au14_-_periodontology_exam_2_20141210195111 Flashcards
1
Q
What 5 features are used to assess inflammation?
A
- color- texture/edema- bleeding- exudate- plaque
2
Q
What 3 ways can you determine whether there is loss of periodontal tissue support?
A
- probing depths- clinical attachment levels- radiographic evaluation
3
Q
What is the purpose of assessing periodontal disease? (What is determined during a perio assessment?)
A
- degree of inflammation of the gingival tissue- degree of periodontal destruction- amount of plaque accumulation- amount of calculus present- treatment needs
4
Q
What is the purpose of a simplified oral hygiene index (OHI-S)? What are the components?
A
- to assess oral cleanliness by estimating the tooth surface covered with debris and/or calculus- components: simplified debris index and simplified calculus index
5
Q
What are the tooth selections for a simplified oral hygiene index?
A
- facial surfaces of #3, 8, 14, 24- lingual surfaces of #19, 30
6
Q
What does each score mean for the simplified debris index?
A
- 0: no debris present- 1: soft debris covering no more than 1/3 of tooth or presence of stains- 2: soft debris covering 1/3-2/3 of the tooth- 3: soft debris covering 2/3+ of the tooth
7
Q
What does each score mean for the simplified calculus index?
A
- 0: no calculus- 1: supragingival calculus covering no more than 1/3 of tooth- 2: supragingival calculus covering 1/3-2/3 of the tooth or individual flecks of calculus subgingivally or both- 3: supragingival calculus covering 2/3+ of tooth or heavy subgingival calculus
8
Q
What does a OHI score of 0 mean? 0.1-1.2? 1.3-3.0? 3.1-6.0? How is the OHI score totaled?
A
- 0: excellent- 0.1-1.2: good- 1.3-3.0: fair- 3.1-6.0: poor- add individual scores of each tooth and divide by the number of teeth scored for the debris and calculus exams separately; add the debris and calculus score together to get OHI score
9
Q
What does the Quigley-Hein plaque index assess? What are the range of the scores?
A
- the amount of plaque at the gingival margin- 0-3
10
Q
What are possible scores for the Turesky Modification of Quigley-Hein Plaque Index?
A
- 0: no plaque- 1: spots of plaque at cervical margin- 2: thin, continuous band of plaque 1 mm but 2/3 of crown height
11
Q
How does the Turesky Modification of the Quigley-Hein plaque index differ from the original Quigley-Hein?
A
- Q-H is biased toward the gingival third- Turesky examines facial and lingual surfaces; plaque is visible with disclosing agent and scored 0-5- Turesky is the most frequently used plaque index
12
Q
What plaque index do we use in the CoD clinic?
A
O’Leary Plaque Index (percentage of tooth surfaces positive for plaque)
13
Q
What are the 3 calculus indices we focused on in class?
A
- simplified oral hygiene index (OHI-S)- probe method (Volpe-Manhold)- NIDR calculus index
14
Q
Describe the scoring of the NIDR calculus index.
A
- O: calculus absent- 1: supragingival calculus, but no subgingival calculus- 2: supragingival and subgingival or subgingival only is present
15
Q
What is the purpose of Volpe-Manhold Index? What tooth surfaces are analyzed? In what situation is it usually used?
A
- determines the quantity of the supragingival calculus- lingual surfaces of lower anteriors (#22-27)- most frequently used calculus index in longitudinal studies
16
Q
How is the Volpe-Manhold index scored?
A
- quantity is determined in mm of calculus along the 2 diagonal and central lines drawn over the lingual surfaces of each tooth- index, expressed in mm, is computed for tooth, subject, or population
17
Q
What does the Papillary-Marginal-Attachment assess? How is it scored?
A
- assesses gingival and/or periodontal inflammation- facial gingival surface is divided in 3 scoring units (PMA); gingival units affected with gingivitis score 1 while those without inflammation score 0; severity component can be considered; score is computed for tooth -> subject -> population
18
Q
What is the Gingival Index used for? How is it scored?
A
- used for the calculation of prevalence and severity in population and individual; frequently used in clinical trials- assessed in 4 areas (distofacial papilla, facial margin, mesiofacial papilla, lingual gingival margin); scored 0-3; bleeding is considered (if bleeding, score is 2+); score for tooth -> subject -> population
19
Q
How is the Modified Gingival Index scored? Describe the appearance of each score.
A
- 0: no inflammation (normal tissue appearance)- 1: mild inflammation of portion of unit (slight change in color, little change in texture)- 2: mild inflammation of entire unit (slight change in color; little change in texture)- 3: moderate inflammation (glazing, redness, edema, and/or hypertrophy)- 4: severe inflammation (marked redness, edema, and/or hypertrophy; bleeding, congestion, or ulceration)
20
Q
How is Bleeding-on-Probing assessed?
A
periodontal probe is inserted to the bottom of the periodontal pocket; bleeding is observed 15 seconds following retraction of probe*NOTE: not to be confused with bleeding as scored in gingival index
21
Q
Bleeding-on-probing is a valid indicator of ___; however, it is a poor indicator of ___.
A
- periodontal stability- periodontal breakdown
22
Q
attachment level = ___ + ___
A
- probing depth (mm)- recession (mm)
23
Q
True or false: There is a variation in probing force.
A
true
24
Q
What are the periodontal indices that were discussed in class?
A
- Extent and Severity Index- Periodontal Index System- Periodontal Disease Index System- CPITN- Periodontal Screening and Recording
25
According to the Extent and Severity Index (ESI), disease is defined as attachment loss >___ mm. What is the definition of extent? Of severity?
- >1 mm- proportion of tooth sites in a patient showing signs of destructive periodontitis- amount of attachment loss at diseased sites, expressed as a mean value
26
How is the Periodontal Index System (PI) scored?
- 0: negative- 1 or 2: gingivitis- 6: gingivitis with pocket formation- 8: advanced destruction with loss of masticatory function- all teeth are examined; the circumference of each tooth is inspected visually and given a score; index computed for subject and population
27
What are the 5 components of the Periodontal Disease Index System?
- gingival status- crevicular measurements- periodontal disease index- plaque criteria- calculus criteria
28
How is the Periodontal Disease Index scored?
- 1, 2, or 3: severity of gingivitis- 4: initial attachment loss (3 mm and s PDI; index computed for subject and population
29
What is the purpose of the Community Periodontal Index of Treatment Needs (CPITN)? How is it done for epidemiology purposes? For individual subjects?
- primarily designed to assess periodontal treatment needs in under-served parts of the world- EPIDEMIOLOGY: 10 index teeth are examined with special probe and worst finding is recorded per sextant- INDIVIDUAL: worst finding of all teeth in a sextant is recorded with special probe, resulting in 6 scores per subject; the worst score determines the treatment needs score
30
Describe the scoring of the Community Periodontal Index of Treatment Needs (CPITN) and the codes for treatment needs.
PERIODONTAL STATUS:- 1: bleeding on gentle probing- 2: calculus felt during probing, crevicular depth 6 mmTREATMENT NEEDS:- code 0: no treatment- code I: improved oral hygiene- code II: I + professional scaling- code III: I + II + complex treatment
31
What is the purpose of the Periodontal Screening and Recording (PSR)? Who endorses it?
- a rapid and effective way to screen patients for periodontal diseases and summarizes necessary information with minimum documentation- the ADA and AAP support the use of PSR by dentists as part of oral examinations
32
How is the Periodontal Screening and Recording scored?
- uses a special probe with color markings- recorded in sextants, but evaluates all sites- 0: colored area visible; no calculus; no BOP- 1: colored area visible; no calculus; BOP- 2: colored area visible; calculus present; +/- BOP- 3: colored area partially visible; +/- calculus; +/- BOP- 4: colored area no visible; +/- calculus; +/- BOP
33
What are the 6 benefits of Periodontal Screening and Recording?
- EARLY DETECTION: evaluates all sites so highly sensitive for detecting deviations from periodontal health; good screening tool for diseases that are site specific and episodic- SPEED: takes only a few minutes- SIMPLICITY: easy to administer and comprehend- COST-EFFECTIVENESS: for equipment, only need special perio probe- RECORDING EASE: only record 6 numbers (one for each sextant)- RISK MANAGEMENT: proper, consistent, and documented use of PSR shows that a dentist is evaluating a patient's periodontal status
34
What are the 3 limitations of the Periodontal Screening and Recording?
- it is designed to DETECT perio diseases, not replace comprehensive perio exam when needed- patients who have been treated for periodontal disease and are in a maintenance phase of therapy require periodic COMPREHENSIVE perio exams- designed to be used for ADULTS, not children/adolescents
35
What are the 2 peri-implant tissues and indices?
- modified PlI- modified GI
36
What is the difference between reliability and validity?
- RELIABILITY: ability of an index to measure a condition in the same subject repeatedly and obtain the same score results every time- VALIDITY: sensitivity and specificity of various diagnostic tools used to create an index
37
What are the 3 potential problems (examiner bias) that can occur when using periodontal indices?
- HALO EFFECT: examiner's general impression of targe distorts his/her perception of the target on specific dimensions- LENIENCY/SEVERITY ERROR: examiner's tendency to be lenient or severe- CENTRAL TENDENCY ERROR: the examiner's reluctance to rate at either the positive or negative extreme so all scores cluster in the middle
38
What are the 2 methods to lessen examiner bias when using indices?
- CALIBRATION: use several examiners at different experience levels on subjects with various disease extents and severity; use follow-up appointments- TRAINING: learning/teaching through hands-on practice
39
What is the difference between sensitivity and specificity? How is each found?
- SENSITIVITY: probability that a test result will be positive when the test is administered to people who actually have the disease in question;found by: (# people who have disease according to test and disease is present) / (total # of people with disease)- SPECIFICITY: probability that a test will be negative when administered to people who are free of the disease in question;found by: (# people who don't have disease according to test and disease is not present) / (total # of people who do not have disease)
40
What is the difference between predictive value positive (PVP) and predictive value negative (PVN)? How is each found?
- PREDICTIVE VALUE POSITIVE: probability of disease in a subject with a positive test result;found by: (# people who have disease according to test and disease is present) / (total # of test-determined positive)- PREDICTIVE VALUE NEGATIVE: probability of not having the disease when the test is negative;found by: (# of people who do not have disease according to test and disease is not present) / (total # of test-determined negative)
41
What are the 4 general categories of dental plaque-induced gingival diseases?
- gingivitis associated with dental plaque only- gingival diseases modified by systemic factors- gingival diseases modified by medications- gingival diseases modified by malnutrition
42
What are the 2 types of gingivitis associated with dental plaque only?
- without other local contributing factors- with other local contributing factors
43
What systemic factors can modify gingival diseases?
ENDOCRINE SYSTEM:- puberty- menstrual cycle- pregnancy- diabetes mellitusBLOOD DYSCRASIAS:- leukemia- acute myeloid leukemia associated with gingival changes- persistent unexplained gingival bleeding may indicate underlying thrombocytopenia- cyclic neutropenia (14-36 day cycles) -> ulcerations
44
How can gingival diseases be modified by medications?
gingival enlargements by:- oral contraceptive-associated gingivitis- anticonvulsants (phenytoin sodium or epinutin)- immunosuppressants (cyclosporin A)- calcium channel blocking agents (nifedipine)* question on the exam?
45
How can gingival diseases be modified by malnutrition?
- ascorbic acid (vitamin C) deficiency gingivitis ("scurvy")- lack of vitamins A, B2, and B12 complex
46
What is gingivitis around implants called?
peri-mucositis (inflammation is limited to mucosa)
47
What are the 6 characteristics common to ALL gingival diseases?
- signs and symptoms limited to gingiva- presence of dental plaque- clinical signs of inflammation- clinical signs and symptoms associated on a periodontium with no attachment loss OR on a stable but reduced periodontium- reversibility of the disease by removing etiology- possible role as a precursor to attachment loss
48
What are the 11 characteristics of plaque-induced gingivitis?
- plaque present at gingival margin- disease begins at the gingival margin- change in color- change in gingival contour- sulcular temperature change- increased gingival exudate- bleeding upon provocation- absence of attachment loss- absence of bone loss- histological changes- reversible with plaque removal
49
How does the color of the gingiva change between normal, inflamed, and severely inflamed? Where do the changes start?
- NORMAL: "coral pink" + pigmentation (tissue's vascularity and overlying epithelial layers)- INFLAMED GINGIVA: red (increased vascularization and decreased epithelial keratinization)- SEVERELY INFLAMED GINGIVA: red and cyanotic (vascular proliferation and reduction in keratinization + venous stasis)- changes start at interdental papillae and gingival margin and spread to attached gingiva
50
How does gingival bleeding change with increasing inflammation?
- dilation and engorgement of the capillaries- thinning or ulceration of the sulcular epithelium
51
Chronic or recurrent bleeding may be provoked by ___. Spontaneous bleeding occurs in ___ and may be related to ___.
- trauma- acute/severe gingival disease- systemic health problems
52
How does the consistency of the gingiva change from normal to inflammation to severe gingival disease? What can chronic inflammation induce?
- NORMAL: firm and resilient- INFLAMMATION: increased extracellular fluid and exudate; degeneration of connective tissues and epithelium; engorged connective tissue and thinning of epithelium; soft, swollen (edema), friable- SEVERE GINGIVAL DISEASE: sloughing with grayish flake-like debris (necrosis)*also, chronic inflammation can induce fibrosis and epithelial proliferation -> firm, leathery gingival tissue consistency
53
How does the surface texture of the gingiva change from normal to inflammation?
- NORMAL: dull surface texture with stippling present in some cases- INFLAMMATION: loss of stippling; smooth and shiny (if exudative changes occur); firm and nodular (if fibrotic changes occur)
54
How does the shape of the gingival margin change from normal to inflammation?
- NORMAL: scalloped with gingiva filling interdental spaces (presence of papilla)- INFLAMMATION: knife-edge gingival adaptation or loose gingival margins; in some cases, clefts or festoons may develop
55
Describe the 2 possible appearances of gingival enlargement.
- clinically deep red lesions with soft, friable, smooth, shiny surface and bleeding tendency- relatively firm, resilient, and pink lesions with greater fibrotic component, abundant fibroblasts and collagen fibers
56
What is the primary etiologic factor of dental plaque-induced gingivitis? The secondary etiological factors?
- PRIMARY: bacterial plaque (duh!)- SECONDARY: calculus; marginal deficiencies in restorations and rough surfaces; malocclusion; tooth/root anomalies (enamel pearls, cemental tears, root fractures, cervical root resorption)
57
What is the biologic width on average? The average sulcus depth? Average epithelial attachment? Average connective tissue attachment?
- biologic width: 2.73 mm- sulcus depth: 0.69 mm- epithelial attachment: 0.97 mm- connective tissue attachment: 1.07 mm
58
The biological width is a minimum dimension of ___ mm coronal to the alveolar crest to permit ___ and ___. Intracrevicular restorative margins at sites of insufficient gingival width and/or thickness can cause ___, ___, or both.
- 3 mm- healing- proper restoration- marginal tissue recession- apical migration of the attachment apparatus
59
True or false: Gingivitis always progresses into periodontitis if left untreated.
FALSE: Gingivitis does not always progress into periodontitis, but periodontitis does start with gingivitis.
60
What is recurrent periodontitis?
recurrent inflammation to sites that were treated for periodontitis*note that this may be confined to gingival tissues and may not cause further attachment loss, but this is still diagnosed as "recurrent PERIODONTITIS"
61
True or false: Plaque is necessary for endocrine-associated gingivitis.
true!
62
What type of bacteria is present in pregnancy associated gingivitis? What type of host response occurs? When does this gingivitis tend to appear?
- microbiota characteristic of gingivitis- exaggerated localized host response modulated by levels of endogenous hormones (androgens, estrogens, and progesterone)- changes often appear during 2nd trimester and regress upon parturition
63
What type of host response occurs during puberty-associated gingivitis? What can be a secondary factor?
- localized host response mediated by high levels of hormone (estrogens, testosterone)- mouth-breathing
64
What type of clinically-detectable changes are found with menstrual cycle-associated gingivitis? What other change is associated with this gingivitis?
- clinically detectable changes do not seem to be associated with menstrual cycle- increase in gingival crevicular fluid by 20% has been described
65
What is pyogenic granuloma of pregnancy? When does it occur?
- a highly vascularized mass of granulation tissue; commonly arises from the proximal gingival tissues and has a pedunculated base- in 2nd or 3rd trimester of pregnancy
66
Who is most susceptible to necrotizing ulcerative gingivitis? Describe the condition. How is the disease resolved?
- adolescents or young adults, smokers, or individuals with often psychological stress- pain, ulceration, and necrosis of the INTERDENTAL PAPILLAE; bleeding- resolution often requires systemic antibiotics
67
Necrotizing Ulcerative Gingivitis often requires a differential diagnosis with what disease?
primary herpetic gingivostomatitis
68
What predisposing factors might make someone more susceptible to necrotizing ulcerative gingivitis? What may it progress to?
- systemic diseases like ulcerative colitis, blood dyscrasias, and nutritional deficiency states- abnormalities of white blood cell function- AIDS- may progress to Noma or cancrum oris (destroyed mucous membranes)
69
What is the differential diagnosis of necrotizing ulcerative gingivitis (NUG) and primary herpetic gingivostomatitis (PHS) in terms of etiology? Symptoms?
ETIOLOGY:- NUG: bacteria- PHS: herpes simplex virusSYMPTOMS:- NUG: ulceration and necrotic tissue, yellowish white plaque- PHS: multiple vesicles which burst, leaving small round fibrin covered ulcers
70
What is the differential diagnosis of necrotizing ulcerative gingivitis (NUG) and primary herpetic gingivostomatitis (PHS) in terms of duration? Contagiousness?
DURATION:- NUG: 1-2 days if treated- PHS: 1-2 weeksCONTAGIOUSNESS:- NUG: no- PHS: yes
71
True or false: Primary herpetic gingivostomatitis is not found in attached gingiva, but necrotizing ulcerative gingivitis is found everywhere.
FALSE: Primary herpetic gingivostomatitis is found everywhere, but necrotizing ulcerative gingivitis is not found in attached gingiva.
72
True or false: Gingival inflammation, clinically presenting as gingivitis, is always due to accumulation of plaque on the tooth surface.
FALSE. Gingival inflammation is NOT always due to plaque.
73
What are the other 6 origins of gingival lesions that are not induced by plaque?
- specific bacterial origin- viral origin- fungal origin- genetic origin- systemic origin- traumatic lesions
74
True or false: Gingival lesions of specific bacterial origin may be accompanied by lesions elsewhere in the body.
true (but also may not necessarily be accompanied by lesions elsewhere)
75
What are the common bacteria involved in gingival lesions of specific bacterial origin?
- Neisseria gonorrhea- Treponema pallidum- Streptococci- Mycobacterium chelonae
76
What are the common clinical presentations of gingival lesions of specific bacterial origin? How are these diagnosed?
CLINICAL PRESENTATION:- fiery red edematous painful ulcerations- asymptomatic chancres (painless ulceration)- mucous patches- atypical non-ulcerated highly-inflammed gingivitisDIAGNOSIS:- biopsy- microbiologic examination
77
What type of herpes virus infection usually causes oral manifestations?
herpes simplex 1
78
What is a primary herpetic gingivostomatitis? What are the symptoms? Characteristics?
- through oral mucosal epithelium, virus penetrates a neural ending and travels to the trigeminal ganglionSYMPTOMS:- painful severe gingivitis with redness- ulcerations with serofibrinous exudate- edema accompanied by stomatitisCHARACTERISTICS:- incubation period is one week- formation of vesicles which rupture, coalesce, and leave fibrin-coated ulcers- healing within 10-14 days
79
How long can the herpes virus stay latent in the trigeminal ganglion? In what types of gingival diseases is the herpes virus found? Who does primary infections mostly affect?
- latent for years- found in gingivitis, necrotizing ulcerative diseases (NUG/NUP), and periodontitis- older ages in industrialized society
80
Recurrent intraoral herpes infections occur in ___% of individuals with primary infection.
20-40%
81
What type of herpes occurs more than per year? Where on the body does it occur? What triggers a recurrent infection? What is the diagnosis?
- herpes labialis- on the vermillion border and/or skin adjacent to it- trauma, UV light exposure, fever, menstruation- generally considered an aphtous ulceration (canker sore); ulcers in attached gingiva and hard palate
82
Herpes labialis is life threatening in what type of patients? How can the virus be sampled? What is the purpose of blood samples? Is histopathology specific?
- immunocompromised patients- aspiration from vesicle- blood samples to determine increased antibody titer against virus (works better for primary infection)- histopathology is not specific
83
How can herpes labialis be treated?
- careful plaque removal to limit bacterial superinfection of the ulcerations- systemic uptake of a antiviral medication such as a aciclovir
84
What is the herpes zoster virus? Where does it lay latent? Does it cause bi- or uni-lateral lesions?
- virocella-zoster virus causes varicella (chicken pox and shingles)- latent in the dorsal root ganglion; 2nd and 3rd branch of the trigeminal ganglion (?)- unilateral lesions
85
How does the herpes zoster virus appear clinically?
- small ulcers usually on the tongue, palate, and gingiva- skin lesions may be associated with intraoral lesions or intraoral lesions may occur alone- initial symptoms are pain and paresthesia (tingling)
86
How is the herpes zoster virus diagnosed? Treated?
- diagnosis: usually obvious due to the unilateral occurrence of lesions associated with severe pain- treatment: soft diet, rest, atraumatic removal of plaque, and diluted chlorhexidine rinses; may be supplemented with anti-viral drug therapy
87
What are the 3 most common fungal infections that may affect the oral cavity?
- candidosis- linear gingival erythema- histoplasmosis
88
What Candida species is the most common the in mouth? What is the oral carriage of this species in healthy adults?
- C. albicans- 3-48%
89
Who is most susceptible to Candidosis? Where is C. albicans frequently isolated from?
MOST SUSCEPTIBLE:- cancer patients with high radiation/chemotherapy- patients with several antibiotics over period of several weeks/months- diabetic patients- women with vaginal candidasis- pregancy and the use of contraceptives- from the subgingival flora of patients with severe periodontitis
90
What is the general clinical appearance of Candidosis?
- painless or slightly sensitive- red and white lesions (redness of attached gingiva, often associated with granular surface)- lesions can be scraped or separated from mucosa
91
How is Candidosis diagnosed? How is it treated?
DIAGNOSIS:- a culture on Nickersons medium at room temperature- microscopic examination of a smear of the material scraped from the lesion and stainedTREATMENT:- use of antimycotic/antifungal agents (ex. Nystatin given as mouthrinse or systemically)
92
What are the 4 different types or oral mucosal manifestations of Candidosis?
- PSEUDOMEMBRANEOUS: whitish patches that can be wiped off- ERYTHEMATOUS: red, associated with pain- PLAQUE TYPE: whitish plaque that cannot be removed; need to differentiate from oral leukoplakia- NODULAR: slightly elevated nodules of white or reddish color
93
How does linear gingival erythema appear clinically?
- distinct linear erythematous band limited to the free gingiva- lack of bleeding- does not respond well to improved oral hygiene or scaling; a disproportion between inflammation and plaque accumulation
94
Of the people who tested positive for C. albicans, what systemic disease was the most prevalent? What is the treatment for linear gingival erythema?
- 50% of HIV-associated gingivitis sites; 26% of unaffected sites of HIV seropositive patients; 3% of healthy sites of HIV negative patients- TREATMENT: conventional therapy plus chlorhexidine 0.12% rinse; anti-mycotic therapy if Candida is detected
95
What bacteria causes histoplasmosis? What are the different types of infections and who is most susceptible?
- Histoplasma capsulatum- acute and chronic pulmonary histoplasmosis or a disseminated form in immunocompromised patients
96
What is the clinical appearance of a histoplasmosis infection? How is it diagnosed? How is it treated?
- nodular or papillary and may be ulcerative type of lesions with pain in any area of the oral mucosa- diagnosed by clinical view and histopathology with systemic manifestations- treatment is systemic anti-fungal therapy
97
What is the gingival lesion discussed in class that is of genetic origin? How does this disease appear clinically?
- hereditary gingival fibromatosis- diffuse gingival enlargement; may interfere with or prevent tooth eruption; may be part of a syndrome (ex. hypertrichosis, mental retardation, epilepsy, hearing loss, growth retardation, abnormalities of extremities)
98
What are the possible mechanisms of hereditary gingival fibromatosis?
- TGF-beta1 favors the accumulation of ECM- may be located on chromosome 2 in humans (defect in the Son of Sevenless-1 gene on chromosome 2p21-22)
99
What are the 2 different types of allergic reactions discussed in class? Describe each.
- TYPE I: immediate; mediated by IgE- TYPE IV: delayed type; mediated by T-cells (12-48 hours following contact with allergens)
100
What are some dental things to have allergies to? How do these allergies clinically present?
- dental restorative materials (type IV contact allergy; mercury, nickel, gold, zinc, chromium, palladium, acrylics, and others); oral hygiene products, chewing gum, and food (generally flavor additives or preservatives)- a diffuse fiery red edematous gingivitis sometimes with ulcerations or whitening
101
What are the 3 categories of traumatic lesions?
- chemical- physical- thermal
102
Describe a chemical traumatic lesion. Give examples. How can this be caused?
- surface etching by various chemical products with toxic properties- ex. chlorhexidine-induced mucosal desquamation, acetylsalicylic acid burn, cocaine burn- incorrect use of caustic by the dentist
103
Give 3 examples of physical traumatic lesions.
- hyperkeratosis, a white leukoplakia-like, frictional keratosis- gingival laceration resulting in gingival recession- traumatic ulcerative gingival lesion (brushing and flossing techniques)
104
Where do people usually get thermal traumatic lesions? Describe their appearance clinically.
- minor burns from hot beverages- mostly seen on palatal and labial mucosa; painful erythematous lesions; vesicles may develop
105
What are foreign body reactions? How are these often detected?
- epithelial ulceration that allows entry of foreign material into gingival connective tissue- foreign body can be generally detected via x-rays (ex. amalgam tattoo, abrasives, toothpick, etc.)
106
What are the 6 mucocutaneous disorders discussed in class?
- lichen planus- pemphigold- pemphigus vulgaris- erythema multiforme- lupus erythematosus- drug-induced mucocutaneous disorders
107
Where does lichen planus usually occur? In what ages? Is it considered a premalignant lesion?
- oral involvement alone is common- prevalence = 0.1-4% in any age, but is rare in children- premalignant potential = 0.5-2%
108
How does lichen planus appear clinically?
- characteristic skin lesions (Wickam striae)- various clinical appearances (papular, reticular, plaque-like, atrophic, ulcerative, bullous)- any area of the oral mucosa
109
Define papula. Reticular. Plaque.
- PAPULA: small inflammatory congested spot on skin; a pimple- RETICULAR: mesh; in the form of network- PLAQUE: patch on the skin or on mucous surface
110
Define atrophy. Ulcerative. Bulla.
- ATROPHY: a wasting; a decrease in size of tissue- ULCERATIVE: affected with an ulcer; open sore or lesion of the skin or mucosa accompanied by sloughing of inflamed necrotic tissue- BULLA: large blister or skin vesicle filled with fluid
111
Papular, reicular, plaque-like forms are generally ___ (symptomatic/asymptomatic).Atrophic, ulcerative, bullous forms are generally ___ (symptomatic/asymptomatic).
- asymptomatic- symptomatic
112
Histologically, describe the appearance of lichen planus (or oral lichenoid).
- subepithelial band-like accumulation of lymphocytes and macrophages characteristic of a type IV hypersensitivity reaction- fibrin in the basement membrane- deposits of IgM, C3, C4, and C5*note: there is a small possibility this may actually be describing oral lichenoid... unclear slide :(
113
What are some examples of oral lichenoid lesions? What is the treatment?
EXAMPLES:- lesions in contact with dental restorations- lesions associated with various types of medications (NSAIDs, diuretics, beta blockers)- group of systemic diseases (liver disease)TREATMENT:- take biopsy- take sample for culture if questioning candida infection (about 38% of OLP cases have secondary infection)- traumatic dental plaque control- topical corticosteroids to control pain, discomfort
114
What is pemphigoid? How does it appear histologically?
- group of disorders in which autoantibodies towards components of the basement membrane result in detachment of the epithelium from connective tissue- autoantibody reactions against hemidesmosome and lamina lucida components; complement-mediated cell destructive processes may be involved in the pathogenesis
115
What are the 3 types of pemphigoid? Who is the most susceptible? What is the telltale sign? How is it treated?
- bullous, benign mucous membrane, cicatricial (scar formation)- female predominance; >50 years of age- NICHOLSKY SIGN (rubbing of gingiva creates bulla formation)- treatment: plaque removal with daily use of chlorhexidine and/or topical corticosteroid
116
What is pemphigus vulgaris? Who is it most prevalent in? How does it clinically appear?
- formation of INTRAEPITHELIAL BULLAE in skin and mucous membranes- strong genetic background (Jewish and Mediterranean); typically in middle age or elderly- painful desquamative lesions, erosions, or ulcerations; chronic course with recurrent bulla formation
117
How does pemphigus vulgaris appear histologically?
- ACANTHOLYSIS: due to destruction of desmosomes- pericellular epithelial depositis of IgG and C3- circulating autoantibodies against interepithelial adhesion molecules
118
What is erythema multiforme? In what age group is it most likely?
- acute, sometimes recurrent, vesiculobullous disease affecting both mucous membranes and skin; oral involvement occurs as much as 25-60% of cases; appears to be a cytotoxic immune reaction towards keratinocytes preciptating by a wide range of factors including HERPES SIMPLEX VIRUS and VARIOUS DRUGS- may occur at any age, but mostly in young individuals
119
How does erythema multiforme appear clinically? What is the treatment?
- SWOLLEN LIPS, often with extensive crust formation of the vermilion border- bullae that rupture and leave extensive ulcers- characteristic skin lesions (iris appearance and bullae)- extensive necrosis (Stevens-Johnson syndrome - oral, ocular, genital, skin)- plaque control, local/systemic
120
What is lupus erythematosus? How does it appear histologically?
- autoimmune connective tissue disorders in which autoantibodies form to various cellular constituents- degeneration of basal cells and increased WIDTH of the basement membrane; deposits of various Ig's, C3, and fibrin along the basement membrane
121
How does lupus erythematosus appear clinically?
- central atrophic area with small white dots surrounded by irradiating fine white striae with a periphery of telangiectasia (vasular lesion formed by dilation of group of small blood vessels)- lesions can be ulcerated and cannot be differentiated from leukoplakia or atrophic oral lichen planus- characteristic skin lesion: BUTTERFLY
122
What are the 5 drug-induced mucocutaneous disorders?
- gingival hyperplasia (enlargement)- erythema multiforme- oral ulceration- epithelial atrophy, superficial sloughing- intense erythema
123
What 6 drugs cause drug-induced mucocutaneous disorders?
- immunosuppressants- calcium channel blockers- anti-epilepsy drugs- anti-malarial drugs- anti-neoplastic drugs (cancer)- methotrexate (leukemia)
124
How does Crohn's disease affect the gingiva?
chronic granulomatous infiltrates of the wall of gastrointestinal tract -> mucosal folding and defective neutrophil functions
125
How does leukemia affect the gingiva? What % of leukemia patients had oral symptoms?
- swelling, ulceration, petecchia, and erythema of gingiva- 69% of patients with acute leukemia had oral signs of leukemia
126
What are the 6 general categories of periodontal tumors?
- reactive processes of periodontal soft tissues- reactive processes of periodontal hard tissues- benign neoplasms of periodontal soft tissues- benign neoplasms of periodontal hard tissues- malignant neoplasm of periodontal soft tissues- malignant neoplasm of periodontal hard tissues
127
What are the 4 reactive processes of periodontal soft tissues?
- fibroma/focal fibrous hyperplasia- calcified fibroblastic granuloma- pyogenic granuloma- peripheral giant cell granuloma
128
What is fibroma/focal fibrous hyperplasia? How does it appear clinically? What is it's differential diagnosis?
- focal fibrous hyperplasia caused by irritation- sessile, well-circumscribed smooth-surfaced nodules; cell-poor, hyperplastic collagenous tissue; may show hyperkeratinization- giant cell fibroma
129
What is calcified fibroblastic granuloma? How does it appear clinically? What is it's differential diagnosis?
- fibrous proliferation in which bone-like or cementum-like hard tissue is formed- often reddish and ulcerated reactive lesion; highly cell-rich areas below ulcerated sites- pyogenic granuloma
130
What is pyogenic granuloma? How does it appear clinically? What is it's differential diagnosis?
- ulcerated (may resemble purulence); gingival margin; reddish or bluish, sometimes lobulated, sessile, or pedunculated; bleeding is common; highly vascular with chronic inflammatory cells- pregnancy tumor
131
What is peripheral giant cell granuloma? How does it appear clinically? What is it's differential diagnosis?
- focal collection of multi-nucleated osteoclast-like giant cells with a richly cellular and vascular stroma separated by collageneous septa; probably originated from periodontal ligament- found anywhere on the gingival mucosa; pedunculated, sessile, red/purple, commonly ulcerated- focal fibrous hyperplasia
132
What is the reactive process of peridontal hard tissue discussed in class? Describe it. What is its differential diagnosis?
- periapical cemental dysplasia- fibrous-osseous cemental lesions; tooth is usually vital; usually asymptommatic; periapical bone is replaced by cellular fibroblastic tissue through cementoblastic phase- cemento-ossifying fibroma and fibrous dysplasia
