Units 1 - 4 Flashcards
(91 cards)
1
Q
What structure surrounds the teeth?
A
Periodontium
2
Q
What is the hardest substance in the body?
A
Enamel which is an epithelial tissue
3
Q
What is the 2nd layer meant to protect pulp. Can be easily penetrated?
A
Dentin
4
Q
What is the hard mineralized connective tissue that covers the root?
A
Cementum
5
Q
What is the space between the tooth and free gingiva?
A
Gingival sulcus
6
Q
What is the flap that surrounds the CEJ that forms a pocket?
A
Free gingiva
7
Q
What outlines and surrounds the CEJ?
A
Crest of alveolar bone
8
Q
What is a thin sheet of fibres?
A
PDL
9
Q
Whats another name for compact bone that holds teeth at the root?
A
Lamina dura
10
Q
What is around the roots of teeth and forms socket counter anchor for PDL?
A
Alveolar bone
11
Q
What separates attached gingival?
A
Mucogingival junction
12
Q
What is the valley like depression that prevents food from sticking between teeth?
A
Col
13
Q
What is the space between the teeth called?
A
Interdental papilla
14
Q
What bone surrounds and supports teeth?
A
Alveolar process
15
Q
What is the ends of PDL that connect alveolar bone and cementum and absorbs shock?
A
Sharpey fibres
16
Q
What is the over growth of cementum called?
A
Hypercementosis
17
Q
Difference between acute and chronic inflammatory response
A
Acute >2 weeks, if antigen eliminated tissue will heal.
Chronic
18
Q
When signs or symptoms disappear
A
Remission
19
Q
When signs or symptoms reoccur in all the severity
A
Exacerbation
20
Q
Function of Monocytes/Machrophages in inflammatory response
A
Slower to arrive, live longer which plays role in periodontists.
Highly phagocytic, more numerous in chronic inflammation.
21
Q
Function of Lymphocytes in inflammatory response
A
Recognize and control antigens
Two main types: B and T.
22
Q
What is the function of antibodies aka immunoglobulins
A
Neautralize MO’s by coating bacteria making them break down easily, activate complement system.
23
Q
What is kind of response is inflammation?
A
Nonspecific response of vascularized tissue trauma.
Complex.
Immediate.
Prevent’s death.
24
Q
How it got started: injury
A
Mode of action
25
Ability to initiate disease
Pathogenicity
26
Degree of pathogenicity
Virulence
27
Power to stimulate antibody response
Antigenicity
28
Degree or extent of being poisonous
Toxicity
29
Define the two different types of inflammatory responses
Cellular: Accumulation of white blood cells at the site of injury which clean up foreign debris,
Vascular: tissue is first injured, the small blood vessels in the damaged area constrict momentarily, a process called vasoconstriction. Then the blood vessels dilate (vasodilation), increasing blood flow into the area.
30
Local signs of inflammation: (5)
```
Edema
Redness
Heat
Pain
Loss of function
```
31
Systemic signs of inflammation: (3)
Fever
Leukocytosis
Lymphadenopathy
32
List the steps of inflammation: (10)
1. Injury
2. Constriction of microcirc.
3. Dilation of sm bv.
4. Increased bv permeability
5. Increased blood viscosity
6. Decreased blood flow through microcirc.
7. Margination and pavementing of WBC's.
8. WBC's leave sm bv and enter tissue
9. WBC's ingest foreign antigens.
10. Debris removed.
33
Cells involved in acute and chronic inflammation:
Leukocytes, Monocytes, Lymphocytes, Plasma cells, Eosinophils, Mast cells
34
Increase vascular dilation and tissue permeability, cause tissue pain and redness, cause changes in CT
Prostaglandins
35
What is an endotoxin?
A powerful chemical mediator
36
How neutrophils damage host tissues
Break down the connective tissue, host contains potent antiproteases to limit effect of proteolytic enzymes. Without them tissue would be destroyed.
37
Tissue destruction in an area surrounding and infection is considered to be what?
A side effect of inflammatory response
38
T cells function is what
intensify the response of the immune cells to the MO's invasion
39
Function of cytokines/inflammatory mediators:
Produced by immune cells, influence other cells, chemical signals, notifies immune system to send more phagocytes.
40
Which prostaglandins are most important and what do they do
D,E,F,H,I, chemical messengers, play role in bone destruction.
41
Function of prostaglandins:
Increase permeability and dilation of b.v's causing redness and edema of CT. Initiate bone destruction.
42
What does MMP stand for ?
matrix metalloproteinases
43
Where are MMP's produced?
Where bacteria inf. present larger quantities dumped into site to kill bacteria. So much that it kills healthy tissues. Extensive collagen destruction occurs when increased amt’s of MMP’s present in periodontal tissues
44
What is the complement system?
Proteins in blood that allow phagocytosis of bacteria.
Recruit PMS/macrophages to site of inf. opsonization of pathogens = coat bacteria for easy recognition and destruction. membrane attack system = puncture some bacteria's cell membranes.
45
Role of bacteria
Lots of plaque may have little/no disease
Little plaque may result in serious CT damage
Untreated gingivitis doesn’t always lead to periodontitis even when those pathogens consistently assoc. with perio are present
46
Phases of periodontal disease
Stage 1 - subclinical gingivitis
Stage 2 - clinical gingivitis - early leasion
Stage 3 - clinical gingivitis - established lesion
Stage 4 - periodontitis
47
Subclinical gingivitis
No sings, all inflammation is at cell/tissue level.
48
Periodontitis
Apical migration of JE - attachment loss
49
How much of tissue damage in periodontal diseases is caused by the host?
A least 80-85%
50
Destructive periodontal diseases in patient who demonstrate continued attachment loss in spite of proper oral hygiene. 90% of smokers. What is it called?
Refractory periodontitis
51
What should be considered when treating a "brittle" diabetic?
prophylactic antibiotics 2 days before continuing through the immediate post-op period.
52
How many time more likely is a smoker to develop periodontitis then a non-smoker and what type of healing?
4X, slow healing and immune response.
53
What does NUG stand for and what does it do and what are the symptoms?
Necrotizing Ulcerative Gingivitis, associated w/ impaired resistance to infection. Painful "punched out" papillae, necrotic slough, fetor oris, metallic taste.
Symptoms: fever, lymphadenopathy, malaise.
54
What does this bacteria cause: Spirochete Borrelia vincentii and Fusiform baciullus?
NUG
55
Bacteria: Mycobacterium tuberculosis
Effect: Primary lung infection rarely with oral lesion but are painful and do not heal. What is it?
Tuberculosis (TB)
56
Bacteria: Staphylococcus aureus, streptococcus pyogenes.
Transmission: Bacteria present on skin, need broken skin for infection.
Clinically: vesicles or bullae.
Symptoms: malaise, fever, lymphadenopathy.
Tx: topical or systemic antibiotics.
What is it?
Impetigo
57
Small vesicles that ulcerate, primary infection involved gingiva, can involve entire oral cavity.
What is it?
Herpes simplex
58
Recurrent herpes simplex infection.
painful eryththematous rupturing ulcers.
What is it?
Primary herpetic gingivostomatitis,
59
What is Varicella-Zoster virus (VZV), tx?
```
Chicken pox (vericella virus), Shingles (herpes zoster).
Tx: antiviral drugs or may resolve on one; steroids may be used to treat neuralgia.
```
60
Found at corners of mouth. Commonly caused by candidiasis. Redness, fissures or cracks.
Angular cheilitis
61
Reticular or erosive. On gingiva: desquamative gingivitis. Lacy, white network of lines = wyckham striae. Chronic oral or skin lesions. May be painful. Tx: erosive= topical steroid or periodic biopsy.
Lichen planus
62
Autoimmune causing xerostomia.
| Tx: treat symptoms, good OH, fluoride.
Sjogrens syndrome
63
"meth" mouth. Rampant decay, periodontitis and gingival keratinization.
Traumatic lesions
64
How does bacteria communicate within the mouth?
Chemical signal
65
How is bacteria in biofilm provided with nutrients?
Fluid chanels
66
How long does it take for the tooth to be colonized with most gram +'ve bacteria?
2 uninterrupted days
67
How does bacteria stink on colonized bacteria on tooth already?
Bacteria are stimulated and excrete gluelike slime, anchors bacteria & provides protective layer.
68
Bacteria in periodontitis is primarily gram what?`
Negative
69
What bacteria is associated with periodontitis?
Actinobacillus actinomycetemcomitans (Aa)
B forsythus
F nucleatum
P gingivalis
70
Actinobacillus actinomycetemcomitans bacteria does what?
25% chronic perio sites, strongly associated with aggressive perio, evades host defense mechanisms, destroys gingival ct and bone.
71
B forsythus bacteria does what?
Commonly in deep PPD's, associated with aggressive perio.
72
F nucleatum bacteria does what?
Capable of initiation early inflammation changes, seen in both ginigivitis and perio.
73
P gingivalis bacteria does what?
Associated with perio, destroys gingival ct and bone, can enter JE and multiply there.
74
Where are the zones of plaque biofilm?
Free/unattached - unorganized and separated from epithelium by layer of leukocytes.
Tooth attached - superficial = gram +, beneath = gram -.
Epithelial attached - invade ct tissues and most likely to cause destruction.
75
What is the primary etiologic risk factor is what?
Bacterial plaque biofilm.
76
What is a suprabony pocket?
PPD is above crestal bone - tends toward horizontal bone loss pattern.
77
What is infrabony pockets?
PPD's are below the crest of alveolar bone
78
How are periodontal pocketed named ?
by the number of remaining walls.
79
What are some symptoms a patient might experience at the time of initial HIV infection?
Mononucleosis-like syndrome with skin rash for 2-4 wks. followed by asymptomatic infection may last 1-20 yrs.
80
Who has higher CD4 count, men or women?
Women, fluctuate with menstrual cycle. Oral contraceptive lower count.
81
Who has higher CD4 count, smoker or non smoker?
smoker.
82
What is Linear Gingival erythema? (LGE)
Red band=like lesion along gingiva, may be painful and bleed, may progress into periodontal disease. Sometimes mistaken for normal gingivitis.
83
What is NUG and NUP collectively called?
Necrotizing periodontal disease. No evidence that they are separate.
84
NUG vs. NUP
NUG may be early stage NUP. Both reflect diminished systemic resistance to bact. infec.
85
Whom is NUG most common in ?
Age 15-25
86
Whom is NUP most common in?
immunosupressed individuals.
87
Seen in HIV + persons, severe pain, spontaneous bleeding. Rapid soft tissue and bone loss. is what?
NUP
88
Symptoms of NUG/NUP
```
Gingival necrosis
Fiery red gingiva
Spontaneous gingival bleeding
Intense oral pain
Fetid odor
Materia alba, plaque, sloughed tissue, blood, stagnant saliva
Excessive salivation
Pseudomembrane easily wiped off, exposing fiery red, shiny gingival tissues
```
89
What is it:
Bacterial infection charaterized by rapid destruction of PDL and supporting bone. High risk for tooth loss, patient have poor respons to therapy, less common.
Aggressive periodontitis.
90
Onset of disease around puberty (but, is not limited to this timeframe)
Rapid tissue destruction around permanent first molars and incisors
Frequently associated with immune dysfunction
Affects females more than males
Previously referred to as localized juvenile periodontitis
Localized aggressive periodontitis
91
Usually occurs in people under age 30 years
Rapid tissue destruction around most teeth
Frequently associated with immune dysfunction
Previously called generalized juvenile periodontitis
Generalized aggressive periodontitis
