OST Exam II Review Flashcards

Question

15) Clinical features of NUG?

Answer 1

● Rapid onset ● Severe pain ● Gingival bleeding; may or may not be spontaneous ● Interdental Crater, punched out papilla, pseudomembrane, fetid (sulfur) breath

Answer 2

``` Host Response: ● Systemic Predisposing Factors ● Immunosuppression-AIDS ● Stress ● Smoking ● Diet ```

Answer 3

● Host resistance and smoking ● Oral hygiene (Pre-existing gingivitis and Opportunistic microorganisms) ● Local irritants

Answer 4

● Zone 1: Bacterial Zone - Superficial, contains bacteria ● Zone 2: Neutrophil-rich Zone - Numerous Leukocytes, mostly PMNs, bacteria, spirochetes ● Zone 3: Necrotic Zone - Dead cells, fibers, spirochetes, and other bacteria ● Zone 4: Zone of spirochetal infiltration - Well-preserved tissue infiltrated with spirochetes

Answer 5

● First treatment- debridement, OHI, evaluate systemic factors ● Recall visit- 1-2 wks, eval. OH, further tx ● Final re-eval- 4-6 wks, consider surgery (gingivectomy) ● If fever present give antibiotics first: Amoxicillin and Metronidazole (G-, bad aftertaste/metallic), take 3x a day for 1 week, no alcohol use while taking (including alcoholic mouthwash) ○ If allergic then prescribed clindamycin

Answer 6

● Essentially the same, except NUP involves bone loss Extraoral and Systemic Signs and Symptoms: ● Patients usually ambulatory w/ no systemic complications ● Locally lymphadenopathy ● Slight elevation in temperature ● Severe cases may have systemic complications: -High fever -Increase pulse rate -Leukocytosis -Loss of appetite -General Lassitude

Answer 7

- Severe, deep pain, & rapid onset - Soft tissue & attachment loss - Exposed bone - Low CD4 & high viral counts ● Consider Antibiotics ● Amoxicillin and/or Metronidazole(Given in severe perio cases, tastes bad, and not to be taken with alcohol)

Answer 8

■ Contagious ■ Herpes Simplex Virus- 1 (HSV-1) ■ can happen in kids and immunocompromised adults ■ occured in bound and unbound tissue: attached gingiva and alveolar mucosa (ex: soft tissue lip, cheeks, palate, mucosa), non-keratinized ■ if young adults contract it, it’s more severe ■ most cases are subclinical (exposure but no S/S) ■ Most adults have developed immunity to HSV with most cases being subclinical ■ Both sexes affected ■ All races affected equally ■ Primary infection- early in life - Children ages 1-10 - More severe in young adults 15-25

Answer 9

■ TX: bed rest, bland mouthwash (no alcohol in them b/c it will burn), fluids, antipyretics (not ASA), lidocaine gel, CHX (chlorhexidine) - Ab: Valacyclovir, Vibraadine, Acyclovir - Topicals: Acyclovir (Zovirax), Penciclovir (Denavir), Docosanol (Abreva - prevents virus getting into the cell, not an antiviral)

Answer 10

■ Prodromal phase: abreva and valacyclovir works at this phase - Fever - Irritability - Headache - Gingival inflammation

Answer 11

■ Active phase - Vesicles rupture, yellow ulcers, red halo - viral shedding (average 12 days) - Mobile and Attached tissue - Heal in 7-14 days with no scarring ■ Latency - Virus resides in ganglia - non-replicating state - latency associated transcripts (LAT) ■ Reactivation - Caused by stress, sun, palatal injections etc. - Put on Ab to prevent outbreak or dec. severity of outbreak

Answer 12

■ Spontaneous or stimuli related ■ Virus migrates ■ Herpes labialis (extra-oral) ■ Virus overwhelms local immune response ■ Intraoral only on Bound down Tissue/ attached gingiva (palate, lip, extra-orally) ■ Herpes will present as more than one dot (grape cluster), looks like outburst of necrotic spots

Answer 13

■ RECURRENT infection ■ fingers and hands ■ latent site- dorsal root ganglion ■ debilitating

Answer 14

■ Sunlight ■ Trauma ■ Fever ■ Stress ○ Treatment ■ Acyclovir Note: aphthous ulcer (immune mediated) is not a virus (non-contagious), it happens on moveable mucosal tissues only, will not be on keratinized attached tissue → looks same as herpes but different etiology, one spot = canker sore

Answer 15

○ Normal Periodontium: ■ Pale pink firm gingiva ■ Either smooth or stippled - stippling found in 35% of children between ages of 5-13 years ■ Interdental gingiva is broad facio-lingually and narrow mesiodistally - No sharp papilla points b/c of tooth spacing ■ Mean gingival sulcus depth average 1mm ■ PDL is wider than the PDL of permanent teeth ■ Radiographically, the trabeculae in the alveolar bone are fewer but thicker than in the adult *The crests of interdental bony septa are flat * Trabeculae in alveolar bone are fewer but thicker than in adult * Calculus can be present, less plaque etiology than adults * BOP(bleeding on probing) and pocketing is less common * Root planing = roots are exposed, most children don’t have exposed roots so would just do scaling on kids * No need to probe deciduous/mixed dentition unless concerns * Malpositioned teeth: - Accumulate more plaque *Localized marginal recession: -tooth position in arch is most important can correct itself as tooth alignment improves -Increased gingivitis with: -excessive overbite/ excessive overjet -Nasal obstruction -Mouth breathing * Disease altering oral mucosa including gingiva - Varicella - Rubeola (measles) - Scarlatina (scarlet fever) - Diphtheria

Answer 16

``` ○ Malpositioned teeth ■ Accumulate more plaque ■ Increased gingivitis with: - excessive overbite - excessive overjet - Nasal obstruction - Mouth breathing ○ Disease altering oral mucosa including the gingiva ■ Varicella ■ Rubeola (measles) ■ Scarlatina (scarlet fever) ■ Diphtheria ```

Answer 17

○ Suprabony - Base of pocket is coronal to level of underlying bone ■ Horizontal bone loss ■ transseptal CT fibers are horizontal ○ Intra(infra)bony - Base of pocket is apical to the level of the adjacent bone ■ Vertical bone loss ■ always have underlying angular defects ■ transseptal CT fibers run length of defect vertically (obliquely)

Answer 18

○ Rationale for pocket reduction is based on the need to eliminate areas of plaque accumulation ○ Pockets create area where daily plaque removal becomes impossible

Answer 19

○ PERIODONTAL ABSCESSES: Acute localized accumulation of viable & nonviable PMNs w/in pocket wall. ■ Extension from infected pocket: G- microorganisms i.e. fusiforms and spirochetes ■ Incomplete removal of calculus ■ Root fracture - Does it hurt? - dull, constant pain, recent origin - Bone Loss? - Bone destruction is responsible for tooth loss ■ Multiple abscesses = uncontrolled/diagnosed DM, immunosuppressive diseases, something is going on systemically ○ GINGIVAL ABSCESSES: Acute localized purulent infection that involves the marginal gingiva and interdental papilla due to bacteria carried into gingival tissue (i.e. popcorn hull, toothbrush bristle, fingernail, dental material) ■ S/S Localized swelling - marginal or interdental Red, smooth, shiny surface May present purulent exudate ``` ■ Treatment If fluctuant, establish drainage Debridement Rinse (saline or CHX) Follow up ``` - Fenestrations - “window” in bone on facial or lingual - places exposed root surface in direct contact with gingiva or alveolar mucosa - Dehiscence - Loss of alveolar bone on the facial (rarely lingual) aspect of a tooth that leaves a characteristic oval, root-exposed defect from cementoenamel junction apically. The defect may be 1-2 millimeters long or extend full length of root. - 3 Features of Dehiscence: 1)gingival recession, 2) alveolar bone loss & 3) root exposure.

Answer 20

1) Crest follows the CEJ and is 1-2mm apical 2) Interproximal higher (more coronal) than facial and lingual 3) Scalloped 4) Related to fenestrations & dehiscences - Fenestrations - “window” of bone loss/absence on facial or lingual - places exposed root surface in direct contact with gingiva or alveolar mucosa - Important to note that this is developmental flaw. Not active PD - Dehiscence - An absence of normal bone growth. Most common on facial (rarely lingual) aspect of a tooth. 5) Related to: interdental septa - Thickness, width, & crestal angulation - “ When attempting to determine if bone morphology is correct, first compare CEJs then compare the bone (and bone loss) to the relationship of the position of the teeth” - Essentially she is saying that bone morphology is unique to the patient.

Answer 21

○ 4 types: 1) Horizontal 2) Vertical 3) Osseous crater 4) Reverse architecture (aka inconsistent margins) ■ PRIMARY Occlusal Trauma: 1. Occurs when EXCESSIVE (GREATER than normal) occlusal forces occlusal forces exerted on a tooth w/ "NORMAL" periodontium 2. NO bone loss, NO perio disease, will have generalized mobile teeth ■ SECONDARY Occlusal Trauma: 1. Occurs when NORMAL or excessive forces are placed on tooth w/ REDUCED periodontium 2. Occurs when there is a compromised periodontal attachment and, thus, a pre-existing periodontal condition. Does occlusal trauma cause periodontal pockets and attachment loss??? NO ○How do you see it on the Radiograph??? *Widened PDL space, *Disruption/ LOSS of lamina DURA, and *ROOT RESORPTION. ``` ○What happens when there is NO occlusal surface ■ HYPO-FUNCTION: 1. a lack of occlusion 2. atrophy of the periodontium 3. narrowing of the PDL space 4. tendency towards extrusion 5. increase in cementum thickness 6. thinning of alveolar bone ``` ○MOST COMMON = HORIZONTAL bone loss ○What regenerates BEST =3 wall defect (vertical bone loss) ○Regenerates LEAST = 1 wall defect (hemiseptum) ○ 4 wall defects= circumferential ■ Does not exist in natural dentition

Answer 22

Scenarios of diagnosis for type of PD - know the numbers associated with each type: ***CHRONIC Periodontitis: Classification based on EXTENT: - Localized is ≤ 30% sites involved - Generalized is > 30% sites involved Classification based on SEVERITY: - Slight (mild) - 1-2 mm CAL - Moderate - 3-4 mm CAL - Severe - > 5 mm CAL * ***AGGRESSIVE Periodontitis: 1) LOCALIZED Aggressive Periodontitis (LAP): - Circumpubertal onset! * Involves NO MORE than 2 teeth other than 1st Molar * Involves no more than 2 teeth other than 1st molars and incisors. 2) GENERALIZED Aggressive Periodontitis (GAP): * Usually < age 30 by may be older * Generalized IP attachment loss * **At least 3 Permanent teeth other than 1st molars and incisors - Familial aggregation - (Based on LOCATION & # of teeth involved. NOT on percentage of sites)

Answer 23

``` ● Porphyromonas gingivalis ● Tannerella forsythia ● Treponema denticola ● Aggregatibacter actinomycetemcomitans ● Prevotella intermedia ```

Answer 24

1) Oral Hairy leukoplakia - Lateral border of tongue - Keratotic area, corrugated, may appear shaggy 2) Oral candidiasis: -Diminished host resistance -Candida albicans Often refractory (meaning it is non-responsive to treatment) 3) Bacilliary (epitheliod) angiomatosis - Infectious vascular disease similar to Kaposi sarcoma - Rickettsia-like organism etiology - Red, purple, blue soft lesion 4) Kaposi sarcoma: can be extra-orally Vascular neoplasm HHV 8 LOCALIZED, slow growing 5) Hyper pigmentation ( from HIV meds) - Seen on PALATE, buccal mucosa, gingiva, tongue AIDS: Periodontal disease 1) NUG 2) NUP 3) NUS (necrotizing ulcerative stomatititis 4) Linear Gingival Erythema: around GM, generalized, diffuse gingivitis -Fiery red, non-painful gingival band -Common in AIDS patients with unpredictable response to Tx -Tx: SRP, polish & re-treat if necessary -May be refractory -May spontaneously remiss does NOT indicate low CD4 count

Answer 25

1) Deposits inconsistent w/ destruction 2) Elevated proportions of A.a 3) In some populations, elevated P.g 4) Phagocyte abnormalities 5) Hyper-responsive macrophage phenotype 6) Elevated levels of PGE2 and IL-1B 7) Progression of attachment loss may be self-limiting Note: generally not universally present

Answer 26

Chronic marginal gingivitis (looks like chronic gingivitis) - Pre-eruption bulge: before crown breaks gingiva, gingiva is blanched, firm and conforms to shape of underlying crown - Gingivitis is associated with tooth eruption → prominent rolled gingival margin, inflamed, edematous - Normal prominence of gingival margin: prominent and rolled esp. in maxillary anterior region - Poor OH with ortho tx → remove brackets/wires until OH improves

Answer 27

● Defense Mechanisms of Gingiva Saliva - Lubrication/Physical protection ● Salivary components: Glycoproteins, mucoids ● Probable mechanism: Coating similar to gastric mucin - Cleansing ● Salivary components: Bicarbonate and phosphate ● Probable mechanism: Antacids - Buffering ● Salivary components: Physical flow ● Probable mechanism: Clearance of debris and bacteria - Antibacterial action ● IgA: Control of bacterial colonization ● Lysozyme: Breaks bacterial cell walls ● Lactoperoxidase: Oxidation of susceptible bacteria

Answer 28

OSSEOUS CRATER ■ concavities in the crest of the alveolar bone ■ confined within facial & lingual walls