White lesion Flashcards
(267 cards)
1
Q
White appearing lesions of the mucosal mucosa from the scattering of light through an altered mucosal surface
A
White Lesion
2
Q
MUCOSAL ALTERATIONS of White Lesion
A
Hyperkeratosis- appears white
Hyperplasia of the stratum malpighi (basale)
Intracellular edema of epithelial cells
Reduced vascularity of subjacent CT
Color of exudate and other surface contaminants
3
Q
Etiology of White Lesion
A
Physical trauma
Tobacco use
Genetic abnormalities
Mucocutaneous diseases
Inflammatory reactions
4
Q
SUBCLASSIFIED ACCORDING TO:
A
Hereditary Conditions
Reactive Lesions
Other mucosal white lesions
Other non epithelial white lesions
Pre-neoplastic & neoplastic lesions
5
Q
WHITE LESIONS HEREDITARY CONDITIONS
A
Leukoedema
White Sponge Nevus
Hereditary Benign Intraepithelial Dyskeratosis (HBID)
Follicular Keratosis
6
Q
Generalized mild opacification of buccal mucosa
Variation of normal
No definitive cause
More prevalent in black population
Shows milder presentation in whites
A
LEUKOEDEMA
7
Q
Etiology of Leukoedema
A
No definitive cause
8
Q
Implicated factors of Leukoedema
A
Smoking
Alcohol Ingestion
Bacterial Infection
Salivary Conditions
Electrochemical Interaction
Poor oral hygiene and abnormal masticatory problems
9
Q
CLINICAL FEATURES OF LEUKOEDEMA
A
Asymptomatic; Symmetrical
Gray-white, diffuse, filmy or milky, opalescent
Exaggerated cases result in wrinkling or corrugation (scalloped shaped areas) of the mucosa
Gentle stroking with gauze pad or tongue depressor will not remove it
Bilateral on the buccal mucosa
10
Q
COMMON LOCATION OF LEUKOEDEMA
A
Bilateral on the buccal mucosa
border of the tongue
11
Q
How to differentiate leukoedema from other white lesions
A
With stretching of the buccal mucosa, the opaque changes will dissipate
12
Q
EPITHELIAL HISTOPATHOLOGY OF LEUKOEDEMA
A
Epithelium is parakeratotic
Epithelium is acantholytic (Irregular thickening of the epidermis/ epithelial layer)
Marked intracellular edema of spinous cells
Enlarged epithelial cells with small pyknotic nuclei in optically clear cytoplasm
13
Q
DIFFERENTIAL DIAGNOSIS OF LEUKOEDEMA
A
Leukoplakia
White Sponge Nevus (Cannon’s Disease)
Hereditary Benign Intraepithelial Dyskeratosis (HBID)
14
Q
TREATMENT OF LEUKOEDEMA
A
No treatment is required
15
Q
PREMALIGNANT BA SI LEUKOEDEMA?
A
No premalignant tendencies
16
Q
Clinical appearance commences during adolescence & has equal predilection for males and females
A
WHITE SPONGE NEVUS (CANNON’S DISEASE)
17
Q
Rare genodermatosis that is inherited as an autosomal dominant trait - defects in the normal keratinization of the oral mucosa
A
WHITE SPONGE NEVUS (CANNON’S DISEASE)
18
Q
Mistaken for leukoplakia
A
WHITE SPONGE NEVUS
19
Q
CLINICAL FEATURES OF WHITE SPONGE NEVUS
A
Typical appearance: white lesion which is elevated and look irregular, have fissures and plaque formation
Painless
Deeply folder, white or gray lesions affecting the mucosa
Bilateral and symmetrical
Appears early in life (adolescence)
Keratosis in the buccal mucosa
Thicker than leukoedema
20
Q
OTHER NAME FOR WHITE SPONGE NEVUS
A
CANNON’S DISEASE
21
Q
HISTOPATHOLOGY OF CANNON’S DISEASE
A
Spongiosis
Acanthosis
Parakeratosis
Pronounced intracellular edema: edematous (fluid accumulation)
Mode of keratinization is characterized by the retention of the nuclei in the stratum corneum
22
Q
DIFFERENTIAL DIAGNOSIS OF CANNON’S DISEASE
A
Hereditary Benign Intraepithelial Dyskeratosis (HBID)
Pachyonychia Congenita
Lichen Planus (Hypertrophy type)
Cheek biting or traumatic/ frictional keratosis
23
Q
Affecting the nails and skin
Blisters in soles on their feet (painful) and palms
White patches on tongue and buccal mucosa
A
Pachyonychia Congenita
24
Q
TREATMENT FOR CANNON’S DISEASE
A
No treatment - self limiting
25
IS WSP MALIGNANT
No malignant tendencies
26
CLINICAL FEATURES OF HBID
Syndrome
Early onset (first yr of life) - gradually intensifies until mid-adolescence
Bulbar Conjunctivitis
Oral lesions
26
Witkop’s Disease
HEREDITARY BENIGN INTRAEPITHELIAL DYSKERATOSIS (HBID)
27
HBID
HEREDITARY BENIGN INTRAEPITHELIAL DYSKERATOS
28
Rare autosomal dominant disorder characterized by elevated epibulbar and oral plaques and hyperemic (increased blood volume) conjunctival blood vessels
HEREDITARY BENIGN INTRAEPITHELIAL DYSKERATOSIS (HBID)
29
foamy plaques - triangular in shape in the eye area (corneal limbus)
Bulbar Conjunctivitis
29
HBID ORAL LESION IS FOUND IN
Buccal and labial mucosa
Labial commissures
Floor of the mouth
Lateral surfaces of the tongue
Gingiva
Palate
Except the dorsum of the tongue
Usually detected within the 1st yr of life
Gradually increase in intensity until mid adolescence
Variations: deeply folded, opaque, white lesions to more delicate, opalescent areas
29
Hypodontia
Accompanied by ocular lesions
HEREDITARY BENIGN INTRAEPITHELIAL DYSKERATOSIS (HBID)
29
Vary seasonally
Patient complain of photophobia, especially in early life
Blindness secondary to corneal vascularization
Spontaneous shedding of the conjunctival plaques occurs on a seasonal basis
Ocular lesions
30
HISTOPATHOLOGY OF HBID
Similarities between oral and conjunctival lesions are noted microscopically
Cell within a cell
Non-dyskeratotic (Enlarged, edematous and elongated)
30
Ocular lesions
Vary seasonally
Patient complain of photophobia, especially in early life
Blindness secondary to corneal vascularization
Spontaneous shedding of the conjunctival plaques occurs on a seasonal basis
31
Similarities between oral and conjunctival lesions are noted microscopically (HBID)
Epithelial hyperplasia
Acanthosis
Significant hydropic degeneration
Enlarged, hyaline, and so called waxy eosinophilic cells present in the epithelium
32
Cell within a cell
Eosinophilic cells within the middle and superficial spinous regions become surrounded by adjacent cells (parang nakasandwich yung cells)
32
Darrier’s Disease / Darrier’s white-disease
FOLLICULAR KERATOSIS
33
TREATMENT OF HBID
No treatment is necessary unless it becomes invasive
Condition is self limiting
34
DIFFERENTIAL DIAGNOSIS OF HBID
White sponge nevus
Pachyonychia Congenita
Hypertrophic Lichen Planus
35
RISK OF MALIGNANCY OF HBID?
No risk of malignant transformation
36
Genetically transmitted disorder with an autosomal dominant mode of inheritance
FOLLICULAR KERATOSIS
37
CLINICAL FEATURES OF DARRIER'S DISEASE/FOLLICULAR KERATOSIS
Onset: childhood or adolescence
accompanied by skin lesions; has a predilections for the skin; 13% of its patients forming oral lesions
Skin manifestations
Oral Lesions
38
SKIN MANIFESTATION OF DARRIER'S DISEASE/FOLLICULAR KERATOSIS
small, skin-colored papular lesions, symmetrically distributed over the face, trunk, and intertriginous areas
Papules eventually coalesce and feel greasy because of excessive keratin production
Finger Nail Changes
Lesions may also occur unilaterally
Hyperkeratosis Palmaris et Plantaris)
39
ORAL LESION MANIFESTATION OF DARRIER'S DISEASE/FOLLICULAR KERATOSIS
Oral lesions closely resemble the cutaneous lesions
Asymptomatic
Favored oral mucosa sites/Predilection: attached gingiva and hard palate
Small, whitish papules producing an overall cobblestone appearance
Papules range from 2 to 3 mm in diameter may become coalescent (dikit-dikit)
40
HISTOPATHOLOGY OF FOLLICULAR KERATOSIS
Suprabasal lacunae (clefts) formation containing acantholytic epithelial cells
Dyskeratotic process characterized by a central keratin plug that overlies epithelium exhibiting a suprabasal cleft
Intraepithelial clefting phenomenon
41
DIFFERENTIAL DIAGNOSIS OF FOLLICULAR KERATOSIS
Dyskeratosis congenita (rare)
Acanthosis nigricans
Condyloma acuminatum
Nicotine stomatitis
Acantholytic dyskeratosis
Hailey-hailey disease
42
TREATMENT OF FOLLICULAR KERATOSIS
Vitamin A/ retinoids used - not advisable for long term therapy because the occurrence of systemic toxicity
Topical corticosteroids and Vitamin A analog retinoic acid
43
Side effects OF CORTICOSTEROIDS
cheilitis,
elevation of serum liver enzymes and triglycerides
severe dryness of the skin.
44
PROGNOSIS OF FOLLICULAR KERATOSIS
The disease is chronic and slowly progressive
Recurrence may be noted in some patient
Non malignant
45
WHAT DISEASE IS MALIGNANT UNDER HEREDITARY WHITE LESION
NONE
46
WHITE LESIONS: REACTIVE LESIONS
Focal (frictional) Hyperkeratosis
White lesions associated with smokeless tobacco
Nicotine stomatitis
Hairy Leukoplakia
Hairy Tongue
Dentifrices associated slough
47
Related to chronic rubbing or friction against an oral mucosa surface
FOCAL (FRICTIONAL) HYPERKERATOSIS
48
Chronic rubbing or friction against an oral mucosal surface — Resulting in Hyperkeratotic white lesion that is analogous to a callus on the skin
FOCAL (FRICTIONAL) HYPERKERATOSIS
48
commonly occur in highly traumatized areas such as the lips, lateral margins of the tongue, buccal mucosa along occlusal line and edentulous ridges
Frictional/Benign Hyperkeratosis
49
Other term: FOCAL (FRICTIONAL) HYPERKERATOSIS
Frictional/Benign Hyperkeratosis
Denture callous or ridge callus
50
Most common white lesion in the oral cavity
FOCAL (FRICTIONAL) HYPERKERATOSIS
51
May form due to chronic lip or cheek chewing that may result to keratinization that present itself as opacification at the affected area
FOCAL (FRICTIONAL) HYPERKERATOSIS
52
ETIOLOGY OF FOCAL (FRICTIONAL) HYPERKERATOSIS
Chronic Irritation
Broken tooth or restoration
Habitual cheek or lip biting
Vigorous tooth brushing
Hyperocclusion
Ill fitting denture
Hyperkeratotic white lesions (analogous to callus on the skin)
Protective action against low grade long term trauma
53
CLINICAL FEATURES OF FOCAL (FRICTIONAL) HYPERKERATOSIS
Lip
Lateral margin of tongue
Buccal mucosa along occlusal line
Edentulous alveolar ridges
Chronic cheek or lip chewing = opacification (keratinization) of the affected area
Chewing on edentulous alveolar ridges produces the same effect
Doesn’t often need biopsy
54
HISTOPATHOLOGY OF FOCAL (FRICTIONAL) HYPERKERATOSIS
Chronic Inflammatory Cells
Hyperkeratosis (thickened layer or keratin) or
Parakeratosis (keratin layers shows remnants of epithelial nuclei)
55
TREATMENT OF FOCAL (FRICTIONAL) HYPERKERATOSIS
Elimination of the cause Repair broken tooth, restoration or ill fitting denture (polish), wear mouth guard
Address the causative habit: encourage the patient to discontinue habit
56
ETIOLOGY OF WHITE LESIONS ASSOCIATED WITH SMOKELESS TOBACCO
Direct contact with smokeless tobacco and contaminants
Snuff form of tobacco
Chemical carcinogens liberated from smokeless tobacco (chewing and snuff)
57
DIFFERENTIAL DIAGNOSIS OF WHITE LESIONS ASSOCIATED WITH SMOKELESS TOBACCO
Frictional Keratosis
Hyperplastic Candidiasis
Leukoedema
Plaque-type Lichen Planus
57
CLINICAL FEATURES OF WHITE LESIONS ASSOCIATED WITH SMOKELESS TOBACCO
Prevalence associated with regional use
Mostly seen in white males
Asymptomatic in mucosa where tobacco is held
Most commonly seen in the mandibular vestibular mucosa (Snuff dipper’s pouch)
Wrinkled appearance
Damage seen in adjacent teeth and periodontium
58
HISTOPATHOLOGY OF WHITE LESIONS ASSOCIATED WITH SMOKELESS TOBACCO
Superficial epithelium may demonstrate vacuolization or edema
Slight to moderate parakeratosis often in form of chevrons (or pires/parulis) acanthosis
Diffused zone of basophilic stromal alterations
Epithelial Dysplasia
58
TREATMENT OF WHITE LESIONS ASSOCIATED WITH SMOKELESS TOBACCO
Smoking cessation (ask px to stop)
Biopsy may be required in persistent lesion, ulcerated and indurated lesions
59
RISK OF MALIGNANCY WHITE LESIONS ASSOCIATED WITH SMOKELESS TOBACCO
Risk of malignant transformation in palate except for reverse smokers
60
ETIOLOGY OF NICOTINE STOMATITIS
Chronic exposure to the heat from tobacco
caused by pipe cigar and cigarette smoking
Most severe changes seen in patients who reverse smoke
Common tobacco related form of keratosis
Opacification on the palate caused by heat and carcinogens
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62
62
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63
CLINICAL FEATURES OF NICOTINE STOMATITIS
Diffuse, white thickening of the palatal mucosa with interspersed elevated white papules with a red central depression
Generalized white changes (hyperkeratosis) seen in hard palate
Red dots in the palate represent inflamed salivary duct orifices
63
PROGNOSIS OF NICOTINE STOMATITIS
Rarely evolves into malignancy
Except in reverse smoking
63
HISTOPATHOLOGY OF NICOTINE STOMATITIS
Hyperkeratosis and acanthosis of surface epithelium
Connective Tissue surrounding exhibits inflammation
Dilated salivary gland with squamous metaplasia of lining
63
TREATMENT OF NICOTINE STOMATITIS
Smoking cessation (ask px to stop)
Condition may regress
Re-evaluation - give them support system
64
Caused by superficial chemical reaction s/a burns, allergic reactions to a component of toothpaste or dentifrice → inclusion of detergents or flavoring compounds → may be related to essential oils
DENTIFRICE ASSOCIATED SLOUGH
64
Common phenomena associated with the use of a certain toothpaste brands
DENTIFRICE ASSOCIATED SLOUGH
64
A painless white lesion that is not known to progress or transform to any significant condition
DENTIFRICE ASSOCIATED SLOUGH
64
ETIOLOGY OF DENTIFRICE ASSOCIATED SLOUGH
Form of chemical burn or a reaction to an ingredient of a dentifrice
Possible causative component (Detergent; flavorings)
Can also be caused by mouthwash with similar causative agents
65
Overgrowth of the filiform papillae on the dorsal surface of the tongue
HAIRY TONGUE
65
PROGNOSIS OF DENTIFRICE ASSOCIATED SLOUGH
Benign white lesion
Lesion will resolve once the dentifrice/mouthwash is discontinued
65
Represents as increased keratin production of a decreased normal keratin production of a decreased normal keratin desquamation
HAIRY TONGUE
65
ETIOLOGY OF HAIRY TONGUE
Used of broad-spectrum antibiotics (like penicillin), systemic corticosteroids, hydrogen peroxide
Intense smoking
Head and neck therapeutic radiation
Not well understood, alteration in oral flora
65
CLINICAL FEATURES OF DENTIFRICE ASSOCIATED SLOUGH
Superficial whitish slough seen on the buccal mucosa
Commonly describe by the patient as “peeling” or “oral peeling”
66
HISTOPATHOLOGY OF HAIRY TONGUE
Presence of elongated filiform papillae, marked hyperkeratosis of filiform papillae with bacterial accumulation on the surface (dorsum of the tongue)
Surface contamination by clusters of microorganisms and fungi
Keratinization may extend into the mid-portions of the stratum spinosum
Mid inflammation occurring in the lamina propria
66
TREATMENT OF HAIRY TONGUE
Elimination of any predisposing factors
Brush, scrape tongue with baking soda
66
DIAGNOSIS OF HAIRY TONGUE
Biopsy is not necessary for confirmation
Clean the area
Know the cause and ask the patient
67
PROGNOSIS OF HAIRY TONGUE
Tongue will return to normal after physical debridement and proper oral hygiene
67
CLINICAL FEATURES OF HAIRY TONGUE
Represents overgrowth of filiform papillae and chromogenic microorganisms
Dense hairy like mat formed by hyperplastic papillae on the dorsal tongue surface
Asymptomatic
May be cosmetically objectionable because of color (usually black)
Extensive elongation of the papillae = gagging or a tickling sensation
Color may range from white to tan to deep brown or black
Depending on the Diet, Oral Hygiene, Oral medications, and the Composition of bacteria
68
White lesions commonly seen along the margins of the lateral borders of the tongue
First case was see in homosexual
HAIRY LEUKOPLAKIA
69
ETIOLOGY OF HAIRY LEUKOPLAKIA
Associated with local or systemic immunosuppression (esp. AIDS and organ transplantation)
Represents an opportunistic infection by Epstein-Barr Virus
Immunosuppression
Organ transplantation (medical induced immunosuppression)
Hematologic malignancy
Long Term use of systemic or topical corticosteroid
Can extend up to dorsal surface of tongue
70
CLINICAL FEATURES OF HAIRY LEUKOPLAKIA
Most commonly seen in lateral tongue, often bilateral
Asymptomatic
Papillary, filiform, or plaque like
May occur before or after the diagnosis of AIDS
May be secondarily infected by candida albicans
71
DIFFERENTIAL DIAGNOSIS OF HAIRY LEUKOPLAKIA
Idiopathic leukoplakia
Frictional hyperkeratosis
Lichen planus
Lupus Erythematosus
Hyperplastic Candidiasis
72
HISTOPATH OF HAIRY LEUKOPLAKIA
Acanthosis parakeratosis edema
Nuclear viral inclusions
EBV in infected nuclei
73
looks similar with fissured tongue
there’s mapping in the tongue
Distinct characteristic: red atrophic center
filiform papillae
Unknown etiolog
GEOGRAPHIC TONGUE
73
Erythema migrans or Benign migratory glossitis
Erythema migrans or Benign migratory glossitis
73
TREATMENT OF HAIRY LEUKOPLAKIA
None, unless cosmetically objectionable
Antiviral and antiretroviral agents likely to cause lesion to regress
Lesions usually improve and resolve with improvement in the patient's immune system
74
WHITE LESIONS: OTHER MUCOSAL WHITE LESION
Geographic tongue
Lichen planus.
Lupus erythematosus
75
ETIOLOGY OF GEOGRAPHIC TONGUE
Numerous theories
emotional stress
fungal infections
bacterial infections
Associated with several different condition
psoriasis
seborrheic dermatitis
reiter’s syndrome
atopy
75
Geographic stomatitis - if its located at different sites
76
CLINICAL FEATURES OF GEOGRAPHIC TONGUE
Ring- shaped/ annular lesion affecting the dorsum and margin of the tongue
Atrophic patches surrounded by elevated keratotic margins
White, yellow, or slightly elevated peripheral zone
Desquamated area appears
Strong association between geographic tongue and fissured tongue
Symptoms may be more common when fissured tongue is present
affecting women slightly more often than men
children may occasionally affected
presence of small, round to irregular areas of dekaratinization and desquamation of filiform papillae
asymptomatic
77
HISTOPATHOLOGY OF GEOGRAPHIC TONGUE
Filiform papillae are reduced in number & prominence
Margins of the lesions demonstrate hyperkeratosis & acanthosis
Presence of neutrophils & lymphocytes
Histologic picture: psoriasiform type of intraoral eruption
77
TREATMENT OF GEOGRAPHIC TONGUE
Not required
Self-limiting & asymptomatic
When symptoms occur, palliative treatment:
Topical steroids, esp. containing antifungal agent
78
DIFFERENTIAL DIAGNOSIS OF GEOGRAPHIC TONGUE
Quite characteristic
Histopathology is rarely needed
79
pre-malignant tendency OF WHITE LESIONS: OTHER MUCOSAL WHITE LESION
LICHEN PLANUS
80
PROGNOSIS OF GEOGRAPHIC TONGUE
Lesion is totally benign
Reassure the patient that this does not represent any serious illness will relieve anxiety
81
TYPES OF LICHEN PLANUS
Reticular form
Plaque type
Erythematous (Atrophic) form
Ulcerative Lesion
Bullous form
Papular type
82
Immune system
Primary role in disease development
Subepithelial band formed infiltrate dominated by T- Lymphocytes and macrophages
Expression of the cell mediated arm of the immune system being involved in the pathogenesis through T- Lymphocyte cytotoxicity directed against antigens expressed by the basal cell layer
multifactorial- many factors that contribute to the condition
83
stress
May establish the inflammatory process
84
Cannot discriminate between inherent molecules of the body and foreign antigens. Activation of these cells may arise in other parts of the body
Autoreactive T lymphocytes
85
CLINICAL FEATURES OF LICEHN PLANUS
Disease of middle age
Affects men & women in equal numbers
The severity of the disease parallels the patient’s level of stress
Prevalence of secondary oral candidiasis in patients with oral lichen planus (50%)
Altered status of cellular immunity may be responsible
most common
Presence of numerous interlacing keratotic lines or striae (Wickham’s striae) that produce an annular or lacy pattern
buccal mucosa
86
most common LICHEN PLANUS
RETICULAR FORM
87
Presence of numerous interlacing keratotic lines or striae (Wickham’s striae) that produce an annular or lacy pattern
RETICULAR FORM
88
Striae may form a network but also show annular (circular) patterns
RETICULAR FORM
89
Primary sites: OF PLAQUE TYPE
dorsum of the tongue & buccal mucosa
89
Can be seen in all regions of the oral mucosa
Fine white lines or striae
RETICULAR FORM
89
Resembles leukoplakia clinically
PLAQUE TYPE
90
Striae display a peripheral erythematous zone which reflects subepithelial inflammation
RETICULAR FORM
90
Most frequently in the buccal mucosa bilaterally
Vermillion border
RETICULAR FORM
90
If in attached gingiva, without papules or striae and presents as
DESQUAMATIVE GINGIVITIS
90
Small white dots, intermingle with the reticular from
PAPULAR TYPE
90
May clinically be very similar to homogeneous oral leukoplakias
Difference is the simultaneous presence of reticular or papular structures in the case of plaque like Oral lichen planus
Smoker
film like material at buccal mucosa
PLAQUE TYPE
90
Initial phase of lichen planus
PAPULAR TYPE
90
Most disabling form
Fibrin coated ulcers are surrounded by erythematous zone displaying radiating white striae
Sharp sensation in conjunction with food intake
ULCERATIVE LESION
90
ERYTHEMATOUS (ATROPHIC) FORM
attached/marginal gingiva
Symptomatic: burning or pain in the area of involvement
Homogenous red area
Buccal mucosa or palate
Striae in the periphery
If in attached gingiva, without papules or striae and presents as DESQUAMATIVE GINGIVITIS
90
HAVE PREMALIGNANT TENDENCIES LICHEN PLANUS?
YES
90
HISTOPATHOLOGY of LICHEN PLANUS
hyperorthokeratosis or hyperparakeratosis
ariable degrees of acanthosis
Within the epithelium, increase in numbers of langerhans cells
lymphocytes, immunoglobulin and fibrinogen
Liquefaction degeneration
Eosinophilic band
Dense subepithelial band shaped infiltrate of lymphocytes and macrophages
90
unusual form
Bullae range from a few mm to cm in diameter
Bullae generally short - lived and or rupturing, leave a painful ulcer
Buccal mucosa: posterior and inferior regions adjacent to the 2nd and 3rd molars
BULLOUS FORM
90
TREATMENT of LICHEN PLANUS
No specific tx
Palliative treatment
Corticosteroids- the single most useful group of drugs
Ability to modulate inflammation & immune response
topical application / local injection of steroids
Vitamin A ( retinoids)- systemic or topical
Cyclosporine –topical
90
release inflammatory or chemotactic factors from mast cells or neutrophils
Dapsone(diaminoiphenylsulfone)
90
the single most useful group of drugs
Ability to modulate inflammation & immune response
Corticosteroids
90
Sub and supragingival plaque and calculus- oral prophylaxis
Optimal oral hygiene prior to steroid treatment
Erythematous OLP
90
PROGNOSIS
Slightly higher rate of oral squamous cell carcinoma
Erosive / atrophic form are more common to develop into malignancy 0.4-2.5 %
90
ETIOLOGY AND PATHOGENESIS
(LUPUS ERYTHEMATOSUS)
Classic prototype of autoimmune disease involving immune complex
Autoimmune disease involving both the humoral and cell-mediated arms of the immune system
Autoantibodies directed against various cellular antigens in both the nucleus and the cytoplasm
90
FORMS OF LUPUS ERYTHEMATOSUS
Systemic (acute) lupus erythematosus (SLE)
Discoid (chronic) lupus erythematosus (DLE)
Subacute lupus (subacute cutaneous LE)
90
Disorders that entail an increased risk of malignant transformation at some site of the oral mucosa, not necessarily associated with a pre existing lesion
Premalignant conditions
90
A lesion that has an inherent increased risk to develop carcinomas compared with the surrounding tissues
Premalignant lesion
90
Less aggressive form OF LUPUS ERYTHEMATOSUS
DISCOID (CHRONIC) LUPUS ERYTHEMATOSUS (SLE)
90
LOCATION OF LUPUSERYTHEMATOUS
Buccal mucosa, gingiva and vermilion
Erythematosus or ulcerative lesions with delicate white, Keratotic striae radiating from the periphery
90
Multisystem autoimmune inflammatory disorder of unknown etiology
SYSTEMIC (ACUTE) LUPUS ERYTHEMATOSUS (SLE)
90
Main feature: SYSTEMIC (ACUTE) LUPUS ERYTHEMATOSUS (SLE)
formation of antibodies to DNA, which may initiate immune complex reactions in particular vasculitis
90
Mild skin and mucosal lesions
Numerous autoantibodies directed against
nuclear and cytoplasmic antigens
Antibodies can cause lesions in nearly any tissue, resulting in a wide variety of clinical signs and symptoms
Affects several organs
SYSTEMIC (ACUTE) LUPUS ERYTHEMATOSUS (SLE)
90
Most aggressive form OF LUPUS ERYTHEMATOSUS
SYSTEMIC (ACUTE) LUPUS ERYTHEMATOSUS (SLE)
90
SYMPTOMS OF SYSTEMIC (ACUTE) LUPUS ERYTHEMATOSUS (SLE)
Fever, weight loss & malaise
With disease progression, many organs systems become involved
90
Common Areas: SYSTEMIC (ACUTE) LUPUS ERYTHEMATOSUS (SLE)
vermillion buccal mucosa,
gingiva, and
palate
90
Involvement of the skin results in an erythematous rash, seen over the malar process and bridge of the nose
Butterfly rash
90
Skin lesions of mild to moderate severity
Mild systemic involvement and the appearance of some abnormal autoantibodies
SUBACUTE LUPUS (SUBACUTE CUTANEOUS LE)
90
Expands peripherally, the center heals, with the formation of scar and loss of pigment
Involvement of hair follicles in permanent hair loss (ALOPECIA)
DISCOID (CHRONIC) LUPUS ERYTHEMATOSUS (SLE)
90
Affecting predominantly the skin rarely progressing to the systemic form
Cosmetic significance because of its predilection for the face
Middle age, especially women
Skin, most commonly on the face and scalp
Oral and vermillion lesions are also commonly seen, but usually in the company of cutaneous lesions
Skin lesions appear as disk shaped erythematous plaques with hyperpigmented margins
DISCOID (CHRONIC) LUPUS ERYTHEMATOSUS (SLE)
91
Intermediate between SLE and DLE
SUBACUTE LUPUS (SUBACUTE CUTANEOUS LE)
91
DIFFERENCE OF DLE FROM SLE IN TERMS OF ORGAN
DLE
Skin and oral only
SLE
Skin, oral, heart, kidneys, joints
91
DIFFERENCE OF DLE FROM SLE IN TERMS OF SYMPTOM
DLE
none
SLE
Fever, malaise, weight loss
91
DIFFERENCE OF DLE FROM SLE IN TERMS OF HISTOPATOLOGY
DLE
Basal cell loss, lymphocytes at interface and prevascular keratosis
SLE
Similar to discoid
91
DIFFERENCE OF DLE FROM SLE IN TERMS OF SEROLOGY
DLE
No detachable antibodies
SLE
Positive ANA, Anti- DNA antibodies
92
SLE diagnosis with 4 of more of 11 criteria present at anytime T/F
TRU
93
Criteria for SLE
Malar rash
Discoid lesions
Photosensitivity
Presence of oral ulcers
Nonerosive arthritis of two joints or more
Serositis
Renal disorder
Neurologic disorder (seizures or psychosis)
Hematologic disorder (hemolytic anemia, leukopenia, lymphopenia, or thrombocytopenia)
Immunologic disorder (anti-DNA, anti-SM, or antiphospholipid antibodies)
93
DIFFERENCE OF DLE FROM SLE IN TERMS OF DIFFERENTIATION
DLE
Granular /linear basement
membrane deposits of IgG and C3
SLE
Similar to discoid
94
DIAGNOSIS OF LUPUS ERYTHEMATOUS
Serologic test- for autoantibodies (+results)
The ANA (antinuclear antibody) test- matic suspecting SLE
94
DLE DIAGNOSIS
Well-demarcated cutaneous lesions with round or oval erythematous plaques with scales and follicular plugging
These lesions may form butterfly-like rashes over the cheeks and nose known as Malar rash
95
HISTOPATHOLOGIC CHARACTERISTICS OF LUPUS ERYTHEMATOUS
Hyperkeratosis with keratotic plugs
Atrophy of the rete pegs/ processes
Deep inflammatory infiltrate
Edema in the lamina propria
Thick patchy or continuous PAS- positive juxta epithelial deposits
96
TREATMENT OF LUPUS ERYTHEMATOUS FOR DLE
topical corticosteroids
96
DIFFERENTIAL DIAGNOSIS OF LUPUS ERYTHEMATOUS
Erosive lichen planus
Erythematous gingival Lupus
97
TREATMENT OF LUPUS ERYTHEMATOUS FOR SLE
systemic steroids
98
TREATMENT OF LUPUS ERYTHEMATOUS FOR Symptomatic intraoral lesions
topical steroids
99
LE tend to be less symmetrically distributed
Keratotic striae of LE show characteristic radiation from a central focus are more delicate and subtle than Wickham’s striae of lichen planus
Erosive lichen planus
99
SIDE EFFECTS OF TREATMENT OF LE
Fungal and viral infections
Immunologic defects
Mucosal ulceration caused by frequent exploitation of NSAIDS
Immunosuppressive drugs used to treat SLE
100
Erythematous gingival Lupus
Mucous membrane pemphigoid
Erythematous lichen planus
Erythematous candidiasis
Contact hypersensitivity
101
OTHER NON-EPITHELIAL WHITE LESIONS
Candidiasis
Mucosal burns
Submucosa fibrosis
Fordyce granules
Ectopic lymphoid tissue
Gingival cysts
Parulis
Lipoma
102
causative agent: ORAL CANDIDIASIS
Candida albicans
102
Most prevalent opportunistic infection affecting the oral mucos
ORAL CANDIDIASIS
103
Common sites ORAL CANDIDIASIS
Mucosal linings
Rare systemic manifestations may have a fatal course
103
accompanied by systemic mucocutaneous manifestations- other areas too & not just in oral region
Secondary infections
103
Restricted to the oral and perioral sites
primary infections
103
Oral candidiasis is divided into
Primary and secondary infections
104
Human immunodeficiency virus (HIV) infections
Steroid inhalers
CHRONIC PSEUDOMEMBRANOUS
104
PSEUDOMEMBRANOUS (CLINICAL FINDINGS)
Loosely attached membranes comprising fungal organisms and cellular debris
Leaves an inflamed, sometimes bleeding area if the pseudomembrane is removed
104
PSEUDOMEMBRANOUS (SYMPTOMS)
Usually asymptomatic
Some discomfort
Brush biopsy
104
TYPES OF ORAL CANDIDIASIS
DENTURE STOMATITIS
CHRONIC PLAQUE
ANGULAR CHEILITIS
CHRONIC PLAQUE
ORAL CANDIDIASIS ASSOCIATED WITH HIV
ERYTHEMATOUS CANDIDIASIS
PSEUDOMEMBRANOUS
104
PSEUDOMEMBRANOUS
ACUTE FORM
Thrush/ Oral thrush
Grouped with the primary oral candidiasis
Classic candida infection
104
Grouped with the primary oral candidiasis
Classic candida infection
whitish
Acute Form
PSEUDOMEMBRANOUS
104
PSEUDOMEMBRANOUS
(PATIENTS)
Medicated with antibiotics or immunosuppressant drugs
Disease that suppresses the immune system
105
reddish
Atrophic oral candidiasis
Erythematous surfac
ERYTHEMATOUS CANDIDIASIS
106
A successor to PC but may also emerge de novo
ERYTHEMATOUS CANDIDIASIS
106
Diffused border- medjo makalat you don’t know where specifically it starts & ends
ERYTHEMATOUS CANDIDIASIS
107
type and Nodular Candidiasis
CHRONIC PLAQUE
108
Inhalation steroids
Palate and dorsum of the tongue
Smoking
Treatment with broad spectrum antibiotics
108
Site DENTURE STOMATITIS
Denture - bearing palatal mucosa
109
White plaque- film like appearance
May be indistinguishable from an oral leukoplakia
Correlation with moderate to severe epithelial
dysplasia
Associated with malignant transformation
Nodular
Can be distinguished through inspection
CHRONIC PLAQUE
109
CAUSE OF DENTURE STOMATITIS
DENTURE
109
Localized to major part erythematous sites caused by trauma from the denture
Type I DENTURE STOMATITIS
110
Protects microorganisms from physical influences such as salivary flow
- not included in the cleansing effect of the saliva
- If the patient doesn’t have good oral hygiene
DENTURE
111
Affects a major part of the denture covered mucosa
Moderate
Type II DENTURE STOMATITIS
111
Microorganisms DENTURE STOMATITIS
Candida
Bacteria from several genera, such as
Streptococcus,
Veillanella,
Lactobacillus,
Prevatella, and
Actinomyces
112
Type II features
Granular mucosa in the central part of the palate
Affecting the granular mucosa and the central part of the palate
Type III DENTURE STOMATITIS
112
mouth area
CHELITIS
112
DIAGNOSIS AND PATHOLOGIC FINDINGS: ORAL CANDIDIASIS
Smear
From the infected area, which compromises
epithelial cells, creates opportunities for detection
of the yeast
Pseudomembranous oral candidiasis and angular cheilitis are suspected
Second scrape
Method is a valuable adjunct in the diagnostic
process of erythematous candidiasis and denture
stomatitis as these infections consist of fairly
homogenous erythematous lesions
Salivary culture techniques
Culture sensitivity testing
Histopathologic exam
Chronic plaque- type and nodular candidiasis,
cultivation techniques
Identify the possible presence of epithelial
dysplasia
112
Causative agents: ANGULAR CHEILITIS
candida and staphylococcus aureus
112
Infected fissures of the commissures of the mouth often surrounded by erythema
ANGULAR CHEILITIS
112
Infection is considered a portent of Aids development
Advice the patient to do a work up
Pseudomembranous candidiasis, erythematous candidiasis, angular cheilitis, and chronic hyperplastic Candidiasis
ORAL CANDIDIASIS ASSOCIATED WITH HIV
112
More than 90% of patients present with AIDS present oral candidiasis during course of HIV infections
ORAL CANDIDIASIS ASSOCIATED WITH HIV
112
MANAGEMENT: ORAL CANDIDIASIS
Antifungal drug
Polyenes or azoles
Azoles
Miconazole for angular cheilitis
Topical treatment biostatic effect on S. Aureus and
fungistatic effect to candida
Systemic azoles for deeply seated primary
candidiasis, such as chronic hyperplastic
candidiasis, denture stomatitis, and median
rhomboid glossitis with a granular appearance
and for therapy- resistant infections, mostly
related to compliance failure
Known to interact with warfarin
Development of resistance is particularly
Compelling for fluconazole in HIV patients
Polyenes
Nystatin and amphotericin B
Negative effect on the production of ergosterol,
which is critical for the candida cell membrane
integrity. Polyenes can also affect the adherence
of the fungi
112
SYMPTOMS: ANGULAR CHELITIS
Dry skin, red areas at the corner of the lips
112
Predilection: CHRONIC PLAQUE
Denture wearers
Inhalation steroids
112
Smokers and denture wearers = increased risk
dorsum of the tongue
Erythematous lesion in the center of the posterior part of the dorsum oval configuration
Atrophy of the filiform papillae
CHRONIC PLAQUE
112
FOUND IN:CHRONIC PLAQUE
dorsum of the tongue w/ MRG
112
Causative agents: CHRONIC PLAQUE
Mixed bacterial/fungal microflora
112
SYMPTOMS: CHRONIC PLAQUE
Concurrent erythematous lesion may be observed in the palatal mucosa ( kissing lesions)
Asymptomatic and management is restricted to a reduction in predisposing factors
112
ETIOLOGY: ANGULAR CHELITIS
Vitamin B12 iron deficiencies and loss of vertical dimension
112
First sign OF SUBMUCOUS FIBROSIS
erythematous lesions
112
Children who chew through electrical cords receive rather characteristic initial burn that are symmetric
Resulting to tissue damage, followed by scarring & reduction in the size of the oral opening
MUCOSAL BURN
112
MANAGEMENT AND PROGNOSIS: Denture Stomatitis
Permanent removal of the denture
Improved denture hygiene and a recommendation not to use the denture while sleeping
If asymptomatic, pt may opt for no treatment
Type III denture stomatitis
112
Surface of these lesions tends to be: thickened slough that extends deep into the surrounding tissue
MUCOSAL BURN
112
MANAGEMENT AND PROGNOSIS: Type III denture stomatitis
Surgical excision if necessary to eradicate microorganisms present in the deeper fissures of the granular tissue
Continuous treatment with topical antifungal drugs
Need to remove because they have deeper
fissures
112
MANAGEMENT AND PROGNOSIS: ANGULAR CHEILITIS
Mild steroid ointment for cases of inflammation
Prognosis is good if predisposing factors associated with the infection are reduced or eliminated
112
MANAGEMENT AND PROGNOSIS: Persistent chronic plaque- type and nodular candidiasis
Increased risk for malignant transformation compared with leukoplakias not allied with candida Infection
Patients with primary candidiasis are also at risk if systemic predisposing factors arise
112
THERMAL BURNS
Hard palatal mucosa
Hot sticky foods
Hot liquids
112
Locations: SUBMUCOUS FIBROSIS
Lips
Buccal mucosa
Retromolar area
Soft palatal mucosa
May extend into pharyngeal region, pharynx and upper ⅔ of esophagus
112
CLINICAL FEATURES: MUCOSAL BURN
Localized erythema
Short- term exposure
White slough or membrane
Long term chemical exposure/ increased concentration of offending agent
Friable and bleeds upon manipulation
With gentle traction, the surface slough will peel from the denuded connective tissue, producing tenderness and pain
112
HAS PREMALIGNANT TENDENCY SUBMUCOUS FIBROSIS?
YES
The development of squamous cell carcinoma
112
ETIOLOGY: MUCOSAL BURN
Topical applications of chemicals:
Aspirin or caustic agents (most common cause)
Chronic abuse of alcohol containing mouth washes
Topical abuse of drugs/medication
Accidental placement of phosphoric acid-etch solutions or gel by dentist
THERMAL BURNS
ELECTRICAL BURNS
112
Electrical burn
MUCOSAL BURN
112
INITIA CHANGE: SUBMUCOUS FIBROSIS
Whitish yellow change
112
HISTOPATHOLOGY: MUCOSAL BURN FOR CHEMICAL BURN
Epithelial component show coagulative necrosis through its entire thickness
Fibrinous exudate is evident
Intensely inflamed underlying connective tissue
112
HISTOPATHOLOGY: MUCOSAL BURN FOR ELECTRICAL BURN
Deep extension of necrosis, often into muscle
112
Chronic, progressive, scarring, high-risk precancerous condition of the oral mucosa seen primarily on the Indian Subcontinent and in Southeast Asia
Areca quid chewing habit
Impaired degradation of normal collagen by fibroblast rather than excess production
Some people have a genetic predisposition for it
SUBMUCOUS FIBROSIS
112
TREATMENT: MUCOSAL BURN FOR ELECTRICAL BURN
Co management
May need the services of pediatric dentist, OMS, and plastic surgeon
112
LATER CHANGE: SUBMUCOUS FIBROSIS
the affected mucosa, especially the soft palate and
the buccal mucosa, loses its resilience and elasticity
fibrous bands are readily palpable in the soft palate and buccal mucosa
the clinical result is significant trismus and considerable difficulty in eating
112
CLINICAL FINDINGS: FORDYCE SPOTS
Multiple areas, often seen in aggregates or in confluent arrangements
Often seen in Buccal mucosa & Vermillion border of the upper lip
Symmetrically distributed
112
TREATMENT: MUCOSAL BURN FOR CHEMICAL BURN
Local symptomatic therapy with or without the use of systemic analgesics
Topical therapy: hydrocortisone acetate with or without benzocaine
Application of dilute solutions of topical anesthetics
112
ETIOLOGY: FORDYCE’S GRANULES
Ectopic sebaceous glands- Normal tissues in an abnormal location; variation of the normal
A.k.a Sebaceous choristomas
Developmental in nature
112
CLINICAL FEATURES: SUBMUCOUS FIROSIS
Fibrotic bands located beneath an atrophic epithelium
Increased fibrosis
112
TREATMENT: SUBMUCOUS FIBROSIS
Cessation of the chewing habits
Eliminate causative agents
Stretching exercise
Intralesional injections of corticosteroids
Local injection of chymotrypsin, hyaluronidase and dexamethasone with placement of placental grafts
Topical and systemic steroids, supplement of vitamins and nutrients, repeated dilatation with physical devices and surgery
112
HISTOPATHOLOGY: SUBMUCOUS FIBROSIS
Principal feature is atrophy of the epithelium and subjacent fibrosis
Epithelial dysplasia may occasionally be evident
Type I collagen predominates in submucosa whereas type III collagen tends to localize at the epithelium- connective tissue interface , and around blood vessels, salivary glands, and muscle
112
DIAGNOSIS: SUBMUCOUS FIBROSIS
Needs to be palpated if its not stretchy as normal mucosa expect that it changed already
Palpable fibrous bands
Mucosal texture feels tough and leathery
Blanching of mucosa together with other histopathologic features
Features consistent with oral submucous fibrosis (atrophic epithelium with loss of rete ridges and juxta epithelial hyalinization of lamina propria)
112
OTHER NAME FOR FORDYCE SPOT
FORDYCE’S GRANULES
112
HISTOPATHOLOGY: FORDYCE SPOTS
Lobules of sebaceous glands aggregated around or adjacent to excretory ducts
Well formed heterotrophic glands and appear functional
112
TREATMENT: FORDYCE SPOTS
Asymptomatic- leave it wag na galawin (not an emergency)
No treatment- removal if the glands would post or show abnormal qualities
112
LOCATION: ECTOPIC LYMPHOID TISSUE
Anywhere in the oral cavity
112
Aggregate of lymphoid tissue commonly seen in the soft palate, floor of the mouth, and tonsillar pillars.
ECTOPIC LYMPHOID TISSUE
112
DIAGNOSIS: ECTOPIC LYMPHOID TISSUE
Entrapped epithelium within lymphoid tissue
Diagnosed on the basis of clinical features alone
112
TREATMENT: GINGIVAL CYSTS
No treatment indicated for infants since it rupture spontaneously early in life
For adults, surgical excision with inclusion of the overlying epithelium is recommended
112
TREATMENT: ECTOPIC LYMPHOID TISSUE
Normal tissue, no biopsy is necessary
112
CLINICAL FEATURES: ECTOPIC LYMPHOID TISSUE
Yellow/yellow-white small dome shape elevations
Posterolateral aspect of tongue
112
Occur in adults as well as infants
Odontogenic origin in adults
Frequency is highest in the neonatal phase- then disappear within 3 months due to rupture or exfoliate
GINGIVAL CYSTS
112
Focus of or accumulation of pus in the gingiva
PARULIS
112
COMMON TERM OF PARULIS
“Gum boil”
112
Cysts noted along the palatal midline that had no relationship to the tooth-forming apparatus
Epstein pearls
112
In neonatal: GINGIVAL CYSTS
Epstein pearls
Bohn’s nodules
112
Cysts noted along the alveolar ridges that were believed to be related to salivary gland remnants
Bohn’s nodules
112
TREATMENT: PARULIS
Treatment of the underlying condition
Know the cause of accumulation of pus
112
CLINICAL APPEARANCE: PARULIS
Yellow-white gingival tumescence with an associated erythema
112
ETIOLOGY: PARULIS
Derived from an acute infection either at the base of the occluded periodontal pocket or at the apex of a nonvital tooth
The path is of the least resistance
Pain is typical until the pus escapes to the surface
112
CLINICAL APPEARANCE: LIPOMA
Asymptomatic
Yellowish submucosal mass
Intact overlying epithelium
Superficial blood vessels evident over the tumor
112
LOCATION: PARULIS
Anywhere in the oral cavity soft tissues
Not expected to recur
Buccal mucosa, tongue, and floor of the mouth
112
LOCATION: LIPOMA
Anywhere in the oral cavity soft tissues
Not expected to recur
Buccal mucosa, tongue, and floor of the mouth
112
A well circumcised, lobulated mass of mature fat cells
LIPOMA
112
DIFFERENTIAL DIAGNOSIS: LIPOMA
Granular cell tumor, neurofibroma
Traumatic Fibroma
Salivary gland lesions (mucocele, and mixed tumor)
112
HAS NO PRE-MALIGNANCY TENDENCIES
Leukoedema
White Sponge Nevus
Hereditary Benign Intraepithelial Dyskeratosis
Follicular Keratosis
Focal Hyperkeratosis
Hairy Leukoplakia
Hairy Tongue
Dentifrice-associated slough
Candidiasis
Mucosal Burns
Gingival cysts
Parulis
Lipoma
Geographic tongue
Lupus Erythematosus
112
TREATMENT: LIPOMA
Excision
112
CLINICAL APPEARANCE: LIPOMA
Asymptomatic
Yellowish submucosal mass
Intact overlying epithelium
Superficial blood vessels evident over the tumor
112
LOCATION: LIPOMA
Anywhere in the oral cavity soft tissues
Not expected to recur
Buccal mucosa, tongue, and floor of the mouth
112
HAS PRE-MALIGNANCY TENDENCIES
Smokeless Tobacco Keratosis
Nicotine Stomatitis
Submucosal Fibrosis
Lichen Planus
