differential diagnosis of clinical red lesions

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

4. Specialized
mucosa
Lining mucosa
Masticatory
mucosa

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.

21.  Slight extravasations
of blood .

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.

26. H/P
Granulomatous tissue
Covering epithelium is usually intact

27. 1. Pyogenic granuloma
2. Hormonal tumor
3. Epulis fissuratum
4. Papillary hyperplasia
5. PGCG
6. Peripheral fibroma with calcification

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.

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.

52. D/D-
Traumatic Erythema
Atrophic Candidiasis
Purpuric macules

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

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

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

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.

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.

80. More pleomorphic cells.
Loss of keratinization and keratin pearl.
Loss of individual cell differentiation.
Increase mitotic figures.

82. D/D-
Inflammatory hyperplasia
Papilloma
Erythroplakia
Leukoplakia

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.

91. Differential diagnosis
Fellatio,
Thrombocytopenic purpura,

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

95. ACUTE ATROPHIC

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

98. CHRONIC ATROPHIC

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

109. Thank you

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