaking down after 2-3 days into ulcerations circumscribed by an erithematousborder.Healing process will take 2 –3 weeks leaving no marks.The location of the lesions on one side only is the main clinical sign of herpes zoster
The most frequent complication of this condition is residual trigeminal neuralgia that can last for weeks or months
Positive diagnosis of oral lesions is established following clinical criteria.
TreatmentTargetsthe reduction of the duration of disease,preventing post-herpetic neuralgia the dissemination in patients with immunodeficiency.Acyclovir<50 years old-200 mg x 5/day, 7-10 days>50 years old-800 mg x 5 /day, 7-10 daysCapsaicina–local therapy Xylineor Novocain infiltration on the affected nerve.
chemical ulcer
1**chemical substances used in dental practice could cause iatrogenic ulcerative lesions of
the oral mucosa when applied incorrectly. Thus,
phenol, trichloroacetic acid eugenol, silver nitrate, formaldehyde, sodium hypochlorite,
etc could cause burns of the oral mucosa and
superficial ulcerations that will heal spontaneously within 4 to 7 days. chemistry
2**there are cases of lesions of the mucosa caused by aspirin or alcohol applied by the patient on the painful tooth. Thus, a tissue necrosis with painful erosions occurs on that specific spot and it will heal in a week time.
Pemphigus vulgaris
Vesicles or bullaspainful erosions that tend to peripheral expansion Eruptions.
Characteristic signs: Nicolsky, Asboe-Hansen
Lesions can be found in any area of the oral mucosa, with a predilection for:-palate -jugalmucosa -lower lip -oral floor
complementary test: Cytological examination -shows the presence of typical acantholyticcells(Tzanckcells) with large, hyperchromaticnuclei.Histopathologicalexaminationfrom a biopsytaken from a perilesionalskin shows the integrity of basal layer and the acantholysisof the spinouslayer.Direct immunofluorescenceIndirect immunofluorescence
Treatament :
sistemic: high doses of prednisone(Prednison) on alternate days with immunosuppressants:Azathioprine, Methotrexate, Cyclophosphamideparenteral administration of gold salts, etretinate, dapsoneand plasmapheresis( in patients refractory to corticosteroid therapy)
local: a rigorous local hygiene ,
mouth rinses with antiseptic solutions-Clorhexidine-0,2%
Topical anesthetics(Lidocaine 5%)
Topical steroids:ELOCOM-crème:3,4 apl./day
major aphthous
SECOND SYPHILIS
2ND SYPHiLIS
dark-red macular eruption -syphilitic rosella, located mainly on the posterior side of the oral cavity. Further on, there will appearmucous plaquesrepresenting the most frequent manifestation of thisstage. From a clinical point of view, they are oval, slightly bolded and turning into opalescent, white-grey plaques and surrounded by an erythematous margin. The superficial layer is removed and slightly painful, possibly bleeding ulcers are revealed
Laboratory examinations-serologic tests are positive-dark field microscopic examination and immunofluorescence examination
treatment : same as other syphilises
acute pseudomembranous candidiasis
in this situation the mouth is dry and burning with dyphagia
white or white yellowish patches that can be easily wiped away to reveal the erythematous beneath
located : can be seen everywhere in oral cavity but mostly palate , tongue , jugal mucosa
C.T: based on clinical examination and culture media on different media and direct microscopic examination
angular chelitis
is a type of chronic candidiasis
bilateral , painful, can be seen yellow-brownish granular nodules or an erythematous cracked zones with peripheral crusts
C.T NO NEED
TREATMENT:MICONAZOLE GEL 2% 4-6 APPLICATIONS A DAY BOTH ON TH MUCOSA and the prosthetic field
antifungal antibiotic therapy
median rhomboid glositis
is a kind of chronic candidiasis
central papillary atrophy of the tongue
clinicalfeatures: first soft red denudated patch located on the median line of the dorsal side of the tongue ,,,,,,,,,,,,,,,,,later it gets hard and lobulated ,,,,,it is - cm oval or rhombic with rounded borders
Kaposi’s sarcoma
its an endothelial cells malignancy
4 types: classic kaposi’s sarcoma (skin lesion)
african kaposi’s sarcoma(skin lesions)
aquired kaposi’s sarcoma (skin)
EPIDEMIC KAPOSI’S SARCOMA :OVER 50% of the patients showed oral manifestation
lesion has 3 stages>>> first its assymptomatic erythematous that dont disappear after pressure >>>then it gets bigger and it will turn into red-blue or purple papular lesion>>> and at the advanced stages sarcoma appears purplish,blue nodules that can bleed and its painful.
located on jugal mucosa, dorsal face of the tongue, half of the palate, on the gingiva
C.T is biopsy
treatment: radiotherapy surgery, chemotherapy Co2 laser
SECONDARY SYPHILIS
2ND SYPHiLIS
dark-red macular eruption -syphilitic rosella, located mainly on the posterior side of the oral cavity. Further on, there will appearmucous plaquesrepresenting the most frequent manifestation of thisstage. From a clinical point of view, they are oval, slightly bolded and turning into opalescent, white-grey plaques and surrounded by an erythematous margin. The superficial layer is removed and slightly painful, possibly bleeding ulcers are revealed
Laboratory examinations-serologic tests are positive-dark field microscopic examination and immunofluorescence examination
treatment : same as other syphilises
pseudomem candid
acute pseudomembranous candidiasis
in this situation the mouth is dry and burning with dyphagia
white or white yellowish patches that can be easily wiped away to reveal the erythematous beneath
located : can be seen everywhere in oral cavity but mostly palate , tongue , jugal mucosa
C.T: based on clinical examination and culture media on different media and direct microscopic examination
measles
Koplik’s spots. This is pathognomonic for measles and it consists of 10-12 isolated or grouped lesions on the buccal mucosa (in the region of the last molars); these lesions are very small, slightly bold, they have a white-bluish colour and are surrounded by a red halo. These formations occur 24-48 hours before the exanthema and quickly disappear leaving hemorrhagic spots on the congested mucosa.
Cutaneous rash occurs 3 –4 days after prodromal phase and it is characterisedby a maculo-papular eruption that starts behind the back of the ears and the frontal region; duringthe next 24 hoursit quickly spreadsto cover the rest of the face, neck, torso and extremities
Positive diagnosisis based on clinical symptoms and signs
Treatmentis supportive and it includes:-hygiene and diet regime-antipyretics-painkillers-cough remediesAntibiotics are recommended only when complications occur.
acute leukemia
clinical signs: hyperplastic swelling of vestibular and oral side of the mouth , pale or purplish gingiva , gingival hyperplasia, dental mobility , tonsil hypertrophy
C.T lab examination of the peripheral blood and bone marrow myelogram or medulogram >>>leukemic cells differentiation
treatment: send the patient to a haemotologist …. any dental procedure needs the approval or presence of the haemotologist.
thrombin sponges in case of gingival bleeding.
reticular form of lichen planus
reticular lichen planus
reticularform of lichen planus
reticular lichen planus
most common tupe of planus
common location: jugal mucosa bilateral , but also on lips tongue , gingiva
clinical aspect: keratotic lesions called wicham straiae (so many)
C.test: histopathalogical test
immunofluorocense tet
treatment: assymptomatic lesion>>no treatment needed
symptomatic lesion>>>> systemic cyclosporine
labial herpes
Clinical aspect:-a discrete congestion and an edema of the vermilion border and the surrounding skin, -vesicle eruption, vesicle has 1-3 mm diameter, while the lesion reaches 1 –2 cm,-people with immunodeficiency will present larger lesions associated with discomfort and physiognomic alterations.The vesicles break down into ulcerations that will get covered by dry scabs and eventually heal in the course of 1 –2 weeks
Positive diagnosis -is based on clinical examination
TreatmentLocal therapy –acyclovir (Zovirax,Euvirox) 5%-ointment x5/day-penciclovir(Denavir)1% ,at 2h,4days-vidarabine3%-idoxuridine3%Systemic -valacyclovir(Valtrex) 4 g ( 2gx2)one doseProphylactic –ointments based on zinc oxide or titanium dioxide
