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AU14 - Perio Exam 2 > au14_-_periodontology_exam_2_20141210195111 > Flashcards

au14_-_periodontology_exam_2_20141210195111 Flashcards

1
Q

What 5 features are used to assess inflammation?

A
  • color- texture/edema- bleeding- exudate- plaque
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2
Q

What 3 ways can you determine whether there is loss of periodontal tissue support?

A
  • probing depths- clinical attachment levels- radiographic evaluation
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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
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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
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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
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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
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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
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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
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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
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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
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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
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12
Q

What plaque index do we use in the CoD clinic?

A

O’Leary Plaque Index (percentage of tooth surfaces positive for plaque)

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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
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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
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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
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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
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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
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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
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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)
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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

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21
Q

Bleeding-on-probing is a valid indicator of ___; however, it is a poor indicator of ___.

A
  • periodontal stability- periodontal breakdown
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22
Q

attachment level = ___ + ___

A
  • probing depth (mm)- recession (mm)
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23
Q

True or false: There is a variation in probing force.

A

true

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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
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25
Q

According to the Extent and Severity Index (ESI), disease is defined as attachment loss >___ mm. What is the definition of extent? Of severity?

A
  • > 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
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26
Q

How is the Periodontal Index System (PI) scored?

A
  • 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
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27
Q

What are the 5 components of the Periodontal Disease Index System?

A
  • gingival status- crevicular measurements- periodontal disease index- plaque criteria- calculus criteria
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28
Q

How is the Periodontal Disease Index scored?

A
  • 1, 2, or 3: severity of gingivitis- 4: initial attachment loss (3 mm and s PDI; index computed for subject and population
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29
Q

What is the purpose of the Community Periodontal Index of Treatment Needs (CPITN)? How is it done for epidemiology purposes? For individual subjects?

A
  • 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
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30
Q

Describe the scoring of the Community Periodontal Index of Treatment Needs (CPITN) and the codes for treatment needs.

A

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

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31
Q

What is the purpose of the Periodontal Screening and Recording (PSR)? Who endorses it?

A
  • 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
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32
Q

How is the Periodontal Screening and Recording scored?

A
  • 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
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33
Q

What are the 6 benefits of Periodontal Screening and Recording?

A
  • 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
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34
Q

What are the 3 limitations of the Periodontal Screening and Recording?

A
  • 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
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35
Q

What are the 2 peri-implant tissues and indices?

A
  • modified PlI- modified GI
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36
Q

What is the difference between reliability and validity?

A
  • 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
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37
Q

What are the 3 potential problems (examiner bias) that can occur when using periodontal indices?

A
  • 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
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38
Q

What are the 2 methods to lessen examiner bias when using indices?

A
  • 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
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39
Q

What is the difference between sensitivity and specificity? How is each found?

A
  • 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)
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40
Q

What is the difference between predictive value positive (PVP) and predictive value negative (PVN)? How is each found?

A
  • 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)
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41
Q

What are the 4 general categories of dental plaque-induced gingival diseases?

A
  • gingivitis associated with dental plaque only- gingival diseases modified by systemic factors- gingival diseases modified by medications- gingival diseases modified by malnutrition
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42
Q

What are the 2 types of gingivitis associated with dental plaque only?

A
  • without other local contributing factors- with other local contributing factors
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43
Q

What systemic factors can modify gingival diseases?

A

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

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44
Q

How can gingival diseases be modified by medications?

A

gingival enlargements by:- oral contraceptive-associated gingivitis- anticonvulsants (phenytoin sodium or epinutin)- immunosuppressants (cyclosporin A)- calcium channel blocking agents (nifedipine)* question on the exam?

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45
Q

How can gingival diseases be modified by malnutrition?

A
  • ascorbic acid (vitamin C) deficiency gingivitis (“scurvy”)- lack of vitamins A, B2, and B12 complex
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46
Q

What is gingivitis around implants called?

A

peri-mucositis (inflammation is limited to mucosa)

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47
Q

What are the 6 characteristics common to ALL gingival diseases?

A
  • 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
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48
Q

What are the 11 characteristics of plaque-induced gingivitis?

A
  • 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
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49
Q

How does the color of the gingiva change between normal, inflamed, and severely inflamed? Where do the changes start?

A
  • 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
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50
Q

How does gingival bleeding change with increasing inflammation?

A
  • dilation and engorgement of the capillaries- thinning or ulceration of the sulcular epithelium
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51
Q

Chronic or recurrent bleeding may be provoked by ___. Spontaneous bleeding occurs in ___ and may be related to ___.

A
  • trauma- acute/severe gingival disease- systemic health problems
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52
Q

How does the consistency of the gingiva change from normal to inflammation to severe gingival disease? What can chronic inflammation induce?

A
  • 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
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53
Q

How does the surface texture of the gingiva change from normal to inflammation?

A
  • 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
Q

How does the shape of the gingival margin change from normal to inflammation?

A
  • 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
Q

Describe the 2 possible appearances of gingival enlargement.

A
  • 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
Q

What is the primary etiologic factor of dental plaque-induced gingivitis? The secondary etiological factors?

A
  • 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
Q

What is the biologic width on average? The average sulcus depth? Average epithelial attachment? Average connective tissue attachment?

A
  • biologic width: 2.73 mm- sulcus depth: 0.69 mm- epithelial attachment: 0.97 mm- connective tissue attachment: 1.07 mm
58
Q

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.

A
  • 3 mm- healing- proper restoration- marginal tissue recession- apical migration of the attachment apparatus
59
Q

True or false: Gingivitis always progresses into periodontitis if left untreated.

A

FALSE: Gingivitis does not always progress into periodontitis, but periodontitis does start with gingivitis.

60
Q

What is recurrent periodontitis?

A

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
Q

True or false: Plaque is necessary for endocrine-associated gingivitis.

A

true!

62
Q

What type of bacteria is present in pregnancy associated gingivitis? What type of host response occurs? When does this gingivitis tend to appear?

A
  • 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
Q

What type of host response occurs during puberty-associated gingivitis? What can be a secondary factor?

A
  • localized host response mediated by high levels of hormone (estrogens, testosterone)- mouth-breathing
64
Q

What type of clinically-detectable changes are found with menstrual cycle-associated gingivitis? What other change is associated with this gingivitis?

A
  • clinically detectable changes do not seem to be associated with menstrual cycle- increase in gingival crevicular fluid by 20% has been described
65
Q

What is pyogenic granuloma of pregnancy? When does it occur?

A
  • 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
Q

Who is most susceptible to necrotizing ulcerative gingivitis? Describe the condition. How is the disease resolved?

A
  • 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
Q

Necrotizing Ulcerative Gingivitis often requires a differential diagnosis with what disease?

A

primary herpetic gingivostomatitis

68
Q

What predisposing factors might make someone more susceptible to necrotizing ulcerative gingivitis? What may it progress to?

A
  • 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
Q

What is the differential diagnosis of necrotizing ulcerative gingivitis (NUG) and primary herpetic gingivostomatitis (PHS) in terms of etiology? Symptoms?

A

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
Q

What is the differential diagnosis of necrotizing ulcerative gingivitis (NUG) and primary herpetic gingivostomatitis (PHS) in terms of duration? Contagiousness?

A

DURATION:- NUG: 1-2 days if treated- PHS: 1-2 weeksCONTAGIOUSNESS:- NUG: no- PHS: yes

71
Q

True or false: Primary herpetic gingivostomatitis is not found in attached gingiva, but necrotizing ulcerative gingivitis is found everywhere.

A

FALSE: Primary herpetic gingivostomatitis is found everywhere, but necrotizing ulcerative gingivitis is not found in attached gingiva.

72
Q

True or false: Gingival inflammation, clinically presenting as gingivitis, is always due to accumulation of plaque on the tooth surface.

A

FALSE. Gingival inflammation is NOT always due to plaque.

73
Q

What are the other 6 origins of gingival lesions that are not induced by plaque?

A
  • specific bacterial origin- viral origin- fungal origin- genetic origin- systemic origin- traumatic lesions
74
Q

True or false: Gingival lesions of specific bacterial origin may be accompanied by lesions elsewhere in the body.

A

true (but also may not necessarily be accompanied by lesions elsewhere)

75
Q

What are the common bacteria involved in gingival lesions of specific bacterial origin?

A
  • Neisseria gonorrhea- Treponema pallidum- Streptococci- Mycobacterium chelonae
76
Q

What are the common clinical presentations of gingival lesions of specific bacterial origin? How are these diagnosed?

A

CLINICAL PRESENTATION:- fiery red edematous painful ulcerations- asymptomatic chancres (painless ulceration)- mucous patches- atypical non-ulcerated highly-inflammed gingivitisDIAGNOSIS:- biopsy- microbiologic examination

77
Q

What type of herpes virus infection usually causes oral manifestations?

A

herpes simplex 1

78
Q

What is a primary herpetic gingivostomatitis? What are the symptoms? Characteristics?

A
  • 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
Q

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?

A
  • latent for years- found in gingivitis, necrotizing ulcerative diseases (NUG/NUP), and periodontitis- older ages in industrialized society
80
Q

Recurrent intraoral herpes infections occur in ___% of individuals with primary infection.

A

20-40%

81
Q

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?

A
  • 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
Q

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?

A
  • immunocompromised patients- aspiration from vesicle- blood samples to determine increased antibody titer against virus (works better for primary infection)- histopathology is not specific
83
Q

How can herpes labialis be treated?

A
  • careful plaque removal to limit bacterial superinfection of the ulcerations- systemic uptake of a antiviral medication such as a aciclovir
84
Q

What is the herpes zoster virus? Where does it lay latent? Does it cause bi- or uni-lateral lesions?

A
  • 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
Q

How does the herpes zoster virus appear clinically?

A
  • 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
Q

How is the herpes zoster virus diagnosed? Treated?

A
  • 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
Q

What are the 3 most common fungal infections that may affect the oral cavity?

A
  • candidosis- linear gingival erythema- histoplasmosis
88
Q

What Candida species is the most common the in mouth? What is the oral carriage of this species in healthy adults?

A
  • C. albicans- 3-48%
89
Q

Who is most susceptible to Candidosis? Where is C. albicans frequently isolated from?

A

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
Q

What is the general clinical appearance of Candidosis?

A
  • 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
Q

How is Candidosis diagnosed? How is it treated?

A

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
Q

What are the 4 different types or oral mucosal manifestations of Candidosis?

A
  • 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
Q

How does linear gingival erythema appear clinically?

A
  • 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
Q

Of the people who tested positive for C. albicans, what systemic disease was the most prevalent? What is the treatment for linear gingival erythema?

A
  • 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
Q

What bacteria causes histoplasmosis? What are the different types of infections and who is most susceptible?

A
  • Histoplasma capsulatum- acute and chronic pulmonary histoplasmosis or a disseminated form in immunocompromised patients
96
Q

What is the clinical appearance of a histoplasmosis infection? How is it diagnosed? How is it treated?

A
  • 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
Q

What is the gingival lesion discussed in class that is of genetic origin? How does this disease appear clinically?

A
  • 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
Q

What are the possible mechanisms of hereditary gingival fibromatosis?

A
  • 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
Q

What are the 2 different types of allergic reactions discussed in class? Describe each.

A
  • TYPE I: immediate; mediated by IgE- TYPE IV: delayed type; mediated by T-cells (12-48 hours following contact with allergens)
100
Q

What are some dental things to have allergies to? How do these allergies clinically present?

A
  • 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
Q

What are the 3 categories of traumatic lesions?

A
  • chemical- physical- thermal
102
Q

Describe a chemical traumatic lesion. Give examples. How can this be caused?

A
  • 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
Q

Give 3 examples of physical traumatic lesions.

A
  • hyperkeratosis, a white leukoplakia-like, frictional keratosis- gingival laceration resulting in gingival recession- traumatic ulcerative gingival lesion (brushing and flossing techniques)
104
Q

Where do people usually get thermal traumatic lesions? Describe their appearance clinically.

A
  • minor burns from hot beverages- mostly seen on palatal and labial mucosa; painful erythematous lesions; vesicles may develop
105
Q

What are foreign body reactions? How are these often detected?

A
  • 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
Q

What are the 6 mucocutaneous disorders discussed in class?

A
  • lichen planus- pemphigold- pemphigus vulgaris- erythema multiforme- lupus erythematosus- drug-induced mucocutaneous disorders
107
Q

Where does lichen planus usually occur? In what ages? Is it considered a premalignant lesion?

A
  • oral involvement alone is common- prevalence = 0.1-4% in any age, but is rare in children- premalignant potential = 0.5-2%
108
Q

How does lichen planus appear clinically?

A
  • characteristic skin lesions (Wickam striae)- various clinical appearances (papular, reticular, plaque-like, atrophic, ulcerative, bullous)- any area of the oral mucosa
109
Q

Define papula. Reticular. Plaque.

A
  • 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
Q

Define atrophy. Ulcerative. Bulla.

A
  • 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
Q

Papular, reicular, plaque-like forms are generally ___ (symptomatic/asymptomatic).Atrophic, ulcerative, bullous forms are generally ___ (symptomatic/asymptomatic).

A
  • asymptomatic- symptomatic
112
Q

Histologically, describe the appearance of lichen planus (or oral lichenoid).

A
  • 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
Q

What are some examples of oral lichenoid lesions? What is the treatment?

A

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
Q

What is pemphigoid? How does it appear histologically?

A
  • 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
Q

What are the 3 types of pemphigoid? Who is the most susceptible? What is the telltale sign? How is it treated?

A
  • 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
Q

What is pemphigus vulgaris? Who is it most prevalent in? How does it clinically appear?

A
  • 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
Q

How does pemphigus vulgaris appear histologically?

A
  • ACANTHOLYSIS: due to destruction of desmosomes- pericellular epithelial depositis of IgG and C3- circulating autoantibodies against interepithelial adhesion molecules
118
Q

What is erythema multiforme? In what age group is it most likely?

A
  • 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
Q

How does erythema multiforme appear clinically? What is the treatment?

A
  • 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
Q

What is lupus erythematosus? How does it appear histologically?

A
  • 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
Q

How does lupus erythematosus appear clinically?

A
  • 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
Q

What are the 5 drug-induced mucocutaneous disorders?

A
  • gingival hyperplasia (enlargement)- erythema multiforme- oral ulceration- epithelial atrophy, superficial sloughing- intense erythema
123
Q

What 6 drugs cause drug-induced mucocutaneous disorders?

A
  • immunosuppressants- calcium channel blockers- anti-epilepsy drugs- anti-malarial drugs- anti-neoplastic drugs (cancer)- methotrexate (leukemia)
124
Q

How does Crohn’s disease affect the gingiva?

A

chronic granulomatous infiltrates of the wall of gastrointestinal tract -> mucosal folding and defective neutrophil functions

125
Q

How does leukemia affect the gingiva? What % of leukemia patients had oral symptoms?

A
  • swelling, ulceration, petecchia, and erythema of gingiva- 69% of patients with acute leukemia had oral signs of leukemia
126
Q

What are the 6 general categories of periodontal tumors?

A
  • 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
Q

What are the 4 reactive processes of periodontal soft tissues?

A
  • fibroma/focal fibrous hyperplasia- calcified fibroblastic granuloma- pyogenic granuloma- peripheral giant cell granuloma
128
Q

What is fibroma/focal fibrous hyperplasia? How does it appear clinically? What is it’s differential diagnosis?

A
  • focal fibrous hyperplasia caused by irritation- sessile, well-circumscribed smooth-surfaced nodules; cell-poor, hyperplastic collagenous tissue; may show hyperkeratinization- giant cell fibroma
129
Q

What is calcified fibroblastic granuloma? How does it appear clinically? What is it’s differential diagnosis?

A
  • 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
Q

What is pyogenic granuloma? How does it appear clinically? What is it’s differential diagnosis?

A
  • 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
Q

What is peripheral giant cell granuloma? How does it appear clinically? What is it’s differential diagnosis?

A
  • 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
Q

What is the reactive process of peridontal hard tissue discussed in class? Describe it. What is its differential diagnosis?

A
  • 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

AU14 - Perio Exam 2 (1 decks)

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