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What is Scaling?
What is Root plaining?
- Scaling is instrumentation of crwon and root to remove plaque, calculus, and stain from these surfaces
- Root plaining is a tx to remove cementum or surface dentin that is rough, impregnated with calculus, or contaminated with toxins or microorganisms.
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Who has NUG?
It is called a "punched out" lesion because of what 3 symptoms??
What is the differential diagnosis?
Wht are 3 predisoposing factors?
How do you treat it?
- *Adolescents or young adults, smokers, individuals under stress
- *Pain, Ulceration, and necrosis of the Inderdental Papilla bleeding
- *Primary Herpetic gingivostomatitis
- *Systemic disease (Ulcerative colitis, blood dycrasis, and nutritional states), Abnormalities of WBC function, Patients with AIDS
- *OHI, Mechanical debridement, systemic AB, Surgical correction of gingival recession
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What medications modifiy plaque induced gingivitis?
- Phenytoin Sodium or epinutin
- Cyclosporin
- Calcium channel blockers such as Nifedipin
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Leukemia modifies plaque induced gingivitis and this results in what changes? What is persistant unexplained gingival bleeding associated with?
Cyclic Neutropenia has _____ as a symptom
- Acute Myeloid leukemia associated with gingival changes
- Thrombocytopenia
- Ulceration
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Plaque induced Gingivitis can be modified by systemic disorders which include ____, _____, and other blood dyscrasias.
Type I Diabetes, Leukemia
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A patient has a granuloma in the interdental Papilla. It has a pedunculated base and is highly vascularized. She's in her 2nd trimester (although same is seen in 3rd) what does she have?
Pyogenic Granuloma
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During menstration the GCF increases by how much? %
20
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Gingivitis is modified by endocrine factors. The host response is exaggerated and modulated by ______.
____ and ____ need to be present as well. In pregnant females the changes being during____ and regress
- Endogenous hormones
- Dental plaque
- microbiota
- 2nd trimester
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What are some common features of Gingivitis on a Reduced Periodontium? (4)
- Previous attachment loss
- disease arrested with treatment
- Gingival margin apical to CEJ and inflammed
- no further attachment loss
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Disease begins where plaque is present--at the gingival margin. What other changes occur?
The absence of ___ and ____ are signs of plaque-induced
- *Color,
- Gingival contour,
- Temperature
- gingival exudate
- BOP
- *Attachment loss and bone loss
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Plaque-induced gingivitis has numerous Characteristics.
Where is it limited to?
What needs to be there?
Inflammation?
Can there be attachment loss?
How do you reverse the disease?
- Gingiva
- Plaque
- Yes
- No, but if on reduced periodontium must be stable
- Remove etiology
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____% of people with Leukemia have oral signs of it. What are these signs?
- 69%
- Swelling, petecchia, ulceration and erythema gingiva
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What are some common physical causes of tramatic lesions?
How do traumatic lesions due to heat look?
- *Gingival laceration (resulting in gingival recession) and brush and floss techniques
- *Seen on palatal and labial mucosa as painful erythmatous lesions. Vesicles may develop.
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What are some common chemical causes for traumatic lesions?
- Chlorohexadine-induced mucosal desquamation
- acetylsalicylic acid burn
- cocaine burn
- incorrect use of caustic material by dentist
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What are the two "Types" of allergic reactions and what are the mediated by?
What are some common allergens?
What are the the signs of an allergic reaction?
- *Type I (immediate) by IgE or Type IV (Delayed) by T-cells
- * Dental restorative materials (Type IV), oral hygiene products, chewing gum, and food (Flavor additives)
- *A diffuse fiery red edematous gingivitis sometimes with ulcerations or whitening
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What are symptons of drug-induced lesions?
- Gingival hyperplasia
- Erythema multiform
- Oral ulceration
- Epithelial atrophy, sloughing, and intense erythema (red)
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What are 3 drugs that can cause lesions in non-plaque induced gingivitis?
- Calcium channel blockers-- (Spelling probably wrong as I wrote what she "said")
- Dilandin
- Cytosphore
- ACE inhibitors
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What happens to the basal cells and with of basement membrane in Lupus?
What is deposited on basement membrane?
- Basal cells degenerate and Basement membrane increases in width
- C3, Igs, and fibrin
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Which tissue does lupus effect?
What are the 2 forms?
How does it present itself clinically?
What does it resemble?
Does it have characteristic skin lesions?
- Connective tissue
- systemic and discoid
- Has a central atrophic area, surrounded by irradiating fine white striae, periphery of telangiectasia (capillary enlargement)
- leukoplakia and atrophic oral lichen planus
- yes
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A patient enters your office with a lesion that is both on their skin and buccal mucosa. There is an extensive crust around lips and they're swollen. They report this has happened before (recurrent). What is it?
How often is there oral involvement with this?
What is causing the extensive ulcers?
- Erythema Multiform
- 25-60%
- Bullae that ruptured
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What is the histological term used to describe the intraepithelial bulla forming?
What deposits are seen?
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Where does pemphigus vulgaris cause pathogenesis of desquamative lesion, erosion, or ulcerations?
Since it's genetic, what groups most affected?
Can this be chronic?
- Intraepithelial bullae in skin and mucous membranes
- Jewish and Mediterranean
- yes
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In Pemphigoid what is the body attacking specifically?
What detaches from what?
What may be the cause of this pathogenesis?
What deposits can be seen?
Shooting air on the epithelium causes it to "bubble" up. What is this "sign" called?
- Hemidesmosomes and lamina lucida
- Epithelium from Connective tissue
- Complement mediated cell destruction
- C3, IgG, and other Igs
- Nikolsky's sign
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Lichen Planus has four histopathology features. Name them.
- Deposits of IgM, C3, C4, C5
- Fibrin in BM
- characterstic of a type IV hypersensitivity
- Subepithelial band-like accumulation of lymphocytes
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What are the characteristic skin lesions of Lichen planus?
What percent of Lichen Planus are premalignant?
Where is it and is it usually orally seen?
- Wickham Striae
- 0.5-2%
- Anywhere in mouth, and oral involvement alone is common
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Name ALL of the lesions of systemic origin
- Mucocutaneous disorders
- Lichen Planus
- Pemphigoid vulgaris
- Pemphigus Multiform
- Lupus erythmatosus
- Drug-induced mucocutaneous disorders
- Allergic Reactions
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The only one known type of lesion from genetic Origin is what?
What are some possible mechanisms for causing this?
- Hereditaty gingival fibromatosis
- TGF-Beta favor the accumulation of ECM
- May be on Chromosome 2 in human
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Histoplasmosis can be Acute, chronis and disseminated (in IC pts). Where is is seen and what does it look like?
ANY area of the mouth; Its granulomatous so caseating necrosis is seem. Originally nodular or papillary and later may because ulcerative type of lesion
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A distinct red band on limited to the free gingiva that does NOT BOP indicates what kind of infection?
Will oral hygiene clear infection?
What is the differential diagnosis?
How can you treat it?
- Linear Gingival Erythema
- NO !
- Oral Lichen planus or Renal insufficiency
- Chlorohexadine rinse and Anti-fungal therapy
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How do you treat candidiasis?
Flucanazole, Nystatin, Amphotericin B (IV)
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Besides Candidiasis, what is another C. albincan infection that is acquired during birth?
What does this look like?
What are some predisposing conditions (5)
- -Thrush
- -pseudomembranous/or erthymatous (white/ or red-yellow), Has bleeding points because of HYPHAE
- -ABs, Immunosuppression, Malnutrition, HIV, Diabetes
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There are many types of Candidiasis. Which is isolated from the the mouth that we are interested in?
How much (%) is in the mouth in normal healthy adults?
Where is it isolated from patients with periodontitis?
What can cause an infection?
- C. albicans.
- 3-48%
- Subgingivally
- Reduced host defense- HIV Smoking antibiotics
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What are the 3 fungi that cause oral lesions?
Candida, Linear Gingival erythema (LGE), and histoplasmosis
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What are common symptoms of Herpes Zoster?
Where is it latent?
What kind of lesions happen due to the neurological aspect?
What does it travel on?
- Small ulcers on tongue, palate and gingiva
- Dorsal root ganglion
- Unilateral lesion
- 2nd and 3rd branch of trigeminal
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What are ways to treat Recurrent HSV patients?
- Limit their baterial superinfection cause they can't brush their teeth by giving mouth wash
- Give ANTIVIRALS to IC patients
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What are common symptoms of Recurrent HSV?
- herpes on the vermillion border of their lip/skin,
- intra-oral ulcers on gingiva and hard palate,
- and a lesion that appears to be apthoous ulcers on their keratinized gingiva
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What are SYMPTOMS expect to see from a patient with a PRIMARY herpes infection (herpetic gingivostomatitis) ? How long is the incubation period? What events take place? how long is healing?
- *Severe gingivitis with Redness
- Ulcerations with serofibronous (Yellow) exudate
- Edema accompanied by stomatitis
- *1 week
- *Formation of vesicles which rupture coalesce and leave fibrin-coated ulcers
- *10-14
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Where does the HSV virus remain latent?
How many cases reactivate?
What triggers this to happen?
- Trigeminal ganglion
- 20-40%
- trauma, fever, UV, menstration
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What are some viruses that can cause lesions in the mouth?
HSV 1 (mostly) and Herpes Zoster.
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A patient comes in with Firey-red edamatous PAINFUL ulcerations, Asymptomatic chancers, some mucous patches, and highly inflammaed gingivitis. What does your patient most likely have? What will you do to Diagnose?
Lesion of bacterial origin. To treat take a Biopsy of ulceration but not mucous patch. Then perform a microbiological examination.
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What are two examples of lesions from bacterial origin? Which bacteria are involved?
Gingivitis and Stomatitis. N. Gonorrhea, Treponema palladium, Streptococci, Mycobacterium chelonae.
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Non-plaque induced gingival lesions can come from what 6 origins?
Viral, Bacterial, fungal, genetic, systemic, trauma
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