More diseaess-Kerr, Dry mouth Flashcards

1
Q

What is this clinical presentation?

A

Homogeneous leukoplakia

○ Thickened leathery, White plaque
○ Well-demarcated, Deepened fissures
○ Non-wipeable white patch

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2
Q

What is this clinical presentation?

A

Homogeneous leukoplakia.

○ Non-wipeable white patch

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3
Q

What is this clinical presentation?

A

homogenous leukoplakia

Just
white color

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4
Q

What is this clinical presentation?

A

Non-homogenous leukoplakia

Nodular leukoplakia ~ Largely white
Verrucous leukoplakia ~ Largely white
Erythroleukoplakia ~ Red and white

Speckled and verrucous leukoplakia have a greater risk for malignant
transformation than the homogeneous form

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5
Q

What is this clinical presentation?

A

Speckled leukoplakia.

Non-homogenous leukoplakia

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6
Q

Leukoplakia

Etiology

A

Etiology

The exact etiology remains unknown. Tobacco, alcohol,
chronic local friction, and Candida albicans are important predisposing
factors. Human papilloma virus (HPV) may also be involved in the
pathogenesis of oral leukoplakia.

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7
Q

Leukoplakia

Treatment

A
  • Biopsy to rule out malignancy
  • Elimination or discontinuation of predisposing factors,
  • systemic retinoid compounds.
  • Smoking cessation (leukoplakias often disappear or become smaller within first year of smoking cessation)
  • Complete removal with surgical excision, electrocautery, cryosurgery, or laser ablation
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8
Q

What is this clinical presentation?

A

Hairy Leukoplakia

corrugated white lesion on the lateral tongue.
• It only occurs on the lateral tongue

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9
Q

What is this clinical presentation?

A

Hairy Leukoplakia

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10
Q

Hairy Leukoplakia

Etiology

A

Epstein–Barr virus seems to play an important role in the
pathogenesis.

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11
Q

Hairy Leukoplakia

Treatment

A
  • Not required
  • however, in some cases aciclovir or valaciclovir
  • can be used with success.
  • Topical retinoids or podophyllum resin for temporary remission
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12
Q

What is this clinical presentation?

A

Proliferative Verrucous Leukoplakia

Patient with proliferative verrucous leukoplakia but manifesting more as
an erythroplakia in multiple sites than a leukoplakia

Proliferative verrucous leukoplakia has very high risk (49.5% in malignant transformation)
almost 10% risk for malignant transformation every year

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13
Q

What is this clinical presentation?

A

Proliferative Verrucous Leukoplakia

Location
○ Gingiva (Frequent)
○ Buccal Mucosa
○ Palatal Mucosa

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14
Q

What is this clinical presentation?

A

Proliferative Verrucous Leukoplakia

Multifocal

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15
Q

Proliferative Verrucous Leukoplakia

Treatment

A

complete removal: excision, electrocautery, cryosurgery, or laber ablation

Lesions rarely regress despite therapy

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16
Q

What is this clinical presentation?

A

Oral lichen planus

White lacy appearance, with
a network reticular appearance (Wickham’s striae)
sometimes punctate or plaque‐like lesions predominate

o Wickham’s striae→ very characteris► white wispy changes

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17
Q

What is this clinical presentation?

A

Oral lichen planus

on the buccal mucosa (most common site

reticular form.

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18
Q

What is this clinical presentation?

A

Oral lichen planus

slightly more red as you move to the left of the picture
● The white lines have small sunburst effect at the periphery
○ Very very characteristic of lichen planus
○ Will never see this in a leukoplakia

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19
Q

What is this clinical presentation?

A

Oral lichen planus

Lichen planus of the dorsum of the tongue

this is a hypertrophic form.

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20
Q

Oral lichen planus

Etiology

A

Although the cause is not well known, T cell-mediated autoimmune
phenomena are involved in the pathogenesis of lichen planus.

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21
Q

Oral lichen planus

Treatment:

A
  • Incisional biopsy on non-keratinized, non-ulcerated mucosa

○ Asymptomatic → no tx
○ Symptomatic → 0.5mg/ml Dexamethasone Elixir.

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22
Q

What is this clinical presentation?

A

Lichenoid Reactions

Contact Lesions

a sensitivity in contact with a dental amalgam
▪ When you replace these amalgams, the lichenoid reaction will typically
disappear

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23
Q

What is this clinical presentation?

A

Oral Lichenoid

Contact lesion

chenoid reaction to dental amalgam and cold: white and erythematous
lesions on the buccal mucosa.

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24
Q

What is this clinical presentation?

pts takes Thiazide Diuretic

A

Oral Lichenoid Drug
Reaction

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25
What is this clinical presentation? pts takes *allopurinol*
Oral Lichenoid Drug Reaction
26
**Oral Lichenoid Contact Lesions** Etiology
**Hypersensitivity** to * dental restorative materials, amalgam or other metal, composite resins * Foods, oral products * Especially cinnamon * dental plaque accumulation are the most common
27
Oral Lichenoid Drug Reaction Etiology
* Lichenoid reactions may develop after exposure to a medication for periods of \> 1 year * May develop very slowly after the problem is initiated so it can be very challenging to connect the dots **Many different medications that can lead to lichenoid reactions** * Beta blockers, ACE inhibitors, Rituxumab etc… * A number of new targeted agents “mabs” and “nibs” can cause lichenoid reactions * In cancer centers, this has become quite a problem because they are taking disease‐modifying drugs
28
Oral lichenoid reaction _Treatment_
**Insicional biopsy Mandated to distinguish from OLP** ○ Biopsy white areas on non-keratinized mucosa NOT ulcerated OR red areas Treatment Replacement of the restorative material, polishing and smoothing, and good oral hygiene are recommended. Topical steroid treatment for a short time is also helpful.
29
What is this clinical presentation?
**Nicotinic Stomatitis** also known as Smoker’s keratosis smoker’s palate * the palatal mucosa becomes diffusely gray or white; numerous slightly elevated papules are noted, usually with punctate red centers
30
What is this clinical presentation?
**Nicotinic Stomatitis** These papules represent _inflamed minor salivary glands_ and their ductal orifices.
31
What is this clinical presentation
Nicotine Stomatitis.
32
Nicotine Stomatitis Treatment
Smoking Cessation. * Nicotine stomatitis is completely reversible, even when it has been present for many decades. * The palate usually returns to normal within 1 to 2 weeks of smoking cessation.
33
Nicotine Stomatitis. Etiology
The elevated temperature, rather than the tobacco chemicals, is responsible for this lesion.
34
What is this clinical presentation?
**Pseudomembranous candidiasis** on the palate. usually caused by Candida albicans Predisposing factors are local (poor oral hygiene, xerostomia, mucosal damage, dentures, antibiotic mouthwashes)
35
What is this clinical presentation?
Geographic tongue/ areata migrans Multiple, well-demarcated zones of erythema (due to filiform atrophy) surrounded by slightly elevated, yellow-white, serpentine/ scalloped border annular - serpiginous - atrophic - Fissured
36
What is this clinical presentation?
Geographic tongue/ areata migrans
37
What is this clinical presentation?
Geographic tongue/ areata migrans
38
What is this clinical presentation?
Geographic tongue/ areata migrans
39
What is this clinical presentation?
Geographic tongue, localized lesion.
40
Geographic tongue/ areata migrans _Treatment_
* Generally no treatment is indicated * Reassuring the patient that the condition is completely benign is often all that is necessary. * In case of tenderness or a burning sensation that is so severe --topical corticosteroids, such as fluocinonide or betamethasone gel, may provide relief
41
Geographic tongue/ areata migrans _Etiology_
The exact etiology remains unknown. It may be genetic.
42
What is this clinical presentation?
**Fordyce’s granules** on the buccal mucosa. a normal anatomical variation. ectopic sebaceous glands of the oral mucosa.
43
What is this clinical presentation?
Leukoedema of the buccal mucosa. Laskaris,
44
Leukoedema Etiology Treatment
Etiology It is due to increased thickness of the epitheliumand intracellular edema of the prickle-cell layer. Treatment No treatment required
45
What is this clinical presentation?
White Sponge Nevus Diffuse, thickened white plaques of the buccal mucosa
46
What is this clinical presentation?
White Sponge Nevus | (Canon disease)
47
**White Sponge Nevus** Etiology
**Autosomal dominant skin disorder** Etiology: ● This condition is due to a defect in the normal keratinization of the oral mucosa in the 30-member family of keratin filaments, the pair of keratins known as **keratin 4 and keratin 13** is specifically expressed in the spinous cell layer of mucosal epithelium.
48
What is this clinical presentation?
**Verrucous Carcinoma** Early verrucous carcinoma of the buccal mucosa.
49
What is this clinical presentation?
**Verrucous Carcinoma** Large, exophytic, papillary mass of the maxillary alveolar ridge.
50
What is this clinical presentation?
**Verrucous Carcinoma** Large, exophytic, papillary mass of the maxillary alveolar ridge.
51
What is this clinical presentation?
Verrucous Carcinoma Extensive papillary, white lesion of the maxillary vestibule
52
**Verrucous Carcinoma** Etiology
a low-grade variant of squamouscell carcinoma. Etiology Leading theories include * human papillomavirus (HPV) infection * chemical carcinogenesis induced by smoking and chewing tobacco * alcohol consumption * betel nut chewing (oral lesions), * chronic inflammation
53
**Verrucous Carcinoma** Treatment
○ Surgical Excision ○ Radiotherapy
54
Traumatic Erythema /Traumatic Hematoma on the lower lip.
55
What is this clinical presentation?
Geographic tongue: well-demarcated red patch on the tongue.
56
What is this clinical presentation?
Median rhomboid glossitis. a Chronic hyperplastic, erythematous candidiasis
57
Median Rhomboid Glossitis Treatment
No treatment is required.
58
Median Rhomboid Glossitis Etiology
**Atrophy of central filiform papillae** Presumably developmental. Candida albicans may also be involved. but smokers, people with xerostomia , who use inhalation steroids and denture wearers are **at increased risk**
59
what is this clinical presentation?
Denture stomatitis.
60
**Erythroplakia** Malignant transformation
Erythroplakia is a high risk for malignant transformation. So, if you encounter an erythroplakia, it's probably already a cancer or it's fast‐tracking towards a cancer
61
What is this clinical presentation?
**Erythroplakia** of the buccal mucosa Well-demarcated erythematous patch or plaque with soft velvety texture
62
What is this clinical presentation?
Erythroplakia of the buccal mucosa.
63
What is this clinical presentation?
**Erythroplakia** of the lateral margin of the tongue. Well-demarcated erythematous patch or plaque with soft velvety texture
64
What is this clinical presentation?
Erythroplakia Firey red Well-demarcated patch or plaque with soft velvety texture transformed into SCC
65
**Erythroplakia** Treatment
○ Biopsy required for diagnosis ○ If a source of irritation can be identified and removed, biopsy may be delayed for 2 weeks to allow lesion to heal ○ Complete excision
66
What is this clinical presentation?
Erythroplakia. Well-circumscribed red patch on the posterior lateral hard and soft palate
67
What is this clinical presentation?
Erythroplakia. Erythematous macule on the right floor of the mouth. Biopsy-- Turned out to be early invasive squamous cell carcinoma.
68
What is this clinical presentation?
Smokeless tobacco keratosis/TOBACCO POUCH KERATOSIS Smokeless Tobacco–related Gingival Recession. Extensive recession of the anterior mandibular facial gingiv
69
What is this clinical presentation?
Smokeless tobacco keratosis/TOBACCO POUCH KERATOSIS Tobacco Pouch Keratosis, Severe
70
What is this clinical presentation?
Smokeless tobacco keratosis/TOBACCO POUCH KERATOSIS Tobacco Pouch Keratosis, Mild. A soft, fissured, gray-white lesion of the lower labial mucosa located in the area of chronic snuff placement.
71
Smokeless tobacco keratosis Treatment:
typically resolves weeks after cessation ○ if persists 6+weeks -\> biopsy to rule out dysplasia + SCC
72
What is this clinical presentation?
**Pemphigus Vulgaris.** . Multiple erosions affecting the marginal gingiva.
73
What is this clinical presentation?
**Pemphigus Vulgaris.** Multiple erosions of the left buccal mucosa and soft palate.
74
What is this clinical presentation?
**Pemphigus Vulgaris.** Large, irregularly shaped ulcerations involving the floor of the mouth and ventral tongue.
75
What is this clinical presentation?
**Pemphigus Vulgaris.**
76
What is this clinical presentation?
**Pemphigus vulgaris** ● Multiple, chronic, mucocutaneous ulcers ● Many patients also have ● Relatively non‐specific ● Very superficial, only in epithelium ● Occur on any mucosal surface: oral, ocular, nasal, GI, esophageal, genital
77
What is this clinical presentation?
**Pemphigus vulgaris** PV Lesions can affect virtually any mucosal surface (oral, nasal, ocular, pharyngeal, esophageal, genital)
78
What is this clinical presentation?
**Pemphigus vulgaris** **usually suffer from Desquamative gingivitis (DG)** More superficial erosion of the marginal gingiva, typically with an intense erythema and inflammation, and very often in the absence of local factors that would typically cause a gingivitis o Hurts to brush their teeth Immediately look for areas where there are no local factors and look for inflammation there o To check the possibility of systemic factors causing local gingivitis
79
What is this clinical presentation?
**Pemphigus vulgaris** Combination of PV inflammation and gingival inflammation accumulating local factors can result in advanced loss of attachment and tooth loss
80
**Pemphigus vulgaris** **Etiology**
Pemphigus vulgaris is not fully understood. Experts believe that it's triggered when a person who has a genetic tendency to get this condition comes into contact with an environmental trigger, such as a chemical or a drug. In some cases, pemphigus vulgaris will go away once the trigger is removed.
81
**Pemphigus vulgaris** **Treatment**
Treatment has 3 stages: **● Stage 1: Control** ○ Suppress inflammation / lesion activity with Systemic **Corticosteroid: Remains initial / 1st‐line treatment…** ○ Then quickly add steroid‐sparing agents (mycophenolate mofetil) to minimize dose and duration of corticosteroid treatment as well as improve disease control **● Stage 2: Consolidation** ○ Reducing auto‐antibody production with the addition of Immunosuppressants ○ Assessed by the lack of development of NEW lesions **● Stage 3. Remission / Maintenance:** ○ achieving complete remission of lesion activity OFF medication is the GOAL ○ When lesion activity OFF medications cannot be achieved, principle of MINIMALLY effective therapy is the goal, typically with combination of immunosuppressant medications **○ RITUXIMAB has become the FIRST CHOICE treatment after ○ the consolidation phase to achieve DISEASE REMISSION** _● TOPICAL / INJECTABLE CORTICOSTEROID MEDICATIONS_ ○ o Can be used to help control limited number of lesions resistant to systemic therapy: it treats ONLY the disease ○ outcome (lesions) and not the systemic illness / pathologic antibody production **○ ex:clobetesol 0. 05% , halbetesol 0.05% (most potent)**
82
**What is this clinical presentation?**
Mucous membrane pemphigoid
83
**What is this clinical presentation?**
Mucous membrane pemphigoid SEVERE/HIGH RISK FORMS OF MMP ▪ Ocular ▪ Esophageal can result in functional blindness
84
**What is this clinical presentation?**
Mucous membrane pemphigoid Oral Hygiene: Plaque related gingival inflammation contributing to continued VB desquamative gingivitis
85
**What is this clinical presentation?**
Mucous membrane pemphigoid REMEMBER: ▪ Plaque and calculus can be the consequence of painful MMP lesions ▪ When assessing MMP lesions/desquamative gingivitis, look for areas of intense inflammation WITHOUT local factors as evidence of VB disease
86
**Mucous membrane pemphigoid** **Etiology**
Mucocutaneous autoimmune disease characterized by sub‐epithelial blisters (bullae) which ruptures to form large, non‐healing ulcerations
87
Mucous membrane pemphigoid _Treatment_
o Approach is similar to PV – but generally not as aggressive unless hi‐risk areas ( ocular, esophageal ) where more intense immunosuppression indicated ▪ NON‐immunosuppressive treatments uniquely effective: * *o** **Dapsone** * *o Tetracycline + nicotinamide**
88
MMP & PV BIOPSY
take two different sites ○ For H&E, still must be perilesional ○ If you get only ulcer just because the clinician thinks ○ that is the pathology → there is no epithelium! ○ The sample is useless and no diagnosis can be made
89
What is this clinical presentation?
Actinic cheilitis (Solar cheilosis) Typical presentation of angular cheilitis with erythema, crusting and mild fissuring of the angles of the mouth bilaterally.
90
What is this clinical presentation?
Actinic cheilitis (Solar cheilosis) Early presetation: Smooth, blotchy, pale, dry areas Diffuse, irregular white plaque around line of the lip Crusted, Scaly **​**
91
**Actinic cheilitis** malignant transformation
Actinic cheilitis has **2 times** of risk for developing SCC of the lip. SCC on the lips is 11 times as likely to metastasize compared to SCC found on other parts of the body
92
**Actinic cheilitis** Etiology
due to chronic ultraviolet light exposure.
93
**Actinic cheilitis** Treatment
* avoid sun exposure * Laser ablation is preferred for severe actinic cheilitis * surgical excision is recommended for severe actinic cheilitis with evidence of high-grade dysplasia * Lip Shaving” (Vermilionectomy) * can also use cryotherapy, electrodesiccation It requires long term follow up and **prognosis is good if caught early**
94
What is this clinical presentation?
**_SCC_** arising from **Actinic Cheilitis**
95
What is this clinical presentation?
**Oral Melanoma** a highly malignant neoplasia, arising from melanocytes, the cells that produce the brownish pigment melanin.
96
What is this clinical presentation?
**Oral Melanoma** an ulcerated, blue-black, slightly elevated lesion in the edentulous, posterior right maxilla. The lesion extends across the residual alveolar ridge onto the palate and onto the facial aspect of the ridge.
97
What is this clinical presentation?
**Oral Melanoma** patient with extensive, black-pigmented and irregularly bordered macule in the maxillary labial mucosa and midline facial gingiva, (teeth 8 and 9). (The patient's fingers are depicted.)
98
What is this clinical presentation?
**Oral Melanoma** Large, blue-black, irregularly bordered lesion on the upper lip of a male Japanese patient. The diagnosis is oral melanoma.
99
What is this clinical presentation?
Amalgam tattoo This image depicts two diffusely bordered, dark gray macules in the left posterior buccal mucosa adjacent to molar teeth that have been restored. .
100
What is this clinica presentation?
Oral melanoacanthoma. the buccal mucosa of a middle-aged, black woman with a brown-black, irregularly bordered macule that arose suddenly. The patient was unaware of its presence.
101
What is this clinical presentation?
**Oral melanotic macule** an irregularly shaped, tan-brown macule on the left hard palate in an edentulous patient.
102
Oral Melanoma ## Footnote **Etiology**
Unknown. Ultraviolet radiation is an important causative factor for skin melanoma **Acute sun damage** can cause it more than chronic exposure
103
Oral Melanoma Risk Factors
Fair skin A history of sunburn Excessive ultraviolet (UV) light exposure. Living closer to the equator or at a higher elevation Having many moles or unusual moles A family history of melanoma Weakened immune system.
104
**Oral Melanoma** Treatment
* Surgical excision * Radiotherapy * Chemotherapy
105
What is this clinical presentation
Oral Melanoma
106
What is this clinical presentation
Oral Melanoma
107
What is this clinical presentation
Oral Melanoma
108
What is this clinical presentation?
Traumatic ulcer caused by sharp or puncturing food stuff
109
What is this clinical presentation?
Traumatic ulcer a chronic ulcer on the left posterior lateral border of the tongue caused by lingually tilted mandibular 3rd molar. Note central ulceration with peripheral keratosis
110
What is this clinical presentation?
Traumatic ulcer Post-anaesthesia traumatic ulcer on lower lip.
111
What is this clinical presentation?
Traumatic ulcer Most often on tongue, lips, buccal mucosa Any sites that may be injured by dentition
112
What is this clinical presentation?
Traumatic Granuloma
113
What is this clinical presentation?
Traumatic Granuloma (traumatic ulcertaive granuloma)
114
What is this clinical presentation?
**Traumatic Granuloma** | ( Traumatic Ulcerative Granuloma)
115
Traumatic ulcer/Traumatic ulcerative granluoma Etiology
**Etiology** * typically caused by trauma. In more than half the cases, the patient does not recall traumatizing the area although this may have occurred during sleep. * Chronic mucosal trauma from adjacent teeth * Some adjacent source of irritation
116
Traumatic ulcer/Traumatic ulcerative granluoma Treatment
**Remove cause of irritation** Topical anesthetic or film for pain relief If there is no obvious cause then ► **biopsy**
117
What is this clinical presentation?
Squamous cell carcinoma on the buccal mucosa)
118
What is this clinical presentation?
**Erythroplakia and Squamous Cell Carcinoma** Erythroplakia is a general term for red, flat, or eroded velvety lesions that develop in the mouth. In this image, an exophytic squamous cell carcinoma on the tongue is surrounded by a margin of erythroplakia
119
What is this clinical presentation?
Leukoplakia and Squamous Cell Carcinoma Leukoplakia is a general term for white hyperkeratotic plaques that develop in the mouth. About 80% are benign. However, in this image, squamous cell carcinoma is present in one of the leukoplakic lesions on the ventral surface of the tongue (arrow).
120
squamous cell carcinoma Risk factors
**HPV + SCC** Area affected: ( Oropharynx cancers largely involved tonsils, . Posterior 3rd of the Tongue) Younger pts, 3:1 Males to females ratio, high socio-eco status Incidence is decreasing less aggressive → higher survival rates ( Better than HPV negative SCC) **HPV - SCC** The chief risk factors for oral squamous cell carcinoma are Smoking (especially \> 2 packs/day) Alcohol use Risk increases dramatically when alcohol use exceeds 6 oz of distilled liquor, 15 oz of wine, or 36 oz of beer/day. The combination of heavy smoking and alcohol abuse is estimated to raise the risk 100-fold in women and 38-fold in men. ( this affects these ares : the tongue, floor of mouth, buccal mucosa, or gingiva) mostly men, low socio-economic factors Incidence is decreasing Very aggressive → lower survival rates
121
SCC treatment
Early stage: Radiation and/or Surgical removal Late stage : combination of surgery, radiation therapy, or chemotherapy
122
What is this clinical presentation?
**Graphite tattoo** Most common location on the palate and gingiva Gray, black, or blue-ish macule
123
What is this clinical presentation?
**Graphite tattoo** Gray, black, or blue-ish macule
124
Graphite tattoo Treatment
If patient is concerned for cosmetic reasons ► then removal of lesion with autogenous graft
125
Graphite tattoo Etiology
result from pencil lead that is traumatically implanted, usually during the elementary school years
126
What is this clinical presentation?
Traumatic ulcer of the tongue.
127
What is this clinical presentation?
**Hemangioma of Infancy** a relatively common benign proliferation of blood vessels that primarily develops during childhood. display a rapid growth phase with endothelial cell proliferation, followed by gradual involution.
128
What is this clinical finding?
Hemangioma of Infancy
129
**Hemangioma of Infancy** Treatment
○ Because most hemangiomas of infancy undergo involution, management often consists of “watchful neglect.”
130
What is this clinical finding?
Necrotizing Sialadenometaplasia an uncommon, usually self-limiting, benign inflammatory disorder of the salivary glands. *Here it is on the palate*
131
What is this clinical finding?
**Necrotizing Sialadenometaplasia** *we see two ulcers on the palate* *Mostly ● Palatal salivary glands ○ Possible for parotid ● 75% of case on posterior palate ● Hard\>Soft palate ● 2/3rd are unilateral*
132
**Necrotizing Sialadenometaplasia** _Etiology_
*The cause is uncertain, although the hypothesis of ischemic necrosis after vascular infarction seems acceptable.*
133
**Necrotizing Sialadenometaplasia** _Treatment_
No Treatment Needed but we need to biopsy to rule out other diseases
134
What is this clinical finding?
**Frictional Keratosis.** There is a rough, hyperkeratotic change to the posterior mandibular alveolar ridge (“alveolar ridge keratosis”), because this area is now edentulous and becomes traumatized from mastication. **Such frictional keratoses should resolve when the source of irritation is eliminated and should not be mistaken for true leukoplakia.**
135
What is this clinical finding?
**Frictional Keratosis** **the white surrounding a a traumatic ulcer** Symptomatic traumatic ulceration of the left mid-ventral tongue associated with a sharp left lower molar. The ulcer has flat edges and is surrounded by an area of frictional keratosis.
136
**Frictional Keratosis.** Differential Diagnosis
Leukoplakia Linea alba Chronic cheek chewing (bite injury) Candidiasis Oral Lichen planus Squamous cell carcinoma
137
What is this clinical finding?
Frictional keratosis on the tongue
138
**Frictional Keratosis** **Etiology**
* Trauma from Sharp cusp & ortho appliance * Chronic mechanical irritation (chronic biting) * Masticatory function * Normal hyperplastic response * Dentures/missing teeth
139
**Frictional Keratosis** **Treatment**
* Remove the cauative factor that caused the trauma * observe large lesion regularly excellent prognosis
140
What is this clinical presentation?
**dry‐mouth** patient a classic example **• Classic fissuring • depapillation of the tongue papilla • some white changes on the tongue.**
141
What is this clinical presentation?
**dry‐mouth** from radiation Note the Ropy, frothiness on the palate. - The tissues are red and irritated due to candida infection as well.
142
What is this clinical presentation?
**dry Mouth** Cervical caries related to radiation. The patient is a smoker and coffee drinker --\> explains the staining
143
What is this clinical presentation?
dry Mouth Incisal caries in a radiation patient: **Incisal caries is a sure sign of severe dry mouth/ significant salivary gland hypofunction**
144
What is this clinical finding?
**Xerostomia-related Caries** **Or** **Dry Mouth** . Extensive cervical caries of mandibular dentition secondary to radiation-related xerostomia.
145
**Dry mouth** Subjective vs Objective
**Xerostomia** The subjective experience of a dry mouth (ie a symptom) **Salivary Hypofunction** The objective measurement of a reduction in salivary flow (a sign)
146
What is the normal rate for **Stimulated Saliva Production**
**Stimulated Saliva Production** **▪ 200+ ml/day ▪ Flow rate: mean 1-2 ml/min, maximum 7 ml/min** o “Normal” range is very wide
147
What is the normal rate for Unstimulated Saliva Production
**300 ml/day ▪ Flow rate: mean 0.3 ml/min**
148
What are Factors affecting unstimulated flow include?
* **Dehydration** * **Medical conditions** * **Body posture** * **Lighting conditions** * **Circadian/circannual rhythm (lowest during)** * **Medications** Age is an independent factor for whole saliva andsubmandibular/sublingual gland secretion (but notparotid).
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What are Factors affecting stimulated flow include:
* **Mechanical stimuli** * **Vomiting** * **Gustatory/olfactory stimuli (acid/smell)** * **Gland size** Age is an independent factor for whole saliva (but not for parotid and minor gland secretions)
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What causes dry mouth?
Central inhibition as a result of connections between the primary salivary centers and the higher centers of the brain.
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● What causes xerostomia in absence of measurable salivary hypofunction?
* **May be a reduction in baseline sialometry which is still above “normal.”** * *If they get a decrease in the salivary flow, they still may be in the normal range, but for them the experience is that they have got dry mouth.* * **Saliva film thickness** * *Palatal mucous gland secretions?* * *Anterior dorsum of tongue?* * **Relative contributions by glands** * Mucins, proteins? * **Alterations in sensory perception?** * **Mental status/central inhibition?**
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What cause Salivary Hypofunction?
**● Dehydration ● Medications (Rx & OTC)** * *Direct damage to glands* * *Head and neck radiotherapy* * *As a result of radiation it’s irreversible damage to the glands* * *Chemotherapy (reversible)* * *Autoimmune diseases* * *Primary vs Secondary Sjögren’s Syndrome, GVHD* * *HIV disease* **● Decreased mastication (tooth loss, soft diet) ● Conditions affecting the CNS:** * Psychologic disorders (depression/anxiety?), Alzheimer’s, Parkinson’s, Cerebral palsy
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To have dry mouth xerostomia what is the rate of Unstimulated and Stimulated Salivary flow **USFR** and **SFR**
**Abnormal unstimulated USFR= \<0.1–0.2ml/min** **Abnormal stiumated SFR = \<0.5ml/min**
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Severity of patients with xerostomia using objective measures
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How to manage with normal USFR and SFR?
* Salivary stimulation (OTC) to stimulate their glands * Salivary lubrication ( to improve it) * Humidification ( like a humidifier in the room at night) * Hydration/prevent dehydration (ie avoid alcohol, caffeine both will act as a * diuretic and lead to dehydration). * Monitor closely to rule out emerging disease ( to see whether they are developing Sjogren’s or something else 􀀀 we want to follow them over time)
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How to manage with abnormal USFR and normal SFR? (respond to stimulated) Abnormal unstimulated USFR= \<0.1–0.2ml/min
* Look for possible causes (major cause will be medications & can dehydration or others) * Restore chewing function (Masticatory issues) * Reduce medication‐induced salivary hypofunction * Prescribe Salivary stimulation OTC, Rx medications, others * Prescribe Salivary lubrication * Humidification ‐use humidifiers * Hydration/prevent dehydration (ie avoid alcohol, caffeine) * Treat oral consequences (such as candidiasis treated with an antifungal or caries with management of caries).
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How to manage with abnormal USFR and abnormal SFR? Abnormal unstimulated USFR= \<0.1–0.2ml/min Abnormal stiumated SFR = \<0.5ml/min
* If dehydrated ► rehydrate or treat underlying condition * People with uncontrolled diabetes, once you control the diabetes‐ their flow comes back. * All we can do is offering Salivary substitutes (sprays, gels, rinses ) * For patients with high dose radiation treatment ► makes sure they get the INRT * Minimizing damage to salivary glands ( there are other strategies for that) * Prevention and treatment of oral complications
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**What are the** **Prescription Medications** for people with low USFR and some oral signs, but responds to stimulation ? (abnormal USFR, Normal/improved SFR) **(include dosage and usage)**
– Muscarinic agonists: – **Pilocarpine** 5‐7.5mg tid & qhs (can go as high as 10mg qid) – **Cevimeline** 30mg tid (can go as high as 60mg tid) _Contradicated for_ : **CV disease, hepatic, renal or respiratory diseases or narrow angle glaucoma** **Pilocarpine affects M1 & M3** _side effects_ (sweating, flushing, rhinitis, increased urination, weakness and some experience the shakes. ) **Cevimeline affects M3 only** fewer side effects
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What is this clinical presentation?
**SJÖGREN’S SYNDROME** Autoimmune exocrinopathy Marked bilateral parotid gland enlargement in a patient with primary Sjögren syndrome Dry mouth and eyes resulting from a chronic progressive loss of secretory function (Slowly but surely, the salivary glands and/or lacrimal glands (some cases are more lacrimal & less salivary or vice versa); slow & progressive Patients with Sjogren’s can have bilateral salivary gland enlargement (parotid) (Sometimes we may see a unilateral enlargement of the salivary glands due to retrograde infections.) **increased risk of lymphoma (MALT type)**
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What is this clinical presentation?
**SJÖGREN’S SYNDROME** _Dry Mouth_ very severe cervical disease & very dry lips
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What is this clinical presentation?
Depapillated & Fissured Tongue ## Footnote **SJÖGREN’S SYNDROME**
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What is this clinical presentation?
a patient with a **_bacterial sialadenitis_** who has **_SJÖGREN’S SYNDROME_** When we examine such patients and ”milk” the gland ► you actually see a purulent drainage from the gland itself.
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**SJÖGREN’S SYNDROME** **Management**
These patients **LOW USFR, no response to stimulation (aka abnormal USFR/SFR)** * Rehydrate if dehydrated * Treat underlying conditions (i.e. DM) * Salivary substitutes (glycerin) * Minimize damage to glands from radiation * Prevention of complications & palliative treatment * Optimal hygiene * Restore caries * Smooth sharp edges in oral cavity * Fluoride therapy * Antifungals * Chlorhexidine rinses w/o alcohol * Sialendoscopy * Salitron - salivary pacemaker * ALTENS (acupuncture like transcutaneous electrical nerve stimulation)
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What is this clinical presentation?
**Sjögren Syndrome** * bilateral enlargement of the submandibular glands * angular cheilitis, dry and cracked lips and fissured and despapilated tongue * severe ocular lesions.