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Presented by
Dr. Shrikant Sonune
Guided by
Dr Ashok Patil,
Dr Shilpa Kandalgaonkar,
Dr Mayur Chaudhary,
Dr Suyog Tupsakhare,
Dr Mahesh Gabhane.
Introduction
Factors affecting color of oral mucosa
Normal variations
Classification of red lesions
Descriptions of all red lesions
Summary
Specialized
mucosa
Lining mucosa
Masticatory
mucosa
Wide spectrum of pink colors varying from a
dark pink(reddish) to a very pale pink(almost
white)
1. Lining mucosa --- Reddish pink
2. Masticatory mucosa--Light pink
Protective layer of keratin
Dense sub epithelial connective tissue
 Deep dusky red in color
contrast to light red
color of surrounding
tissue.
 Painless red macular
bands may present
 Richer blood supply
 Individual normal
variation
Vascularity
Thickness & degree of keratinization
Presence of pigmentation
Presence of inflammation
Duration
Associated with pain
Associated with habit
Other systemic manifestations
Any known cause
SOLITARY GENERALIZED RED TONGUE LESIONS
1. Traumatic erythematous macules &
erosions
2. Purpuric macules(early stage)
3. Inflammatory fibrous hyperplasia lesions
4. Nonpyogenic soft tissue odontogenic
infections
5. Chemical or thermal erythematous
macule
6. Nicotine Stomatitis
8) Erythroplakia
9) Carcinoma in situ
10) Red macular Squamous cell carcinoma
11) Candidiasis (atrophic / erythematous,
denture Stomatitis, angular Cheilitis)
12) Macular hemangioma & telangiectasia
13) Allergic macules
14) Vesiculobullous disease
15) Metastatic tumor of soft tissue
Vascular dilations from
a. Inflammation (Erythema)
b. Congenital defects(e.g. hemangioma)
 Extravasations of blood (e.g. trauma
hemostatic disease or both)
 Atrophy or erosion of mucosa
 Marked increase in hemoglobin
concentration of circulating blood
 Inflammation
(Erythema)
 Mechanical trauma
 Thermal trauma
 Chemical trauma
 Infections
 Ulcer with inflamed rim
 Congenital defects(e.g.
hemangioma)
 Erythematous macule
 Erosion
 The purpuric macule
 Granulomatous stage of inflammatory
hyperplasia
Etiology --Produce by low grade, usually
chronic physical insult
 Sharp margins of teeth & restorations
 Ill-fitting prosthesis
 Self inflected trauma
 Habits
Clinical feature (c/f)
 Erythematous macule are
on
 Anterior & lateral border of
tongue
 Cheek mucosa
 Lip mucosa
 Margins may or may not be
sharply defined
 Mild tenderness
 Digital pressure may
cause blanching
 Regress quickly
after removal of
cause
H/P
Inflamed lamina propria
Slightly thinned or Eroded stratified
Squamous epithelium
D/D
 Purpuric macule h/o trauma
 Purpuric macule of oral sex
 Macular hemangioma
 Atrophic Candidiasis
 Mononucleosis
 Herpangina (not transient)
 Caused due to blunt trauma which is sufficient
force to cause the extravasations of blood.
 Soon after the traumatic damage, lesion is red
afterwards converts into blue color.
 Borders are poorly demarcated
 Blanching on pressure does not usually occur
 May also have secondary inflammatory
component.
 Slight extravasations
of blood .
 The purpuric macule
due to oral
sexual practices.
 Reddish
 Elliptical
 Purpuric macule
 Occurring on palatal mucosa
 near the junction of the hard & soft palate.
 Disappear within 2 to 3 days
 Judicial history with confidential setting revel
the true identity.
D/D
 Traumatic Erythematous macule h/o
 Purpuric macule of oral sex trauma
 Macular hemangioma
 Atrophic Candidiasis
 Mononucleosis
 Herpangina
Traumatic origin
Prolonged chronic physical stimulus can
induce the production of granulation tissue
Mass of inflamed granulation tissue &
clinically appears as soft & vary red.
Reversible lesion up to this stage.
H/P
Granulomatous tissue
Covering epithelium is usually intact
1. Pyogenic granuloma
2. Hormonal tumor
3. Epulis fissuratum
4. Papillary hyperplasia
5. PGCG
6. Peripheral fibroma with calcification
Excisional biopsy
Elimination of irritant
(priority depends on clinical judgment)
Caustic drugs or hot foods or beverages
Depends on duration & intensity of stimuli
Stimuli may produce coagulative necrosis
of superficial tissues that appears white
After scraping off that white layer it may
produce clinically appreciable red lesion
Ulceration & properly stripping off mucosa
Tender to painful
May blanch on pressure
Size & shape varies depend on stimuli.
D/d
Erythema from mechanical trauma
Purpuric macule
Erythroplakia
Atrophic Candidiasis
Other names
 Leukokeratosis nicotina palati,
 Smokers palate,
 Nicotine palatinus
Conventional smokers
Is seen primarily on the palate of pipe
smokers.
Also seen in bidi smoker
Does not having premalignant nature
It develops in response to heat rather than
tobacco.
Appears red in initial stage
In later keratotic
stage minor salivary
duct orifices
appear red
Men , 4-5 decade
 H/p
 Hyperkeratosis
 Acanthosis
 Squamous metaplasia
 Chronic inflammation of subepithelial
connective tissue
 Inflammatory exudate within duct
D/d
Lesions associated with reverse smoking
Denture Stomatitis
Atrophic Candidiasis
Erythroplakia
• Commonly seen on buccal mucosa , floor of mouth,
tongue
Definition –
Persistent velvety red patch that can not be
identified as any other specific red lesion such as
inflammatory Erythema or those produce by blood
vessel anomalies or infection.
It appear red because
Absences of surface keratin layer
Connective tissue papillae, containing
enlarge capillaries, project close to the
surface.
C/F-
• Velvety red or
granular red macules.
• Varies greatly in size
• Borders may be
well defined
• Painless
• Drying of the mucosa will intensify the red colour
Types
Homogenous erythroplakia
Erythroplakia interspread with patches of
Leukoplakia
Speckled erythroplakia
The lesion may have an irregular, red
granular surface interspersed with white
or yellow foci, which may be described as
granular erythroplakia.
There may be numerous, small irregular
foci of leukoplakia dispersed in the
erythroplakic patch, and this has been
called speckled leukoplakia.
Oral erythroplakia is soft to palpation and
does not become indurated or hard until an
invasive carcinoma develops.
 Histopathologically
erythroplakia almost
always show dysplasia,
carcinoma in situ or
invasive squamous cell
carcinoma.
 Epithelium is frequently
atrophic with lack of
keratin production.
 The connective tissue
demonstrates chronic
inflammation.
If the lesion persist for more than 21 days
after all local trauma & infections foci have
been eliminated, biopsy is mandatory.
D/D-
Traumatic Erythema
Atrophic Candidiasis
Purpuric macules
Malignant epithelial neoplasm exhibiting
Squamous differentiation as characterized
by formation of keratin & / or presence of
intercellular bridges
(pinborg JJ 1997)
Annually, nearly 30,000 new cases of oral
and oropharyngeal cancer are expected to
occur in men and women in the United
Sates.
The ratio of cases in men and women is
now about 2 to 1.
Tobacco,
Typically mixed with areca (betel) nut,
Slaked lime,
All forms of tobacco smoking
Reverse smoking
Alcohol
Poor nutritional status
HPV 16 & 18 has some role in the
development of OSCC.
Ultraviolet (UV) light
 A compromised immune system
 Chronic irritation
The first is loss of cell cycle control through
increased proliferation and reduced
apoptosis.
The second stage is increased tumor cell
motility, leading to invasion and
metastasis.
 Carcinoma of the Lips:
 Carcinomas of the lower lip are far more
common than upper lip lesions.
 Pipe smoking, uv light exposure.
 The growth rate is slower for lower lip
 Favorable prognosis
 Account for 25% to 30% of all oral cancers
Lesions arise on the vermilion surface
Appear as a chronic non healing ulcer
(Exophytic ,verrucous type may present)
Deep invasion -- later in the course of the
disease.
Metastasis to local submental or
Submandibular lymph nodes is uncommon
One of the most common intraoral
malignancy.
Predilection for men (6-8th decade)
However, lesions may uncommonly be
found in the very young.
Exhibit a particularly aggressive behavior.
Lingual carcinoma is typically
asymptomatic.
As deep invasion occurs, pain or dysphagia
may be a prominent patient complaint.
Appear in one of four ways:
 indurated, nonhealing ulcer,
 a red lesion,
 a white lesion,
 a red-and-white lesion.
The neoplasm may occasionally have a
prominent exophytic, as well as
endophytic, growth pattern
The most common location of cancer of the
tongue is the posterior-lateral border.
Specific reason is due to chronic irritation
because of tooth
Approximately 1/4th of tongue cancers
occur in the posterior one third or base of
the tongue.
 Metastases from tongue cancer are relatively
common.
 The first nodes to become involved are the
submandibular lymph node.
 Uncommonly, distant metastatic deposits may
be seen in the lung or the liver.
Second most common intraoral location of
squamous cell carcinomas.
Predominantly in older men,
 Painless, nonhealing, indurated ulcer.
 It may also appear as a white or red patch.
 May widely infiltrate the soft tissues of the floor
of the mouth,
 Decreased mobility of the tongue.
 Metastasis to Submandibular lymph nodes is
common
Predominantly in Men
Clinical appearance varies from a white
patch to a nonhealing ulcer to an exophytic
lesion.
It is slow growing
Usually well differentiated,
Rarely metastasizes,
Has a favorable prognosis
Palatal squamous cell carcinomas
generally present as asymptomatic red
or white plaques or as ulcerated and
keratotic masses
1. Well differentiated:
 It consists of sheets and nests of cells of
squamous epithelium.
 Cells are large and show distinct cell
membrane but intercellular bridges or
tonofibrils are not seen.
 Pleomorphic nuclei and becomes
hyperchromatic.
Mitotic figures are seen but not numerous.
Individual cell keratinization and
formation of numerous keratin pearl.
Group of cells invades underlying
connective tissue.
Shape of cells and their arrangement may
be altered.
The growth rate of individual cells is more
rapid and this is reflected in the greater
numbers of mitotic figures.
Keratin pearl formation may or may not be
seen.
More pleomorphic cells.
Loss of keratinization and keratin pearl.
Loss of individual cell differentiation.
Increase mitotic figures.
D/D-
Inflammatory hyperplasia
Papilloma
Erythroplakia
Leukoplakia
 Coxsackie virus A4 -cause a majority of cases
of Herpangina,
 Types A1 to A10, A16 to A22
 Herpangina may be seen more than once in
the same patient.
 Herpangina frequently occurs in epidemics
 The majority of cases affect young children
adolescents.
Clinical Manifestations.
After a 2- to 10-day incubation period,
The infection begins with generalized
symptoms of fever, chills, and anorexia.
The fever and other symptoms are
generally milder than those experienced
with primary HSV infection.
The patient complains of sore throat,
dysphagia, and occasionally sore mouth.
 Lesions start as punctate macules, which
quickly evolve into papules and vesicles
involving the posterior pharynx, tonsils,
faucial pillars, and soft palate.
 Lesions are found less frequently on the
buccal mucosa, tongue, and hard palate.
Within 24 to 48 hours, the vesicles rupture,
forming small 1 to 2 mm ulcers.
The disease is usually mild and heals
without treatment in 1 week.
Definition Infectious mononucleosis is an acute,
self-limited infectious disease that primarily affects
children.
Etiology
Epstein–Barr virus transmitted through saliva
transfer,
Cytomegalovirus (CMV)
CMV is the major cause of non-Epstein-Barr virus
infectious mononucleosis in the general
population.
The oral manifestations are early and
common, and consist of
 palatal petechiae,
 uvular edema,
 tonsillar exudate,
 gingivitis,
 rarely ulcers
Generalized
 lymphadenopathy,
 hepatosplenomegaly,
 maculopapular skin rash,
 sore throat are common.
 Prodromal symptoms such as anorexia,
malaise, headache, fatigue, and later fever
occur before the clinical manifestations.
Differential diagnosis
Fellatio,
Thrombocytopenic purpura,
Caused by Nonpyogenic bacteria
Prepyogenic
Postpyogenic state
 It is the infection with yeast like fungus Candida albicans
 Earlier termed moniliasis
 Types
ACUTE CHRONIC
Psuedomembranous Hyperplastic
Atrophic Mucocutaneous
Atrophic
Candidiasis
clinical type Appearance
Erythematous Red
Atrophic Red
Hyperplastic White, red raised
Mixed Red/ white keratotic / white necrotic
Mucocutaneous Lip/ angles
Psuedomembranous White lesion
ACUTE ATROPHIC
Acute atrophic Candidiasis/Antibiotic sore
mouth
Painful mucosa due to broad spectrum
antibiotics
Angular Cheilitis- Erythema, fissuring of
angles of mouth
D/D-
 Chemical burn
 Drug reactions
 Syphilitic mucous patches
 Necrotic ulcers
 Traumatic ulcer
 Contact allergy
CHRONIC ATROPHIC
Due to denture cuts off the underlying
mucosa from the protective action of
saliva.
The erythema is sharply limited to the area
of mucosa occluded by a well-fitting upper
denture or even an orthodontic plate.
Hyphae proliferates in denture mucosal
interface
Gram staining shows gram +ve hyphae.
It is red colored unraised area usually
present on buccal mucosa.
It is usually capillary type,
Also occur as port wine stain on skin.
History of long duration
It is non tender
Even no inflammatory component
Absence of recurrent traumatic episode
References-
 Text book of oral and maxillofacial
pathology- Neville
 Differential diagnosis of oral lesions by-
Wood and Goaz, Fifth Edition
 Shafer’s textbook of oral pathology 6th
edition .
 Textbook of oral medicine Burkait 10th
edition .
1. Traumatic erythematous macules & erosions
2. Purpuric macules(early stage)
3. Inflammatory fibrous hyperplasia lesions
4. Nonpyogenic soft tissue odontogenic
infections
5. Chemical or thermal erythematous macule
6. Nicotine Stomatitis
7. Erythroplakia
8. Carcinoma in situ
9. Red macular Squamous cell carcinoma
10. Candidiasis (atrophic / erythematous,
denture Stomatitis, angular Cheilitis)
16. Actinomycosis
17. Anemia (solitary red patch)
18. Amyloidosis
19. Angiosarcoma
23. Blastomycosis
24. Candidiasis endocrinopathy syndrome
25. Crohn’s disease
25. Coccidiodimycosis
26. Dermatitis herpetiformis
27. Erysipelas
28. Exfoliative Cheilitis
29. Gonococcal infection
30. Graft – versus – host disease (GVHD)
31. Herpangina
32. Histoplasmosis
33. Hyperemic oral tonsils
34. Larva migrans
35. Lichen planus
36. Lupus erythematous
37. Ludwig’s angina
38. Lymphonodular pharyngitis
39. Multinucleate cell angiohistiocytoma
40. Mycosis fungoides
41. Non- Hodgkin's lymphoma
42. Peripheral Ameloblastoma
43. Plasma cell gingivitis
44. Psoriasis
45. Sarcoidosis
46. Secondary syphilis
47. Self mutilation
48. Subacute necrotizing sialadenitis
49. Tuberculosis
50. Tumoral calcinosis
Thank you
Increase Vascularity
Decrease thickness of epithelium
Decrease keratinization
Inflammation
Mechanical trauma
Increase Hb content
 extravasations of blood
Connective tissue papillae, containing
enlarge capillaries, project close to the
surface.
Blood supply
Thick cortical plate
Gravity
Food lodgment
Dysplasia involving full vertical & horizontal
thickness of epithelium along with basilar
hyperplasia

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Red lesion of oral mucosa

  • 1. Presented by Dr. Shrikant Sonune Guided by Dr Ashok Patil, Dr Shilpa Kandalgaonkar, Dr Mayur Chaudhary, Dr Suyog Tupsakhare, Dr Mahesh Gabhane.
  • 2. Introduction Factors affecting color of oral mucosa Normal variations Classification of red lesions Descriptions of all red lesions Summary
  • 3.
  • 5. Wide spectrum of pink colors varying from a dark pink(reddish) to a very pale pink(almost white) 1. Lining mucosa --- Reddish pink 2. Masticatory mucosa--Light pink Protective layer of keratin Dense sub epithelial connective tissue
  • 6.  Deep dusky red in color contrast to light red color of surrounding tissue.  Painless red macular bands may present  Richer blood supply  Individual normal variation
  • 7. Vascularity Thickness & degree of keratinization Presence of pigmentation Presence of inflammation
  • 8. Duration Associated with pain Associated with habit Other systemic manifestations Any known cause
  • 9. SOLITARY GENERALIZED RED TONGUE LESIONS
  • 10. 1. Traumatic erythematous macules & erosions 2. Purpuric macules(early stage) 3. Inflammatory fibrous hyperplasia lesions 4. Nonpyogenic soft tissue odontogenic infections 5. Chemical or thermal erythematous macule 6. Nicotine Stomatitis
  • 11. 8) Erythroplakia 9) Carcinoma in situ 10) Red macular Squamous cell carcinoma 11) Candidiasis (atrophic / erythematous, denture Stomatitis, angular Cheilitis) 12) Macular hemangioma & telangiectasia 13) Allergic macules 14) Vesiculobullous disease 15) Metastatic tumor of soft tissue
  • 12. Vascular dilations from a. Inflammation (Erythema) b. Congenital defects(e.g. hemangioma)  Extravasations of blood (e.g. trauma hemostatic disease or both)  Atrophy or erosion of mucosa  Marked increase in hemoglobin concentration of circulating blood
  • 13.  Inflammation (Erythema)  Mechanical trauma  Thermal trauma  Chemical trauma  Infections  Ulcer with inflamed rim  Congenital defects(e.g. hemangioma)
  • 14.  Erythematous macule  Erosion  The purpuric macule  Granulomatous stage of inflammatory hyperplasia
  • 15. Etiology --Produce by low grade, usually chronic physical insult  Sharp margins of teeth & restorations  Ill-fitting prosthesis  Self inflected trauma  Habits
  • 16. Clinical feature (c/f)  Erythematous macule are on  Anterior & lateral border of tongue  Cheek mucosa  Lip mucosa  Margins may or may not be sharply defined
  • 17.  Mild tenderness  Digital pressure may cause blanching  Regress quickly after removal of cause
  • 18. H/P Inflamed lamina propria Slightly thinned or Eroded stratified Squamous epithelium
  • 19. D/D  Purpuric macule h/o trauma  Purpuric macule of oral sex  Macular hemangioma  Atrophic Candidiasis  Mononucleosis  Herpangina (not transient)
  • 20.  Caused due to blunt trauma which is sufficient force to cause the extravasations of blood.  Soon after the traumatic damage, lesion is red afterwards converts into blue color.  Borders are poorly demarcated  Blanching on pressure does not usually occur  May also have secondary inflammatory component.
  • 22.  The purpuric macule due to oral sexual practices.  Reddish  Elliptical  Purpuric macule  Occurring on palatal mucosa  near the junction of the hard & soft palate.  Disappear within 2 to 3 days  Judicial history with confidential setting revel the true identity.
  • 23. D/D  Traumatic Erythematous macule h/o  Purpuric macule of oral sex trauma  Macular hemangioma  Atrophic Candidiasis  Mononucleosis  Herpangina
  • 24. Traumatic origin Prolonged chronic physical stimulus can induce the production of granulation tissue
  • 25. Mass of inflamed granulation tissue & clinically appears as soft & vary red. Reversible lesion up to this stage.
  • 27. 1. Pyogenic granuloma 2. Hormonal tumor 3. Epulis fissuratum 4. Papillary hyperplasia 5. PGCG 6. Peripheral fibroma with calcification
  • 28.
  • 29.
  • 30.
  • 31.
  • 32.
  • 33.
  • 34. Excisional biopsy Elimination of irritant (priority depends on clinical judgment)
  • 35. Caustic drugs or hot foods or beverages Depends on duration & intensity of stimuli Stimuli may produce coagulative necrosis of superficial tissues that appears white After scraping off that white layer it may produce clinically appreciable red lesion
  • 36. Ulceration & properly stripping off mucosa Tender to painful May blanch on pressure Size & shape varies depend on stimuli.
  • 37.
  • 38. D/d Erythema from mechanical trauma Purpuric macule Erythroplakia Atrophic Candidiasis
  • 39. Other names  Leukokeratosis nicotina palati,  Smokers palate,  Nicotine palatinus
  • 40. Conventional smokers Is seen primarily on the palate of pipe smokers. Also seen in bidi smoker Does not having premalignant nature It develops in response to heat rather than tobacco.
  • 41. Appears red in initial stage In later keratotic stage minor salivary duct orifices appear red Men , 4-5 decade
  • 42.  H/p  Hyperkeratosis  Acanthosis  Squamous metaplasia  Chronic inflammation of subepithelial connective tissue  Inflammatory exudate within duct
  • 43. D/d Lesions associated with reverse smoking Denture Stomatitis Atrophic Candidiasis
  • 44. Erythroplakia • Commonly seen on buccal mucosa , floor of mouth, tongue Definition – Persistent velvety red patch that can not be identified as any other specific red lesion such as inflammatory Erythema or those produce by blood vessel anomalies or infection.
  • 45. It appear red because Absences of surface keratin layer Connective tissue papillae, containing enlarge capillaries, project close to the surface.
  • 46. C/F- • Velvety red or granular red macules. • Varies greatly in size • Borders may be well defined • Painless • Drying of the mucosa will intensify the red colour
  • 47. Types Homogenous erythroplakia Erythroplakia interspread with patches of Leukoplakia Speckled erythroplakia
  • 48. The lesion may have an irregular, red granular surface interspersed with white or yellow foci, which may be described as granular erythroplakia. There may be numerous, small irregular foci of leukoplakia dispersed in the erythroplakic patch, and this has been called speckled leukoplakia.
  • 49. Oral erythroplakia is soft to palpation and does not become indurated or hard until an invasive carcinoma develops.
  • 50.  Histopathologically erythroplakia almost always show dysplasia, carcinoma in situ or invasive squamous cell carcinoma.  Epithelium is frequently atrophic with lack of keratin production.  The connective tissue demonstrates chronic inflammation.
  • 51. If the lesion persist for more than 21 days after all local trauma & infections foci have been eliminated, biopsy is mandatory.
  • 53. Malignant epithelial neoplasm exhibiting Squamous differentiation as characterized by formation of keratin & / or presence of intercellular bridges (pinborg JJ 1997)
  • 54. Annually, nearly 30,000 new cases of oral and oropharyngeal cancer are expected to occur in men and women in the United Sates. The ratio of cases in men and women is now about 2 to 1.
  • 55. Tobacco, Typically mixed with areca (betel) nut, Slaked lime, All forms of tobacco smoking Reverse smoking Alcohol Poor nutritional status HPV 16 & 18 has some role in the development of OSCC. Ultraviolet (UV) light
  • 56.  A compromised immune system  Chronic irritation
  • 57. The first is loss of cell cycle control through increased proliferation and reduced apoptosis. The second stage is increased tumor cell motility, leading to invasion and metastasis.
  • 58.  Carcinoma of the Lips:  Carcinomas of the lower lip are far more common than upper lip lesions.  Pipe smoking, uv light exposure.  The growth rate is slower for lower lip  Favorable prognosis  Account for 25% to 30% of all oral cancers
  • 59. Lesions arise on the vermilion surface Appear as a chronic non healing ulcer (Exophytic ,verrucous type may present) Deep invasion -- later in the course of the disease. Metastasis to local submental or Submandibular lymph nodes is uncommon
  • 60.
  • 61. One of the most common intraoral malignancy. Predilection for men (6-8th decade) However, lesions may uncommonly be found in the very young.
  • 62. Exhibit a particularly aggressive behavior. Lingual carcinoma is typically asymptomatic. As deep invasion occurs, pain or dysphagia may be a prominent patient complaint.
  • 63. Appear in one of four ways:  indurated, nonhealing ulcer,  a red lesion,  a white lesion,  a red-and-white lesion.
  • 64. The neoplasm may occasionally have a prominent exophytic, as well as endophytic, growth pattern
  • 65. The most common location of cancer of the tongue is the posterior-lateral border. Specific reason is due to chronic irritation because of tooth Approximately 1/4th of tongue cancers occur in the posterior one third or base of the tongue.
  • 66.  Metastases from tongue cancer are relatively common.  The first nodes to become involved are the submandibular lymph node.  Uncommonly, distant metastatic deposits may be seen in the lung or the liver.
  • 67. Second most common intraoral location of squamous cell carcinomas. Predominantly in older men,
  • 68.  Painless, nonhealing, indurated ulcer.  It may also appear as a white or red patch.  May widely infiltrate the soft tissues of the floor of the mouth,  Decreased mobility of the tongue.  Metastasis to Submandibular lymph nodes is common
  • 69.
  • 70. Predominantly in Men Clinical appearance varies from a white patch to a nonhealing ulcer to an exophytic lesion.
  • 71. It is slow growing Usually well differentiated, Rarely metastasizes, Has a favorable prognosis
  • 72.
  • 73. Palatal squamous cell carcinomas generally present as asymptomatic red or white plaques or as ulcerated and keratotic masses
  • 74. 1. Well differentiated:  It consists of sheets and nests of cells of squamous epithelium.  Cells are large and show distinct cell membrane but intercellular bridges or tonofibrils are not seen.  Pleomorphic nuclei and becomes hyperchromatic.
  • 75. Mitotic figures are seen but not numerous. Individual cell keratinization and formation of numerous keratin pearl. Group of cells invades underlying connective tissue.
  • 76.
  • 77. Shape of cells and their arrangement may be altered. The growth rate of individual cells is more rapid and this is reflected in the greater numbers of mitotic figures. Keratin pearl formation may or may not be seen.
  • 78.
  • 79.
  • 80. More pleomorphic cells. Loss of keratinization and keratin pearl. Loss of individual cell differentiation. Increase mitotic figures.
  • 81.
  • 83.  Coxsackie virus A4 -cause a majority of cases of Herpangina,  Types A1 to A10, A16 to A22  Herpangina may be seen more than once in the same patient.  Herpangina frequently occurs in epidemics  The majority of cases affect young children adolescents.
  • 84. Clinical Manifestations. After a 2- to 10-day incubation period, The infection begins with generalized symptoms of fever, chills, and anorexia.
  • 85. The fever and other symptoms are generally milder than those experienced with primary HSV infection. The patient complains of sore throat, dysphagia, and occasionally sore mouth.
  • 86.  Lesions start as punctate macules, which quickly evolve into papules and vesicles involving the posterior pharynx, tonsils, faucial pillars, and soft palate.  Lesions are found less frequently on the buccal mucosa, tongue, and hard palate.
  • 87. Within 24 to 48 hours, the vesicles rupture, forming small 1 to 2 mm ulcers. The disease is usually mild and heals without treatment in 1 week.
  • 88. Definition Infectious mononucleosis is an acute, self-limited infectious disease that primarily affects children. Etiology Epstein–Barr virus transmitted through saliva transfer, Cytomegalovirus (CMV) CMV is the major cause of non-Epstein-Barr virus infectious mononucleosis in the general population.
  • 89. The oral manifestations are early and common, and consist of  palatal petechiae,  uvular edema,  tonsillar exudate,  gingivitis,  rarely ulcers
  • 90. Generalized  lymphadenopathy,  hepatosplenomegaly,  maculopapular skin rash,  sore throat are common.  Prodromal symptoms such as anorexia, malaise, headache, fatigue, and later fever occur before the clinical manifestations.
  • 92. Caused by Nonpyogenic bacteria Prepyogenic Postpyogenic state
  • 93.  It is the infection with yeast like fungus Candida albicans  Earlier termed moniliasis  Types ACUTE CHRONIC Psuedomembranous Hyperplastic Atrophic Mucocutaneous Atrophic Candidiasis
  • 94. clinical type Appearance Erythematous Red Atrophic Red Hyperplastic White, red raised Mixed Red/ white keratotic / white necrotic Mucocutaneous Lip/ angles Psuedomembranous White lesion
  • 96. Acute atrophic Candidiasis/Antibiotic sore mouth Painful mucosa due to broad spectrum antibiotics Angular Cheilitis- Erythema, fissuring of angles of mouth
  • 97. D/D-  Chemical burn  Drug reactions  Syphilitic mucous patches  Necrotic ulcers  Traumatic ulcer  Contact allergy
  • 99. Due to denture cuts off the underlying mucosa from the protective action of saliva. The erythema is sharply limited to the area of mucosa occluded by a well-fitting upper denture or even an orthodontic plate.
  • 100. Hyphae proliferates in denture mucosal interface Gram staining shows gram +ve hyphae.
  • 101. It is red colored unraised area usually present on buccal mucosa. It is usually capillary type, Also occur as port wine stain on skin.
  • 102. History of long duration It is non tender Even no inflammatory component Absence of recurrent traumatic episode
  • 103. References-  Text book of oral and maxillofacial pathology- Neville  Differential diagnosis of oral lesions by- Wood and Goaz, Fifth Edition  Shafer’s textbook of oral pathology 6th edition .  Textbook of oral medicine Burkait 10th edition .
  • 104. 1. Traumatic erythematous macules & erosions 2. Purpuric macules(early stage) 3. Inflammatory fibrous hyperplasia lesions 4. Nonpyogenic soft tissue odontogenic infections 5. Chemical or thermal erythematous macule 6. Nicotine Stomatitis 7. Erythroplakia 8. Carcinoma in situ 9. Red macular Squamous cell carcinoma 10. Candidiasis (atrophic / erythematous, denture Stomatitis, angular Cheilitis)
  • 105. 16. Actinomycosis 17. Anemia (solitary red patch) 18. Amyloidosis 19. Angiosarcoma 23. Blastomycosis 24. Candidiasis endocrinopathy syndrome 25. Crohn’s disease
  • 106. 25. Coccidiodimycosis 26. Dermatitis herpetiformis 27. Erysipelas 28. Exfoliative Cheilitis 29. Gonococcal infection 30. Graft – versus – host disease (GVHD) 31. Herpangina
  • 107. 32. Histoplasmosis 33. Hyperemic oral tonsils 34. Larva migrans 35. Lichen planus 36. Lupus erythematous 37. Ludwig’s angina 38. Lymphonodular pharyngitis 39. Multinucleate cell angiohistiocytoma
  • 108. 40. Mycosis fungoides 41. Non- Hodgkin's lymphoma 42. Peripheral Ameloblastoma 43. Plasma cell gingivitis 44. Psoriasis 45. Sarcoidosis 46. Secondary syphilis 47. Self mutilation 48. Subacute necrotizing sialadenitis 49. Tuberculosis 50. Tumoral calcinosis
  • 110. Increase Vascularity Decrease thickness of epithelium Decrease keratinization Inflammation Mechanical trauma Increase Hb content  extravasations of blood Connective tissue papillae, containing enlarge capillaries, project close to the surface.
  • 111. Blood supply Thick cortical plate Gravity Food lodgment
  • 112. Dysplasia involving full vertical & horizontal thickness of epithelium along with basilar hyperplasia